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The skin changes in pregnancy can be either physiological (hormonal), changes in pre-existing skin diseases or development
of new pregnancy specific dermatoses. Pregnancy-specific skin dermatoses include an ill-defined heterogeneous group
of pruritic skin eruptions which are seen only in pregnancy. These include Atopic eruption of pregnancy, Polymorphic
eruption of pregnancy, Pemphigoid gestationis and intrahepatic cholestasis of pregnancy. Atopic eruption of pregnancy
is the most common of these disorders. Most skin eruptions resolve postpartum and require only symptomatic treatment.
Antepartum surveillance is recommended for patients with pemphigoid gestationis and intrahepatic cholestasis of
pregnancy as they carry fetal risk. This article deals with the classification, clinical features and treatment of the specific
dermatoses of pregnancy.
raised total serum IgE levels. The eruption was seen more immunoflourosecence studies are negative. The lesions
commonly in primigravida with single gestation pregnancy resolve near term or in the early postpartum period. The
and skin lesions started during early pregnancy in first and maternal and fetal prognosis is excellent.14,15
second trimester. The skin eruption affected all parts of the
body, including face, palms, and soles. 3. Pemphigoid gestationis (herpes gestationis)
Prurigo of pregnancy: Prurigo of pregnancy has been Pemphigoid gestationis is a rare autoimmune disorder
reported to occur in approximately one in 300 pregnancies.6 occurring in approximately one in 50,000 pregnancies,
It is characterized by pruritic, often excoriated papules and and begins in the second or third trimester. The condition
nodules on the extensor surfaces of the legs and upper has been linked to the presence of HLA-DR3 and HLA-
arms. The abdomen can also be involved. The time of DR4 and has a rare association with molar pregnancies and
onset is variable and it has been reported to occur in all choriocarcinoma has been reported.16 It has been suggested
trimesters. The etiology and pathogenesis is not known, that the disease could be triggered by a placental antigen
although there is sometimes a history of atopy.4 There are that causes cross-reaction with skin antigens. This explains
no recognized adverse effects for the mother or fetus. the onset of the disease in the periumbilical region. The
skin lesions are pruritic, urticarial and vesiculobullous.
Pruritic folliculitis: This rare dermatosis occurs in the Histologically, it is characterized by subepidermal vesicle
second and third trimester of pregnancy and affects an formation, and immunopathologically by deposition
estimated one in 3,000 pregnancies.7 Contrary to its name, of complement 3 along the basement membrane zone.
pruritus is not a major feature and it may be mistaken These features are shared by another skin disease bullous
for acne or microbial folliculitis.8,9 It is characterized by pemphigoid which suggests that herpes gestationis may
an acneiform eruption consisting of multiple, pruritic, be a related entity.17 The condition may resolve late in
2- to 4-mm, follicular papules or pustules typically on pregnancy, but classically flares up again at delivery. Fetal
the shoulders, upper back, arms, chest, and abdomen. risk has not been substantiated, although immunoglobulin
The diagnosis is made clinically after excluding other, G autoantibodies cross the placenta, and 5 to 10 percent
more common rashes. The skin lesions usually resolve of newborns have urticarial, vesicular or bullous lesions.18
spontaneously one to two months following delivery. Small Mild placental failure has been associated with premature
case series have failed to implicate immunologic dysfunction deliveries and newborns that are small for gestational
or elevated androgen levels.10-12 On histopathology, an acute age. Therefore, antenatal surveillance is advised. Affected
sterile folliculitis is evident and direct immunofluorescence patients may have nongestational recurrences triggered by
stains are negative. The disorder is not associated with any oral contraceptives and menstrual cycles.6
maternal or fetal morbidity, although one small series of
patients showed a reduction in fetal birth weight.12 4. Pruritus gravidarum (intrahepatic cholestasis of
pregnancy) (ICP)
2. Polymorphic eruption of pregnancy (Syn. late -
The two terms term pruritus gravidarum and intrahepatic
onset prurigo of pregnancy) cholestasis of pregnancy (ICP) have been used
Polymorphic eruption of pregnancy also known as pruritic interchangeably in the literature.7 While pruritus gravidarum
urticarial papules and plaques of pregnancy (PUPPP), is classically associated with itching, without any skin lesions
occurs with an incidence of one in 160 pregnancies4 and and occurs in the first trimester, ICP also called obstetric
is the second most common skin dermatosis in pregnancy cholestasis is seen in third trimester and is characterized by
after atopic eczema. It is associated with multiple gestation pruritus with or without jaundice, absence of primary skin
and increased maternal weight gain. The exact etiology lesions, and with laboratory markers of cholestasis.19 The
is not known. It has been proposed that stretching of the skin lesions are usually secondary linear excoriations and
skin damages the connective tissue causing subsequent excoriated papules, which are caused by scratching and are
conversion of nonantigenic molecules to antigenic ones, localized on the extensor surfaces of the limbs, abdomen and
leading to skin eruption.13-14 PUPPP usually occurs in back. The severity of skin lesions correlates with the duration
primigravidas in the third trimester and recurrence in of pruritus.3 The etiology of ICP remains controversial.
subsequent pregnancies is unusual. The eruption may first A family history of the condition is common, and there
appear in postpartum period. PUPPP has a marked pruritic is an association with the presence of human leukocyte
component and the onset of pruritis coincides with the skin antigen-A31 (HLA-A31) and HLA-B8. The condition tends
lesions which are seen as polymorphous, erythematous, to recur in subsequent pregnancies.7,19 Patients may have a
nonfollicular papules, plaques, and sometimes vesicles. The family history of cholelithiasis and a carry higher risk of
eruption begins over the abdomen, commonly involving gallstones.20,21 Laboratory markers include elevated serum
striae gravidarum with sparing of the periumbilical region. bile acid levels (4.08 mcg per mL [10 μmol per L] or more)
It may spread to the breasts, upper thighs, and arms. and alkaline phosphatase levels with or without elevated
The face, palms, soles, and mucosal surfaces are usually bilirubin levels. The condition is associated with a higher risk
spared. Histopathologic findings are nonspecific and the of premature delivery, meconium-stained amniotic fluid, and
Author Query??????
PE Please confirm the style given for heading level three is fine throughout the issue.
Background: The etiology and pathophysiologic mechanism of vitiligo are still unclear. The relationship between
increased oxidative stress due to the accumulation of radicals and reactive oxygen species and the associated changes in
blood and epidermal component of vitiliginous skin have been reported many times. We investigated the possible changes
of plasma malondialdehyde, glutathione, selenium, hydroxyproline and glutathione peroxidase activity levels in patients
with vitiligo in order to evaluate the relationship between oxidative stress and etiopathogenesis of vitiligo. Materials and
Methods: Plasma malondialdehyde, glutathione, hydroxyproline and glutathione peroxidase activity levels were measured
by spectrophotometric methods, and HPLC was used for measurement of selenium concentrations. Results: Our results
showed increased malondialdehyde, hydroxyproline and glutathione peroxidase activity levels in plasma of vitiligo group
(P < 0.05). Conclusion: Support of antioxidant system via nonenzymatic antioxidant compounds and antioxidant enzymes
may be useful to prevent of melanocyte degeneration which occur due to oxidative damage in vitiligo.
University, Faculty of Pharmacy, Malatya/Turkey. 2Department possible degradation of collagen caused by ROS in vitiligo
of Chemistry, Firat University, Faculty of Science, Elazig/Turkey. diseases hence we measured hydroxyproline levels in blood
3
Department of Dermatology, Acibadem Hospital, Bursa/Turkey. samples with vitiligo patients.
4
Inonu University, Faculty of Medicine, Public Health Department,
Malatya/Turkey. Address correspondence to: Dr. Kadir Batcioglu, In this study, we investigated the possible changes of plasma
Inonu University Faculty of Pharmacy, Biochemistry Dep., 44280 MDA, GSH, GSSG, Se, hydroxyproline and glutathione
Malatya/Turkey. E-mail: kadirbatci@inonu.edu.tr peroxidase activity levels in patients with vitiligo in order
to evaluate the relationship between oxidative stress and and centrifuged at 500 g. To 1 ml of TCA extract (the
etiopathogenesis of vitiligo. supernatant) 0.25 ml TBA was added and heated in a water
bath at 958C for 1 h till a faint pink color appeared. After
Materials and Methods cooling, the color was extracted in 1 ml butanol and the
Experiment groups intensity was read at 532 nm. 1,1,3,3 tetra ethoxypropane
(1-100 nmol/ml) was used as the standard.
Thirty (19 male, 11 female) patients with generalized stable
vitiligo, and thirty (12 male, 18 female) healthy controls Measurement of glutathione levels
were included in this study. The ages of the patients ranged
Total glutathione: Glutathione was assayed according to
from 16 to 43 years old (23.6 ± 7.4). The control group
modified Owens17 method. Previously, plasma treated with
consisted of healthy volunteers, whose ages ranged from
meta phosphoric acid and centrifuged at 4000 g. to obtained
16 to 52 (27.9 ± 7.1). The Ethic Committee approved the
deproteinized samples. Then, supernatants mixed with 5,5’-
protocol for this study; all subjects gave his/her protector
dithiobis-2-nitrobenzoat, NADPH2 and oxidized glutathione
informed consent. They were not under a therapeutic
reductase in a sodium potassium phosphate buffer. The
regimen for the previous 2 months and had not received
samples were incubated in a water bath at 30 °C for
drugs containing iron and/or vitamins. All individuals with
15 min, and absorbance was read spectrophotometrically at
any history of smoking and alcohol habits were excluded.
412 nm.
Chemicals Oxidized glutathione: Previously, supernatants were
All chemicals were purchased from Sigma Chemical treated with 2-vinylpyridine to prevent present reduced
Company (St. Louis, MO, USA). glutathione interference. Then, each sample was mixed
with high concentrations of NADPH2 and GSSG reductase
Preparation of plasma samples in the sodium potassium phosphate buffer. The change in
All blood samples were drawn at the same time. Ten ml absorbance was observed spectrophotometrically at 340 nm.
blood was drawn from cubital median vein of the patients When all the GSSG was run out, a constant absorbance
and control group into tubes that were washed with heparin. was recorded.
The blood samples were centrifuged at 1000 × g for 10 min
Measurment of selenium levels
at +4°C, and upper plasma phase was drawn with pipette
Q2 and transferred to into polypropilen tubes, and stored at Plasma samples were digested in a teflon bomb according
−40°C. to Breyer and Gilbert.18 Each sample was diluted with (v/
v:1/3) 1.00 N HNO3/1.00 N HClO4 and left in the teflon
Determination of protein levels bomb at 120°C for 12 h. After coolin to room temperature,
Protein determinations in plasma were done according to Se6+ was reduced to Se4+ by addition of HCl to a final
modified micro method of Lowry et al.,14 using BSA as concentration of 4N and the samples kept at 90°C in
standard. a water-bath for 15 min. After returning to the room
temperature, to each sample 5 ml of 0.1 M EDTA was added
Estimation of glutathione peroxidase enzyme activity and mixed thoroughly. Two ml of 2.5 M HCOOH and 2 ml
GSHPx activity measurements were conducted according of 1500 ppm. 3,3-diaminobenzidine (DAB) were added to
to Lawrence and Burk.15 900 μL of 50 mM PBS solution each sample and the mixtures were left in a dark place for
(pH 7.4), including 5 mM EDTA, 2 mM NADPH, 20 mM 60 min. The pH was adjusted to 7.0 with 4N NH3 and the
GSH, 10 mM NaN3 and 23 mU of GSSG reductase Se-DAB complex was extracted with 5 ml of of toluene.
were incubated at 37°C for 5 min. Fifty μL of 0.25 mM These samples were analysed according to Watkinson19 and
H2O2 solution and 50 μL of samples were added to the Whetter and Ullrey20 using a Perkin Elmer 100 Flouresans Q4
assay mixture. The change in absorbance at 340 nm was Spectrophotometer with excitation at 420 nm and emission
Q3 monitored for 3 min. A blank with all ingredients except at 570 nm.
supernatant was also monitored. Specific activity was
Measurment of hydroxyproline levels
calculated as U/mg protein for plasma samples.
Hydroxyproline (HyPro) levels were measured by the
Measurement of MDA levels method described by Bergman and Loxley.21 One mililiter
Lipid peroxidation products were quantified by the of plasma samples were sealed in small Pyrex test tubes and
thiobarbituric acid (TBA) method.16 Malondialdehyde is hydrolyzed for 12 hours at 110°C by adding 5 mL of 6N
formed as an end product of lipid peroxidation which reacts HCl. The hydrolysates were neutralized by 2.5 N NaOH and
with TBA reagent under acidic conditions to generate a 0.25 mL was used for analyses. Hydroxyproline oxidation
pink-colored product. Plasma (0.5 ml) was made up to was initiated by adding chloramine T and the tube content
1 ml with saline and an equal volume of trichloroacetic were kept at room temperature for 5 min. Chloramine T
acid (TCA) was added and incubated at 378C for 20 min was then removed by adding 3.15 M perchloric acid. After
5 min, 3.25 mL of Ehrlich’s reagent was finally added; not play an important role in protecting blood cells against
the mixture was shaken, and the tubes were placed in a endogenous H2O2. Rather, thay concluded glutathione
60°C water bath for 25 min. They were then cooled in tap peroxidase is the major route for disposing of H2O2. We
water for 5 min. The absorbance values of the solutions know that concentration of H2O2 is high in vitiligonous
were determined at 558 nm. The hydroxyproline values area, and the diffusion of H2O2, which is thought to be
calculated from L-hydroxyproline standard curve. in high concentration in the lesion area, into plasma
will be more limited, but significant; but significantly as
Results and Discussion statistically GSHPx activity elevated in response to possible
Results are tabulated in Table 1. All results were expressed low concentration of H2O2 in plasma will be able to lead to
as mean + SD. the detoxification of H2O2. Ines et al.30 reported decreased Q5
Table 1: Activity of GSHPx, and MDA, GSH,GSSG, Se and HyPro levels in vitiligo and control samples
MDA GSHPx Se GSH GSSG HyPro
(nmol/mL) (U/mg prot) (ppb) (nmol/mL) (nmol/mL) (mg/L)
Vitiligo (n = 30) 0.642 ± 0.110a 0.550 ± 0.077a 122.333 ± 30.173 4.497 ± 0.486 4.45 × 102− ± 0.6 × 102− 16.841 ± 1.856a
Control (n = 30) 0.494 ± 0.085 0.439 ± 0.075 120.766 ± 21.802 4.567 ± 0.497 4.66 × 10 ± 0.55 × 10
2− 2−
15.013 ± 2.231
P < 0.05, vitiligo group was compared to control group
a
nonenzymatic antioxidant system and substrate for GSHPx. Lipid peroxidation, free radical production and antioxidant status
Passi et al.37 showed that the epidermal GSH levels of active in breast cancer. Breast Cancer Res Treat 2000;59:163-70.
vitiligo patients were significantly lower when compared 14. Lowry OH, Rosebrough NJ, Farr AL, Randall RI. Protein
with the controls. Park et al.38 reported that glutathione measurement with the folin phenol reagent. J Biol Chem
1951;193:265-75.
prevented dopamine-induced apoptosis of melanocytes.
15. Lawrence RA, Burk RF. GSHPX activity in rat liver. Biochem
In conclusion, vitiligo effects not only skin but also Biophys Res Commun 1976;71:952-8.
other components of organism such as blood. However, 16. Gavino VC, Miller JS, Ikharebha SO, Milo GE, Cornwall DG.
the effects on plasma is lower than skin. In addition, Effects of polyunsaturated fatty acids and antioxidants on lipid
we believe that the support of antioxidant system via peroxidation in tissue cultures. J Lipid Res 1981;22:763-9.
nonenzymatic antioxidant compounds and antioxidant 17. Owens CW, Belcher RV. A colorimetric micro-method for the
enzymes may be useful in the prevention of melanocyte determination of glutathione. Biochem J 1965;94:705-10.
degeneration, which occurs due to oxidative damage in 18. Breyer PH, Gilbert BP. Determination of selenium differantial
vitiligo. pulse voltametry of the 3,3’-diaminobenzidine piazselenol. Anal
Chem Acta 1987;201:23-32.
