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Background/Aims: The ideal end point of treatment for chronic hepatitis B virus (HBV) infection is sustained off-therapy hepatitis B surface antigen (HBsAg) loss with or even without seroconversion to anti-HBs. We investigated the role of adding PEGylated interferon (PEG IFN) to ongoing tenofovir treatment in chronic HBV patients for achieving HBsAg clearance. Patients and Methods: In this randomized controlled trial, chronic HBV patients who have been receiving tenofovir for >6 months with HBV viral load

BACKGROUND AND OBJECTIVES: The epidemiology, clinical characteristics, and natural course of inflammatory bowel disease (IBD) in Saudi Arabia are still largely unknown. Hence, we decided to conduct a large retrospective, cohort study to determine these features of the disease. DESIGN AND SETTING: Retrospective study conducted in a tertiary care hospital in Riyadh from January 1970 to December 2008. PATIENTS AND METHODS: We reviewed all the cases of IBD diagnosed and collected all data pertaining to patients with IBD. RESULTS: A total of 312 patients with IBD were included for this analysis, including 197 (63%) patients with Crohn disease (CD) and 115 (37%) patients with ulcerative colitis (UC). The mean age (standard deviation) of patients with IBD was 25.5 (10.6) years; 152 (48.7%) were males and 160 females. The referral rate in the past 10 years was 72.1% compared with preceding 20 years, and 56% (n=178) of patients with IBD were from the central region of Saudi Arabia. The patients were followed up for a mean duration of 9.5 years; during their follow-up, 206 patients (66%) required hospital admission and 9 patients (2.9%) with UC developed colon cancer. A total of 6 patients died during the follow-up. Fifty-three percent (n=104) of the patients with CD underwent surgeries as part of their treatment, whereas only 20% (n=23) of the patients with UC underwent colectomy. CONCLUSIONS: The incidence of IBD has been gradually increasing in Saudi Arabia over the years. Clinical features and morbidity in patients are not different from patients with IBD seen in the West.

Chronic hepatitis C is common in Saudi Arabia and most often presents in an advanced stage. To assess the response of patients to interferon, a randomized placebo-controlled double-blind study was undertaken. All but 1 patient had cirrhosis or fibrosis before interferon. After a 24-week observation period patients received alpha 2a interferon, 3 mega units sc tiw or placebo for 24 weeks, then the opposite treatment for another 24 weeks followed by 24 weeks of observation. Liver biopsies were performed before and after each of the treatment phases. Twenty-two out of 24 patients completed the study. The mean alanine aminotransferase (ALT) levels fell from 150.7 +/- 118.7 units/l to 91.0 +/- 42.6 units/l after 6 months interferon treatment (P = 0.03) but only 3 patients (14%) had complete normalization of mean ALT levels and 4 (18%) had50% reduction. The mean hepatitis activity index fell from 12.2 +/- 2.6 immediately before to 11.6 +/- 2.5 just after interferon (P = 0.4). After interferon there was an insignificant raise in 6-month mean ALT. Hepatitis C virus-RNA was positive in all 17 patients tested and remained so after treatment. Side-effects were mild and well tolerated. Alpha interferon 3 mega units tiw for 24 weeks is not an effective treatment of histologically advanced chronic hepatitis C.

It is well known that Helicobacter pylori (H. pylori ) infection of the gastroduodenal mucosa causes chronic active gastritis and may dispose to peptic ulcer disease. Several invasive and noninvasive methods to detect H. pylori infection of the stomach have been described in the literature. Until recently, the practice has mainly been focused on the detection of H. pylori by endo scopic biopsy of the gastric mucosa, and documentation of its presence, either by histological identification of H. pylori or culture of antral biopsies. We know that H. pylori produces large amounts of urease, which buffer surrounding hydrogen ions by the production of ammonia and bicarbonate.

We report the case of a 65-year-old patient who was diagnosed with large-cell lymphoma arising and remaining localized in the porta hepatis, causing obstructive jaundice, and resulting into ascending cholangitis, septicemia, and acute renal failure. We discuss how jaundice can be a manifestation of both Hodgkins and non-Hodgkins lymphoma.

Chronic non-A, non-B hepatitis occurs in 50% of Saudi patients with end-stage renal failure and requires long-term hemodialysis since it is a contraindication to renal transplantation. Thirteen patients with biochemical and histological documented chronic non-A, non-B hepatitis (11 with HCV antibodies) entered a double-blind placebo controlled cross-over study, in which Roferon A 3 MU or placebo were administered subcutaneously 3 times weekly after hemodialysis for 6 months. The mean ALT fell significantly from pretreatment levels of 74.7 (95% confidence interval (CI) 54.7, 92.5) (13 patients in the 6-month run-in period) and 66.8 (CI 47.7, 85.8) (7 patients in the run-in period + 6 patients in the placebo period) (difference NS) to 37.6 (CI 21.0, 54.2) during interferon treatment (P0.005). In 10/13 patients (77%) ALT levels became normal. In the 6-month follow-up period immediately after therapy, the mean ALT was 45.2 (CI 28.0, 62.0). Although this change was not significant (P = 0.49), only 7 of these 10 patients sustained biochemical remission in the 6-month follow-up period. The corresponding total Histological Activity Index improved from 8.9 (CI 7.5, 10.3), 8.9 (CI 7.2, 10.7) (difference NS) to 6.2 (CI 3.9, 8.5) (P0.05; P = 0.052, respectively). Intralobular inflammation and periportal inflammation showed the most significant changes. Five of 13 (39%) and 2/13 patients (15%) had complete resolution of piecemeal necrosis and intralobular inflammation, respectively. Toxic effects of interferon were mild, early and self-limiting.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic hepatitis C virus (HCV) infection affects approximately 300 million people worldwide and currently is the most frequent cause for liver transplantation in the United States and Europe.[1] Natural history studies suggest that up to 20% of chronic HCV patients develop liver cirrhosis after 20 years of infection. Moreover, the incidence of chronic liver failure is expected to increase over the next 10 years as a result of the “silent epidemic” of HCV infection.[2] The recommended treatment for patients with HCV genotypes 1 and 4 is pegylated interferon plus ribavirin for 48 weeks.[3] Such treatment has yielded overall sustained viral response (SVR) rates of 54–63% in randomized controlled phase III clinical trials.[4–6] However, treatment responses are not uniform across all populations,[7] and are dependent on various viral and host factors. The majority of studies conducted worldwide have assessed the predictors of SVR in patients infected with HCV genotypes 1, 2, and 3, and showed that the factors independently associated with a favorable treatment result include serum HCV-RNA levels below 2 million copies/mL (800,000 IU/mL), body weight