Hubungan stroke dan SGOT

1. In this study the prognostic value of various routine clinical and biochemical parameters has been
evaluated. The only clinical parameter evaluated in our study was the GCS score to quantify the
level of consciousness. Like several studies in the past,[5],[6] our study also suggested that a low
GCS score was predictive of poor outcome.
Possibly, changes in hematological parameters at the onset of stroke play an important role in altering
the cerebral blood flow. Czlonkowska et aldemonstrated the importance of hematocrit as a predictive
factor of 30-day fatality.[4] In our study, hemoglobin, platelet counts and platelet aggregation analysis
did not show any significant difference amongst expired patients and survivors. In another study,
platelet count obtained within 48 hours was significantly lower in patients of ischemic stroke than the
control group. The platelet count was also significantly lower in patients who later expired than who
survived.[8] Leukocytosis also influences the prognosis. Several mechanisms by which leukocytes may be
implicated in parenchymal brain injury include vessel plugging, release of hydrolytic enzymes, oxygen
free radicals or initiation of thrombosis.[9] Leukocytosis might also be a manifestation of some common
causes of fever (e.g., pulmonary or urinary tract infections, sepsis, or pulmonary embolism from deep
vein thrombosis). Czlonkowska et al[4] have also demonstrated leukocytes as an independent predictor
of 30-day case fatality in stroke patients. In our study, total leukocyte counts were significantly higher in
expired patients, both on univariate and multivariate analysis. A high ESR value has been associated with
large ischemic lesions and more severe deficits.[3] An elevated ESR value may indicate a greater increase
in the concentration of fibrinogen; a more pronounced reduction in the cerebral blood flow, a larger
lesion and a poor outcome.[10] Like other studies in the past, [4] in our study, a high ESR was associated
with a poor prognosis.
Elevated blood glucose has been implicated as a poor prognostic factor for cerebral ischemia and
hemorrhage.[11] Animal studies have demonstrated the aggravation of ischemic injury by
hyperglycemia.[12] Diabetes predisposes to occlusive vascular disease but not to intracerebral
hemorrhage.[13] However, in hemorrhagic strokes it predisposes to larger size of hematoma and
increased mortality at 30 days.[14],[15] In diabetics, ischemic strokes are often associated with large
infarct size and poor outcome due to decreased autoregulation and changes in blood coagulability.[13]
Even in non-diabetic patients with hyperglycemia, the size of the lesion and neurological deficit were
worse.[16] Many studies deny the prognostic significance of elevated blood glucose.[17],[18] Our study
also did not observe prognostic significance of blood sugar. In our series, on univariate analysis, blood
urea and creatinine levels were found significantly higher in patients who later expired. High creatinine
significantly affected poor outcome on multivariate analysis. No independent effect of urea was noted
on mortality. Woo et al have demonstrated that higher plasma urea and creatinine levels are associated
with more severe stroke and a low GCS score, however, these parameters have no independent effect
on mortality. [18] We could not observe any prognostic value of electrolyte estimations. Among liver
function tests serum transaminases and globulin levels were found to be significantly associated with
poor outcome on univariate analysis. After multivariate analysis, only SGPT correlated with poor
outcome. Low albumin levels were related to increased incidence of hemorrhagic stroke.[19] Low
albumin, globulin ratio was found to predispose to recurrent strokes.[20]
Serum lipids have been linked to a higher risk of ischemic stroke. [21] An inverse association exists for
total cholesterol and cerebral hemorrhage. A greater mortality is observed from hemorrhagic stroke
with serum cholesterol levels under 160 mg/dL.[22] In a recent study total cholesterol measured within
24 hours suggested that higher levels of cholesterol were associated with a favorable early outcome
after ischemic stroke.[23] We could not establish any prognostic significance of cholesterol levels.
In conclusion, a high ESR, total leukocyte count, creatinine and SGPT and a low GCS score at admission
are independent predictors of 30-day fatality in acute stroke
Dalam penelitian ini nilai prognostik berbagai parameter klinis dan biokimia rutin telah dievaluasi . Satu-
satunya parameter klinis dievaluasi dalam studi kami adalah skor GCS untuk mengukur tingkat
