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HUBUNGAN ANTARA INTERLEUKIN- 6 DAN C-REACTIVE PROTEIN PADA SIROSIS HATI DENGAN PERDARAHAN SALURAN MAKANAN BAGIAN ATAS Mariadi, I Ketut; Wibawa, I Dewa Nyoman
journal of internal medicine Vol. 9, No. 3 September 2008
Publisher : journal of internal medicine

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Variceal bleeding is a frequent complication of liver cirrhosis. Upper gastrointestinal (GI) bleeding is a risk factor forinfection. The severity of liver cirrhosis was correlated with infection and GI bleeding. Bacterial infection and endotoxin promotecytokine proinflammation (IL-6) release from monocyte. IL-6 stimulates the liver to produce CRP. Does liver cirrhosisaffect the CRP production? Recently, there are no data about the correlation of IL-6 and CRP in liver cirrhosis with uppergastrointestinal bleeding. A cross-sectional analytic study was performed to describe the correlation between IL-6 and CRP inliver cirrhosis patient with upper gastrointestinal bleeding.We performed a cross-sectional analytic study in 52 liver cirrhosis patients. The liver cirrhosis patients with uppergastrointestinal bleeding in last 14 days, absence of steroid and statin treatment, without hepatoma, and GFR 15 ml/mnt/1.73m2, were collected consecutively. The correlation of IL-6 and CRP was analyzed with Pearson correlation test, mean differenceof CRP between Child Turcotte Pugh (CTP) group was analyzed by Ancova test continued with post hoc Tamhane test, the effectof CTP on CRP production was analyzed with Ancova test.Seventy-five percent out of 52 samples were male and the rest were female. Two of them (3.8%) with CTP score A, 20(38.5%) CTP score B and 30 (57.7%) CTP score C. Mean of IL-6 was 28.29 ± 34.60. Mean of CRP was 17.17 ± 28.80 mg/L. Wefound strong positive correlation between IL-6 and CRP (r = 0.610; p<0.001). CTP score didnt have significant independenteffect on correlation of IL-6 and CRP level (F=2.33; p=0.108). Significant mean difference of CRP was found between CTP scoregroup (F=4.27; p=0.02).In conclusion, Interleukin-6 has a strong correlation with CRP in liver cirrhosis with upper GI bleeding. CRP level issignificantly higher in severe liver cirrhosis. And the degree of liver damage doesnt have significant independent effect oncorrelation of IL-6 and CRP level. These results show us that hepatocyte in liver cirrhosis still adequately produce CRP.

ASOSIASI CA 125 DENGAN RESPON TERAPI PADA PENDERITA LIMFOMA NON-HODGKIN AGRESIF YANG MENDAPAT KEMOTERAPI CYCLOPHOSPHAMIDE, DOXORUBICIN, VINCRISTINE, PREDNISONE (CHOP) S, Merlyna; Mulyono, Adi; -, Ugroseno; Putra Sedana, Made; Ashariati, Ami; -, Sugianto; -, Boediwarsono; -, Soebandiri
journal of internal medicine Vol. 12, No. 3 September 2011
Publisher : journal of internal medicine

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Cancer antigen (CA) 125 is a glycoprotein produced by epithelial ovarium tumors and mesothelial cells, its levels alsohave been shown to be elevated in patients with Non-Hodgkin!s Lymphoma (NHL). Several papers have reported anassociation of high CA 125 serum levels with advanced NHL as well as relationship between high CA 125 values and pooroutcome. This study aimed to determine association between CA 125 levels (> 35 U/ml) with normal CA 125 ( 35 U/ml)to the respone of NHL patients receiving chemotherapy CHOP. An observational analytic prospective study was done in40 patients with NHL at Dr Soetomo Hospital Surabaya. The patient were recruited from both inpatient and outpatientclinic and the initial CA 125 level had determined before the patients received chemotherapy with Cyclophosphamide,Doxorubicin, Vincristine and Prednisone (CHOP). Of the 40 patients who included in this study, 62.5% were male, 37.5%were female, the average age 43,45 years, the most kind of histophatology result were diffuse large cell, cleaved or noncleaved cell (47.5%). There was a signiÞ cant association between CA 125 levels with therapy respone groups (responiveand unresponive), with signiÞ cancy 0.001 (OR 23.22; CI 95%), and with therapy respone groups (CR, PR, NC, PD) withsigniÞ cancy 0.013. The group with normal CA 125 levels ( 35 U/ml), had better respone, it was around 95% responive(CR = 35%, PR = 60%) and 5% unresponive (NC = 5%, PD = 0%) than the group who had high CA 125 levels (> 35U/ml), it was only 45% responive (CR = 15%, PR = 30% and 55% unresponive (NC = 50%, PD = 5%). As a conclusion,levels of CA 125 (> 35 U/ml) perhaps could be a negative prognostic factor to predict the CHOP chemotherapy responein NHL patients.