35. Halliwell B, Gutteridge JM. Ischemia/reoxygenation injury. In: Epidermal oxidative stress in vitiligo. Pigment Cell Res
Halliwell B, Gutteridge JM, editors. Free radicals in biology 1998;2:81-5.
and medicine, 2nd ed. Oxford: Clarendon Press; 1985. p. 38. Park ES, Kim SY, Na IM, Ryu SH, Youn SW, Kim DS,
163-78. et al. Glutathione prevented dopamine-induced apoptosis of
36. Teherani DK, Nagy-Vezekenyi K. Neutron activation analysis melanocytes and its signaling. J Dermatol Sci 2007;47:141-9.
of some trace elements (selenium, chromium, cobalt and
nickel) in the blood of vitiligo patients. J Radioanal Nucl Chem Received: December, 2007. Accepted: January, 2008.
1986;104:53-8. Source of Support: Inonu University Research Fund,
37. Passi S, Grandinetti M, Maggio F, Stancato A, De Luca C. Conflict of Interest: Nil.
Author Queries??????
Q1 check change
Q2 polypropylene?
Q3 a control?
Q4 flourescent?
Q5 This will statistically correspond to the elevation of GSHPx activity in response to the possibly low concentration
of H2O2 in plasma, which in turn will lead to the detoxification of H2O2. Please check if we can revise the
sentence like this.
Q6 misture of?
Background: Despite worldwide prevalence of hirsutism studies on hirsutism in Indian patients are not many. Aims: This
retrospective study was carried out to assess the clinico-investigative profile of patients presenting with hirsutism.
Materials and Methods: Medical records of 82 hirsutism patients diagnosed consecutively during July 2005 to October
2007 were analyzed. Results: The complete data of 50 patients aged between 13 and 47 years were available. Fifty
percent patients were aged 20 to 30 years. The average F-G score was 10.3 ± 2.46. Associated signs of hyperandrogenism
were acne (64%), oligomenorrhea or menstrual irregularities (36%), androgenetic alopecia (16%), acanthosis nigricans
(6%) and seborrhea (4%). Polycystic ovaries were detected in 30% patients and 22% patients had elevated serum free
testosterone levels. Family history of hirsutism was present in 18% patients. Conclusion: Hirsutism in Indian patients is
not uncommon. Adolescent patients appear to be more concerned about hirsutism as compared to those in the older age
group who were more often worried of late onset acne. All patients, however, were more concerned for facial hair than
those on other body areas signifying that facial hair need be given higher than current value in F-G score.
25.84 ± 8.30) years, 25 (50%) of them were in age group It can be classified as androgenic and non-androgenic
of 20-30 years. The maximum hirsutism F-G score was hirsutism. Hirsutism can be caused by abnormally high
17 with an average of 10.3 ± 2.46. Acne was found to be androgen levels or by hair follicles which are more
associated in 32 (64%) patients aged between 15-41 years. sensitive than usual to normal androgen levels. Biologically
Other signs of hyperandrogenism were acanthosis nigricans active free testosterone is responsible for hair growth and
in 3 (6%) and seborrhea in 2 (4%) patients respectively. is regulated by sex hormone-binding globulin. The causes
Oligomenorrhea or irregular menstrual cycles was reported of androgenic hirsutism can be exogenous due to drugs
by 18 (36%) patients; 10 of them had PCO as well. (testosterone, dehydroepiandrosterone sulfate, danazol,
Androgenetic alopecia was observed in 8 (16%) patients. corticotropin, high-dose corticosteroids, metyrapone,
Nine (18%) patients had history of hirsutism in first degree phenothiazine derivatives, anabolic steroids, androgenic
relatives; 2 of them showed no investigative abnormality. progestin, and acetazolamide) or excess endogenous
Eleven (22%) patients had no investigative/menstrual androgen of adrenal or ovarian origin. Various causes of
abnormality except for a family history of hirsutism in first ovarian hyperandrogenism are PCOS and virilizing ovarian
degree relatives of 2 of these patients. None of the patients neoplasia (Luteoma of pregnancy, arrhenoblastomas, leydig
was obese, hypertensive, diabetic or had clinical/laboratory cell tumors, hilar cell tumors, thecal cell tumors, etc.).
evidence of adrenal, thyroid or Cushing’s disease. No However, PCOS alone accounts for 75-80% cases of
patient had history of any drug intake. hyperandrogenism.4,6 Clinically the most common sign of
hyperandrogenism in PCOS is hirsutism. The prevalence
Serum free testosterone levels were elevated in 11 (22%)
of hirsutism in PCOS varies between 17% and 83%.7
patients and 10 (20%) patients had elevated serum prolactin
Polycystic ovaries were detected in our 30% patients.
levels. LH/FSH ratio was increased in 17 (34%) patients, 9 of
However by using Rotterdam criteria for diagnosing PCOS,2
them had normal serum free testosterone levels and menstrual
17 (64%) of our patients had clinical hyperandrogenism.
cycles. Fifteen (30%) patients revealed polycystic ovaries on
Acne appears another consistent feature and was found
pelvic USG. In total 17 (34%) patients fulfilled Rotterdam
in 64% patients across all age groups followed by
criteria2 for hyperandrogenism of polycystic ovarian syndrome
oligomenorrhea in 18% and androgenetic alopecia in
origin and 9 of them also had anovulatory menstrual cycles.
16% patients respectively. Acanthosis nigricans (6%) and
seborrhea (4%) appear other but less common signs of
Discussion
hyperandrogenism in our patients. Since gonadotrophins
Hirsutism affects 5-10% of women of reproductive age.1 are released in a pulsatile manner their concentration varies
over the menstrual cycle and a single measurement of LH while patients in the adolescent group showed more concern
and/or FSH may not be a sensitive method for diagnosis.5 for their facial hair than acne, the patients in the older age
This is also evident in our17 patients having abnormal LH group had worries more often for late onset acne signifying
to FSH ratio but elevated serum free testosterone levels and a varied perception of the same problem. However, all
abnormal menstrual cycles, features of hyperandrogenism, patients were more concerned for facial hair than those on
were observed in 11 and 9 patients only. other body areas. We feel that facial hair be given higher
than current value in F-G scoring system in view of the
Adrenal hyperandrogenism is uncommon and seen
psychological/cosmetic embarrassment it causes.
in congenital adrenal hyperplasia, late-onset adrenal
hyperplasia, Cushing’s syndrome, pituitary adenomas that References
produce excess corticotropin or prolactin and acromegaly.
1. Hatch R, Rosenfield RL, Kim MH, Tredway D. Hirsutism:
None of our patients had adrenal abnormality. Hirsutism
implications, etiology and management. Am J Obstet Gynecol
in 8 of 10 patients having raised serum prolactin levels 1981;140:815-30.
appears to be more of PCOS associated hyperandrogenism
2. Rotterdam ESHRE/ASRM sponsored PCOS consensus workshop
in view of additional features such as elevated free group 2004 revised 2003 consensus on diagnostic criteria and
serum testosterone, LH-FSH ratio, oligomenorrhea and/or long term health risk related to polycystic ovary syndrome. Hum
polycystic ovaries. Reprod 2004;19:41-7.
3. Balen AH, Laven JS, Tan SL, Dewally D. Ultrasound assessment
The non-androgenic causes of hirsutism may be familial,
of the polycystic ovary: International consensus definition. Hum
idiopathic or due to drugs like cyclosporine, phenytoin, Reprod Update 2003;9:505-14.
diazoxide, triamterene-hydrochlorothiazide, minoxidil, 4. Carmina E, Rosato F, Janni A, Risso M, Longo RA. Relative
hexachlorobenzene, penicillamine and psoralens. Other less prevalence of different androgen excess disorders in 950 women
common causes include anorexia nervosa, hypothyroidism referred because of clinical hyperandrogenism. J Clin Endocrinol
and porphyria. Idiopathic hirsutism, also called simple or Metab 2006;91:2-6.
peripheral hirsutism, is diagnosable in women who have 5. Ehrmann DA. Polycystic ovary syndrome. N Engl J Med
normal ovulatory function and normal androgen profile. 2005;32:773-7.
Only 5-15% of hirsute women qualify for this diagnosis 6. Azziz R, Sanchez LA, Knochenhauer ES, Moran C, Lazenby
by these criteria.4,7,8 Except for our two patients who had J, Stephens KC, et al. Androgen excess in women: Experience
hirsutism in first degree relatives other 4 patients with with over 1000 consecutive patients. J Clin Endocrinol Metab
2004;89:453-62.
normal investigative profile can be considered to be of
7. Carmina E. Prevalence of idiopathic hirsutism. Eur J Endocrinol
idiopathic origin.
1998;139:421-3.
Despite limitations of small number of patients and lack of 8. Azziz R, Carmina E, Sawaya ME. Idiopathic hirsutism. Endocr
long-term follow-up in most patients, the study indicates Rev 2000;21:347-62.
that hirsutism in Indian women is not uncommon. Although
its clinical presentation does not differ from its description
in the literature, hirsutism of adrenal or thyroid origin does Received: November, 2007. Accepted: April, 2008.
not appear to be common in our patients. Interestingly, Source of Support: Nil, Conflict of Interest: Nil.
Context: Tinea versicolor is a common fungal disease. Many topical and systemic drugs have been used for the treatment
of Tinea versicolor. But more or less the treatment results had been similar with high recurrence rates. Aims: The aim
of this study was to compare the therapeutic effects of topical Artremisia sieberi 5% lotion with topical clotrimazole 1%
lotion in the treatment of pityriasis versicolor. Settings and Design: This was a descriptive study which was conducted
in Sanandaj. Materials and Methods: This was a double-blind clinical trial. 100 patients with pityriasis versicolor and
microscopic identification of Malassezia furfur were randomly assigned to treatment with either topical Artemisia sieberi
5% lotion (group 1) or topical clotrimazole 1% lotion (group 2) for 2 weeks. Group 1 and group 2 consisted of 51 and 49
patients respectively. The patients were evaluated both clinically and mycologically at baseline and every 2 weeks for a
period of 4 weeks. Statistical Analysis Used: The data were processed with SPSSwin13 software and data analysis was
performed by means of independent t test, X2, and Fisher’s exact test. Results: In this study, at the end of the second
week, clinical cure rates were 86.3% and 65.3% for group 1 and group 2 respectively (P < 0.01), but at the same time
mycological cure rate was 92.2% for group 1 and 73.5% for group 2 (P < 0.05), which revealed significant differences
clinically and mycologically. At the end of the fourth week (2 weeks after cessation of the treatments), clinical cure
rates were 86.3% and 59.2% for group 1 and group 2 respectively (P < 0.01), and at the same time mycologic cure rate
was 96.1% for group 1 and 65.3% for group 2 (P < 0.01), which demonstrated significant differences, clinically and
mycologically. Conclusions: The results of this study demonstrated that Artemisia sieberi 5% lotion was more effective
than clotrimazole 1% lotion in the treatment of pityriasis versicolor and the recurrence rate with clotrimazole lotion was
high but in the Artemisia sieberi group no recurrence was detected.
Key Words: Artemisia sieberi lotion, clotrimazole lotion, pityriasis versicolor, recurrence ratre
Materials and Methods There were 27 (27%) female and 73 (73%) male patients;
sex distribution was similar in both groups (70.6% male in
The study was a randomized, double-blind clinical trial.
group 1 and 75.5% male in group 2) (P = 0.65).
After informed consent, 102 patients with pityriasis
versicolor were enrolled in the study. The diagnosis The mean age of the patients was 26.5 ± 9.8 (range
was made on clinical examination and confirmed with 15-45 years) (P = 0.26). The mean numbers of weekly
microscopic examination of scales soaked in 10-15% baths were 1.5 ± 0.2 and 1.8 ± 0.25 for group 1 and
potassium hydroxide. group 2 respectively. The mean values for disease duration
in group 1 and group 2 were 3.09 ± 0.43 and 3.61 ± 0.51
This study was approved by Ethical Review Committee of
months respectively.
Kurdistan University of Medical Sciences and conformed to
the ethical guidelines of the 1975 Declaration of Helsinki. From the occupational point of view, no significant
difference was noted between the two groups (P = 0.31).
Inclusion criteria were as follows: clinical diagnosis of
Distributions of lesions over different parts of the body
pityriasis versicolor and its confirmation with microscopic
(Neck, chest, abdomen, back arms…) was similar in both
examination in patients between 15 and 45 years of age,
groups (P = 0.67).
and involvement of less than 10% of the total body surface
by skin lesions. 19.6% of the patients of group 1 and 16.3% of the patients
of group 2 had positive family history of pityriasis
Pregnant and lactating women were excluded from the
versicolor (P = 0.76).
study. The patients were randomly divided into two groups.
Group 1 used 1-2 ml of Artimisia sieberi 5% topical lotion Clinical assessment of the patients, after two weeks
produced by Barij Essence Pharmaceutical Company in revealed that 86.3% of the patients of group 1 and 65.3%
Iran, twice daily and group 2 applied 1-2 ml of clotrimazole of the patients of group 2 achieved success, which was
topical lotion on the lesions twice daily, for two weeks. statistically significant (P < 0.05). Mycological examination
of the skin smears at the same time demonstrated cure rates
Of 102 patients, 100 completed the treatment course
of 92.2% and 73.5% for group 1 and group 2 respectively,
(51 patients in group 1 and 49 patients in group 2 respectively).
which showed a significant difference (P < 0.05).
Two patients were lost to follow-up and excluded from the
study. Disappearance of all skin lesions on inspection was After four weeks (2 weeks after cessation of the treatments)
our criterion for clinical cure and negative direct smear in clinical cure rates were 86.3% and 59.2% (P < 0.01) and
microscopic study was regarded as mycological cure.17 mycological cure rates at the same time were 96.1% and
65.3% (P < 0.01) for group 1 and group 2 respectively
Skin assessment and microscopic examination of skin
[Table 1].
smears were performed at baseline, after completion of the
two-week treatment course, and two weeks after cessation Among the cured patients, the recurrence rates clinically
of the topical agents. The phone numbers and addresses (assessed only by inspection of the skin) and mycologically
of the patients were recorded in their files. One of our (assessed by microscopic examination of the skin smears)
colleagues was responsible to call the patients to remind were 9.4% and 11.1% respectively, in the patients of
them of the follow-up visits, but in the event they did not group 2. However we noticed no recurrence of the skin
come, he referred to them to take skin smear and evaluate lesions, clinically and mycologically in the patients of the
the patients for clinical cure rate (assessment of the group 1, which was statistically significant (P < 0.01).
clinical cure rate for all of the patients was performed by
the same person). Results of the clinical and microscopic Discussion
examinations and demographic data of the patients were
recorded in a check- list for each of the patients. At the end of the second week of this study, clinical
assessment demonstrated a higher cure rate in Artemisia
The data were processed with SPSS Win13 software and sieberi group than clotrimazole group (P < 0.05). At the
data analysis was performed by means of independent t test, same time, in microscopic study, rate of negative direct
Chi- square tests, and Fisher’s exact test. smears was higher in group 1 (P < 0.05).
