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"Patients with liver cirrhosis frequently have infection which can deteriorate further the already impaired liver function. The most common form of infection in this particular patients are spontaneous bacterial peritonitis, urinary tract infection, and respiratory infection. Causative organism mostly Gram negative micro organism and originate from the gastrointestinal tract. The weaken of immune defense mechanism and also the altered gastrointestinal tract motility can explained most of these infection. This paper will review the bacterial infection in liver cirrhosis with some guidance in the management."

"Small intestinal bacterial overgrowth is a condition where the proximal small intestine harbours more than 10 organisms/ml intestinal fluid for a long period. Bacterial overgrowth could be found in patients with certain clinical conditions, such as intestinal anatomical disorders, intestinal motility disorders, and several diseases including liver cirrhosis. It was reported that the prevalence of bacterial overgrowth in patients with liver cirrhosis was around 30%-75%. Small intestinal bacterial overgrowth could induce various clinical conditions from mild to severe cases, therefore it is important to recognise its signs and symptoms, diagnosis, and management. This article will also review the clinical management of small intestinal bacterial overgrowth in liver cirrhosis."

"Spontaneous bacterial peritonitis (SBP) is one of serious complication of liver cirrhosis. Most of the patient with SBP have severe reduced liver function that clasified as Child Plugh class C. There are other risk factors for SBP such as poor nutritional status, GI bleeding, intravascular catheter insertion, ascites fluid protein concentration of less than I g/L, large volume paracentesis, urinary tract infection and respiratory tract infection. The management of SBP is mainly the administration of proper antibiotics. The antibiotic of choice for the emperial treatment is cefotaxim."

"Latar Belakang: Kondisi dekompensata tanpa infeksi bakteri pada pasien sirosis hati dapat meningkatkan kadar prokalsitonin (PCT). Belum ada penelitian yang secara khusus membandingkan kadar PCT berdasarkan kompensasi hati dan ada tidaknya infeksi bakteri. Tujuan: Mengetahui peran PCT dalam membantu menegakkan diagnosis infeksi bakteri pada pasien sirosis hati. Metode: Studi potong lintang dilakukan terhadap pasien sirosis hati yang berobat jalan dan dirawat inap di RSUPNCM Jakarta dari April sampai Mei 2016. Pada pasien dilakukan pemeriksaan PCT dan penentuan ada tidaknya infeksi bakteri berdasarkan pemeriksaan standar sesuai jenis infeksi yang dicurigai. Dilakukan analisis untuk mengetahui perbedaan rerata kadar PCT pada pasien sirosis hati yang tidak terinfeksi bakteri dan yang terinfeksi bakteri, serta pencarian nilai titik potong PCT untuk mendiagnosis infeksi bakteri pada sirosis hati dekompensata dengan menggunakan receiver operating curve (ROC). Hasil: Didapatkan 55 pasien sirosis hati, pria sebanyak 65,5%, dengan rerata usia 55,34±1,308 tahun. Sebanyak 38 (69,1%) pasien sirosis hati dekompensata yang 22 (57,9%) diantaranya tidak terinfeksi bakteri dan 16 (42,1%) terinfeksi bakteri. Pada pasien yang tidak terinfeksi bakteri terdapat perbedaan rerata kadar PCT yang bermakna antara pasien dekompensata (0,738ng/mL±1,185) dibandingkan dengan 17 pasien kompensata (0,065ng/mL±0,022). Rerata kadar PCT pasien dekompensata yang terinfeksi bakteri (3,607ng/mL±0,643) lebih tinggi bermakna dibandingkan dengan yang tidak terinfeksi bakteri(0,738ng/mL±1,185). Dari kurva ROC, kadar PCT pada pasien sirosis hati dekompensata didapatkan area under curve (AUC) 0,933 (IK 0,853-1,014) untuk diagnosis infeksi bakteri. Nilai titik potong kadar PCT untuk mendiagnosis infeksi bakteri pada pasien sirosis hati dekompensata adalah 2,79ng/mL dengan sensitivitas 87,5% dan spesifisitas 86,4%. Kesimpulan: Pada pasien sirosis hati yang tidak terinfeksi bakteri, kadar PCT pasien dekompensata lebih tinggi dibandingkan dengan yang kompensata. Kadar PCT pasien sirosis hati dekompensata yang terinfeksi bakteri lebih tinggi dibandingkan dengan yang tidak terinfeksi bakteri. Sementara nilai titik potong kadar PCT untuk mendiagnosis infeksi bakteri pada pasien sirosis hati dekompensata adalah 2,79ng/mL.

