Annals of PIMS-Editorial Board

In vitro experiments show strong antiviral effects of fluvastatin against hepatitis C virus. Fluvastatin used as monotherapy in vivo showed suppressive effects of HCV clinically that are modest, variable, and often short-lived. Statins and fluvastatin, in particular, appear to be safe for use in hepatitis C⁴. It has recently been observed that a proportional relationship is found between serum lipid profiles and hepatitis C viral load in patients with genotype 2 infection; however, whether manipulation of lipid profiles would improve the response to current anti-HCV therapy is to be determined in further studies⁵. Further it has been investigated that in chronic hepatitis C serum ferritin is a useful marker for assessing disease duration and progression before starting treatment and for predicting therapeutic response while on therapy. Serum ferritin rise during antiviral therapy is largely independent of hemolysis and likely indicates activation of macrophages in response to antivirals⁶. Over a million persons die annually due to HBV related complications around the world^7&8.In patients coming with one hepatic infection, other viral infections should be sought as they share a common mode of spread and may affect the overall response to treatment⁹. Mild ascites is hard to notice, but severe ascites leads to abdominal distension. Peritoneal fluid of less than 2 L is difficult to detect clinically, and ultrasound is useful in defining small amounts of ascites. A pleural effusion is found in a small percentage of patients with ascites, usually on the right side. This is due to the presence of a diaphragmatic defect that allows ascitic fluid to pass into the pleural cavity. Patients with ascites generally will complain of progressive abdominal heaviness and pressure as well as shortness of breath due to mechanical impingement on the diaphragm. Ascites is detected on physical examination of the abdomen by visible bulging of the flanks in the reclining patient ("flank bulging"), "shifting dullness" or in massive ascites with a "fluid thrill". Other signs of ascites may be present due to its underlying etiology. For instance in portal hypertension, patients may also complain of pedal edema, bruising, gynecomastia, hematemesis, or mental changes due to encephalopathy. The study has documented that in current clinical practice the classical signs of cirrhosis expected to be present in advanced cases are observed quite infrequently and therefore, cannot be relied upon in clinical diagnosis of the disease alone. The diagnosis of cirrhosis should be supported by other means including ultrasound examination of the abdomen etc¹⁰. An other study shows that the frequency of some of the clinical features of cirrhosis likes jaundice, pyrexia, spider angiomas, gynecomastia, palmer erythema and dupuytren`s contracture is different in our population as compared to that reported in western literature. It could be due to difference in etiology of cirrhosis (alcohol in the west and viral hepatitis in our population)¹¹. Both ALT/AST ratio reversal (AST/ALT>1) and prolonged prothrombin time are separate indicators of hepatic cirrhosis. The high positive predictive value here shows that almost all the patients with reversed ratio and prolonged PT will have cirrhosis¹². Further it was found that the platelet count less than 65 x 10³/mm³ serum albumin less than 2.2 g/dl and portal vein diameter more than 13 mm on ultrasound are independent and significant predictors of esophageal varices on endoscopy¹³.
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