After four weeks from the start of the treatment regimens
Results clinical re-evaluation of the patients revealed a higher cure
Analysis of the two treatment groups at baseline, as rate in group 1 than group 2 (P < 0.01). At the same time
explained in the following paragraphs revealed no significant a higher number of the patients of group 1 had negative
differences between the group 1 and group 2 patients in direct smears, compared with group 2 patients (P < 0.01). In
relation to age, sex distribution, number of weekly baths, this study the results of clinical evaluation and microscopic
distribution and location of the skin lesions, occupation, examination showed that Artemisia sieberi lotion was
disease duration, and family history of the patients; superior to clotrimazole lotion in the treatment of pityriasis
suggesting that the randomized arms were equivalent. versicolor. It is likely that active antifungal constituent(s)
Table 1: Comparison of the therapeutic effects of Artemisia sieberi lotion with clotrimazole lotion based on clinical
examination and skin smear after 2 and 4 weeks of the treatment regimens
Group Improvement N (%) Lack of improvement N (%) X2 P
Clinical examination
2 weeks
Artemesia 44 (86.3) 7 (13.7) 6.1 0.01
Clotrimazol 32 (65.3) 17 (34.7)
4 weeks
Artemesia 44 (86.3) 7 (13.7) 9.3 0.002
Clotrimazol 29 (59.2) 20 (40.8)
Skin smear
2 weeks
Artemesia 47 (92.2) 4 (7.8) 6.43 0.01
Clotrimazol 36 (13) 13 (26.5)
4 weeks
Artemesia 49 (96.1) 2 (3.9) 15.3 0.000
Clotrimazol 32 (65.3) 17 (34.7)
of Artemisia sieberi persisted in the superficial layer of skin variety of plants including Artemisia species, sage and
for a longer period than did clotrimazole and prevented the Thuja tree.14,16 Alpha- thujone has also antihelminthic,
early recurrence of pityriasis versicolor. insecticidal, and antinociceptive properties.14,18,19
In a similar double-blind clinical trial, by Mansouri and
her colleague’s significant clinical improvement, after two Conclusion
weeks was observed in 77.4% and 60.7%, and after 4 weeks This double- blind clinical trial shows that Atremisia sieberi
in 93.5% and 57.1% of the patients in Artemisia sieberi 5% lotion is more effective than clotrimazole 1% lotion
group and clotrimazole group respectively. After two weeks in the treatment of pityriasis versicolor. According to the
Mansouri found negative direct smears in 87.1% and 69%, results of our study, recurrence rate is expected to be much
and after four weeks in 100% and 61.5% of the patients lower with Artemisia sieberi 5% lotion than clotrimazole
in Artemisia group and clotrimazole group respectively.9 In 1% lotion after cessation of the therapeutic agents. This
the above mentioned study the results of clinical assessment study emphasizes the need for definitive studies to address
and microscopic examination were compatible with those this issue in the future.
of our study.
Clinical cure rates after two and four weeks were lower References Q4
than mycological cure rates at the same time periods. 1. Savin R. Diagnosis and treatment of tinea versicolor. J Fam Pract
Therefore accuracy of the laboratory- based care rates was 1996;43:127-32.
higher than that of clinically- assessed cure rates. 2. Faergemann J. Management of seborrheic dermatitis and
pityriasis versicolor. Am J Clin Dermatol 2000;1:75-80.
Occasionally in the pale type of pityriasis versicolor white
3. Thoma W, Krämer HJ, Mayser P. Pityriasis versicolor alba. J Eur
marks are permanent for unknown reasons, persisting long Acad Dermatol Venereol 2005;19:147-52.
after the scaling and yeasts have gone and despite exposure
4. Faergemann J. Pityrisis versicolor. Semin Dermatol 1993;12:276-9.
to the sun.3
5. Montero-Gei F, Robles ME, Suchil P. Fluconazole vs itraconazole
In such cases results of the direct smear of the in the treatment of tinea versicolor. Int J Dermatol 1999;38:601-3
hypopigmented lesions are negative and clinically these 6. Farshchian M, Yaghoobi R, Samadi K. Fluconazole versus
patients may be misdiagnosed as cases of untreated pityriasis ketoconazole in the treatment of tinea versicolor. J Dermatol
versicolor. Therefore sometimes clinical assessment and Treat 2002;13:73-6.
laboratory results may be incompatible. It is very likely 7. Chu AC. Comparative clinical trial of bifonzole solution versus
that antifungal effect of Artemisia sieberi lotion is due to selenium sulphide shampoo in the treatment of pityriasis
versicolor. Dermatologica 1984;169:81-6.
alpha- thujone.
8. Vander Straten, Hossain MA, Ghannom MA. Cutaneous infection,
The mechanism by which alpha- thujone is of therapeutic dermatophytosis, onychomycosis and tinea versicolor. Infect Clin
benefit in pityriasis versicolor is unclear at present. Alpha- North Am 2003;17:87-112.
thujon is a constituent of essential oils derived from a 9. Mansouri P, Kashanian M, Bekhradi R, Hakmat H. Artemesia
sieberi lotion 5% compared with clotrimazole lotion in the internet. N Engl J Med 1997;337:825-7.
treatment of tinea versicolor. Iran J Pharma Res 2004;2:38. 16. FEMA. FEMA Database: Thujone. Washington, DC: Flavor and
10. Habibi R, Shakoei M. Ecological regions of Iran vegetation Extract Manufacturer’s Association; 1997. p. 12.
types of Tehran area. 1382. Available from: http:/www.rifr-ac.ir/ 17. Delescluse J. Itraconazole in tinea vesicolor: A review. J Am
English/books/details.aspx?id=1000019. Acad Dermatol 1990;23:551-4.
11. Tavili A, Jafari M. Comparing artemisisa sieberi besser and 18. Lee s, Tsao R, Peterson C, Coats JR. Insecticidal activity
artemisia scoparia waldst and kit: Elemental content grown on of monoterpenoids to western corn rootworm (Coleoptera:
crusted and uncrusted soils. Pak J Nutr 2006;5:10-3. Chrysomelidae), twospotted spider mite (Acari: Tetranychidae),
12. Sirisoma NS, Höld KM, Casida JE. Alpha- and beta- Thujones and house fly (Diptera: Muscidae). J Econ Entomol 1997;90:
(herbal medicines and food additives): Synhthesis and analysis 883-92.
of hydroxy and dehydro metabolites. J Agric Food Chem 19. Rice KC, Wilson RS. (-)-3-Isothujone, a small nonnitrogenous
2001;49:1915-21. molecule with antinociceptive activity in mice. J Med Chem
13. Arnold WN. Absinthe. Sci Am 1989;260:112-7. 1976;19:1054-7.
14. Lachenmeier DW, Walch SG, Padosch SA, Kroner LU. Absinthe:
A review. Crit Rev Food Sci Nutr 2006;46:365-77.
15. Weisbord SD, Soule JB, Kimmel PL. Poison on line- acute Received: October, 2007. Accepted: April, 2008.
renal failure caused by oil of worm wood purchased through the Source of Support: Nil, Conflict of Interest: Nil.
Author Queries??????
Q1 Approximately 250 words
Q2 Include why this study was conducted, what were the aims and objectives of the study.
Q3 Should this be deleted?
Q4 Follow the punctuation marks carefully. Do not include unnecessary bibliographic elements such as issue number,
month of publication, etc. Include names of six authors followed by et al if there are more than six authors.
Background and Aim: Herpes Zoster (HZ) is reactivation of latent varicella-zoster virus that involves dermatomes. Aging
and immunosupressed states are among the main risk factors. Some investigations showed that HZ is more common in
diabetic patients than in normal population. Aim: To determine whether undiagnosed DM is more common in patients
with HZ than in those without it. Materials and Methods: In this study 103 patients with HZ (cases) and 142 as control
participated. They had no history of DM. Both groups were matched according to age, gender and family history of DM.
Fasting plasma glucose was checked for all participants. DM was defined when the fasting plasma glucose was equal
or more 126 mg/dl. Results: 35.9% of patients with HZ and 19.7% of the control group had DM. There was significant
association between HZ and undiagnosed DM (OR = 2.28, 95% CI: 1.28-4.06). Conclusion: Our findings indicate that
the prevalence of undiagnosed DM is more common in HZ patients and supports the policy to investigate patients with
HZ for the presence of undiagnosed DM.
Background: Acne vulgaris is one of the most common skin disorders in youth especially during the puberty. Objective: This
in vitro study was performed to determine the antibiotic resistance and sensitivity in acne vulgaris. Materials and
Methods: Samples were collected from normal skin and nodulocystic and pustular skin lesions of one hundred youngsters
(64 girls, 36 boys) among college students in the age range of 18-24 years old. The specimens were cultured individually
on blood agar and Muller-Hinton media. The cultures were then incubated under both aerobic and anaerobic conditions for
2 to 7 days. Bacteria were identified and their resistance to common antibiotics was evaluated according to the standard
procedures. Results: In aerobic culture of pustular and nodulocystic skin lesions, Staphylococcus aureus was present in
41% of subjects, Staphylococcus epidermidis in 53% and Micrococcus spp in 45% of subjucts. In anaerobic bacterial
culture of pustular and nodulocystic skin lesions, Staphylococcus aureus was present in 39%, Propionibacterium acne
in 33% and Staphylococcus epidermidis in 21% of subjects. The results of present study revealed that clindamycin and
erythromycin were the least effective antibiotics for Propionibacterium acne while tetracycline was the least effective for
Staphylococcus aureus in vitro. A synergic effect of benzoyl peroxide, erythromycin or clindamycin was noticed. Rifampin
was the most effective antibiotic in vitro. Conclusion: Our results showed that rifampin was the most sensitive antibiotic
in vitro for acne vulgaris. To achieve a better treatment, a combination of rifampin with other antibiotics may be more
efficient. We suggest in vivo studies for better evaluation and treatment of acne patients with rifampin.
Dermatol Online J 2003;9:8. effectiveness. In: Diagnosis microbiology. 8th ed. The CV Mosby
2. Webster GF, Leyden JJ, Nilsson UR. Complement activation in Company; 1990. p. 171-94.
acne vulgaris: Consumption of complement by comedones. Infect 13. Toyoda M, Morohashi M. An overview of topical antibioticforacne
Immun 1979;26:183-6. treatment. Dermatology 1998;196:130-4.
3. Simpson NB. Disorders of the sebaceous glands. In: Burn T, 14. Rodriguez-Cavallini E, Vargas-Dengo P. Etiologyia bacteriana y
Breathnach S, Cox N, Grifiths C, editors. Rook’s Textbook of susceptiblidad a antibioticos en pacientes con acne. Rev Biomed
Dermatology. 7th ed. Oxford Blackwell Science; 2004. p. 43.15. 2004;15:101-6.
4. Firooz A, Sarhangnejad R, Davoudi SM, Nassiri-Kashani M. Acne 15. Thiboutot D. New treatments and therapeutic strategies for acne.
and smoking: Is there a relationship? BMC Dermatol 2005;24;5:2. Arch Fam Med 2000;9:179-87.
5. Adebamowo CA, Spiegelman D, Berkey CS, Danby FW, Rockett 16. Leyden JJ. Effect of topical benzoyl peroxide-clindamycin
HH, Colditz GA, et al. Milk consumption and acne in adolescent versus topical cindamycin and Propionibacterium acnes. Cutis
girls. Dermatol Online J 2006;12:25. 2002;69:475-80.
6. Smith RN, Mann NJ, Braue A, Mäkeläinen H, Varigos GA. 17. Ross JI, Eady EA, Cove JH, Ratyal AH, Cunliffe WJ. Resistance
A low-glycemic-load diet improves symptoms in acne vulgaris to erythromycin and clindamycin in cutaneous propionibacteria
patients: A randomized controlled trial. Am J Clin Nutr is associated with mutations in 23S rRNA. Dermatology
2007;86:107-15. 1998;196:69-70.
7. Gollnick HP, Krautheim A. Topical treatment in acne: current 18. Bowe WP, Filip JC, DiRienzo JM, Volgina A, Margolis DJ.
status and future aspects. Dermatology 2003;206:29-36. Inhibition of propionibacterium acnes by bacteriocin-like
8. Stein RH, Lebwohl M. Acne therapy: Clinical pearls. Semin inhibitory substances (BLIS) produced by Streptococcus
Cutan Med Surg 2001;20:184-9. salivarius. J Drugs Dermatol 2006;5:868-70.
9. Zaenglein AL, Thiboutot DM. Acne vulgaris. In: Bolognia JL, 19. Cunliffe WJ, Baron SE, Coulson IH. A clinical and therapeutic
Jorizzo JL, Rapini RP, editors. Dermatology. 2nd ed. Toronto: study of 29 patients with infantile acne. Br J Dermatol
Mozby; 2003. p. 532. 2001;145:463-6.
10. Ashkenazi H, Malik Z, Harth Y, Nitzan Y. Eradication of 20. Noyon V, Legallou F, Richet H, Dreno B. The resistance of
Propionibacterium acnes by its endogenic porphyrins after Propionibacterium acnes and Staphylococcus epidermidis to
illumination with high intensity blue light. FEMS Immunol Med cyclones. Ann Dermatol Venereol 1998;125:885-7.
Microbiol 2003;35:17-24. 21. Tan HH, Goh CL, Yeo MG, Tan ML. Antibiotic sensitivity of
11. Ross JI, Snelling AM, Eady EA, Cove JH, Cunliffe WJ, Propionibacterium acnes isolates from patients with acne vulgaris
Leyden JJ, et al. Phenotypic and genotypic characterization of in a tertiary dermatological referral centre in Singapore. Ann
antibiotic-resistant Propionibacterium acnes isolated from acne Acad Med Singapore 2001;30:22-5.
patients attending dermatology clinics in Europe, the USA, Japan
and Australia. Br J Dermatol 2001;144:225-7. Received: November, 2007. Accepted: April, 2008.
12. Baron EJ, Finegold SM. Methods for testing antimicrobial Source of Support: Nil, Conflict of Interest: Nil.
Author Queries??????
Background: Onychomycosis is a difficult condition to treat and cure rates are disappointing. Moreover fungicidal action
of antifungal agents in NCCLS assays and their rapid accumulation in nails in vivo are not compatible with the duration
of treatment. Aims: This study aimed to find the effectiveness of 4 different antifungal agents in an in vitro model with
some similarities to in vivo conditions. Materials and Methods: Strains of Trichophyton rubrum I-III, Trichophyton
mentagrophytes (usual form), Trichophyton mentagrophytes 73, Epidermophyton Flucosom, Microsporum Canis, and
Trichophyton Schoenleini which were isolated from the nails of patients, were hired. Inocula suspensions were prepared
from 7 to 14 day-old cultures of dermatophytes. Antifungal agents including fluconazole, ketoconazole, terbinafine, and
griseofulvin were obtained as standard powders. For each antifungal agent, initial MIC was calculated by registering the
optical density for 10 two-fold serially diluted forms which was incubated with diluted fungal suspensions with RPMI
1640. Human nail powder inoculated with different strains and incubated in RPMI 1640 and different concentrations of
antifungal drugs for 4 weeks. Final MIC at different steps of 1, 2, 3 and 4 weeks were investigated. Results: The final
MIC that resulted from the incubation of dermatophytes with nail powder was much more than the initial which was
concluded from conventional MIC assay. Terbinafine had the lowest rate of initial and final MICs. Conclusion: The
model described here may present more similar conditions to clinical fungal infections; therefore the results such as MIC
may be more helpful for hiring the most effective antifungal agent.
carefully with the tip of a Pasteur pipette. Heavy particles find the amount of reduction in turbidity as compared to
of the suspension were allowed to settle for 3 to 5 min. The that of the drug-free control tube. MIC at which 50% of
final inoculum size was adjusted with a spectrophotometer the isolates are inhibited (MIC50) was determined.
at a wavelength of 530 nm to a transmittance of 95%.
Preparation of nail powder:5,10 Human nail Clippings
These suspensions were diluted in RPMI 1640 test medium
from several healthy volunteers previously found free from
(1:50) to obtain a cell number ranging from 0.5 × 104 to
fungi when examined in 10% KOH were used. The samples
5 × 104 CFU/ml.
were cleaned with 70% ethanol, dried in a sterile Petri dish
Antifungal agents: They were obtained as standard at 37°C, and ground with using a stainless steel peppermill.
powders. The powder of fluconazole 99.7% (Pars Daru, The powder was autoclaved at 121°C for 20 min.
Iran), ketoconazole 98.43% (Rooz Daru, Iran), terbinafine
Nail model culture: After finding the primary MIC for each
99.6% (Behvarzan, Iran), and griseofulvin 99.3%
microorganism, 6 tubes containing MIC tube, 2 tubes with
(Daroopakhsh, Iran) were used in this study.
higher dilution and 2 tubes with lower dilution, respectively
Stock solutions were prepared by dissolving and two-fold plus another tube as the control tube were selected.
serially dilution of drugs in Methanol 0.1 percent, by using Autoclaved nail powder was added, at approximately
Broth microdilution method. 10× dilutions were prepared 10 mg per tube. 0.9 cc of Inocula suspensions were added
for each drug Tested concentrations for fluconazole ranged directly onto the nail powder. The tubes were left at 37°C
from 0.187-96.0 μg/ml, and for ketoconazole, terbinafine for 10 days. After 10 days the mycelium were attached
and griseofulvin from 0.125-64.0 μg/ml. Stock solutions to nail particles which established the sufficiency of the
were prepared by dissolving and two-fold serially dilution growth time. 0.1 cc of antifungal agents were added to the
of drugs in Methanol 0.1 percent. culture according to the calculated MIC, and the cultures
were returned to 37°C. Final MIC 4 weeks after incubation
Determination of initial MIC: For each fungal strain with nail powder was investigated.