NUTRISI PADA PENDERITA SAKIT KRITIS Wiryana, Made
journal of internal medicine Vol. 8, No. 2 Mei 2007
Publisher : journal of internal medicine

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Malnutrition is always been being associated with the increase of morbidity and mortality rate due to lack of immunesystem, depending on ventilator, high rate of infection, and delayed healing process, so it will increase the cost and length of stayof the patients. Clinician need to have right information about how to manage nutrition for critical ill patient because it willinfluence the outcome of ICU patient.Objective measurement nutritional status of the patient is difficult because process of illnesses itself will disturb themethod that will be used in the population. Nutritional status is multidimension phenomenon that need several methods formeasurement, including associated factors of nutrition, nutrition intake, and energy expenditure.Nitrogen balance can be used to determine effectiveness of nutritional therapy. Nitrogen balance can be counted by formulathat count nitrogen in 24 hours from patch urine, especially urine urea nitrogen (UUN), minus nitrogen intake from the food.Resting Energy Expenditure (REE) must be determined for nutritional therapy in critical ill patients. Acuracy estimation REE willhelp to reduce complications due to overfeeding, such as infiltration fat to liver and pulmonyary compromise. Several methods areavailable to predict REE such as Calorimetry, and Harris-Benedict equation.The goal in nutritional therapy in critical ill patient is to support metabolic, not to complete their need in that time. Becausein critical ill patient there is no metabolic condition is able to metabolize total amount of calories to fulfill lack of energy expenses.Ideally the route of nutritional therapy is able to supply nutrition with minimal morbidity. Each routes (parenteral andenteral) have advantages and disadvantages, and the choice is depend on patient condition. In critical ill patient care, enteralnutrition is always being the first choice and parenteral nutrition become the next alternative.

INTERLEUKIN 8 BERHUBUNGAN DENGAN DERAJAT GASTRITIS PADA PASIEN TERINFEKSI HELICOBACTER PYLORI Mariadi, IK; Kurniari, PK; Wibawa, IDN; Purwadi, N; Suryadarma, IGA
journal of internal medicine Vol. 12, No. 2 Mei 2011
Publisher : journal of internal medicine

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Helicobacter pylori infection induces a local pro-inflammatory cytokine response. The secretion of IL-8 by epithelialcells is probably a key factor in host defenses at mucosal sites, permitting a rapid polymorph response against infectious agents.Interleukin-8 is an important chemotactic and activating factor for neutrophils. If defense mechanisms fail and chronic infectionresults, continued up regulation of IL-8 and neutrophil activation could lead to mucosal damage and increased free radicalformation. Mucosal IL-8 production in Helicobacter pylori infection may be an important factor in the immunopathogenesisof gastritis and peptic ulcer disease. This study aim to investigate correlation between IL-8 and severity of gastritis in ourpopulation. We performed a cross-sectional analytic study in Helicobacter pylori infected patients. Severity of gastritis wasdetermined base on The Updated Sydney System. IL-8 level was analyzed from gastric mucosa biopsy using ELISA method.We included 65 samples. 31 (47.7%) men and the rest was women. Base on Kruskalwallis test we found significant associationbetween IL-8 gastric mucosa and severity of gastritis (x2 = 12.8; p = 0.002). We also found significant association between IL-8gastric mucosa and density of H pylori infection (x2 = 10.6; p = 0.01), severity of atrophy (x2 = 9.4; p = 0.02) and neutrophilscount (x2 = 11.0; p = 0.01). But notmethaplasia (x2 = 3.3; p = 0.18). Base on this study we concluded that IL-8 was associatedwith severity of gastritis in Helicobacter pylori infected patients.