kesadaran . Seperti beberapa penelitian di masa lalu , [ 5 ] , [ 6 ] penelitian kami juga menunjukkan
bahwa skor GCS yang rendah adalah prediksi dari hasil yang buruk .
Mungkin , perubahan parameter hematologi pada awal stroke memainkan peran penting dalam
mengubah aliran darah otak . [ 3 ] , [ 4 ] , [ 7 ] Czlonkowska et al [ 4 ] menunjukkan pentingnya
hematokrit sebagai faktor prediktif dari 30 hari kematian . [ 4 ] Dalam studi , hemoglobin , jumlah
trombosit dan analisis agregasi platelet tidak menunjukkan perbedaan yang signifikan antara pasien
kadaluarsa dan selamat . Dalam studi lain, jumlah trombosit diperoleh dalam waktu 48 jam secara
signifikan lebih rendah pada pasien stroke iskemik daripada kelompok kontrol . Jumlah trombosit juga
secara signifikan lebih rendah pada pasien yang kemudian berakhir daripada yang selamat . [ 8 ]
Leukositosis juga mempengaruhi prognosis . Beberapa mekanisme yang leukosit dapat terlibat dalam
cedera otak parenkim termasuk plugging kapal , pelepasan enzim hidrolitik , oksigen radikal bebas atau
inisiasi trombosis . [ 9 ] Leukositosis mungkin juga merupakan manifestasi dari beberapa penyebab
umum dari demam ( misalnya , paru atau saluran kemih infeksi saluran , sepsis , atau emboli paru dari
deep vein thrombosis ) . Czlonkowska et al [ 4 ] juga telah menunjukkan leukosit sebagai prediktor
independen dari 30 hari kasus kematian pada pasien stroke. Dalam penelitian kami , jumlah total
leukosit secara signifikan lebih tinggi pada pasien kadaluarsa , baik pada analisis univariat dan
multivariat . Nilai ESR tinggi telah dikaitkan dengan lesi iskemik besar dan defisit yang lebih parah [ 3 ]
Sebuah nilai ESR tinggi dapat menunjukkan peningkatan yang lebih besar dalam konsentrasi fibrinogen .
; penurunan lebih jelas dalam aliran darah otak , lesi yang lebih besar dan hasil yang buruk . [ 10 ] Seperti
penelitian lain di masa lalu , [ 4 ] dalam penelitian kami , ESR tinggi dikaitkan dengan prognosis yang
buruk .
Glukosa darah telah terlibat sebagai faktor prognosis yang buruk untuk iskemia otak dan perdarahan . [
11 ] Penelitian pada hewan telah menunjukkan kejengkelan cedera iskemik oleh hiperglikemia . [ 12 ]
Diabetes merupakan predisposisi oklusif penyakit pembuluh darah tetapi tidak untuk perdarahan
intraserebral . [ 13 ] Namun, dalam stroke hemoragik itu merupakan predisposisi ukuran yang lebih
besar dari hematoma dan peningkatan kematian pada 30 hari . [ 14 ] , [ 15 ] pada penderita diabetes ,
stroke iskemik sering dikaitkan dengan ukuran infark yang besar dan hasil yang buruk akibat penurunan
autoregulasi dan perubahan koagulabilitas darah [ 13 ] . Bahkan pada pasien non - diabetes dengan
hiperglikemia , ukuran lesi dan neurologis defisit yang lebih buruk. [ 16 ] Banyak penelitian menyangkal
signifikansi prognostik glukosa darah . [ 17 ] , [ 18 ] studi kami juga tidak mengamati makna prognostik
gula darah . Dalam seri kami , pada analisis univariat , urea darah dan kreatinin tingkat ditemukan secara
signifikan lebih tinggi pada pasien yang kemudian berakhir . Kreatinin tinggi secara signifikan
mempengaruhi hasil yang buruk pada analisis multivariat . Tidak ada efek independen urea tercatat
pada kematian . Woo et al telah menunjukkan bahwa lebih tinggi plasma urea dan kreatinin tingkat
berhubungan dengan stroke yang lebih parah dan skor GCS rendah, namun , parameter ini tidak
memiliki efek independen terhadap mortalitas . [ 18 ] Kita tidak bisa mengamati nilai prognostik estimasi
elektrolit . Di antara tes fungsi hati transaminase serum dan kadar globulin ditemukan secara signifikan
berhubungan dengan hasil yang buruk pada analisis univariat . Setelah analisis multivariat , hanya SGPT
berkorelasi dengan hasil yang buruk . Tingkat albumin rendah berhubungan dengan peningkatan
kejadian stroke hemoragik . [ 19 ] Rendah albumin , globulin ratio ditemukan predisposisi stroke
berulang . [ 20 ]
Lipid serum telah dikaitkan dengan risiko lebih tinggi stroke iskemik . [ 21 ] Hubungan terbalik ada untuk
kolesterol total dan pendarahan otak . Sebuah kematian yang lebih besar diamati dari hemorrhagic
stroke dengan kadar kolesterol serum di bawah 160 mg / dL . [ 22 ] Dalam sebuah studi baru-baru total
kolesterol diukur dalam waktu 24 jam menunjukkan bahwa kadar kolesterol dikaitkan dengan hasil awal
yang menguntungkan setelah stroke iskemik . [ 23 ] Kita tidak bisa membangun apapun signifikansi
prognostik kadar kolesterol .
Sebagai kesimpulan, ESR tinggi , jumlah total leukosit , kreatinin dan SGPT dan skor GCS yang rendah
saat masuk adalah prediktor independen dari 30 - hari kematian pada stroke akut