13 tubes with the volume of 10 ml, were prepared. 0.1 cc of
each antifungal agent dilutions were added to tubes 1 to 10. Statistical analysis
Then 0.9 cc of diluted fungal suspensions with RPMI 1640
Initial and final MICs were assessed 2 times for each
was added to each tube. The eleventh tube contained a 0.9 ml
sample and presented as means. ANOVA besides Tukey
volume of inoculum suspension and a 0.1 ml volume of drug-
test was hired to analyze MICs in each subgroup. Pearson
free medium (To assess the inhibitory effect of medium on
correlation was used in order to find any correlation
fungal growth). The twelfth tube (growth control) consisted
between initial and final MICs. Paired t-test was used for
of fungal suspensions with RPMI 1640. A sterility control
comparing between initial and final MICs.
(the thirteenth tube) was run in parallel by including a 1 ml
volume of uninoculated, drug-free medium.
Results
Tubes were incubated at 30°C for 48h. Growth control
Initial MICs [before culturing on nail powder] for each
tubes were observed for the presence or absence of visible
subgroup are presented in Table 1.
growth. When growth was visible, the growth in each tube
was compared with that of the growth control tube. Optical Grisofulvin and ketoconazole had the same rate of initial
density (OD) of each tube which was obtained from a MICs, which were statistically different from fluconazole
spectrophotometer at a wavelength of 530 nm was used to with the highest rate of initial MIC and terbinafine with
Table 1: Initial MIC* for different antifungal agents according to the type of dermatophytes
Ketoconazole Fluconazole Terbinafine Grisofulvin
Dermatophytes
T. rubrum I 32 48 2 32
T. rubrum II 16 24 4 16
T. rubrum III 32 48 2 32
T. mentagrophytes 16 48 0.125 8
T. mentagrophytes73 32 48 1 32
T. schoenleini 0.5 48 4 0.5
E. flucosom 1 48 2 16
M. canis 8 24 8 16
M. gypseum 16 24 8 64
MIC range 0.5-32 24-48 0.125-8 0.5-32
*μg/ml
Table 2: Final MIC for different antifungal agents according to the type of dermatophytes
Ketoconazole Fluconazole Terbinafine Grisofulvin
Dermatophytes
T. rubrum I 64 96 4 32
T. rubrum II 16 48 8 32
T. rubrum III 64 96 4 32
T. mentagrophytes 64 96 1 16
T. mentagrophytes73 - 96 4 32
T. schoenleini 2 96 16 1
E. flucosom 2 96 2 32
M. canis 16 48 16 16
M. gypseum 32 - 32 -
the lowest rate of initial MIC respectively (ANOVA, nutrition by activation of keratinases secretion. In this
P = 0.0001). in vitro model, using its natural substrate, the dermatophytes
act with more similarity to in vivo clinical condition.5,10,15,16
After incubation with nail powder we found that final MICs
Therefore, response to antifungal agents which is normally
statistically increased in comparison with initial MICs
reported as MIC reached form NCCLS models would reach
(Initial MIC: 19.42 ± 17.21 μg/ml, final MIC 36.72 ± 33.77
more relevant and practical result.
μg/ml, paired t-test, P value = 0.0001) [Table 2].
Due to our findings, the final MIC which resulted after
There was a direct correlation between initial and final
the incubation of dermatophytes beside nail powder was
MICs which was statistically significant (R = 0.95,
much more than the initial which was concluded from
P value = 0.0001).
conventional MIC assay. In addition Osborne et al,10 found
that terbinafine Nail-MFCs obtained from in vitro method
Discussion
using nail powder were much higher than MFC values
Griseofulvin and newer antifungal drugs such as obtained after conventional assays. Also, they found that
ketoconazole, fluconazole and terbinafine, are the major the cidal action of terbinafine was much slower than in
systemic drugs applied to treat onychomycosis.11 Griseofulvin conventional assays. Therefore the current model of culture
was the first systemic antifungal drug but nowadays it is may show the needs for high dose and long duration of
not used in a widespread way.12 Ketoconazole was the first antifungal treatment for OM.
orally active imidazole but it is known for its hepatotoxicity
as well.7 Terbinafine is highly effective against dermatophyte On the other hand, by comparing the efficacy of the
infections and acts by blocking ergosterol synthesis.10 assessed antifungal drugs, we found that terbinafine
inhibited the growth of dermatophytes in the in vitro model
Studies which compared the effectiveness of different more effectively. Osborne et al, concluded similarly.10
antifungal agents in treatment of onychomycosis at the The higher activity of terbinafine in comparison to other
same time7 are scarce. Moreover, treatment of OM is a tested antifungal drugs has been established during in vitro
problematic issue in clinical practice.1,10 studies.7,17 Therefore our finding in this regard is not new
Santos et al,7 tried to study in vitro susceptibility of rather than higher MIC which had been also achieved by
52 isolates of Trichophyton rubrum and 40 of Trichophyton Osborne et al.10
mentagrophytes to griseofulvin, terbinafine, itraconazole, In conclusion, the model described here offers a clinically
ketoconazole, fluconazole and cyclopiroxolamine. They mimicking condition for measuring the efficacy of different
used modified NCCLS approved procedure M38-A. Finally, antifungal drugs for the treatment of onychomycosis. Future
they concluded that terbinafine was the most effective studies on dermatophytes using other biomaterials such as
in vitro against all isolates, followed by itraconazole, hair powder as a part of culture medium may be useful for
cyclopiroxolamine, ketoconazole and fluconazole. other clinical conditions.
Conidial suspensions or mixed suspension of mycelial
fragments and conidia growing in a rich medium are used References
in the NCCLS methodology for antifungal testing makes 1. Blumberg M, Kantor GR. (Internet): Onychomycosis. Available
use of.13,14 Employing nail powder for antifungal testing,10 from: http://www.emedicine.com/derm/topic300.htm.
mimics the course of a natural nail fungal infection, with 2. Faergemann J, Baran R. Epidemiology, clinical presentation and
antifungal treatment starting only after mycelial growth. diagnosis of onychomycosis. Br J Dermatol 2003;149:1-4.
In this method the fungi must use the nails as their only 3. Osborne CS, Leitner I, Favre B, Ryder NS. Antifungal drug
Background: Cutaneous Leishmaniasis (CL) is a parasitic disease characterized by single or multiple ulcerations.
Secondary bacterial infection is one of the complications of the disease that can increase the tissue destruction and
the resulting scar. Objective: To effectively determine the incidence of real secondary bacteria infection in cutaneous
leishmaniasis, we designed the current study. Methods and Materials: This was a cross-sectional study performed in
Skin Diseases and Leishmaniasis Research Centre, Isfahan, Iran. In this study, 854 patients with confirmed CL were
enrolled. Samples were taken from all the patients. Sterile swaps were achieved for the ulcer exudates and scraping was
used for nonulcerated lesions. All the samples were transferred to tryptic soy broth medium. After 24 h of incubation in
37°C, they were transferred to eosin methylene blue agar (EBM) and blood agar. Laboratory tests were used to determine
the species of bacteria. All of the collected data were analyzed by SPSS software and chi-square. Results: Among
854 patients with confirmed cutaneous leishmaniasis, 177 patients (20.7%) had positive cultures for secondary bacterial
infection. Bacteria isolated from the lesions were as follows: Staphylococcus aureus - 123 cases (69.4%), coagulase
negative Staphylococcus - 41 cases (23.1%), E. coil - 7 cases (3.9%), Proteus - 3 cases (1.7%) and Klebsiella - 3 cases
(1.7%). Conclusions: The incidence of secondary bacterial infection in lesions of CL was 20.7%. The most common
isolated pathogen was Staphylococcus aureus. The incidence of secondary bacterial infection was significantly more in
the ulcerated lesions as compared with nonulcerated lesions (P = 0.00001).
ulcerated lesions and samples were collected aseptically In the another study, bacteria including Proteus
by scraping the nonulcerated lesions. All the samples valguries, Pasteurella multisided, Staphylococcus aureus, Q1
were transferred to tryptic soy broth medium. After 24-h Staphylococcus albus, E. coli and Pseudomonas aurogenosa Q2
incubation in 37°C, the samples were transferred to eosin were isolated from clinically infected lesions.6
methylene blue agar (EMB) and blood agar.
In another study that was performed in the impetiginized
Gram staining, oxidase test, indole test, urease test, catalase forms of leishmaniasis, Staphylococcus aureus was
test and coagulase test were used to determine the species recognized to be the responsible pathogen.4
of bacteria.
In a study performed in the Yucantan peninsula of
Statistical analysis Mexico, some pathogenic bacteria were detected from
All of the collected data were analysed by SPSS and Chi- the skin lesions of patients with chiclero’s ulcers (a form
squared test. of cutaneous leishmaniasis due to Leishmania mexicana)
reluctant to antimonial treatment, and the results of
Results this study suggested the need to eliminate bacterial
infections by antibiotic therapy before starting antimonial
In this study, 854 patients who confirmed CL were enrolled.
administration.7
The age range of patients was 2 months to 85 years and the
mean age of the patients was 27.21 years. Among them, In our study, out of the 854 patients with confirmed
320 patients (37.5%) were women and 534 (62.5%) were cutaneous leishmaniasis, 177 patients (20.7%) had
men. The results of the culture were positive in 20.7% confirmed secondary bacterial infection.
of the patients (177 patients). Bacteria isolated from the
The most common bacterial isolate was Staphylococcus
lesions were as follows: Staphylococcus aureus - 123 cases
aureus. Other pathogens included coagulase negative
(69.4%), coagulase negative Staphylococcus - 41 cases
Staphylococcus, E. coli, Proteus vulgaris and Klebsiella.
(23.1%), E. coil - 7 cases (3.9%), Proteus - 3 cases (1.7%)
and Klebsiella - 3 cases (1.7%). There was no significant association between the prevalence
The distribution frequency of the isolated bacteria by the distribution of the isolated bacteria with the age, sex,
clinical from of the leishmaniasis lesions are shown in location, number and duration of the disease (P > 0.05).
Table 1. However, there was a significant association between
the clinical form of the disease and the isolated bacteria
Discussion (P = 0.00001).
Secondary bacterial infection is one of the complications All the lesions that had secondary bacterial infection were
of CL. Although some authors emphasize on the rarity of ulcerated. There was no bacterial isolates from the lesions
this finding,3 our clinical findings are in contrast to this. that were not ulcerated. With regard to these facts, we can
In our practice, we encounter many cases of the infected conclude that destruction of the epidermis in the ulcerated
leishmaniasis ulcers. In fact, secondary bacterial infection lesions had predisposed the patients to the secondary
can exacerbate the disease and the final scar because it will bacterial infection.
increase the tissue destruction and necrosis. In these cases,
Regarding the results of our study, we suggest that topical
painful ulcers with purulent discharges and with surrounding
antiseptic solutions are need for ulcerated lesions of the
inflammation may occur. In addition, the duration of disease
cutaneous leishmaniasis to prevent the secondary bacterial
would be prolonged.4 The appropriate use of antibiotics will
infection that may accelerate tissue destruction.
decrease the resultant infection in these cases. One study in
Sudan has shown the prevalence of the secondary infection In addition in the case of secondary bacterial infection
to be 18% of the 736 evaluated patients. The pathogenic symptoms and signs, the use of antibiotics particulary
organism was not identified in this study.5 against staphylococcus would be logical.
Author Queries??????
Q1 vulgaris?
Q2 Pseudomonas aeruginosa?
Background: In recent years, skin diseases in wrestling have finally received the attention they deserve. Outbreaks of tinea
corporis are often associated with sports involving extensive bodily contact; such sports include wrestling. Tinea corporis
gladiatorum is primarily caused by Trichophyton tonsurans, infecting wrestlers at alarming rates. The management of
skin infections in wrestlers and other athletes in sports involving skin-to-skin contact entails numerous challenges, from
making an accurate diagnosis to determining eligibility for playing the sports. To control outbreaks, we conducted an
epidemiologic investigation. The purpose of this article is to determine the prevalence of tinea corporis gladiatorum in
wrestlers in Tehran, Iran. Materials and Methods: A study of dermatophytosis was carried out during the period of
March 2004 to December 2005 on 612 mycological proven cases of dermatophytosis found in male wrestlers in Tehran.
Mycological examination consisted of culturing of pathologic material followed by direct microscopic observation.
Diagnosis was based on macroscopic and microscopic characteristics of the colonies. Result: T. tonsurans was the
predominant dermatophyte, accounting for >90% of all tinea corporis gladiatorum isolates during the 2 year analysis. Tinea
corporis gladiatorum was found to be more frequent in individuals between the ages of 10 and 20 years of age (72.7%).
Wrestlers with tinea corporis gladiatorum were predominantly from wrestling clubs in southern and southeastern Tehran.
Transmission of tinea corporis is primarily through skin-to-skin contact. Conclusion: Rapid identification and treatment
of tinea corporis gladiatorum is required to minimize the disruption of team practices and competitions. Infection with
dermatophytes can disqualify a wrestler from competing in matches, and thus, vigilant surveillance and rapid initiation of
treatment is important to prevent the suspension of team practices and competitions.
Key Words: Dermatophytosis, infection control, Iran, tinea corporis, tinea gladiatorum, trichophyton tonsurans, wrestling
and currently accounts for >95% of tinea capitis in the We need to study all aspects of this infection in this
United States.18-19 population in order to develop strategies to deal with it.
Because infection with dermatophytes can disqualify a
Since the 1950s, T. tonsurans has spread to North America.19
wrestler from competing in matches, vigilant surveillance,
A rapid increase in the incidence of T. tonsurans resulting
prevention, rapid identification and treatment of tinea
in tinea capitis has been noted in Canada. Canadian studies
gladiatorum is vital to reduce the suspension of a team’s
reported an incidence of 9% in 1985 and 76% in 1996.26 In
practice and competition.
Europe, an increasing number of T. tonsurans infections in
recent years suggest its return to this area. In 1999, Fitowski Good personal hygiene helps prevent the spread of
and Ratka27 reported an epidemic outbreak of T. tonsurans ringworm. Showering thoroughly after practices and
in 23 village children in Poland. In 1995, an outbreak of competitions and washing uniforms after they are used with
tinea corporis occurred in members of a wrestling team antibacterial detergent is an effective means in achieving
in Sweden. Wrestlers from a USA team visiting Sweden appropriate hygiene.6,35 Furthermore, uniforms and practice
were the suspected source of this epidemic.28 Recently, clothing should not be shared among wrestlers.35
T. tonsurans was also reported to occur in the United
Tinea corporis gladiatorum can be found quite frequently
Kingdom and was found to be the predominant cause of
among high school wrestlers. Without a thorough knowledge
tinea capitis, accounting for 72% of the observed infections
of tinea gladiatorum, wrestling is compromised as a sport.
in Birmingham.29 Other outbreaks of T. tonsurans were also
Vigilant surveillance and rapid initiation of therapy is
reported in southeastern London (United Kingdom) 30 and
important to prevent suspension of team practices and
among school children in Spain.31
competitions due to infection with dermatophytes. Awareness
This particular study focuses on its occurrence in wrestlers of these infections may facilitate the implementation of
in Tehran during recent years. In this study, incidence of early treatment and preventive measures.35
tinea corporis gladiatorum occurred in males between the
We suggest focusing our efforts on studying the
ages of 10and 20 years. Occlusion has been postulated to
person-to-person transmission, studying when return to
increase hydration of the underlying skin and emission
competition techniques such as the use of skin barriers34
of carbon dioxide from the skin, which could favor
and pharmacologic prophylaxis.37,38 We would suggest
dermatophyte growth.32,33 Tinea corporis in 64 cases (10.8%)
the continuation of common-sense hygiene measure,
was documented among the family members of infected
including showering after very encounter, washing practice
wrestlers. Most of our patients came from wrestling clubs
clothes daily and disinfecting mats daily.36 Until we have
in southern and southeastern Tehran. This is the first and
more definitive answers about ringworm in wrestlers,
largest outbreak of tinea corporis gladiatorum to be reported
it is impossible to have sufficient infection control and
in Tehran. Appropriate control measures have not yet been
prevention plans.
established.
