Kasus 1 Seorang laki-laki 30th pekerjaan buruh tani datang ke puskesmas dengan keluhan nyeri dan bengkak di semua

sendi jari-jarinya. Keluhan ini sudah sering dialami, hilang timbul. Keluhan ini sering kambuh jika dia mengkonsumsi kacang-kacangan dan jeroan. Beberapa orang anggota keluarganya juga mengalami keluhan yang sama. Hasil pemeriksaan isik didapatkan tanda radang !!!, teraba massa keras di sendi-sendi jari, jari-jari sulit digerakkan karena nyeri dan massa tersebut. "anda #ital dalam bats normal. $pd% gastritis. &ermasalahan dan 'iagnosis 1. (yeri dan bengkak semua sendi. ). (yeri hilang timbul dan kambuh jika makan kacang dan jeroan. 3. &emeriksaan isik% peradangan, massa keras di sendi, dan sendi sulit digerakkan akibat nyeri dan massa. *. +danya ri,ayat gastritis. 'iagnosis -out arthritis. "ujuan &engobatan .

-out -out is a metabolic disease most o ten a ecting middle-aged to elderly men and postmenopausal ,omen. /t is the result o an increased body pool o urate ,ith hyperuricemia. /t is typically characteri0ed by episodic acute and chronic arthritis, due to deposition o 1S2 crystals in joints and connecti#e tissue tophi, and the risk or deposition in kidney interstitium or uric acid nephrolithiasis 34hap. 3536. +cute and 4hronic +rthritis +cute arthritis is the most re7uent early clinical mani estation o gout. 2sually, only one joint is a ected initially, but polyarticular acute gout can occur in subse7uent episodes. "he metatarsophalangeal joint o the irst toe is o ten in#ol#ed, but tarsal joints, ankles, and knees are also commonly a ected. 8specially in elderly patients or in ad#anced disease, inger joints may be in#ol#ed. /n lamed Heberden9s or Bouchard9s nodes may be a irst mani estation o gouty arthritis. "he irst episode o acute gouty arthritis re7uently begins at night ,ith dramatic joint pain and s,elling. :oints rapidly become ,arm, red, and tender, ,ith a clinical appearance that o ten mimics cellulitis. 8arly attacks tend to subside spontaneously ,ithin 3;10 days, and most patients ha#e inter#als o #arying length ,ith no residual symptoms until the ne<t episode. Se#eral e#ents may precipitate acute gouty arthritis% dietary e<cess, trauma, surgery, e<cessi#e ethanol ingestion, hypouricemic therapy, and serious medical illnesses such as myocardial in arction and stroke. + ter many acute mono- or oligoarticular attacks, a proportion o gouty patients may present ,ith a chronic nonsymmetric syno#itis, causing potential con usion ,ith rheumatoid arthritis 34hap. 31*6. .ess commonly, chronic gouty arthritis ,ill be the only mani estation and, more rarely, the disease ,ill mani est only as periarticular tophaceous deposits in the absence o syno#itis. =omen represent only 5;)0> o all patients ,ith gout. &remenopausal gout is rare? it is seen mostly in indi#iduals ,ith a strong amily history o gout. Kindreds o precocious gout in young emales caused by decreased renal urate clearance and renal insu iciency ha#e been described. 1ost ,omen ,ith gouty arthritis are postmenopausal and elderly, ha#e osteoarthritis and arterial hypertension causing mild renal insu iciency, and are usually recei#ing diuretics. .aboratory 'iagnosis 8#en i the clinical appearance strongly suggests gout, the diagnosis should be con irmed by needle aspiration o acutely or chronically in#ol#ed joints or tophaceous deposits. +cute septic arthritis, se#eral o the other crystalline-associated arthropathies, palindromic rheumatism, and psoriatic arthritis may present ,ith similar clinical eatures. 'uring acute gouty attacks, strongly bire ringent needle-shaped 1S2 crystals ,ith negati#e elongation are typically seen both intracellularly and e<tracellularly 3@ig. 3)A-16. Syno#ial luid cell counts are ele#ated rom )000 to B0,000C .. 8 usions appear cloudy due to the increased numbers o leukocytes. .arge amounts o crystals occasionally produce a thick pasty or chalky joint luid. Bacterial in ection

can coe<ist ,ith urate crystals in syno#ial luid? i there is any suspicion o septic arthritis, joint luid must also be cultured. @igure 3)A-1

