Kg Sajith

Recurrent acute pancreatitis: clinical profile and an approach to diagnosis.

Background and AimsThough recurrent acute pancreatitis is often seen in clinical practice, there are few comprehensive articles on this entity. The aim of this study therefore was to assess the etiological and clinical profile as well as diagnostic yield of non-invasive and invasive tests in this group of patients.MethodsAll patients with recurrent acute pancreatitis seen from 2002 to 2007 were included in the study, retrospectively. Clinical information, investigation, and treatment data were collected for all patients by a standardized review of medical charts. Diagnostic tests were grouped into level one (non-invasive) and level two (invasive) tests and their yield was assessed. Comparison was made between the group with known etiology and idiopathic group to look for significant differences.ResultsA total of 188 patients with recurrent acute pancreatitis were seen during the study period. Common etiological factors were biliary disease (37%), pancreas divisum (8.5%) and alcohol (6.4%). Multiple etiologies were seen in 7% of cases, and no cause was found in 32.4%. The diagnostic yield of level-one investigation (non-invasive) was 29.3%. Level-two tests (invasive) identified presumptive etiologies in 38.3% of cases. Complications developed in 12.2% and there was no mortality. Clinical features and complications were similar in the idiopathic group and those with known etiology.ConclusionsEtiological diagnosis was obtained in 67.6% of patients after comprehensive diagnostic work up. Diagnosis in the majority of patients could only be reached after invasive tests (bile crystal analysis, EUS, ERCP). Early diagnosis and etiology-based therapy is the key to optimum patient outcome.

Duodenal villous morphology assessed using magnification narrow band imaging correlates well with histology in patients with suspected malabsorption syndrome

Narrow band imaging with magnification enables detailed assessment of duodenal villi and may be useful in predicting the presence of villous atrophy or normal villi. We aimed to assess the morphology of duodenal villi using magnification narrow band imaging and correlate it with histology findings in patients with clinically suspected malabsorption syndrome.

Hepatocellular carcinoma continues to be diagnosed in the advanced stage: profile of hepatocellular carcinoma in a tertiary care hospital in South India

Summary This report is an analysis of 231 patients with hepatocellular carcinoma (HCC) from a tertiary care hospital in India. Most of the HCCs were diagnosed in cirrhotics and at an advanced stage which limited the therapeutic options. Physician awareness of this complication of cirrhosis and regular ultrasound screening of cirrhotic patients will help in detection of early stage cancers and, thus, enhance the survival rates.

Plasma von Willebrand factor levels predict in-hospital survival in patients with acute-on-chronic liver failure

Background and AimsCirculating levels of von Willebrand factor (vWF) predict mortality in patients with cirrhosis. We hypothesized that systemic inflammation in acute-on-chronic liver failure (ACLF) will stimulate endothelium, increase vWF levels, and promote platelet microthrombi causing organ failure.MethodsIn this prospective study, we correlated plasma vWF levels with organ failure, liver disease severity, sepsis, and systemic inflammatory response syndrome (SIRS) and also analyzed if vWF levels predicted in-hospital composite poor outcome (i.e. death/discharged in terminal condition/liver transplantation) in consecutive ACLF patients.ResultsTwenty-one of the 50 ACLF patients studied had composite poor outcome. ACLF patients had markedly elevated vWF antigen and activity (sevenfold and fivefold median increase, respectively) on days 1 and 3. Median ratio of vWF to a disintegrin and metalloprotease with thrombospondin type 1 motif, member 13 (ADAMTS13) activity on day 1 was significantly higher in ACLF patients (11.2) compared to 20 compensated cirrhosis patients (3.3) and healthy volunteers (0.9). On day 1, area under ROC curve (AUROC) to predict composite poor outcome of hospital stay for ACLF patients for vWF antigen, vWF activity, and model for end-stage liver disease (MELD) score were 0.63, 0.68, and 0.74, respectively. vWF activity correlated better with liver disease severity (MELD score, ACLF grade) and organ failure (Sequential Organ Failure Assessment [SOFA] score) than vWF antigen; in contrast, neither vWF antigen nor activity correlated with platelet count, sepsis, or SIRS.ConclusionsvWF levels are markedly elevated, correlate with organ failure, and predict in-hospital survival in ACLF patients. This data provides a mechanistic basis for postulating that vWF-reducing treatments such as plasma exchange may benefit ACLF patients.