Attention should be focused on primary and secondary
Tinea corporis is spread through direct contact with
prevention as well as treatment. Educating wrestlers,
infected individuals and may also occur due to contact with
coaches, parents and members of the medical community
infectious spores on inanimate objects such as clothing,
about skin infections and their prevention, recognition and
mats, etc. However, the presence of a dermatophyte on
treatment is crucial and a part of our continuing effort. The
a fomite or as part of a carrier sate does not affirm it
prevention of tinea should be a major priority in wrestling.
as the definitive source. The principles of an infectious
Prevention begins with cleaning all the mats before and
disease require a viable organism, a susceptible host
after practices with a hospital grade disinfectant. Secondly,
and an appropriate environment for clinical infection to
wrestlers should be educated on symptoms and trained
occur. Several authors suggest that some wrestlers may
to inspect their own bodies daily. Thirdly, wrestlers must
be asymptomatic carriers and act as reservoirs.6-34-35 Tinea
wash all workout equipment daily and be sure to wash
gladiatorum is highly contagious and is a result of the
knee pads and headgear twice a week. Fourth, wrestlers
presence of T. tonsurans. As infection with dermatophytes
should shower and use an antibacterial soap and selenium
can disqualify a wrestler from competing in matches,
shampoo immediately after workouts. It is also important to
vigilant surveillance, prevention, rapid identification;
avoid drying of skin as it is more susceptible to infection.
further, treatment of tinea gladiatorum is vital to reduce the
Finally, when a lesion is noticed, the individual must consult
suspension of team practice and competition. Appropriate
their physician or allelic trainer and use the appropriate
treatment can mitigate an infection and potentially prevent
medication. The lesion should be covered prior to wrestling
recurrence. In addition, physicians must know when
according to NCAA guidelines outlined below.39
to disqualify a wrestler and how to prevent an outbreak
through appropriate hygienic and immediate diagnostic Hygienic measures, such as mandatory showers before and
measures.36,37 In recent decades, the improvement of after practice, use of antibacterial soaps and daily washing
hygiene standards and earlier treatment may have decreased of practice gear, may be the most effective means in
widespread infections. preventing skin infections.
This study highlights a common problem in many areas Septembre 2004-avril 2005. Bull Epidemiol Hebdomadaire
of the world and suggests that further measures regarding 2005;34:171-2.
public health and personal hygiene must be undertaken 10. Estève E, Poisson DM. Trichophyties cutanées et sports de
in order to reduce the risk of tinea gladiatorum.5,40 In combat. Science Sports 2005;20:241-6.
particular, greater and more efficient sanitary control 11. Ergin S, Ergin C, Erdoğan BS, Kaleli I, Evliyaoğlu D. An
experience from an outbreak of tinea capitis gladiatorum due to
should be implemented in communal environments such
Trichophyton tonsurans. Clin Exp Dermatol 2006;31:212-4.
as gymnasia, farms, factories, swimming pools, changing
12. Poisson DM, Rousseau D, Defo D, Estève E. Outbreak of tinea
rooms of sports clubs and public showers.
corporis gladiatorum, a fungal skin infection due to Trichophyton
More research concerning different treatment regimens in tonsurans, in a French high level judo team. Euro Surveill
the wrestling environment is needed to define the optimal 2005;10:187-90.
treatment to quickly return wrestlers to competitions 13. Kasai T. Epidemiological survey of Trichophyton tonsurans
infection in Tohoku district and its clinical problems. Nippon
without placing other wrestlers at risk of infection.
Ishinkin Gakkai Zasshi 2005;46:87-91.
Intuitive hygiene practices have been suggested to
14. Mochizuki T, Tanabe H, Kawazaki M, Anzawa K, Ishizaki H.
prevent the spread of infection, but have not yet been Survey of Trichophyton tonsurans infection in the Hokuriku
substantiated.36 and Kinki region of Japan. Nippon Ishinkin Gakkai Zasshi
2005;46:99-103.
Knowledge of the most common agents producing infectious
disease outbreaks in specific sports can be used to guide 15. Hirose N, Shiraki Y, Hiruma M, Ogawa H. An investigation of
Trichophyton tonsurans in university students participating in
targeted prevention efforts. Surveillance of the frequency sports clubs. Nippon Ishinkin Gakkai Zasshi 2005;46:119-23.
of infections per team each season will also allow athletic
16. Nishimoto K, Honma K, Shinoda H, Ogasawara Y. Survey of
staff to identify outbreaks.1 Trichophyton tonsurans infections in the Kyushu, Chugoku
In conclusion, these data reiterate the continued predominance and Shikoku areas of Japan. Nippon Ishinkin Gakkai Zasshi
2005;46:105-8.
of T. tonsurans as the principal pathogens in cutaneous fungal
infections in Tehran. Trichophyton tonsurans remain the most 17. Himura M, Shiraki Y, Nihei N, Hirose N, Sugunami M.
Questionnaire investigation of incidence of Trichophyton
prevalent pathogen as tinea gladiatorum in wrestlers. The tonsurans infection in Dermatology Clinics in the Kanto area.
most prevalent fungal pathogen was T. tonsurans (92.6%), Nippon Ishinkin Gakkai Zasshi 2005;46:93-7.
followed by T. rubrum, T. mentagrophytes, E. floccosum, 18. Babel DE, Baughman SA. Evaluation of the adult carrier state
T. violaceum and T. verrucosum and M. canis. in juvenile tinea capitis caused by Trichophyton tonsurans. J Am
Acad Dermatol 1989;21:1209-12.
Acknowledgment 19. Grissey JT, Martin R. A new form of scalp ringworm in western
New York. N Y State J Med 1960;60:679-82.
The authors are grateful to Miss Nazanin Hakimzadeh-Jahromi
for her help during this research. 20. Shiraki Y, Hiruma M, Hirose N, Sugita T, Ikeda S. A nationwide
survey of Trichophyton tonsurans infection among combat sport
club members in Japan using a questionnaire form and the
References hairbrush method. J Am Acad Dermatol 2006;54:622-6.
1. Kohl TD, Giesen DP, Moyer J Jr, Lisney M Tinea gladiatorum: 21. Rebell G, Taplin D. Dermatophytes. Their recognition and
Pennsylvania’s experience. Clin J Sport Med 2002;12:165-71. identification. 2nd ed. Coral Gables, University of Miami Press.
2. Nelson M. Stopping the spread of herpes simplex: A focus on 22. Bobel DE, Rogers AL, Benede ES. Dermatophytosis of the scalp:
wrestlers. Physician Sportmed 1992;20:116-27. Incidence, immune response and epidemiology. Mycopathologia
3. William L, Dienst Jr, Dightman L, Dworkin MS. Diagnosis, 1990;109:69-73.
treatment and pinning Down skin Infections: Diagnosis, treatment 23. Jahromi ShB, Khaksar AA. Aetiologic agents of tinea capitis in
and prevention in wrestlers. Physician Sportsmed 2005;25:12. Tehran, Iran. Mycoses 2006;49:65-7.
4. el Fari M, Gräser Y, Presber W, Tietz HJ. An epidemic of Tinea 24. Shiraki Y, Soda N, Hirose N, Hiruma M. Screening examination
corporis caused by Trichophyton tonsurans among children and management of Dermatophytosis by Trichophyton tonsurans
(wrestlers) in Germany. Mycoses 2000;43:191-6. in the judo club of a university. Nippon Ishinkin Gakkai Zasshi
5. Ghannoum M, Isham N, Hajjeh R, Cano M, Al-Hasawi F, 2004;45:7-12.
Yearick D, et al. Tinea capitis in Cleveland: Survey of elementary 25. Hedayati MT, Afshar P, Shokohi T, Aghili R. A study on tinea
school students. J Am Acad Dermatol 2003;48:189-93. gladiatorum in young wrestlers and dermatophyte contamination
6. Kohl TD, Lisney M. Tinea gladiatorum: Wrestling’s emerging of wrestling mats from Sari, Iran. Br J Sports Med 2007;41:
foe. Sports Med 2000;29:439-47. 332-4.
7. De Hoog, Guarro J, Gene J, Figueras MJ. Atlas of clinical Fungi, 26. Gupta AK, Summerbell RC. Increased incidence of Trichophyton
2nd ed. Centraalbureau Vor Schimmelcultures: Utrecht; 2000. tonsurans tinea capitis in Ontario, Canada between 1985 and
8. Campbell Ck, Johnson EM, Philpot CM, Warnock DW. The 1986. Med Mycol 1998;36:55-60.
dermatophytes. In: Identification of pathogenic Fungi. PHLS: 27. Fitowski JA, Ratka P. An epidemic of superficial dermatophytosis
London; 1996. p. 26-68. caused by trichophyton tonsurans in 23 village children. Pediatr
9. Estève E, Defo D, Rousseau D, Poisson DM. Épidémie de Dermatol 1992;9:314-5.
trichophyties cutanées chez les judokas du pôle France d’Orléans: 28. Haradil E Hersle, Nordin P, Faergemann J. An epidemic of tinea
corporis caused by Trichophyton tonsurans among wrestler in 35. Kohl TD, Martin DC, Nemth R, Hill T, Evans D. Fluconazole
Sweden. Acta Dermatol Venerol 1995;75:305-6. for the prevention and treatment of tinea gladiatorum. Pediatr
29. Leeming JG, Elliott TS. The emergence of Trichophyton Infact Dis J 2000;19:717-22.
tonsurans tinea capitis in Birmingham, UK. Br J Dermatol 36. Hand JW, Wroble RR. Prevention of tinea corporis in collegiate
1995;133:929-31. wrestlers. J Athl Train 1999;34:350-2.
30. Fuller LC, Child FC, Higgins EM Tinea capitis in South-East 37. Hazen PG, Weil ML. Itraconazole in the prevention and
London: An outbreak of Trichophyton tonsurans infection. Br J management of dermatophytosis in competitive wrestlers. J Am
Dermatol 1997;136:139. Acad Dermatol 1997;36:481-2.
31. Cuctara MS, Del Palacio A, Percito M, Noricga AR. Prevalence 38. Kohl TD, Martin DC, Nemeth R, Evans DL. Wrestling mats:
of undetected tinea capitis in a prospective survey in Madrid: Are they a source of ringworm infections? J Athl Train 2000;35:
Emergence of new causative fungi. Br J Dermatol 1998;138: 427-30.
658-60. 39. Stiller MJ, Klein WP, Dorman RI, Rosenthal S. Tinea corporis
32. King RD, Cunico RL, Maibach HI, Greenberg JH, West ML, gladiatorum: An epidemic of Trichophyton tonsurans in student
Jeppsen JC. The effect of occlusion carbon dioxide emission wrestlers. J Am Acad Dermatol 1992;27:632-3.
from human skin. Acta Dermatol Venereol 1978;58:135-8. 40. Adams BB. Tinea corporis gladiatorum. J Am Acad Dermatol
33. Ripen JW. Medical mycology. 2nd ed. WB Saunders: 2002;47:286-90.
Philadelphia, A; 1982. p. 154-248.
34. Nenoff P, Handrick W, Haustein UF. Sport-induced infections. Received: October, 2007. Accepted: December, 2007.
Wien Med Wochenschr 2002;152:574-7. Source of Support: Nil, Conflict of Interest: Nil.
Author Queries??????
Q1 tinea corporis gladiatorum - Please check if we shuld use the full name throughout
Q2 Should this be ‘submerged’?
Q3 100%?
Q4 Should this part be deleted?
Q5 or skin-to-skin?
Development of skin neoplasms is one of the most important chronic complications of radiation therapy. Basal
cell carcinoma (BCC) is the most frequent carcinoma occurring at the region of the body to which radiotherapy was
delivered. The aim of this study was to evaluate clinical and histological aspects of basal cell carcinoma in patients with
a history of radiotherapy. Materials and Methods: Medical records and microscopic slides of 80 patients with basal cell
carcinoma who had received radiotherapy (1996-2006) were reviewed in pathology department of Imam Reza hospital
of Mashhad, Iran. Collected data were analyzed statistically using descriptive test. Results: 60 men and 20 women were
included, majority of them in their sixties. Plaque was the most common clinical pattern of basal cell carcinoma. Fift one
percent of the patients had pigmented and 42.5% had multiple lesions. Scalp was the most common site of involvement.
Histologically, macronodular and pigmented carcinoma were the most predominant forms of basal cell carcinoma.
Discussion: Majority of patients had scalp involvement and multiple lesions. Nodular and pigmented forms were the
most common histological findings. We suggest the need for close supervision in patients with a history of radio therapy
in the past.
ulcer, histologic pattern and pigmentation were reviewed BCC was 30 to 70 years in our cases. The average patients’
using microscopic slides. age at the time of irradiation was 12 ± 6 years and 5 to
17 years in Maalej’s and Mseddi’s studies respectively.3,11
Collected data were analyzed statistically by SPSS software
(version 13) using qui-square, T-student and Man-Whitney Majority of our cases were irradiated at less than 12 years
tests with 95% confidence interval. of age. Among all 648 patients suffering from BCC,
80 cases (12.5%) had a history of radiation therapy. This
Results was 41% in Akhyani’s study17 which can be explained by
Among 80 patients with positive history of radiation the professional aspects of Razi hospital and also division of
therapy, 60 (75%) were men and 20 (25%) were women our patients in 2 major dermatologic centers in Mashhad.