HEPCIDIN PADA ANEMIA OF CHRONIC DISEASE Agustriadi, Ommy; Suega, Ketut
journal of internal medicine Vol. 7, No. 2 Mei 2006
Publisher : journal of internal medicine

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Anemia of chronic disease (ACD) induce dysregulation of iron homeostasis. A hallmark of anemia of chronic disease is thedevelopment of disturbances of iron homeostasis, with increased uptake and retention of iron within cells of thereticuloendothelial system (RES), that leads to a diversion of iron from the circulation into storage sites of RES, and decreasedintestinal iron absorption, subsequent limitation of the availability of iron for erythroid progenitor cells, and iron-restrictederythropoiesis. A new small peptide called hepcidin was found. It is strongly suggest that hepcidin play role on the pathogenesisof ACD. Hepcidin expression is induced by inflammation/infection (by lipopolysaccharide and interleukin-6) and iron overloadcondition, it is strongly suggest that hepcidin induced dysregulation of iron homeostasis by inhibit iron efflux from macrophagedan RES (causing iron retention in turn) and decrease intestinal iron absorption. In the aggregate, the increase of hepcidinproduction suppress erythropoiesis by iron starvation strongly suggest that hepcidin is the key mediator of ACD. If hepcidinfollows the pattern of other peptide hormones or cytokines, its actions will be mediated by cell surface receptors. Elucidation ofthe receptor and its transduction pathways should lead to the development of hepcidin antagonists, some of which could be usefulin treatment of ACD, along with it's underlying disease.

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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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.

HUBUNGAN ANTARA KADAR LEPTIN DAN ADIPONEKTIN PLASMA PADA PASIEN DENGAN DIALISIS RUTIN Raka Widiana, I Gde; Kandarini, Yenny; Suwitra, Ketut
journal of internal medicine Vol. 9, No. 2 Mei 2008
Publisher : journal of internal medicine

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Leptin and adiponectin (ADPN) are adipokines with respective pro-atherogenic and anti atherogenic properties. In nonrenalpatients, both hyperleptinemia and hypoadiponectinemia are associated with cardiovascular complication. Relationshipsbetween serum leptin and ADPN in patients with dialysis is not consistently reported.Objective of this study is evaluate relationships between serum ADPN and leptin in patients with dialysis. A cross sectionalstudy was performed in and 54 HD and 22 CAPD patients.Seventy six patients were enrolled this study, M/F 41/76, aged 48.4±11.4 year, BMI 21.4±2.7 kg/m2, haemoglobin (Hb)7.9±1.5 mg/dL, blood sugar 94.8±33.5 mg/dL, albumin 4.1±0.4 g/dL, total-cholesterol 177.9±46.3 mg/dL, triglyserida 164.4±104.8mg/dL, SC 14.3±3.8 mg/dL, TNF 14.40±7.43 pg/mL, ADPN 17.6±7.6 µg/mL, leptin 13068±23589 µg/mL (log leptin 3.7±0.59µg/ml). Using Spearmans rho analysis there were negative correlation between log-leptin and ADPN (r= -0.39, p= 0.00), andpositive correlation between log leptin and Hb (r= 0.25, p= 0.04), insulin(r= 0.44, p = 0.00), total-cholesterol (r= 0.34, p = 0.003),triglyserida (r= 0.41, p= 0.00), and BMI (r= 0.41, p= 0.00), but there was no correlation between log-leptin and albumin, bloodsugar, SC and TNF alfa. Using multiple regression to analyze relationship between ADPN and leptin, insulin, Hb, and dialysismodality, we found log leptin independently correlated with ADPN (B= -0.402, p= 0.01, 95%CI B: -1.24 to -0.32). Using multipleregression to analized relationship between ADPN with log-leptin, BMI, total cholesterol, and triglyserida, we found log leptin(beta= -0.3, p= 0.01, 95%CI B: -0.98 to -0.13) and triglyserida independently correlated with ADPN (beta= -0.5, p= 0.00, 95%CIB: -0.008 to -0.003).Serum leptin and triglyseride relate with ADPN. Some metabolic parameters such as insulin resistance, anemia, dialysismodality, nutritional status (BMI and total cholesterol) have indirect relationship with ADPN may be through leptin secretion.

THROMBOPHILIA KARENA DEFISIENSI PROTEIN C DAN PROTEIN S Rama Putra, I Made; Suega, Ketut
journal of internal medicine Vol. 11, No. 2 Mei 2010
Publisher : journal of internal medicine