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Background: Liver decompensated without bacterial infection may increase procalcitonin (PCT) level in liver cirrhosis patients. Previous studies did not provide conclusive results about the differences of PCT level due to specific liver compensation and bacterial infection.

Objective: To examine the role of PCT in assisting the diagnosis of bacterial infection in liver cirrhosis patients.

Methods: A cross sectional study was conducted in liver cirrhosis patients who were outpatients and admitted to Cipto Mangunkusumo Hospital, Jakarta between April and May 2016. Procalcitonin were examined and bacterial infection were identified using standard criteria for each type of infection being suspected. Analysis were performed to determine differences in the level of PCT among liver cirrhosis patients without bacterial infection and with bacterial infection, also to get cut off point of PCT for bacterial infection diagnosis in decompensated liver cirrhosis patients using receiver operating curve (ROC).

Results: There were 55 patients with liver cirrhosis, 65,5% male, with mean of age 55,34±1,308 years. A total of 38 (69,1%) patients had decompensated liver cirrhosis, while 22 (57,9%) of them without bacterial infection and 16 (42,1%) with bacterial infection. In the absence of bacterial infection, there was significant difference between PCT level in decompensated patients (0,738ng/mL±1,185) and 17 compensated patients(0,065ng/mL±0,022). Decompensated patients with bacterial infection (3,607ng/mL±0,643) had significantly higher PCT levels than those without bacterial infection(0,738ng/mL±1,185). From ROC, level of PCT for bacterial infection in decompensated liver cirrhosis was area under curve (AUC) 0,933 (IK 0,853-1,014). Cut off point of PCT for bacterial infection diagnosis in decompensated liver cirrhosis patients was 2,79ng/mL with a sensitivity of 87.5% and specificity of 86,4%.

Conclusion: In the absence of bacterial infection, PCT levels of decompensated patients was higher than compensated ones. Procalcitonin levels of decompensated liver cirrhosis patients with bacterial infection was higher than those without bacterial infection.Cut off point of PCT for bacterial infection diagnosis in decompensated liver cirrhosis patients was 2,79ng/mL."

"Since the limulus test, a method for the evaluation of endotoxin levels using extract from horsehoc crabs (limulus, spp), was developed in the year 1969 by Levin and Bang, there have been reports on endotoxin from portal blood without negative gram bacterial infection, a condition known as endogenous endotoxemia."

"LATAR BELAKANG : Sirosis hati merupakan salah satu masalah kesehatan di Indonesia. Penyakit ini merupakan penyakit hati yang sering dijumpai selain hepatitis virus akut dan kanker hati. Komplikasi sirosis hati yang tersering adalah asites. Adanya asites merupakan prognosis yang buruk karena hanya sekitar 50% penderita sirosis hati dengan asites dapat bertahan hidup dalarn waktu 2 tahun. Asites juga merupakan faktor predisposisi terjadinya komplikasi berbahaya seperti Peritonitis Bakteri Spontan (PBS).BAHAN DAN METODE : 74 subyek penelitian penderita sirosis hati dengan asites. Pada cairan asites dilakukan biakan aerob-anaerob, pemeriksaan hitung leukosit dengan alat hitung sel otomatis Sysmex XT2000i®, hitung jenis leukosit dengan mikroskop dan uji leukosit esterase carik celup urin sedangkan pemeriksaan albumin, protein dan LDH dilakukan untuk serum dan cairan asites.HASIL : Pada penelitian ini didapatkan penderita PBS sebanyak 14 orang (18.92%). Pada kelompok PBS didapatkan netrositik asites sebanyak 12 orang (85.71%). Dari hasil biakan yang positif pads kelompok penderita PBS berhasil diisolasi dua jenis kuman golongan Enterobacteriaceae yaitu Escherichia call dan Enterobacter aerogenes. Kedua kuman ini diduga menghasilkan Extended Spectrum Beta Lactamase (ESBL). Dengan menggunakan cara perhitungan stastistik menurut Bland-Altman didapatkan bahwa hasil hitung jumlah leukosit pada cairan asites dengan menggunakan alat otomatis Sysmex XT2000P tidak berbeda bermakna dengan cara manual. Untuk memperkirakan jumlah PMN cairan asites ? 250 sellpL maka cut off point untuk MuitistixlOSG® adaiah pada skala trace sedangkan untuk Comburl4M® adalah pada skala positif-2. Sebagian besar cairan asites pada penderita PBS termasuk transudat berdasarkan kriteria Light (85.71 %). Pada 92.86 % penderita PBS mempunyai SAAG > 1.1 g/dL.KESIMPULAN : Pada penelitian ini diperoleh proporsi PBS sebesar 18.92 % dan proporsi netrositik asites sebesar 85.71%. Kedua jenis kuman batang Gram negatif diduga menghasilkan ESBL sehingga resisten terhadap Sefotaksim. Hitung leukosit cairan asites dapat dilakukan dengan alat penghitung sel otomatis Sysmex XT2000i. Leukosit esterase carik celup urin Multistixi OSG® dan Comburl0M@ dapat digunakan untuk memperkirakan jumlah PMN cairan asites > 250 sellpL. Cairan asites pada penderita PBS temasuk transudat menurut modifikasi kriteria Light. PBS tidak mempengaruhi SAAG.SARAN : Parasentesis diagnostik harus dilakukan sebelum pemberian antibiotik empirik. Leukosit esterase carik celup urin dapat digunakan sebagai salah satu cara untuk memdiagnosis PBS secara "bedside". Penelitian lanjutan untuk mendapatkan pola dan kepekaan antibiotika kuman penyebab PBS.