(male: female ratio was 3:1). Predominantly, BCC had been Ron and colleagues reported that the average radiation dose
developed in 5th (28/75%), 6th (42.5%) and 7th (18.75%) for treatment of tinea capitis was 7GY. The relative risk of
decades of age. Average age of our cases was 56 years. radiogenic skin cancer did not differ significantly between
Plaques (74%), papules (13%), nodules (10%) and patches men or women or by time since exposure but was greatest
(3%) were the most common clinical patterns of basal cell following exposures in early childhood. The estimated
carcinoma. Fifty one percent of the patients had pigmented excess relative risk was 0.7 per Gy.10
lesions and clinical ulcer was detected in 53%. Forty six Shore’s study showed a relative risk of 3.6 (95% confidence
cases had only one lesion but 18 cases had two, 8 cases interval, 2.3-5.9) for BCC of the head and neck among
had three and 8 cases had five lesions. The mean of lesions irradiated Caucasians in response to a dose of about 4.8Gy to
Q1 number was 1.83 per patient. Scalp (71%), forehead (6%), scalp. Children irradiated at young ages had the highest BCC
nose (5%) and periorbital area (5%) were the most common risk. He also mentioned that low ages at the time of exposure
sites of involvement. and UV radiation increase the relative risk of BCC.18
Histologically, nodulocystic (60%) and micronodular Radiation induced BCC usually occurs with low to
(17.5%) carcinoma were the most predominant forms of moderate doses of radiation for treatment of tinea capitis,
BCC. 37.5% had ulcers and 72% had pigmentation. hypertrophic tonsillitis, acne vulgaris, atopic dermatitis and
hyperthyroidism. But SCC seems to develop after high-
Discussion dose radiation.2,4,7
Different types of neoplasms such as skin cancers,
In 1987 Vloten et al, examined 605 patients treated by
angiosarcoma, malignant fibrous histiocytoma, thyroid
irradiation for benign diseases in the head and neck region.
carcinoma and brain tumors may occur following
They reported 30 skin tumors mainly BCC and mentioned
radiotherapy.2,4 BCC (70-100%)11 and then SCC are the most
that severity of radiodermatitis is associated with a higher
common malignancies in patients receiving radiation.3,4
prevalence of skin cancer and the number of radiation-
Karagas suggests that exposure to therapeutic radiation is induced skin cancers rises with the post-treatment time.2
associated with BCC but not with SCC.1 These neoplasms
The mean age of our cases was 56 years (ranged 40 to 80)
usually occurs after radiation therapy for treatment of tinea
that is higher than Maalej’s cases in which patient’s age at
capitis, hypertrophic tonsillitis4 acne vulgaris,1,4 atopic
diagnosis of malignancy varied from 20 to 83 years with
dermatitis and hyperthyroidism4 and rarely following
an average of 47 years.3
cancer of cervix and nasopharynx,12 neck lymph node
tuberculosis,5 medulloblastoma,13 ankylosing spondylitis,14 Among 98 patients of Maalej’s study, in 61 patients (62%),
hemangioma15,16 and hirsutism.7 A recent report suggested the scalp appeared normal and in 38% radio dermatitis was
an increased risk of nonmelanoma skin cancer among the noted. Basal cell carcinomas were the most frequent tumors
latest Japanese atomic bomb survivors.1 arising on chronic radiodermatitis.3 The radiogenic BCCs
tend to be multiple and they manifest as conventional
Arai et al, defined radiation-associated second cancer using
nodular BCC, superficial BCC and rarely, fibroepithelioma
the following criteria:1 difference of histologic type from
Pinkus and keloidal types.7 Also, linear BCC can develop
the primary cancer2 latency period of at least 2 years after
rarely in the irradiated areas.19
radiation therapy and3 development site in the irradiated
field.4 Majority of our cases were men (75%) similar to Mseddi’s
study.11 It can be due to higher prevalence of tinea in
Regarding to Maalej and colleagues report the average
leading to higher radiation therapy in men. Moreover,
latency period between irradiation and cancer occurrence
occupation and sunlight exposure are also important
was 36 ± 14 years.3 Meseddi’s report suggests that the
risk factors. In Mseddi’s study 40% of BCC occurred on
interval between irradiation and the onset of carcinoma
the occipital area and 65% were in the scalp site. The
varied between 21 and 51 years.11
number of lesions varied from 1 to 5 and the size from
The time between receiving radiation therapy and onset of 2 to 45 mm.11 About 41% of Akhyani’s cases had a positive
history of irradiation. This rate was 90% in patients with 6. Iwamoto I, Endo M, Kakinuma H, Suzuki H. Multiple basal cell
BCC on head, ear helices and neck. Also number of lesions carcinoma developing two years after 60Co irradiation. Eur J
Dermatol 1998;8:180-2.
was higher in cases having received previous radiation.17
7. Misago N, Ogusu Y, Narisawa Y. Keloidal basal cell carcinoma
Scalp was the main area of involvement in our cases (71%) after radiation therapy. Eur J Dermatol 2004;14:182-5.
and 42.5% had multiple lesions varying from 3 mm to 8. Marín-Gutzke M, Sánchez-Olaso A, Berenguer B, González B,
8 × 4 cm. Rodríguez P, De Salamanca JE, et al. Basal cell carcinoma in
childhood after radiation therapy: Case report and review. Ann
Also Shore reported several cancers in irradiated patients.9,18 Plast Surg 2004;53:593-5.
About 40% of his irradiated cases have had multiple 9. Shore RE, Albert RE, Reed M, Harley N, Pasternack BS. Skin
BCCs.18 The average of lesions number was 1.8 per patient cancer incidence among children irradiated for ringworm of the
in our study, 1.5 per patient in Maalej’s study and 1.76 per scalp. Radiat Res 1984;100:192-204.
patients in Mseddi’s study.3,11 In Mseddi’s study, nodular 10. Ron E, Modan B, Preston D, Alfandary E, Stovall M, Boice JD.
BCC and pigmentation was detected in 51% 64% of cases Radiation-induced skin carcinomas of the head and neck. Radiat
clinically but histological study showed a nodular pattern Res 1991;125:318-25.
in 76% and pigmentation in 63% of cases.11 Despite of 11. Mseddi M, Bouassida S, Marrekchi S, Khemakhem M,
Akhyani’s report in which noduloulcerative BCC was the Gargouri N, Turki H, et al. Basal cell carcinoma of the scalp after
radiation therapy for tinea capitis: 33 patients. Cancer Radiother
main clinical from (30.5%),17 the most common forms
2004;8:270-3.
in our study were plaque (74%) and pigmented (51%).
12. Badri T, Zeglaoui F, Kochbati L, Kooli H, El Fekih N, Fazaa B,
The most frequent histological type in both Akhyani’s et al. Multiple basal cell carcinomas following radiation therapy
and Malekzadeh’s studies was solid tumors (53.5% and for nasopharyngeal cancer. Presse Med 2006;35:55-7.
30%).17,20 Microscopic study revealed 72% pigmentation 13. Atahan IL, Yildiz F, Ozyar E, Uzal D, Zorlu F. Basal cell
in our study which was higher than Mseddi’s (62%)11 and carcinomas developing in a case of medulloblastoma associated
Malekzadeh’s (44%) reports.20 with Gorlin’s syndrome. Pediatr Hematol Oncol 1998;15:187-91.
14. Beswick SJ, Garrido MC, Fryer AA, Strange RC, Smith AG.
Conclusion Multiple basal cell carcinomas and malignant melanoma
following radiotherapy for ankylosing spondylitis. Clin Exp
Periodical lifetime examination of irradiated areas in Dermatol 2000;25:381-3.
addition to scalp and ear helices is indicated for patients
15. Eggers G, Flechtenmacher C, Kurzen H, Hassfeld S. Infiltrating
with a history of radiation. Moreover, it is very important to basal cell carcinoma of the neck 34 years after irradiation
create awareness in patients of referring to their physician of an haemangioma in early childhood: A case-report.
for any suspicious lesions. J Craniomaxillofac Surg 2005;33:197-200.
16. Bucher S, Guerra M, Corrias F, Ribuffo D. Basal cell carcinoma
References of the nose requiring amputation arising after irradiation for
1. Karagas MR, McDonald JA, Greenberg ER, Stukel TA, childhood hemangioma. Anticancer Res 2006;26:4767-70.
Weiss JE, Baron JA, et al. Risk of basal cell and squamous cell 17. Akhyani M, Ghaninezhad Ahary H, Safaie Naraghi Z, Rezaie A.
skin cancers after ionizing radiation therapy. J Natl Cancer Inst An epidemiologic clinical and pathological study of basal cell
1996;88:1848-53. epithelioma (BCE) in Razi Dermatological Hospital. J Tehran
2. Ekmekçi P, Bostanci S, Anadolu R, Cengizhan Erdem C, Faculty Med 1977;5:48-52.
Gürgey E. Multiple basal cell carcinomas developed after 18. Shore RE, Moseson M, Xue X, Tse Y, Harley N, Pasternack BS.
radiation therapy for tinea capitis: A case report. Dermatol Surg Skin cancer after X-ray treatment for scalp ringworm. Radiat Res
2001;27:667-9. 2002;157:410-8.
3. Maalej M, Frikha H, Kochbati L, Bouaouina N, Sellami D, 19. Chopra KF, Cohen PR. Linear basal cell carcinomas: Report of
Benna F, et al. Radio-induced malignancies of the scalp about 98 multiple sequential tumors localized to a radiotherapy port and
patients with 150 lesions and literature review. Cancer Radiother review of the literature. Tex Med 1997;93:57-9.
2004;8:81-7. 20. Malek Zadeh F. The comparison of pathological BCC variation
4. Handa Y, Miwa S, Yamada M, Ono H, Suzuki T, Tomita Y. with previous history of radiotherapy versus patients without
Multiple pigmented basal cell carcinomas arising in the normal- history of radiotherapy. Sci J Hamadan Univ Med Sci Health
appearing skin after radiotherapy for carcinoma of the cervix. Services 1978;14:16-8.
Dermatol Surg 2003;29:1233-5.
5. Misago N, Ogusu Y, Narisawa Y. Keloidal basal cell carcinoma Received: August, 2007. Accepted: April, 2008.
after radiation therapy. Eur J Dermatol 2004;14:182-5. Source of Support: Nil, Conflict of Interest: Nil.
Author Query??????
Basal cell carcinoma (BCC) is the most common malignant skin tumor, amongst which the nodular, nodulo ulcerative
and superficial types comprise nearly 80% of all BCCs. Topical Imiquimod, an immune response modifier has been found
to be effective in superficial and nodular types of BCC with histological clearance rates of up to 100%. We report our
experience of treatment a large pigmented BCC on the face with topical Imiquimod 5% cream.
Fig. 1: Hyperpigmented plaque with raised borders Fig. 3: Photomicrograph showing close up of basaloid cells with peripheral
palisading 40×
Fig. 2: Photomicrograph showing nests of basaloid cells in continuity with Fig. 4: Post-treatment photograph showing resolution of pigmentation
the epidermis 20× from the periphery
Mycophenolate Mofetil has been tried in 20 cases of chronic relapsing ENL reaction where long use of systemic steroid
produce complications or are contraindicated. Excellent results have been observed in all the cases to arrest the reaction
followed for a period of six to eight months duration.
Conclusion
Mycophenolate Mofetil may be an important steroid
sparing agent for ENL reactions where systemic cortisone
is contraindicated for producing quick control of symptoms
and remission lasting over 6 to 8 months.
References
1. Karat AB. Complications of leprosy, a window on leprosy. In:
Chatterjee BR, editor. Calcutta: Statesman Commercial Press;
1978. p. 128-32.
2. Thangaraj RH. Reactions in leprosy, A manual of leprosy. South
Asia: The Leprosy Mission; 1983. p. 160-5.
Q1 Fig. 1: Missing???
3. Waters MF. A window on leprosy. In: Chatterjee BR, editor.
Calcutta: Statesman Commercial Press; p. 124-7.
4. Schnuelle P, van der Heide JH, Tegzess A, Verburgh CA, LC,
lymphocytes are more dependent on this path way that van der Woude FJ, et al. Open randomized trial comparing early
alters cell types. MPA is five times more potent inhibitor of withdrawal of either cyclosporine or Q2
Author Query??????
We describe a 76-year-old man presenting with a chronic, non-healing ulcer of six-year duration on his left zygomatic
area. The skin biopsy specimen taken from the lesion, showed increased vascular proliferation, edematous endothelial
cells in the dermal blood vessels and perivascular eosinophilic/lymphocytic infiltration. The routine and specific blood
tests were unremarkable. On the basis of these features, the patient was diagnosed as having angiolymphoid hyperplasia
with eosinophilia (ALHE). We present the case because of its rarity in older people, atypical clinical appearance; and
stress the consideration of ALHE in the differential diagnosis of chronic non-healing superficial ulcers confined to face
and neck.
References
1. Wells GC, Whimster IW. Subcutaneous angiolymphoid
hyperplasia with eosinophilia. Br J Dermatol 1969;81:1-14.
2. Zarrin-Khameh N, Spoden JE, Tran RM. Angiolymphoid
hyperplasia with eosinophilia associated with pregnancy:
A case report and review of the literature. Arch Pathol Lab Med
2005;129:1168-71.
3. Olsen TG, Helwig EB. Angiolymphoid hyperplasia with
eosinophilia: A clinicopathologic study of 116 patients. J Am
Acad Dermatol 1985;12:781-96.
4. Hollo P, Marschalko M, Sikos G, Harsing J, Horvath A.
Angiolymphoid hyperplasia with eosinophilia in pregnancy. J Eur
Acad Dermatol Venereol 2005;19:645-6.
5. Azizzadeh M, Namazi MR, Dastghaib L, Sari-Aslani F.
Fig. 2: Dense chronic inflammation and vascular network in dermis. Angiolymphoid hyperplasia with eosinophilia and nephrotic
(H&E, ×20) syndrome. Int J Dermatol 2005;44:242-4.
6. Moy RL, Luftman DB, Nguyen QH, Amenta JS. Estrogen
receptors and the response to sex hormones in agiolymphoid
hyperplasia with eosinophilia. Arch Dermatol 1992;128:825-8.
7. Aoki M, Kimura Y, Kusunoki T, Tahara S, Kawanah S.
Angiolymphoid hyperplasia with eosinophilia associated with
anomalous dilation of occipital artery: IL-5 and VEGF expression
of lesional mast cells. Arch Dermatol 2002;138:982-4.
8. Calonje E, MacKie RM. Soft-tissue tumors and tumor-like
conditions. In: Breathnach S, Cox N, Griffiths C, editors.
Textbook of dermatology, 7th ed. Oxford: Blackwell Publishing;
2004. p. 20.
9. David J, Leffell L. A fitzgerald basal cell carsinoma Fitzpatrick’s
Dermatology in General Medicine. In: Freedberg IM, Eisen ZA,
Wolff K, Austen KF, Goldsmith LA, Katz SI, et al, editors.
Fitzpatrick. 5th ed. New York: McGraw Hill Company; 1999.
p. 857-64.
10. Meyerle CH., Glusac E.: Angiolymphoid hyperplasia with
Fig. 3: Prominent histiocyte-like endothelial cells and chronic inflammatory eosinophilia. eMedicine. [cited on 2006]. Available from:
cells (eosinophils and neutrophils) around vessels. (H&E, x40) http://www.emedicine.com/derm/topic30.htm. [last accessed on
2006 Dec 14].
localization and association with lymphadenopathy.
Histologically, it contains sclerosis at any stage, but does Received: July, 2007; Accepted Date: October, 2007.
not have epithelioid endothelial cells.8 Source of Support: Nil, Conflict of Interest: Nil.
Metastatic Crohn’s disease is an uncommon extraintestinal manifestation of Crohn’s disease. Its hallmark features include
the presence of cutaneous noncaseating granulomas that are noncontiguous with the gastrointestinal tract or fistula. We
report a rare case of metastatic Crohn’s disease involving the external genitalia in a 14-year-old girl. Diagnosis was based
on skin biopsy. Patient had complete recovery on treatment with oral and topical steroids along with azathioprine.
Key Words: Extraintestinal manifestation of IBD, metastatic Crohn’s disease, noncaseating granuloma
Conclusion
Metastatic Crohn’s disease is a disfiguring illness and often
Fig. 2: Skin biosy showing multinucleate giant cell and epitheloid cells
(H&E, ×400)
refractory to treatment. A thorough evaluation including
biopsies is required to make a definite diagnosis. Ours is
a case of metastatic Crohn’s disease involving external
genitalia and it responded to oral and topical steroids along
with azathioprine.
References
1. Goyal A, Mansel RE, Young HL, Douglas-Jones A. Metastatic
cutaneous Crohn’s disease of the nipple: Report of a case. Dis
Colon Rectum 2006;49:132-4.
2. Burgdorf W. Cutaneous manifestations of Crohn’s disease. J Am
Acad Dermatol 1981;5:689-95.
3. Parks AG, Morson BC, Pegum JS. Crohn’s disease with
cutaneous involvement. Proc R Soc Med 1965;58:241-2.
4. Mountain JC. Cutaneous ulceration in Crohn’s disease. Gut
1970;11:18-26.
5. Guest GD, Fink RL. Metastatic Crohn’s disease: Case report
Fig. 3: Skin biopsy showing noncaseating granuloma (H&E, ×100) of an unusual variant and review of the literature. Dis Colon
Rectum 2000;43:1764-6.
6. Sangueza OP, Davis LS, Gourdin FW. Metastatic Crohn’s
Metastatic Crohn’s disease can have a varied presentation. disease. South Med J 1997;90:897-900.
It can present as cutaneous ulcerations, plaques, papules 7. Hackzell-Bradley M, Hedblad MA, Stephansson EA. Metastatic
and nodules.6 Lesions usually have a predilection for skin Crohn’s disease: Report of 3 cases with special reference to
folds, infra-mammary area and the limbs. Biopsies from histopathologic findings. Arch Dermatol 1996;132:928-32.
8. Burgdorf W, Orkin M. Granulomatous perivasculitis in Crohn’s of severe refractory metastatic Crohn’s disease to infliximab.
disease. Arch Dermatol 1981;117:674-5. J Gastroenterol Hepatol 2001;16:940-2.