ORIGINAL ARTICLE
Year : 2004 | Volume : 52 | Issue : 2 | Page : 220-223
Predictive value of routine hematological and biochemical parameters on 30-
day fatality in acute stroke

RS Bhatia, RK Garg, S PS Gaur, AM Kar, R Shukla, A Agarwal, R Verma
Department of Neurology, King George's Medical University, Central Drug Research Institute, Lucknow, India
Correspondence Address:
Department of Neurology, King George's Medical University, Lucknow - 226 003, India
garg50@yahoo.com



2. J W Norris, V C Hachinski, M G Myers, J Callow, T Wong and R W Moore
Serum cardiac enzymes in stroke.
Print ISSN: 0039-2499. Online ISSN: 1524-4628
Copyright 1979 American Heart Association, Inc. All rights reserved.
is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Stroke
doi: 10.1161/01.STR.10.5.548
1979;10:548-553 Stroke.
http://stroke.ahajournals.org/content/10/5/548
World Wide Web at:
The online version of this article, along with updated information and services, is located on the


SUBARACHNOID hemorrhage produces a variety of cardiac disturbances in both animals and man. These
include electrocardiogram (ECG) changes, disturbances of cardiac function, focal myocardial necrosis,
and an increase in circulating catechol-amines. Although similar cardiac changes occur in other forms of
intracranial hemorrhage, the occurrence of similar cardiac changes in non-hemorrhagic forms of stroke
is less certain.Raised levels of serum cardiac enzymes serum glutamic oxalo-acetic transaminase
(SGOT), lactate dehydrogenase (LDH) and creatine phospho-kinase(CK) have been reported in the
initial phase of stroke
Myocardial dysfunction with intracranial hemorrhage is well documented, and includes evolving
"ischemic" changes on ECG, a rise in serum cardiac enzymes and elevated serum catecholamine levels.
Although autopsy examination of the heart in such patients may be suprisingly normal, subendocardial
lesions are sometimes found. These myocardial changes have been attributed to increased sympathetic
activity and can be produced experimentally in animals by infusion of catecholamines, and by
stimulation of certain areas of the brain. Although cerebral infarction is a more common form of stroke
than cerebral hemorrhage, similar acute cardiac dysfunction has seldom been described. In 231
neurosurgical autopsies, had focal myocytolysis but only one had cerebral infarction. However, raised
serum CK levels with ischemic changes on ECG were associated with significantly in- creased mortality in
78 patients with ischemic strokes. Meyer et al. 20 found an increase in serum and CSF catecholamines in
a relatively small number of patients with acute cerebral infarction only when hypertension was also
present. They concluded that the catecholamine increase resulted from the non- specific effect of stress
and hypertension rather than the cerebral lesions themselves. We also found significantly higher levels
of plasma catecholamines in patients with acute cerebral infarction compared to control (non-stroke)
patients. Further, plasma catecholamine levels were significantly elevated in both normotensive and
hypertensive stroke groups. The significant elevations of serum SGOT, LDH and CK found in 8% of our
patients with stroke, suggests a much higher myocardial involvement in ischemic or hemorrhagic stroke,
than hitherto believed. The progressive ischemic changes on ECG and the timing of elevated cardio-