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Protein C is a natural anticoagulant, inhibits thrombin generation. Protein C de! ciency, is associated with a variablyincreased risk of thrombosis. Incidence of symptomatic protein C de! ciency is approximately 1 in 16,000 to 1 in 32,000 persons,similar in men and women. Morbidity in protein C de! ciency greatly increases with advancing age, when patients are at greaterrisk for thrombotic events such DVT, PE, postphlebitic and blindness secondary to vitreous hemorrhages may occur in patientswith these severe conditions. The etiology can be inherited and acquired in a number of clinical scenarios include meningococcalseptic shock; DIC; liver disease; or chemotherapy. Diagnostic base on personal history of venous thrombosis, thromboembolicevents, abnormal laboratory coagulation tests. The laboratory workup should include haemostatic parameters, coagulationsystem such aPTT, PT, ! brinogen level and D-dimer test. A decreased protein C activity level is required. Imaging studies areappropriate for assessing the presence of thrombotic disease in a particular vessel. The treatment depends largely on a particularpatient?s disease manifestations. Surgical treatment may be appropriate in some circumstances.We reported, a male Balinese 62 years old came with complain red vision and dull feeling since a moth prior toadmission. No historical medical problem found. Physical exam found hypertension and laboratory ! nding showed slightdyslipidemia. Ophthalmologic examination revealed BRVO (Branch Retinal Vein Occlusion) ocular sinistra. Hypercoagulablaestate are suspected. Hematologic exam revealed light hyperagregation and low level of protein C and protein S. Treated withheparin 5000 unit intravenously followed by drip 1000 unit per hour for 3 day continued with warfarin 4 mg OD reach INR 1.5? 2.5. Good resulted base on patient?s good compliance.

KADAR ADIPONEKTIN PLASMA PADA PASIEN YANG MENJALANI HEMODIALISIS DI RUMAH SAKIT SANGLAH DENPASAR Sanjaya, Surya; Suwitra, Ketut
journal of internal medicine Vol. 11, No. 1 Januari 2010
Publisher : journal of internal medicine

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Adiponectin, a cytokine with anti-inß ammatory properties that is secreted from adipose tissue. Adiponectin has beenshown to be a predictor of cardiovascular events in the general population and patients who undergoing hemodialysis. The aimof this study is to evaluate serum adiponectin in patient undergoing regular hemodialysis.A cross sectional study involved 53 reguler hemodialysis patient at Sanglah hospital. Inclusion criteria was patientundergoing regular hemodialysis more than three month and twice a week. We exclude severe infections, abnormality of liverfunctions test, malignancies and diabetes mellitus.The mean of age and abdominal circumference was 48.01 ± 12.3 years old and 79.5 ± 9.99 cm. Systolic and diastolicblood pressure pre hemodyalisis was 140 ± 20.7 mmHg and 83.3 ± 10.7 mmHg. Systolic and diastolic blood pressure posthemodialysis was 148.6 ± 23.6 mmHg and 85.6 ± 11.5 mmHg, respectively. We found serum level of calcium 9.5 ± .97 mmol/l,inorganic phospat 6.4 ± 2.1 mmol/l, BUN 84.8 ± 19.9 mg/dl, serum creatinin 16.1 ± 3.9 mg/dl, hemoglobine levels 7.7 ± 1.4 g/dland blood glucose levels 92.9 ± 1.4 mg/dl. Serum levels of adiponectin was 15.4 ± 5.98 mg/l compare with normal levels 5.52mg/l. Levels of serum adiponectin in regular hemodialysis patients is three fold higher than normal population.

PROFIL PENDERITA SEPSIS AKIBAT BAKTERI PENGHASIL ESBL Irawan, Danny; -, Hamidah; -, Purwati; EA, Triyono; -, Bramantono; V, Arfianto; U, Hadi; -, Nasronudin; -, Suharto; E, Soewandojo
journal of internal medicine Vol. 13, No. 1 Januari 2012
Publisher : journal of internal medicine

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Extended Spectrum !-Lactamases (ESBL) is plasmid enzyme which catalyzing hydrolysis and inactivation !-lactamantibiotic, including third generation of Cephaloporin, penicillin and aztreonam. This enzyme is mutation of !-lactamaseTEM-1, TEM-2, and SHV-1 which commonly found in Enterobacteriaceae and normally have resistance to penisillin andrst generation celaphorin. The incidence of infection cause by ESBL bacterial is increasing worldwide. AntimicrobialResistance in Indonesia: prevalence and prevention (AMRIN study) is showed incidence of infection ESBL bacterial 29%E. coli, and 36% K. pneumonia. This study is descriptive and restrospectively learn about prole of DMK with septicemiapatient caused by ESBL bacterial in Internal Medicine Ward RSUD Dr Soetomo within 1st January 2010 until 30th June2011. Sixty four patient were recruited and 48 patients with ESBL bacterial positive. Mortality rate is 16.7%, severe septiccondition 27.08%, septic shock 14.58%. The result of positive ESBL bacterial was found from urine culture (37.5%).Sensitivity of antibiotics results are meropenem (98.07%), amikacin (88.46%).

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