The liver plays a central role in the control of haemostasis being the site of synthesis of most of the coagulation factors and natural anticoagulants, as well as fibrinolytic factors except the main activators of the fibrinolytic system (t-PA and u-PA). The liver also clears many of the activated clotting and fibrinolytic factors, as well as haemostatic activation complexes (TAT and PAP) and end product of fibrin degradation, FDP. Therefore, liver disease results in a complex and multifactorial pattern of defects in haemostatic function in the form of: (i) decreased synthesis of coagulation factors (ii) Abnormal protein synthesis e.g. dysfibrinogen (iii) Deficiency of natural anticoagulants (iv) Enhanced fibrinolytic activity (v) Quantitative and qualitative platelet defects (vi) Consumptive coagulopathy as in advanced liver disease. These abnormalities of haemostasis, which often occurs in the form of multiple defects, underlie the haemorrhagic diathesis, which often complicates liver disease. In the same manner, measurement of various haemostatic factors can be employed to reflect the degree of liver damage

Background: Chronic hepatitis B (CHB) in Oman is similar to the Mediterranean Region with significant number of HBeAg negative patients. Interferon therapy is less effective in these patients and lamivudine is an alternative treatment. Patients and Methods: Thirty patients (16 HBeAg positive), who received lamivudine were studied retrospectively over 27 months. End of treatment (after 52 weeks) and sustained responses were analyzed for both HBe-antigen positive and negative patients. Results: Of the thirty patients, who received lamivudine, 22 patients (73%) completed 52 weeks therapy. Eight patients had previously received interferon treatment. The overall end-of-treatment (ET) biochemical response was 81.8% and virological response was 45%. Among patients who were HBeAg positive and HBeAg negative, similar proportion of patients achieved end-of-treatment biochemical responses (80% Vs 83.3%) and virological responses (40% Vs 50%) respectively. Sustained biochemical and virological response was achieved in four patients, two each in both groups. Of the nine patients currently receiving treatment, six of them had normalization of ALT and two had undetectable HBV DNA. Conclusion: Almost 50% of patients with CHB in Oman have HBeAg negative hepatitis. Therapy with lamivudine is effective in both HBeAg positive and negative cases

Aim: The aim of this study is to determine the frequency of celiac disease (CD) in a group of children with juvenile rheumatoid arthritis (JRA) and determine the correlation between the presence of the serologic markers and the histological diagnosis of CD. Patients and Methods : Forty-two children (24 females) with JRA, aged between 5-15 years underwent study of serologic markers for CD (gliadin-IgA, gliadin-IgG, reticulin and endomysium-IgA antibodies). Endoscopic intestinal biopsy was performed in patients who had positive serologic markers for CD. The diagnosis of CD was based on the classic finding of villous atrophy and crypt hypertrophy. Results: Eighteen patients (42.8%) had serologic markers for CD; ten of them with a systemic form, five with a polyarticular form and three with a pauciarticular form of JRA. Levels of AGA ­IgG were high in 14 patients (77.8%), four patients (22.2%) had high levels of AGA-IgA and seven patients (38.9%) had anti-endomysium antibodies (AEA). One patient had anti-reticulin antibodies (ARA) 5.5%. Sixteen patients underwent intestinal biopsy; in only one patient with AEA antibodies (2.38%), biopsy revealed typical finding of CD. The patient with CD showed improvement in both growth parameter as well as articular symptoms after starting gluten-free diet Conclusion: Our study shows that the screening for silent CD among children with JRA may be useful. Those patients with AEA need further follow up since these antibodies are quite sensitive and specific for CD