specific CK iso enzyme are further evidence that these cardiac changes follow closely upon the heels of
the acute cerebrovascular lesion. Also, the increased incidence of cardiac arrhythmias found in Group II
is consistent with our previous finding 10 of increased arrhythmias in a group of patients with acute
stroke matched for age, sex and duration of stay in the Unit against a control group. The cerebral lesions
themselves, however, do not appear to elevate serum cardiac enzyme levels in the absence of cardiac
lesions or other causes known to affect these enzymes. The incidence of raised cardiac enzyme levels
was the same whether the lesion was ischemic or hemorrhagic so that embolism of a mural thrombus to
the brain is unlikely to be the explanation. In any case, the massive cerebral ischemic lesions
encountered can scarcely be attributed to the small subendocardial lesions as indicated by the minor
serum enzyme elevations, since the degree of serum CK-MB rise is proportional to the volume of
infarcted cardiac muscle. Although the specificity of the MB isoenzyme for cardiac muscle is
controversial, it still remains the most sensitive indicator of acute myocardial necrosis. Circulating
levels of serum CK-BB could not be detected by earlier workers but increasingly sensitive fiuorometric
and radioimmunoassay techniques have shown that trace amounts do exist and may rise following a
variety of cerebral lesions. The early peak (within a few hours) and transient nature of the brain iso-
enzyme in the blood may explain our in ability to detect it in our patients. The present findings indicate
that acute ischemic and hemorrhagic strokes may be accompanied byacute myocardial ischemia or
infarction with raised serum cardiac enzyme levels and associated with cardiac arrhythmias. These
coincidental findings raise the possibility that the acute cardiac abnormalities sometimes seen in stroke
patients are a direct consequence of the neurological lesion

3. In many Exertional heat strok (EHS)cases, Tre is not measured on site. In some cases, although Tre
probably exceeds the critical temperature at the moment of collapse, heat illness might not be
diagnosed. The discrepancies in Tre between the measurements may be significant and Shibolet et
al. reported a 3.3C difference in Tre on site of collapse and at the emergency room. This may lead
to a misdiagnosis of the real condition. In addition, many of the EHS patients arrive at the
emergency room after being treated on site. The treatment, which usually includes fluid
replacement, will result in a hematological picture within a normal range. Specific dynamics were
noted for CPK and sGOT. The former peaked at 24 h of hospitalization andthe latterpeakedat 12 h
andthen at 72 h. The firstsGOTpeak is concomitant with rhabdomyolysis and correlates with
elevated CPK. The second peak of sGOT reflects an acute hepatic dysfiroction that develops in some
cases during a later phase of exertional heat stroke. The results from this study, along with other
works, confirm that peak values of CPK occur 24 to 48 h after EHS collapse (7). Although the
dynamics in CPK levels are not pathognomonic, it is mostly helpful in differential diagnosis of heat
stroke because in most other febrile states enzyme levels will be within a normal range. Moreover,
since CPK levels correlate with the severity of the medical condition it is also a good indicator of the
level of this ergonomic maladaptation.

