I Wayan Dary
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DIAGNOSIS DAN PENATALAKSANAAN ARTRITIS SEPTIK Dary, I Wayan; Raka Putra, Tjokorda
journal of internal medicine Vol. 10, No. 1 Januari 2009
Publisher : journal of internal medicine

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Abstract

Septic arthritis which caused by bacterial infection is a serious disease and still as challenge to physician because theprognosis has not improved significantly over the past two decades. The route of spread infection to joint through hematogenousor other routes include direct inoculation through joint prosthetic. The most often aetiology is Staphylococcus aureus. The processof native joint infection can be divided into three steps: bacterial colonization, establishing an infection, and induction ofhost inflammatory response. The diagnosis of septic arthritis rests on isolation of the pathogen from joint fluid. If we find classicsign and symptoms associated septic arthritis should not to delay the diagnosis of septic arthritis. Once septic arthritis is suspectedand the proper sample for microbiologic studies are collected, appropriate antibiotic treatment and adequate joint drainage shouldbegin immediately. The aim management of septic arthritis mainly are joint decompression, joint sterilization, and reserve jointfunction. Sterilization joint with empirical antibiotic based on gram stain and co-morbid disease and than adjusted base onbaterial culture result. Antibiotic should be administrated intravenously at least 2 weeks than continued orally. Joint decompressioncan be achieved by a variety methods include closed-needle aspiration, tidal irrigation, arthroscopy, and arthrotomy. Prophylacticuse of antibiotics is controversial for events posing a risk of haematogenous bacterial arthritis through transientbacteraemia. Prognosis of septic arthritis is poor since a permanent reduction in joint function is seen in approximately 30% ofpatients.
KORELASI ANTARA DERAJAT GASTRITIS DAN RASIO PEPSINOGEN I/II PADA PENDERITA GASTRITIS KRONIS Dary, I Wayan; Wibawa, I Dewa Nyoman
journal of internal medicine Vol. 10, No. 2 Mei 2009
Publisher : journal of internal medicine