Maintenance zinc therapy after initial penicillamine chelation to treat symptomatic hepatic Wilson’s disease in resource constrained setting

BackgroundExperience with zinc in treating symptomatic hepatic Wilson’s disease (WD) is limited.AimTo study the efficacy of Penicillamine followed by zinc in treating symptomatic hepatic Wilson’s disease.MethodsWe retrospectively analyzed case records of 31 symptomatic hepatic WD patients for whom disease severity scores (Child’s, model for end-stage liver disease (MELD), Nazer’s, and New Wilson Index (NWI) score) and 24-h urinary copper were compared at 3-time points—baseline at presentation, at transition from penicillamine to zinc and at end of follow up.ResultsThirty-one patients (median age 11 [5–24] years) with symptomatic hepatic WD were studied; ten had associated neuropsychiatric manifestations of WD. Penicillamine was changed to zinc sulfate either due to financial constraints (28 patients) or due to adverse effects of penicillamine (3 patients). At presentation (baseline), six patients belonged to Child’s class A, five to Child’s B, and 17 to Child’s C. Duration of initial penicillamine chelation therapy was 134 (2–320) weeks, and of subsequent zinc therapy was 363 (35–728) weeks. There was a significant improvement in liver function tests and disease severity scores (Child’s, MELD, Nazer’s, and NWI score) at the transition from penicillamine to zinc compared to baseline. This improvement was maintained until the end of study period with 90% survival at 10 (2–20) years. Fifteen of the 17 Child’s C cirrhotic patients showed significant improvement in disease severity scores from baseline until end of follow up.ConclusionsPenicillamine followed by zinc may be a safe and effective treatment in resource-constrained setting for symptomatic hepatic WD patients in all grades of baseline disease severity. Some patients with decompensated cirrhosis due to WD may be managed with medical treatment, avoiding liver transplantation.

Maintenance Zinc Therapy After Initial Penicillamine Chelation to Treat Symptomatic Hepatic Wilson's Disease in Resource Constrained Setting

Background Experience with zinc in treating symptomatic hepatic Wilson’s disease (WD) is limited.

Is empiric therapy with fluconazole appropriate for esophageal candidiasis

We studied the prevalence of fluconazole resistance in esophageal candidiasis. Patients with suspected esophageal candidiasis during gastroscopy underwent culture of white plaques. Minimum inhibitory concentration (MIC) >64 μg/mL of fluconazole for Candida was indicative of resistance. Sensitivity of itraconazole was tested in a subset of resistant strains. Sixty-five patients were included. Mean (SD) age was 50.03 (13.5) years and 67.7 % were males. Predisposing factors for candidiasis were found in 42 (64.6 %) patients. C. albicans was identified in 64 (97.4 %) patients and C. glabrata in one patient. Fluconazole resistance was seen in 38 (59.4 %) patients with C. albicans and also in the one patient with C. glabrata. All the fluconazole resistant isolates of C. albicans had MIC >128 μg/mL suggesting very high resistance. Twelve patients with fluconazole resistance had itraconazole resistance as well. The study shows a high rate of fluconazole resistance in patients with esophageal candidiasis.

Erythrocytosis as a cause of false increase in prothrombin time and activated partial thromboplastin time.

Editor: Prothrombin time (PT) as an index of liver dysfunction is well-established. Abnormal PT in a patient with acute hepatitis alerts us to the possibility of impending liver failure and mandates much closer monitoring. We present a case where PT was falsely elevated. A 23-year-old gentleman, with ventricular septal defect, severe pulmonary hypertension, and reversal of shunt, was referred for opinion on deranged liver function. He had no jaundice, prodrome, ascites, or signs of liver decompensation. On examination, his vital parameters were normal. There was clubbing and cyanosis with normal neck veins. Abdominal examination showed no organomegaly or free fluid. He was on digoxin and diuretics and was not anticoagulated. He had erythrocytosis [hemoglobin of 23.3 g/dL (mean corpuscular volume, 92.6 fL; packed cell volume, 74 %)] with normal total white blood cell and platelet counts. He had mild indirect hyperbilirubinemia (serum total bilirubin, 1.6 mg/dL; direct fraction, 0.3 mg/dL), mildly elevated liver enzymes (serum alanine aminotransferase, 75 U/L; serum aspartate aminotransferase, 57 U/L), and normal serum albumin (5 g/dL). His PT was prolonged, 26.3 s, i.e. 14 s above the normal upper limit with an international normalized ratio (INR) of 2.37. Activated partial thromboplastin time (aPTT) was also prolonged, 58.9 s, i.e. 19 s above the normal upper limit. The PT and aPTT values were repeated on two different occasions with similar results. Etiological evaluation of liver disease, in the form of HBsAg, HCV antibody, serum ceruloplasmin, and serum ferritin, was unyielding. His liver on ultrasound appeared normal. The presence of coagulopathy was the only factor alarming in what looked like a nonspecific liver function abnormality. The tests were repeated on the same day after adding excess blood (7 mL) to the same amount of citrate thus maintaining the normal bloodto-anticoagulant ratio (Table 1). The corrected PT and aPTT were 11.6 s (INR, 1.08) and 29.4 s, respectively. The patient was reassured at that point and asked to review later. The patient was unable to come for reassessment, but on telephonic follow up at 6 months from the initial visit, he remained well and anicteric.

32 LOW SERUM CHOLINESTERASE LEVELS-CAN DIFFERENTIATE BETWEEN WELL COMPENSATED AND DECOMPENSATED CIRRHOSIS

S 20TH ANNUAL CONFERENCE OF INASL, MARCH 2–4, 2012 S20