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Cirrhosis is identified as one of major health problems in Indonesia. It is found to be the most prevalent liver disease in addition to acute viral hepatitis and liver cancer. Ascites is the most common complication associated with cirrhosis. About 50% of patients with cirrhosis who develop ascites die within 2 years of diagnosis. Ascites also predisposes life-threatening complication such as Spontaneous Bacterial Peritonitis (SBP).

Materials and Methods. 74 cirrhosis patients who develop ascites were included in the study. The ascitic fluid was cultured in aerobic and anaerobic media. Leukocytes were evaluated for leukocytes count using Sysmex XT2000iT"" automatic cell counter, leukocytes differential count was observed under the microscope, and dip stick urine of leukocyte esterase test. Moreover, albumin, protein, and LDH level were assessed for both serum and ascitic fluid.

Results. Spontaneous Bacterial Peritonitis was diagnosed in 14 subjects (18.92%). Twelve subjects (85.71%) within this group developed neutrocytic ascites. Enterobacteriaceae pathogens, i.e. Eschericiiia coil and Enterobacter aerogerles, had been isolated from the ascitic fluid culture. These pathogens were suspected for producing Extended Spectrum Beta Lactamase (ESBL). Using Bland-Altman test, it was discovered that there were no significant differences in leukocytes count of ascitic fluid either measured with Sysmex XT2000iT"' automatic cell counter or conventional method. The cut-off point for MultistixlOSGTm was set on trace scale, whereas the ComburlOMTM was set on scale positive-2 to obtain a number of PMN leukocytes count of more than 250 cellslpL. Based on Light criteria, 85.71% of ascitic fluid from the SBP patients were considered as transudates. Meanwhile, 92.86% of SBP group showed an SHAG ? 1.lg/dL.

Conclusions. The study reveals that the proportion of SBP is 18.92% and neutrocytic ascites is 85.71%. Both of the Gram-negative bacteria are considered producing ESBL that induce resistance to Cefotaxime. Leukocytes count of ascitic fluid can be measured using Sysmex XT2000iTM automatic cell counter. To predict PMN leukocyte count of more than 250 cells/pL, the dip stick urine leukocytes esterase test using MultistixlOSGT"^ and ComburlOMTM are available. The ascitic fluid in SBP patients are classified as transudates, based on Light criteria. SBP has no effect against SAAG.

Suggestions. A diagnostic paracentesis should be performed prior to empirical antibiotics therapy. The dip stick urine leukocytes esterase test can be use as an alternative method to diagnose SBP along with the other bedside techniques. Further study is required to attain pattern and sensitivity of SBP pathogens."

"The recent advances of endoscopic examination had proven that source of upper gastrointestinal bleeding in liver cirrhosis is not always caused by esophageal varices rupture but also gastric mucosal lesion. The prevalence of gastric ulcer in patients with liver cirrhosis is higher than healthy individuals. Imbalance of defensive and aggressive factors of gastric mucosa may involve in development of portal hypertensive gastropathy (PHG). Several studies reported hemodynamic changes associated wuth portal hypertension causing decreased mucus layer thickness as one of mechanism of PHG. Other dialogic factors of PHG were hypoacidity, hypergastrinemia, reduced hexosamin concentration, mucus metabolic function associated with decreased prostaglandin E2, and increased nitric oxyde which had caused mucus wall thickness changes. Gastric mucus damage induced by portal hypertension has important role in the pathogenesis of gastric ulcer in liver cirrhosis."