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Abstract

Chronic gastritis is a histopathological entity characterized by chronic inflammation of the stomach mucosa. Chronicgastritis tend to damage stomach mucosa and be atrophy sequence to change gastric physiology. Pepsinogen (PG) can be used asÔserologic biopsy,Õ as clinical application for evaluating gastric inflammations. The different cellular origins of PG I and PG II areimportant because alteration in their serum concentration can be correlated with some histological gastric anomalies. To determinethe correlation between grade of gastritis and PG I/II ratio (PGR) in chronic gastritis patients, we conducted an analyticcross sectional study in 64 gastritis patients whom enrolled consecutively. Gastric mucosal of dyspeptic patients who had uppergastrointestinal endoscopy biopsy 2 at anthrum and 2 at corpus were examined histologically using the Updated Sydney System(USS) by two pathologists independently, and also the serum examined for PG I, PG II, and IgG H. pylori. Degree of gastritis wascounted with the USS method. Pepsinogen examination used ELISA method, however IgG H. pylori examanition usedimmunochromatographic test (ICT) method with local reagen. H. pylori positive if serologically H. pylori positive and or histologicallyH. pylori positive. Interobserver agreement for histopatology abnormalities were examined by using kappa test. Thedifference PGR and severity of gastritis between subjectswith H. pylori positive and H. pylori negative were identified by usingMann-Whitney U test. Correlation between the severity of gastritis and PGR was identified by using spearmanÕs test and theeffect of total USS score and H. pylori to PGR was identified by using dummy regression, also to know the effect of PGR and H.pylorito total USS score was identified by using dummy regression. Pvalue of less than 0.05 was considered statistically significant.There were 64 chronic gastritis whom mean age 45.9 ± 15.5 year, consisted of 44 male and 20 female. The level of PG I218.70 (53,90 Ð 530.00) mg/L, PG II 15.72 (2.84 Ð 59.25) mg/L, dan PGR 12.66 (28.97 Ð 5.80). Interobserver agreement of gastrichistologic examanation shown moderate to substantial criteria (k = 0.590 Ð 0.795) with polymorphonuclear activity k = 0.795,glandular atrophy k = 0.591, density of H. pylori k = 0.727, chronic inflammation k = 0.629, and intestinal metaplasia k = 0.778.The frequency of abnormalities gastric mucosa as infected H. pylori 28.1%, inflammation 100.0%, polymorphonuclear activity22.8%, atrophy 37.5%, and intestinal metaplasia 6.2%. Total USS score from 1 to 9 and most of them had score 1 and 2 withfrequency 17 (26,6%) and 15 (24,4%) respectively. Subjects with H. pyloriinfection had lower PGR than uninfected subjects(11.2 ± 4.3 mg/L vs 15.0 ± 5.1 mg/L, p = 0.001; Mann-Whitney U test), and also subjects with H. pyloriinfection had higherseverity of gastritis than uninfected subjects either degree of inflammation, activity polymorphonuclear, and atrophy (p = 0.000,p = 0.004, p = 0.041 respectively; Mann-Whitney Utest). There was significant inversed correlation between total USS score andPGR (r = -0.470, p < 0.0001; SpearmanÕs tes). Significant effect of total USS score and positivity H. pylori to PGR (F = 7.015, p = 0.002; dummy regression), but only coefficient of total USS score significantly (t = -2.030, p = 0.047), however positvity H.pylori didnÕt influence PGR significatly (t = -1.199, p = 0.235). Total USS score influences PGR as much as 15,4% (adjusted R2= 0.154, F = 12.504, p = 0.001; linier regression) with regression coefficient -0,933 (t = -3.536, p = 0.001). H. pylori serology andPGR can be used to determine total USS score significantly (F = 9.498, p < 0.0001; dummy regression) and both of regressioncoefficient were significant (t = -3.417, p = 0.001; t = 2.360, p = 0.021 respectively; dummy regression) how ever can be madeÔserologic biopsyÕ with formula Ôtotal USS score = 6.786-0.169.PGRÕ for H. pylori positive subjects and Ôtotal USS score = 5.258Ð 0.169.PGRÕ for H. pylori negative subjects. In conclusion that there was a significant inversed correlation between total USSscore and PGR, formula Ôserologic biopsyÕ to determine total USS score were Ôtotal USS score = 6.786 Ð 0.169.PGRÕ for H. pyloripositive subjects and Ôtotal USS score = 5.258 Ð 0.169.PGRÕ for H. pylori negative subjects.
DIAGNOSIS DAN PENATALAKSANAAN PNEUMONITIS HIPERSENSITIVITAS Dary, I Wayan; Ngurah Rai, Ida Bagus
journal of internal medicine Vol. 9, No. 3 September 2008
Publisher : journal of internal medicine

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Abstract

Hypersensitivity pneumonitis (HP), or extrinsic allergic alveolitis, is a group of immunologically mediated lung diseasesin which the repeated inhalation of certain finely dispersed antigens of a wide variety, mainly including organic particles or lowmolecular weight chemicals, provokes a hypersensitivity reaction with granulomatous inflammation in the distal bronchioles andalveoli of susceptible subjects. HP can be classified as acute, subacute, and chronic form. Clinically its presented as fever, fatique,myalgia, cough and shortness of breath after exposured and physical finding with fever, takipneu, diffuse rhales bibasal. Chestradiograph showed diffuse micronodular pattern or ground-glass appearance on lower and mid field lung only found on tenperse10%n of cases. HRCT can show more specific abnormalities of the lung. Lung function test describe restrictive type.Hystopathologic features are noncaseating granulomas, giant cells with a lot of nucleus, and mononuclear cells infiltration. Themost diagnostic criteria used is made by Richerson et al. the history and physical findings and pulmonary function tests indicatean interstitial lung disease, the X-ray film is consistent, there is exposure to a recognized cause, and there is antibody to thatantigen. Being an immune reaction in the lung, the most obvious treatment of HP is avoidance of contact with the offendingantigen. Systemic corticosteroids represent the only reliable pharmacologic treatment of HP but do not alter the long-term outcome.On the acute HP, prednisone administrate 1 mg/kgBW/day or its equivalent dose for 7 ? 14 days than tapering off foe 2 ? 6 weeks.