BIOCHEMICAL PROFILE CHANGES DURING
EXERTIONAL HEAT STROKE
D.S. Moran, Y. Epstein and Y. Shapiro
Heller Institute of Medical Research, Sheba Medical Center, Tel-Hashomer
52621, Department of Physiology, Sadder Faculty of Medicine, Tel-Aviv
University, Israel.

4. During ischemic stroke, glutamate is highly released into the extracellular space leading
to a marked increase in intracellular calcium, followed by the activation of intracellular
enzymes, which provokes neuronal death. As glutamate has a central role in the
ischemic cascade, this neurotransmitter represents a good target in the search for
neuroprotective agents in ischemic stroke. In this sense, calcium and glutamate
antagonists have been attractive tools used as neuroprotective agents in experimental
studies of cerebral ischemia, but they failed when tested in clinical trials and many of
them also showed adverse effects (Ginsberg, 2008). Nevertheless, the relevant role of
glutamate in the ischemic cascade of stroke makes it necessary to look for new
neuroprotective strategies based in glutamate. In experimental models, the capacity of
the enzyme GOT to remove glutamate from the brain by means of blood glutamate
degradation has been shown to be an efficient and novel neuroprotective strategy
against ischemic damage; however, the beneficial effects of this enzyme have not yet
been tested in stroke patients (Gottlieb et al, 2003; Teichberg et al, 2009; Zlotnik et al,
2007). Glutamate oxaloacetate transaminase is an enzyme that is normally expressed in
the liver and heart cells and released into blood under different kinds of pathologies
(Ladue et al, 1954; Lin et al, 2010). Owing to the effect of GOT on glutamate
metabolism, we hypothesize that high blood levels of GOT could correlate with a better
functional outcome and lower infarct volume in ischemic stroke patients. To prove the
association between blood GOT levels and clinical outcome in ischemic stroke patients,
we carried out two clinical independent and observational studies, the primary end
point of which was functional outcome at 3 months. We found that patients with poor
outcome showed higher glutamate levels and lower GOT levels in blood at admission.
Higher GOT levels at admission were independently associated with good functional
outcome at 3 months. This favorable effect on the primary variable was also supported
by positive effects on the reduction of lesion volume. The confirmation of these clinical
results in another independent cohort of ischemic stroke patients shows a clear
association between high blood glutamate levels and worse outcome and vice versa for
GOT, presumably explained by the capacity of this enzyme to metabolize blood
glutamate. According to this, in a previous experimental study with animal model of
cerebral ischemia by means of a middle cerebral arterial occlusion and following the
Stroke Therapy Academic Industry Roundtable (STAIR) group guidelines (Campos et al,
2011), we observed that oxaloacetate-mediated GOT activation inhibits the increase in
blood and cerebral glutamate after middle cerebral arterial occlusion, inducing a
reduction of infarct size, smaller edema volume, and lower sensorimotor deficits with
regard to controls, thus showing the neuroprotective effect of the enzyme GOT.
Attending to these experimental results and these clinical findings, it is tempting to
postulate that the administration of GOT might be an effective therapy in ischemic
stroke because of its capacity to decrease blood and brain glutamate. In fact, previous
studies by our group have shown that neurologic deterioration and infarct growth in
acute ischemic stroke is associated with higher glutamate levels in blood (Castellanos et
al, 2006; Castillo et al, 1996, 1997). However, as the inclusion of patients was not
randomized, our study has some limitations, such as the different percentages of
cardioembolic patients observed in both cohorts, 37.8% versus 54.1%. Nevertheless, this
limitation has not affected the aim of this study. In conclusion, these clinical findings
show a clear association between low blood glutamate levels and high blood GOT levels
with good outcome, probably mediated by the capacity of this enzyme to metabolize
blood glutamate. In this regard, further clinical trials based on the administration of
GOT or agents that can increase GOT expression or activity are necessary to show the
neuroprotective effects of GOT in stroke patients.