9. Perret CM, Bahmer FA. Extensive necrobiosis in metastatic 14. Escher JC, Stoof TJ, van Deventer SJ, van Furth AM. Successful
Crohn’s disease. Dermatologica 1987;175:208-12. treatment of metastatic Crohn disease with infliximab. J Pediatr
10. Brady CE 3rd, Cooley BJ, Davis JC. Healing of severe perineal Gastroenterol Nutr 2002;34:420-3.
and cutaneous Crohn’s disease with hyperbaric oxygen. 15. Rispo A, Lembo G, Insabato L, Cozzolino A, Pesce G,
Gastroenterology 1989;97:756-60. Castiglione F. Successful treatment of therapy-resistant metastatic
11. Williams N, Scott NA, Watson JS, Irving MH. Surgical Crohn’s disease with infliximab. Br J Dermatol 2004;150:1045-6.
management of perineal and metastatic cutaneous Crohn’s 16. Graham DB, Jager DL, Borum ML. Metastatic Crohn’s disease
disease. Br J Surg 1993;80:1596-8. of the face. Dig Dis Sci 2006;51:2062-3.
12. van Dullemen HM, de Jong E, Slors F, Tytgat GN, van 17. Konrad A, Seibold F. Response of cutaneous Crohn’s disease to
Deventer SJ. Treatment of therapy-resistant perineal metastatic infliximab and methotrexate. Dig Liver Dis 2003;35:351-6.
Crohn’s disease after proctectomy using anti-tumor necrosis
factor chimeric monoclonal antibody, cA2: Report of two cases.
Dis Colon Rectum 1998;41:98-102. Received: October, 2007. Accepted: December, 2007.
13. Miller AM, Elliott PR, Fink R, Connell W. Rapid response Source of Support: Nil, Conflict of Interest: Nil.
Tuberculosis, one of the oldest diseases known to affect humans is caused by the bacteria mycobacterium tuberculosis. The
disease usually affects the lungs, although, in up to one third of cases, other organs are involved. Metastatic tuberculosis
abscess is a rare form of skin tuberculosis. It is characterized by nodule and abscess formation throughout the body
after hematogenous spread of mycobacterium tuberculosis from a primary focus during a period of impaired immunity.
Tuberculosis osteomyelitis is also a rare form of extrapulmonary tuberculosis in pediatric age group. Skeletal tuberculosis
pathogenesis is related to reactivation of hematogenous foci or spread from adjacent paravertebral lymph nodes. Weight-
bearing joints are affected most commonly. Bilateral hand and foot bone involvement is rarely reported. We present a
five-year-old girl with two very rare presentations of the disease such as osteomyelitis and metastatic skin abscess.
Skin tuberculosis, a form of the extrapulmonary Dermatologic examination revealed widespread dusky
tuberculosis, occurs in 1% of all tuberculosis cases. red nodules. The lesions were fluctuating and non-tender
Metastatic tuberculosis abscess is a rare form of cutaneous without redness or local warmth on the overlying skin.
tuberculosis resulting in single or multiple cutaneous and The left fourth finger, right elbow, left ankle and bilateral
subcutaneous lesions on trunk, extremities, or head.3,8,9 dorsal foot regions were swollen and painful. Regional
lymphadenopathy was not detected. The other physical
Skeletal involvement occurs in approximately 1-3% of
findings were normal.
patients with tuberculosis. The most frequently involved
site is vertebrae followed by pelvis and knee joints. Few Her weight and height were 15 kg and 100 cm respectively
cases are reported in the literature that showed involvement (both below the third percentile). There was history of
of tarsal and carpal bones.3,8,10-12 progressive weight loss. She had no previous history of
skin injury or immunosuppressive therapy. The family
history revealed a past occurrence of treated pulmonary
From Departments of Pediatry, 1Dermatology, 2Plastic and
Reconstructive Surgery and 3Pathology, Cerrahpasa Medical
tuberculosis in one of the house members. She did not
School, Istanbul, Turkey. Address correspondence to: Dr. have BCG vaccine. A quantative reading of PPD (purified
Selma Sönmez Ergün, Bahçeşehir Emlak Bankası Konutları, protein derivate) skin test was positive with 22 × 29 mm of
B 18 D3 C020403 34 900, Büyükçekmece/Istanbul/Turkey. induration at the 72nd hour. Erythrocyte sedimentation rate
E-mail: selmasonmezergun@yahoo.com was 102 mm/hr. Blood count showed signs of pancytopenia
(HGB: 9.2 gr/dl, WBC: 3260/mm³, PLT: 100 000/mm³). humerus, left distal fibula and tibia and bilateral calcaneus
CRP was 4.05 mg/dl (usual value 0-1 mg/dl). Serology for [Figs. 4-6]. The findings on the bone scan were suggestive
antibodies to HIV was negative. of osteomyelitis.
The chest roentgenogram was normal. The roentgenograms Skin biopsy specimen was taken from the margin of the
of the extremities showed a periosteal reaction in the left active skin lesion. Large areas of necrosis, surrounded
fourth metacarpal bone, right proximal ulna, right proximal by palisading epithelioid histiocytes, Langhans-type
multinucleated giant cells and lymphocytes were detected
in this skin biopsy [Fig. 7]. Using Ehrlich-Ziehl-Neelsen
stain, acid-fast bacilli were not seen.
On the basis of clinical-pathological findings, positive
tuberculine skin test, and history of close contact with
tuberculosis patient in her family, a final diagnosis of
extrapulmonary tuberculosis was made.
Abscesses were drained and treatment with isoniazid (INH)
15 mg/kg/day, rifampicin (RMP) 15 mg/kg/day, ethambutol
(EMB) 15 mg/kg/day and pyrasinamid (PZA) 20 mg/kg/
day were started. The lesions regressed within two months.
After two months EMB and PZA were discontinued. INH
and RMP were given for 16 more months.
children, tuberculous dactylitis can produce spina ventosa presentations of tuberculosis is essential for early diagnosis
like our patient, a pattern of chronic osteitis characterized and proper therapy. Therefore physicians must have a high
by central defect, soft tissue swelling, and exuberant index of suspicion with regard to tuberculosis.
periosteal reaction.
The most common radiologic finding is that of osteoporosis, References
which may be intense cancellous bone involvement 1. Braun-Falco O, Plewing G, Wolff HH, Winkelman R.
and may present as a cystic lesion with or without Dermatology. 4th ed. Berlin: Springer-Verlag; 2000.
sequestrum.7,10,12,15 2. Munoz FM, Starke JR. Mycobacterial infections. In: Behrman
RE, Kliegman RM, Jenson HB, editors. Nelson’s texbook of
Roentgenograms, CT or MRI reveal the characteristic lesion pediatrics.17th ed. Philadelphia: WB Saunders Company; 2004.
and suggest its etiology, although the differential diagnosis p. 958-78.
includes other infections and tumors. Aspiration of the 3. Mert A, Tabak F, Dumankar A, Öztürk R, Aktuğlu Y. Derialtı
abscess or bone biopsy confirms the tuberculous etiology, abseleri gelisen dissemine tüberküloz olgusu. Turk J Infect
as histologic findings are highly typical and cultures are 1997;11:157-8.
usually positive; however skeletal and skin tuberculoses are 4. Kivanç-Altunay I, Baysal Z, Ekmekçi TR, Köslü A. Incidence of
paucibacillary lesions and it is difficult to demonstrate or cutaneous tuberculosis in patients with organ tuberculosis. Int J
Dermatol 2003;42:197-200.
culture acid-fast mycobacteria from these lesions like our
patient.22 5. Maltezou HC, Spyridis P, Kafetzis DA. Extra-pulmonary
tuberculosis in children. Arch Dis Child 2000;83:342-6.
The incidence of active pulmonary tuberculosis associated 6. Kumar B, Rai R, Kaur I, Sahoo B, Muralidhar S, Radotra BD.
with skin or skeletal tuberculosis is reported as 50-65% Childhood cutaneus tuberculosis: A study over 25 years from
in the literature. The concomitant presentations of skin northern India. Int J Dermatol 2001;40:26-32.
and skeletal tuberculosis is a very rare condition. Kıvanc- 7. Starke RS. Tuberculosis. In: Gerson AA, Hotez PJ, Katz SL,
Altunay et al, reported that 61% of skin tuberculosis cases editors. Krugman’s infectious diseases of children. 11th ed.
had pulmonary involvement whereas no skeletal tuberculosis Philadelphia: Mosby Co; 2004. p. 731-65.
was encountered. Kumar et al, reported that four patients 8. Tappeiner G, Wolff K. Tuberculosis and other mycobacterial
out of 75 with skin tuberculosis had skeletal tuberculosis infections. In: Fitzpatrick TB, Freedberg IM, Eisen AZ, Wolff
K, editors. Dermatology in general medicine. 4th ed. New York:
and only one had tuberculous dactylitis. Although active McGraw-Hill Company; 1999. p. 2274-92.
pulmonary tuberculosis was not present in our case, two
9. Darmstadt GL, Sidbury R. The skin. In: Behrman E, Kliegman
rare presentations of tuberculosis, skin tuberculosis and RM, Jenson HB, editors. Nelson Texbook of Pediatrics. 17th ed.
skeletal tuberculosis were concomitantly observed.4,6 Philadelphia: WB Saunders Company; 2004. p. 2153-250.
The histological findings of metastatic tuberculous abscess 10. Mittal R, Gupta V, Rastogi S. Tuberculosis of the foot. J Bone
involve massive necrosis and abscess formation with or Joint Surg Br 1999;81:997-1000.
without acid fast bacilli. No bacilli were shown among 11. Ray M, Kataria S, Singhi P. Unusual presentation of disseminated
typical necrotising granulomas in our case. The culture tuberculosis. Indian Pediatr 2002;39:88-91.
and PCR results were also negative for tuberculosis in our 12. Engin G, Acunaş B, Acunaş G, Tunaci M. Imaging of
extrapulmonary tuberculosis. Radiographics 2000;20:471-88.
case. In endemic regions, the clinical features, radiological
appearance and elevated ESR are sufficient to diagnose 13. Baykal C, Deri Tüberkülozu: 64 olgunun retrospektif
değerlendirilmesi. Türkderm 2001;35:103-7.
tuberculosis and begin treatment.10,15,23,24 Considering
positive family history with a patient having cavernous 14. Kumar B, Muralidhar S. Cutaneous tuberculosis: A twenty-year
prospective study. Int J Tuberc Lung Dis 1999;3:494-500.
tuberculosis in the same home environment, strong positive
15. Vanmarsenille JM, de Berg B, Houssiau FA, de Selys J. Unusually
PPD results, X-ray findings and necrotising granulomas in
prolonged course of tuberculous dactylitis with osteitis. Joint
histology, metastatic tuberculous abscesses and tuberculous Bone Spine 2003;70:535-7.
osteomyelitis were diagnosed in our case. Immune
16. McNally L, Al-Ansari H, Novelli V. Mycobacterial infections
suppression due to malnutrition was the explanation for the of the skin. In: Haiper J, Orange A, Prose N, editors. Text book
clinical situation. of pediatric dermatology. Oxford: Blackwell Science; 2000.
p. 401-10.
In conclusion, tuberculosis incidence has increased in
industrialized countries, which is attributed to several factors 17. Combalia A, Sastre S, Esteban P. Tuberculous osteomyelitis of
the knee. Arch Orthop Trauma Surg 2004;124:708-10.
such as immigration from countries with a high prevalence
18. Martinez SF, Canale ST. Tuberculosis and other unusual infections.
of tuberculosis, infection with HIV, emergence of multi-drug
In: Canale ST editor. Campbell’s operative orthopaedics. 10th ed.
resistant tuberculosis, and social problems such as poverty, Philadelphia: Mosby Company; 2003. p. 713-27.
homelessness and drug abuse.22 Rare extrapulmonary 19. Lin YS, Huang YC, Chang LY, Lin TY, Wong KS. Clinical
tuberculosis cases are seen more frequently as a result of this. characteristics of tuberculosis in children. J Pediatr Orthop
The possibility of tuberculosis must always be kept in mind 1999;19:151-5.
in subcutaneous abscess and nodule cases non-responsive to 20. Wang MN, Chen WM, Lee KS, Chin LS, Lo WH. Tuberculous
non-spesific therapy, and drainage. Awareness of the unusual osteomyelitis in young children. J Pediatr Orthop 1999;19:151-5.
21. Çaksen H, Arslan S, Oner AF, Kuru M, Karakök M, Odabaş tuberculosis in children. Pediatr Dermatol 1999;16:264-9.
D. Multiple metastatic tuberculous abscesses in a severly 24. Uzel M, Garipardic M, Cetinus E, Bilgic E, Karaoguz A,
malnourished infant. Pediatr Dermatol 2002;19:90-1. Boran C, et al. Tuberculosis of knee in a child. J Trop Pediatr
22. Raviglione MC, O’Brien RJ. Tuberculosis. In: Braunwald E, 2004;50:182-4.
Hauser SL, Fauci AS, Longo DL, Kasper DL, Jameson JL,
editors. Harrison’s Principles of Internal Medicine. 15th ed.
Philadelphia: McGraw-Hill; 2001. p. 1024-35. Received: May 2007. Accepted: July 2007.
23. Ramesh V, Misra RS, Beena KR, Mukherjee. A study of cutaneous Source of Support: Nil, Conflict of Interest: Nil.
A 55-year-old female patient presented to our outpatient department with complaints of persistent erythema, oozing and
crusting restricted to the left breast over the last 6 months. The patient underwent investigations to rule out the possibility
of mammary Paget’s disease, all of which were negative. A possibility of contact dermatitis to topical medication was
considered and confirmed by patch testing.
Key Words: Allergic contact dermatitis, patch testing, topical steroids, Paget’s disease
initially patch tested the patient with the commercial budesonide and need to be tested in suspected cases, either
products she was using, including brands of fluticasone as a patch test in an ethanol base or as an intradermal test
and betamethasone. Interestingly all the products showed in saline.7-9 Nonhalogenated topical steroids are considered
a strong positive reaction after 48h. We then patch-tested to be more frequent sensitizers than halogenated molecules.7
the patient with multiple antigens including topical This case was published to highlight the importance of
antibiotics, preservatives and bases. The patch tests thinking of an allergic contact dermatitis to topical agents Q1
showed a strongly positive reaction to propylene glycol, in lesions stimulating a chronic eczematous dermatitis.
parabens and chlorocresol and a moderate reaction to
both neomycin and gentamycin. We also carried out an References
intradermal test with hydrocortisone and betamethasone 1. García M, del Pozo MD, Díez J, Muñoz D, de Corrès LF.
solutions in saline, which gave a negative result. Based Allergic contact dermatitis from a beeswax nipple-protective.
on the patch test findings we asked the patient to stop Contact Dermatitis 1995;33:440-1.
all topical preparations and started the patient on saline 2. McGeorge BC, Steele MC. Allergic contact dermatitis of the
compresses and plain Vaseline along with a short course nipple from Roman chamomile ointment. Contact Dermatitis
1991;24:139-40.
of systemic steroids. The lesions improved and by the
end of two weeks had subsided almost entirely with only 3. Lamb SR, Ardley HC, Wilkinson SM. Contact allergy to
propylene glycol in brassiere padding inserts. Contact Dermatitis
a mild residual hyperpigmentation [Fig. 2]. 2003;48:224-5.