Extracellular and intracellular monosodium urate crystals, as seen in a resh preparation o syno#ial luid, illustrate needle- and rod-shaped strongly negati#e bire ringent crystals 3compensated polari0ed light microscopy? *00<6. 1S2 crystals can also o ten be demonstrated in the irst metatarsophalangeal joint and in knees not acutely in#ol#ed ,ith gout. +rthrocentesis o these joints is a use ul techni7ue to establish the diagnosis o gout bet,een attacks. Serum uric acid le#els can be normal or lo, at the time o the acute attack, as in lammatory cytokines can be uricosuric and e ecti#e initiation o hypouricemic therapy can precipitate attacks. "his limits the #alue o serum uric acid determinations or the diagnosis o gout. (e#ertheless, serum urate le#els are almost al,ays ele#ated at some time and are important to use to ollo, the course o hypouricemic therapy. + )*-h urine collection or uric acid can, in some cases, be use ul in assessing the risk o stones, in elucidating o#erproduction or undere<cretion o uric acid, and in deciding i it might be appropriate to use a uricosuric therapy 34hap. 3536. 8<cretion o DE00 mg o uric acid per )* h on a regular diet suggests that causes o o#erproduction o purine should be considered. 2rinalysis, serum creatinine, hemoglobin, ,hite blood cell 3=B46 count, li#er unction tests, and serum lipids should be obtained because o possible pathologic se7uelae o gout and other associated diseases re7uiring treatment, and as baselines because o possible ad#erse e ects o gout treatment. $adiographic @eatures 8arly in the disease radiographic studies may only con irm clinically e#ident s,elling. 4ystic changes, ,ell-de ined erosions ,ith sclerotic margins 3o ten ,ith o#erhanging bony edges6, and so t tissue masses are characteristic radiographic eatures o ad#anced chronic tophaceous gout. -out% "reatment +cute -outy +rthritis "he mainstay o treatment during an acute attack is the administration o anti-in lammatory drugs such as nonsteroidal anti-in lammatory drugs 3(S+/'s6, colchicine, or glucocorticoids. (S+/'s are most o ten used in indi#iduals ,ithout complicating comorbid conditions. Both colchicine and (S+/'s may be poorly tolerated and dangerous in the elderly and in the presence o renal insu iciency and gastrointestinal disorders. /n attacks in#ol#ing one or t,o joints, intraarticular glucocorticoid injections may be pre erable and e ecti#e. /ce pack applications and rest o the in#ol#ed joints can be help ul. 4olchicine gi#en orally is a traditional and e ecti#e

treatment, i used early in the attack. Fne to t,o 0.B-mg tablets can be gi#en e#ery B;E h o#er se#eral days ,ith subse7uent tapering. "his is generally better tolerated than the ormerly ad#ised hourly regimen. "he drug must be stopped promptly at the irst sign o loose stools, and symptomatic treatment must be gi#en or the diarrhea. /ntra#enous colchicine is occasionally used, e.g., as pre- or postoperati#e prophyla<is in 1- to )-mg doses ,hen patients cannot take medications orally. .i e-threatening colchicine to<icity and sudden death ha#e been described ,ith the administration o D* mgCd /G. "he /G colchicine should be gi#en slo,ly through an established #enous line o#er 10 min in a soluset. "he total dose should ne#er e<ceed * mg. (S+/'s gi#en in ull anti-in lammatory doses are e ecti#e in HI0> o patients, and the resolution o signs and symptoms usually occurs in 5;E days. "he most e ecti#e drugs are any o those ,ith a short hal -li e and include indomethacin, )5;50 mg tid? ibupro en, E00 mg tid? or diclo enac, 50 mg tid. Fral glucocorticoids such as prednisone, 30;50 mgCd as the initial dose and gradually tapered ,ith the resolution o the attack can be e ecti#e in polyarticular gout. @or single or e, in#ol#ed joints intraarticular triamcinolone acetonide, )0;*0 mg, or methylprednisolone, )5;50 mg, ha#e been e ecti#e and ,ell tolerated. +drenocorticotropic hormone 3+4"H6 as an intramuscular injection o *0;E0 /2 in a single dose or e#ery 1) h or 1; ) days can be e ecti#e in patients ,ith acute polyarticular re ractory gout or in those ,ith a contraindication or using colchicine or (S+/'s. Hypouricemic "herapy 2ltimate control o gout re7uires correction o the basic underlying de ect, the hyperuricemia. +ttempts to normali0e serum uric acid to J300;3B0 molC. 35.0;B.0 mgCd.6 to pre#ent recurrent gouty attacks and eliminate tophaceous deposits entail a commitment to long-term hypouricemic regimens and medications that generally are re7uired or li e. Hypouricemic therapy should be considered ,hen, as in most patients, the hyperuricemia cannot be corrected by simple means 3control o body ,eight, lo,-purine diet, increase in li7uid intake, limitation o ethanol use, and a#oidance o diuretics6. "he decision to initiate hypouricemic therapy is usually made taking into consideration the number o acute attacks 3urate lo,ering may be cost e ecti#e a ter t,o attacks6, serum uric acid le#els Kprogression is more rapid in patients ,ith serum uric acid D535 molC. 3DI.0 mgCd.6L, patient9s ,illingness to commit to li elong therapy, or presence o uric acid stones. 2rate-lo,ering therapy should be initiated in any patient ,ho already has tophi or chronic gouty arthritis. 2ricosuric agents, such as probenecid, can be used in patients ,ith good renal unction ,ho undere<crete uric acid, ,ith JB00 mg in a )*-h urine sample. 2rine #olume must be maintained by ingestion o 1500 m. o ,ater e#ery day. &robenecid can be started at a dosage o )50 mg t,ice daily and increased gradually as needed up to 3 g in order to maintain a serum uric acid le#el J300 molC. 35 mgCd.6. &robenecid is

generally not e ecti#e in patients ,ith serum creatinine le#els o D1AA molC. 3).0 mgCd.6. "hese patients may re7uire allopurinol or ben0bromarone 3not a#ailable in the 2nited States6. "he latter is another uricosuric drug that is more e ecti#e in patients ,ith renal ailure. $ecent reports ha#e identi ied that losartan, eno ibrate, and amlodipine ha#e some mild uricosuric e ects.