J Cereb Blood Flow Metab. Jun 2011; 31(6): 13871393.
Published online Jan 26, 2011. doi: 10.1038/jcbfm.2011.4
PMCID: PMC3130328
Francisco Campos,
1,*
Toms Sobrino,
1
Pedro Ramos-Cabrer,
1
Mar Castellanos,
2
Miguel Blanco,
1
Manuel
Rodrguez-Yez,
1
Joaqun Serena,
2
Rogelio Leira,
1
and Jos Castillo
1,*


5. Before the 1959 discovery that Glu plays a central role as an excitatory neurotransmitter
(9), and the subsequent developments on synaptic activity and excitotoxicity
(8, 20, 28, 32, 39, 40, 42, 44), Glu was viewed as a major metabolic fuel for the brain
(30, 41, 45). Resting on that foundation this work proposes a paradigm shift claiming
that correction of hypoxia in an ischemic brain injury setting can help clear extracellular
neurotoxic Glu by enabling utilization of this amino acid as a metabolic fuel to support
survival of the stroke-affected brain tissue. Brain ATP levels decrease by one-third
within the first 15 min of cerebral ischemia (21). During ischemic brain injury hypoxia
and hypoglycemia represent two major components of insult resulting in accumulation
of excitotoxic levels of extracellular Glu (11,12, 17, 29). To date, strategies to mitigate
extracellular Glu-mediated neurodegeneration have primarily focused on blocking
receptor-mediated excitotoxicity (i.e., NMDA and calcium antagonists) (43). This
approach has failed in clinical trials (1, 14, 15). In this work we introduce the concept
that under hypoglycemic conditions extracellular Glu can be transformed from a
neurotoxin to a survival factor, provided there is sufficient oxygen to sustain cellular
respiration.
From the work of Sir Hans Krebs in 1963 we know that GOT metabolism of Glu generates
TCA cycle intermediates under hypoglycemic conditions in brain tissue (18). GOT catalyzes
transfer of the amino group from Glu to the 4-carbon TCA cycle intermediate oxaloacetate
to generate aspartate and the 5-carbon TCA cycle intermediate -ketoglutarate (18, 41).
Under conditions of stroke, the brain tissue cannot rescue itself from the insult of
hypoglycemia by turning to Glu as an alternate source of energy because of inadequate
tissue oxygenation. This work demonstrates that the oxidative pathway of Glu metabolism
by GOT, as proposed by Krebs, can be utilized as a survival mechanism during stroke as
long as tissue hypoxia is corrected. Transamination of Glu by GOT will, on the one hand,
clear toxic extracellular Glu from the ischemic site while also feeding cellular respiration to
generate energy in glucose-starved energy-deprived cells. Interestingly, strategies to
scavenge neurotoxic brain Glu to blood by increasing GOT activity have been shown to
protect against stroke in rat (5). Although blood Glu scavenging addresses the problem of
neurotoxic Glu handling in brain tissue, it does not resolve the problem of energy deficiency.
The current work addresses Glu handling during stroke by repurposing neurotoxic Glu as
energy substrate to glucose-starved stroke-affected brain tissue. Taken together, outcomes
of the current work suggest a pivotal role for brain GOT in enabling the functional switch of
Glu from neurotoxin to survival factor. Findings of this work also recognize brain GOT
activity as a therapeutic target in managing stroke outcomes.

Antioxid Redox Signal. May 15, 2011; 14(10): 17771785.
doi: 10.1089/ars.2011.3930
PMCID: PMC307850

Cameron Rink, Surya Gnyawali, Laura Peterson, and Savita Khanna
Oxygen inducible glutmate oxaloacetate transaminase as protective switch transforming
neurotoxic glutamate to metabolic feul during acute ischemic stroke