Discussion 4. Novick NL. Unilateral, circumscribed, chronic dermatitis of
the papillary-areolar complex: Case report and review of the
Contact dermatitis of the breast area can be due to a number literature. Mt Sinai J Med 2001;68:321-5.
of factors including topical applications of various types.1-3 5. Krupa Shankar DS, Shrestha S. Relevance of patch testing in
In our case the unilateral presentation and the apparent lack patients with nummular dermatitis. Indian J Dermatol Venereol
of response to topical steroids made us think on the lines of Leprol 2005;71:406-8.
mammary Paget’s. Most eczematous lesions of the breast 6. Dogra A, Minocha YC, Sood VK, Dewan SP. Contact dermatitis
due to cosmetics and their ingredients. Indian J Dermatol
tend to be bilateral like seborrheic and atopic dermatitis
Venereol Leprol 1994;60:72-5.
though there have been reports of chronic unilateral
7. English JS. Corticosteroid-induced contact dermatitis: A pragmatic
dermatitis of the nipple areolar complex.4 The diagnosis of
approach. Clin Exp Dermatol 2000;25:261-4.
mammary Paget’s was excluded in our case based on the
8. Seukeran DC, Wilkinson SM, Beck MH. Patch testing to
cytology, mammography and histopathology findings. The detect corticosteroid allergy: Is it adequate? Contact Dermatitis
history of apparent worsening of the lesions after an initial 1997;36:127-30.
improvement made us think of a possibility of an allergic 9. Isaksson M, Andersen KE, Brandão FM, Bruynzeel DP, Bruze
contact dermatitis to the topical applications used by the M, Camarasa JG, et al. Patch testing with corticosteroid mixes in
patient. Ointment bases and vehicles are known to cause Europe: A multicentre study of the EECDRG. Contact Dermatitis
various kinds of contact allergies, prominent among them 2000;42:27-35.
being those due to chlorocresols, parabens and propylene
glycol.5,6 Topical corticosteroids per se can also cause an Received: August, 2007. Accepted: October, 2007.
allergic contact dermatitis, especially tixocortol pivalate and Source of Support: Nil, Conflict of Interest: Nil.
Author Query??????
Q1 Matter missing?
Our literature search on FDE due to fluconazole revealed in tapering doses which resulted in complete healing of the
that all cases reported so far had limited cutaneous or erosions within a month.
mucosal lesions. In contrast, our patient had extensive
Localized bullous pemphigoid (LBP) is a rare autoimmune
generalized lesions with many bullous lesions, a unique
subepidermal blistering disease of the elderly characterized
presentation of fixed drug eruption due to fluconazole
by chronic intermittent eruptions affecting only a restricted
which has not been described in the literature so far. With
area of the body. Though it accounts for 16% to 29%
widespread use of any drug, new adverse effects come to
of all cases of bullous pemphigoid, the true incidence
light and hitherto unknown adverse effect may become
may be greater as it is often misdiagnosed and is highly
more common occurrence. We recommend that fluconazole
responsive to topical steroids. LBP has got similar clinical,
be included in the list of drugs causing multifocal bullous
histopathological and immunofluorescence features to
FDE so that similar cases may be diagnosed more often.
generalized bullous pemphigoid.1 Three types have been
References identified which include: 1.) mucous membrane pemphigoid
or cicatricial pemphigoid 2.) localized scarring pemphigoid
1. Konnikov N, Raynham H. Oral antifungal agents. In:
or Brunsting Perry pemphigoid affecting the head and
Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA,
Katz SI, editors. Fitzpatrick’s Dermatology in General Medicine, neck 3.) localized non scarring pemphigoid usually seen
6th ed. New York: McGraw-Hill; 2003. p. 2443-8. over the pretibial region, vulva, breast and the soles. The
2. Amichai B, Grunwald MH. Adverse drug reactions of the new diagnosis of this last entity tends to be delayed because
oral antifungal agents-terbinafine, fluconazole and itraconazole. it can mimic other localized vesicobullous diseases and
Int J Dermatol 1998;37:410-5. dyshidrotic eczema.2 While the pathogenesis of generalized
3. Mahendra A, Gupta S, Gupta S, Sood S, Kumar P. Oral fixed bullous pemphigoid is well elucidated, it is unknown why
drug eruption due to fluconazole. Indian J Dermatol Venereol patients with LBP have limited disease. The pathogenesis
Leprol 2006;72:391. most likely could be similar to that of generalized bullous
4. Ghislain PD, Ghislain E. Fixed drug eruption due to fluconazole: pemphigoid because patients in both the groups recognize
A third case. J Am Acad Dermatol 2002;46:467.
5. Shukla P, Prabhudesai R. Fixed drug eruption to fluconazole.
Indian J Dermatol 2005;50:236-7.
6. Sehgal VN, Srivastava G. Fixed drug eruption (FDE): changing
scenario of incriminating drugs. Int J Dermatol 2006;45:897-908.
the same BP antigens.3 LBP has been documented following case of mango dermatitis. A 42-year-old female presented
radiotherapy,4 PUVA therapy, trauma,5 sunexposure,6 to the physician at a health unit with a one-day history of
split skin grafting for burns,7 around peristomal lesions8 patchy pruritic erythema of the face, and extremities with
and several authors have thus postulated that these local periorbital edema. Periorbital edema was present without
factors might play a role in the induction of lesions in intraoral abnormalities or laryngeal changes. The patient
immunologically susceptible individuals. In a study on the denied any history of contact urticaria or new household
distribution of bullous pemphigoid antigens in normal human or personal hygiene contactants. She gave the history of
skin the greatest expression was seen in the skin obtained this illness as a common episode after ingestion of peeled
from the flexor aspect of arms, legs and thighs9 which mangoes. In the Health Unit, the patient was administered
probably explains the predominant flexural localization of a single 50 mg dose of oral prednisone. She continued
lesions in our case. Whether the ACE inhibitors contributed treatment with a five-day course of prednisone, 50 mg
in triggering the bullous eruption here is not clear as the daily, with chlorphemiramine, 8 mg daily. Symptomatic
patient had been taking the above medications for almost a improvement was seen over seven days. Patch testing
year. Nevertheless this case emphasizes the need to follow- using mango skin and mango flesh gave positive reactions.
up such patients regularly as they are at risk of developing a Complete avoidance of mango is suggested to this patient.
generalized eruption later in life. Adding to the previous report of Weinstein et al,1 this is the
second reported positive patch test to the mango flesh.
References
1. Tran JT, Mutasim DF. Localized bullous pemphigoid: References
A commonly delayed diagnosis. Int J Dermatol 2005;44:942-5. 1. Weinstein S, Bassiri-Tehrani S, Cohen DE. Allergic contact
2. Scola F, Telang GH, Swartz C. Dyshidrosiform pemphigoid. dermatitis to mango flesh. Int J Dermatol 2004;43:195-6.
J Am Acad Dermatol 1995;32:516-7. 2. Paschke A, Kinder H, Zunker K, Wigotzki M, Steinhart H,
3. Soh H, Hosokawa H, Miyauchi H, Izumi H, Asada Y. Localized Wessbecher R, Vieluf I. Characterization of cross-reacting
bullous pemphigoid shares the same target antigen as bullous allergens in mango fruit. Allergy 2001;56:237-42.
pemphigoid. Br J Dermatol 1991;125:73-5.
4. Leconte-Boulard C, Dompmartin A, Verneuil L, Thomine E,
Joly P, Rogerie MJ, et al. Localized bullous pemphigoid IN HERPETIFORM PEMPHIGUS
following radiotherapy. Ann Dermatol Venereol 2000;127:70-2.
5. Vermeulen C, Janier M, Panse I, Daniel F. Localized bullous
CLINICALLY RESEMBLING
pemphigoid induced by thermal burn. Ann Dermatol Venereol BULLOUS PEMPHIGOID
2000;127:720-2.
6. Lee CW, Ro YS. Sun induced localized bullous pemphigoid. Vandana Mehta, C Balachandran,
Br J Dermatol 1992;126:91-2. Sudhir Nayak
7. Hafejee A, Coulson IH. Localized bullous pemphigoid 20 years
after split skin grafting. Clin Exp Dermatol 2005;30:187-8. Indian J Dermatol 2008:53(3):00-00******
8. Torchia D, Caproni M, Ketabchi S, Antiga E, Fabbri P. Bullous From the Department of Skin and STD, Kasturba Medical College,
pemphigoid initially localized around a urostomy. Int J Dermatol Manipal, Karnataka, India. E-mail: vandanamht@yahoo.com
2006;45:1387-9.
9. Hamm G, Wozniak KD. Bullous pemphigoid antigen
Herpetiform pemphigus was first introduced by Jablonska in
concentration in normal skin: relation to body area and age. Arch 1975, as a variant of pemphigus that combines the clinical
Dermatol Res 1988;280:416-9. features of dermatitis herpetiformis with the immunological
features of pemphigus.1 Because of its rare and atypical
clinical presentation, patients are often initially diagnosed as
Dermatitis herpetiformis, Linear IgA bullous disease, Bullous
MANGO DERMATITIS pemphigoid or Pemphigus foliaceus. We report a case of
herpetiform pemphigus in an elderly lady which was initially
Viroj Wiwanitkit
misdiagnosed as bullous pemphigoid, however histology and
Indian J Dermatol 2008:53(3):00-00****** immunofluorescence helped in clinching the diagnosis.
From Health Unit, Chulalongkorn University; Department of A 75-year-old woman presented with a one year history of
Laboratory Medicine, Faculty of Medicine, Chulalongkorn an intensely pruritic eruption which began on her extremities
University, Bangkok, Thailand - 10330. E-mail: wviroj@yahoo.com
and later expanded to involve the trunk with only partial
Mango, Mangifera indica, is a common tropical fruit. It is response to topical corticosteroids and antihistamines. She
a favorable sweet for millions of people living in several was otherwise healthy with no accompanying constitutional
tropical countries.1 Mango Dermatitis’ is the common term symptoms and not on any other medications. Cutaneous
given to allergic contact dermatitis to the sap or skin of the examination revealed a symmetric polymorphous eruption
fruit of mango. This type of allergic reaction is rare but has of old and new lesions, comprising of erythematous
become increasingly important.2 Here, the author reported a urticarial papules and plaques studded with clear and
cloudy vesicles [Fig. 1], ulcerated and crusted lesions of IgG to the upper epidermis as was seen in our case. Why
arranged in herpetiform groups. Oral and genital mucosa the auto-antibodies in PH and pemphigus vulgaris give rise
were normal. Clinically a differential diagnosis of bullous to different clinical presentations could be explained by
pemphogoid was entertained, however a Tzanck smear from their preferential binding to different epitopes on the same
a clear vesicle showed abundant neutrophils, with only antigen molecule.4
few eosinophils. Biopsy for histopathology showed mild
In our case, the presence of severe pruritus in an elderly
epidermal hyperplasia with a subcorneal blister containing
female with blisters and absence of mucosal involvement
neutrophils and few acantholytic cells. Predominant areas
made us think of bullous pemphigoid, however, to our
of neutrophilic spongiosis with a superficial perivascular
surprise the histology and immunofluorescence turned out
infiltrate of eosinophils and neutrophils were seen in the
to be PH. Patient was started on oral steroids along with
papillary dermis. Direct and indirect immunofluorescence
dapsone and is currently under follow-up.
demonstrated strong intercellular deposits of IgG and
C3 in the upper epidermis. Based on the histology and References
immunofluorescence findings, the diagnosis was revised
1. Jablonska S, Chorzelski TP, Beuther EH, Chorzelska J.
to herpetiform pemphigus and patient was started on oral
Herpetiform pemphigus: A variable pattern of pemphigus. Int J
steroids. Dermatol 1975;14:353-9.
Pemphigus herpetiformis (PH) is recognized as a distinct 2. Robinson ND, Hashimoto T, Amagai M, Chan LS. The new
subset of pemphigus by its pruritus, rarity of mucosal pemphigus variants. J Am Acad Dermatol 1999;40:649-71.
involvement, invariable presence of eosinophils on histology 3. Huhn KM, Tron VA, Nguyen N, Trotter MJ. Neutrophilic
and its tendency to respond to sulfones. Various terms that spongiosis in pemphigus herpetiformis. J Cutan Pathol
1996;23:264-9.
have been used to describe it are acantholytic herpetiform
4. Ishii K, Amagai M, Komai A, Ebihara T, Chlorzelski TP,
dermatitis, pemphigus controlled by sulfapyridine, mixed
Jablonska S, et al. Desmoglein 1 and desmoglein 3 are the
bullous disease and eosinophilic spongiosis in pemphigus. target autoantigens in herpetiform pemphigus. Arch Dermatol
Clinically patients present with severe intractable pruritus 1999;135:943-7.
and erythematous urticarial papules and plaques with
occasional vesicles in a herpetiform arrangement. Even
though the clinical picture is reminiscent of dermatitis
herpetiformis, the histological findings are variable and IDIOPATHIC VULVAR CALCINOSIS:
include eosinophilic spongiosis, subcorneal pustules with
minimal or no apparent acantholyis.2 Though eosinophilic THE COUNTERPART OF
spongoisis is classically seen in pemphigus herpetiformis, IDIOPATHIC SCROTAL CALCINOSIS
neutrophilic spongiosis may also be encountered and
should be recognized as an important diagnostic clue3 as Vandana Mehta, C Balachandran
was seen in our case. Definitive diagnosis is established by
Indian J Dermatol 2008:53(3):00-00******
immunopathology which shows in vivo bound IgG deposits
on the keratinocyte cell surface primarily in the upper From the Departments of Skin and STD, Kasturba Medical College,
epidermis. The auto-antibodies in most patients of PH target Manipal, Karnataka, India. E-mail: Vandanamht@yahoo.com
desmoglein 1 and because desmoglein 1 is predominantly Calcinosis cutis is characterized by the deposition of
located in the upper epidermis, there is preferential binding hydroxyapatite crystals of calcium phosphate in the skin. It
is commonly encountered as a consequence of connective
tissue disease or metabolic abnormalities but sometimes
could be idiopathic. We report a case of idiopathic
calcinosis cutis of the vulva in a healthy woman.
A 35-year-old woman presented with multiple asymptomatic
yellowish nodules on the external genitalia of one year
duration. A few of the nodules broke down spontaneously
discharging a chalky white material. She was otherwise
healthy and had no systemic complaints. There was
neither a history of trauma nor any inflammatory process
in the vulvar skin prior to the development of lesions.
The hematologic and biochemistry panel such as liver and
renal function, serum calcium, phosphorous, electrolytes,
uric acid and parathyroid hormone levels were normal. An
excision biopsy of the nodule showed features suggestive
Q2 Fig. 1: Caption missing?????? of calcinosis cutis.
References
Cutaneous calcification may be divided into four
major categories: dystrophic, metastatic, iatrogenic and 1. Angamuthu N, Pais AV, Chandrakala SR. Calcinosis cutis:
idiopathic.1 Though dystrophic calcinosis is fairly common, A report of four cases. Trop Doct 2003;33:50-2.
idiopathic calcification is rare, and usually no underlying 2. Walsh JH, Fairley JA. Calcifying disorders of the skin. J Am
Acad Dermatol 1995;33:693-706.
cutaneous cause can be identified. It commonly presents as
painless, firm papules and nodules that appear in childhood 3. Ozçelik B, Serin IS, Başbuğ M, Oztürk F. Idiopathic calcinosis
cutis of the vulva in an elderly woman: A case report. J Reprod
and adolescence and gradually increase in number and Med 2002;47:597-9.
size. Lesions may be solitary or pedunculated and are
4. Aksoy HM, Ozdemir R, Karaaslan O, Tiftikcioglu YO, Oruç M,
initially skin-colored, but as they grow larger they become Kocer U. Incidental idiopathic calcinosis cutis in a rhytidectomy
yellowish and lobulated breaking down spontaneously patient. Dermatol Surg 2004;30:1145-7.
or when compressed to produce a chalky white material. 5. Sánchez-Merino JM, Bouso-Montero M, Fernández-Flores A,
Microscopic examination typically shows large granular García-Alonso J. Idiopathic calcinosis cutis of the penis. J Am
deposits of deeply basophilic material which stains black Acad Dermatol 2004;51:S118-9.
with Von Kossa stain for calcium.2 6. Oh CK, Kwon KS, Cho SH. Idiopathic calcinosis of the areola
of the nipple. J Dermatol 2000;121-2.
The pathogenesis of idiopathic vulvar calcinosis is highly
7. Yahya H, Rafindadi AH. Idiopathic scrotal calcinosis: A report
disputed. The principle debate concerning the cause of four cases and review of the literature. Int J Dermatol
is whether calcium is deposited at the site of inflamed 2005;44:206-9.
epidermal cysts or whether the calcific nodules are truly 8. Cornelius CE, Tenenhouse A, Weber JC. Calcinosis cutis.
idiopathic. Although several authors have suggested that Metabolic, sweat, histochemical, X- Ray diffraction and electron
vulvar calcinosis results from dystrophic calcification of microscopic study. Arch Dermatol 1968;98:218.
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