"he <anthine o<idase inhibitor allopurinol is by ar the most commonly used hypouricemic agent and is the best drug to lo,er serum urate in o#erproducers, urate stone ormers, and patients ,ith renal disease. /t can be gi#en in a single morning dose, 100;300 mg initially and increasing up to E00 mg i needed. /n patients ,ith chronic renal disease, the initial allopurinol dosage should be lo,er and adjusted depending on the serum creatinine concentration? or e<ample, ,ith a creatinine clearance o 10 m.Cmin, one ,ould generally use 100 mg e#ery other day. 'oses can gradually be increased to reach the target urate le#el? ho,e#er, more studies are needed to pro#ide e<act guidance. &atients ,ith re7uent acute attacks may also re7uire lo,er initial doses to pre#ent e<acerbations. "o<icity o allopurinol has been recogni0ed increasingly in patients ,ith renal ailure ,ho use thia0ide diuretics and in those patients allergic to penicillin and ampicillin. "he most serious side e ects include skin rash ,ith progression to li e-threatening to<ic epidermal necrolysis, systemic #asculitis, bone marro, suppression, granulomatous hepatitis, and renal ailure. &atients ,ith mild cutaneous reactions to allopurinol can reconsider the use o a uricosuric agent or undergo an attempt at desensiti0ation to allopurinol. "hey can also pay increased attention to diet and should be a,are o ne, alternati#e agents under in#estigation 3see belo,6. 2rate-lo,ering drugs are generally not initiated during acute attacks but a ter the patient is stable and lo,-dose colchicine has been initiated to decrease the risk o lares that o ten occur ,ith urate lo,ering. 4olchicine prophyla<is in doses o 0.B mg one to t,o times daily is usually continued, along ,ith the hypouricemic therapy, until the patient is normouricemic and ,ithout gouty attacks or B months or as long as tophi are present. (e, urate-lo,ering drugs undergoing in#estigation include a &8-ylated uricase and a ne, speci ic <anthine o<idase inhibitor, ebu<ostat.

Fbat-obat 2rikosurik a. 8 ikasi% obat ini direabsorbsi secara lengkap oleh tubulus ginjal dan dimetabolisme sangat lambat, akan tetapi cepat dieksresi oleg ginjal. 1eningkatnya eksresi asam urat melalui urin, jumlah timbunan asam urat menurun, ,alaupun kadar dalam plasma sedikit berkurang. b. Suitability% teraoi urikosurik dimulai jika timbul beberapa serangan akut arthritis gout jika tampak adanya to i, atau jika kadar asam urat dalam plasma tinggi sehingga kerusakan jaringan hamper tak dapat dielakkan. "etapi tidak boleh )-3 minggu setelah serangan akut. c. Sa ety% menyebabkan iritasi saluran cerna, dermatitis alergi, rash. &emakaian lama menimbulkan sindrom ne rotik. 'apat menimbulkan anemia aplastik, tetapi sangat langka. (ama-nama Fbat 2rikosurik 1. &robenesid a. 8 ikasi% &robenesid dan sul inpyra0one meningkatkan klirens ginjal untuk mengeluarkan asam urat dengan menghambat reabsorbsi asam urat di tubular ginjal. &robenesid diberikan dengan dosis a,al )50 mg dua kali sehari selama 1-) minggu, kemudian 500 mg dua kali sehari selama ) minggu. b. Suitability% dirancang untuk menurunkan simpanan jaringan asam urat dengan meningkatkan eksresi asam urat ginjal murah menginhibisi reabsorbsi dari tubuler. c. Sa ety% kontra indikasi untuk pasien yang hipersensiti#itas terhadap obat ini, anak J) tahun, insu isiensi renal, baju ginjal. d. Harga% $p.110.000C100 "ab, $p. 1.100C"ab. ). Sul inpira0on a. 8 ikasi% &robenesid dan sul inpyra0one meningkatkan klirens ginjal untuk mengeluarkan asam urat dengan menghambat reabsorbsi asam urat di tubular ginjal. b. Suitability% mencegah serta mengurangi kelainan sendi dan to i pada penyakit gout kronik berdasarkan reabsorbsi tubuler asam urat. Sul inpira0on kurang e ekti dalam menurunkan kadar asam urat dibandingkan dengan alopurinol dan tidak berguna pada gout akut. c. Sa ety% kontra indikasi untuk ulkus lambung dan penyakit kanker gastrointestinal, hipersensiti#itas terhadap deri#ati pira0olon, kerusakan hati dan ginjal berat.

d. Harga%