ABSTRACT
AIM: This study was conducted to assess the predictive value of coagulation abnormalities in determining disease severity and prognosis of acute pancreatitis (AP). METHODS: Patients of AP and 25 healthy volunteers were included in this prospective observational study. The final outcomes were disease severity assessed by Computed Tomography Severity Index, Acute Physiological Assessment and Chronic Health Evaluation--II, presence of organ failure and mortality. Prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), fibrinogen, antithrombin-III (AT-III), protein-C, and protein-S levels were assessed on day 0, 3 and 7 of admission. RESULTS: Of the 38 patients included, 13 died. Mean PT and TT were similar between patients and controls on any given day. PTT showed elevation on day 3 and 7 (p = 0.001) compared to controls, although fibrinogen and D-dimer were significantly higher in patients on all days. Protein C and AT-III were significantly lower in patients and more so in non survivors ( (p = 0.001)) than controls. Multiple logistic regression analysis revealed D-dimer levels > or = 400 - 800 ng/ml and AT- III level of < 71% at admission were associated with high mortality (OR 11.2, AUROC 0.70 and OR 16.6, AUROC 0.82 respectively) as well as predicted organ failure. CONCLUSION: Serum D-dimer and antithrombin-III levels can be used to assess disease severity and predict outcome of patients with acute pancreatitis.
Subject(s)
Blood Coagulation Factors/metabolism , Pancreatitis/blood , Severity of Illness Index , Adult , Aged , Antithrombin III/metabolism , Female , Fibrin Fibrinogen Degradation Products/metabolism , Fibrinogen/metabolism , Humans , Male , Middle Aged , Partial Thromboplastin Time , Predictive Value of Tests , Prognosis , Prospective Studies , Protein C/metabolism , Protein S/metabolism , Prothrombin Time , Thrombin TimeABSTRACT
The present report is a review article on various aspects of Hepatitis C virus (HCV) genotypes and their subtypes. HCV has six genotypes and several subtypes showing important epidemiological and clinical implications. The information based on previous studies and presented through this article highlight the origin, classification and causes of genetic diversity, global status, detection assays, pathogenicity and response to treatment of HCV-genotypes. The six genotypes differ in 30-35% of nucleotide sites over the complete genome. The difference in genomic composition of sub-types of genotype is usually found to be 20-25%. The variability remains more frequent in structural genes as compared to non-structural or untranslated genes. Both genotypes and their sub-types show a varied prevalence globally and raise several issues related to their transmission and treatment of HCV-infection. All this information has a great significance while planning future strategies for eradication and therapeutic management of HCV. In addition, these reports produce a further scope for more studies to unravel the mystery behind HCV-genotypes and formulate guidelines to resolve this public health problem noted worldwide.
