Kayhan B

Increased prevalence of hepatitis C virus antibodies in patients with diabetes mellitus

DEAR SIR, hyperglycaemia and glucose intolerance are frequently observed in patients with chronic liver disease [l. 21. Taliani et al. [3] found the prevalence of diabetes mellitus to be 18.7% amongst patients with chronic hepatitis C virus (HCV) infection. In this study, we investigated hepatitis virus markers in 100 patients with diabetes mellitus. One hundred patients (42 men and 58 women) with diabetes mellitus diagnosed by conventional criteria [4] were studied. Their mean age was 50 (range 20-75) years and mean duration of diabetes was 8.1 (range 6 months-27) years. Twenty-five patients with type 1 diabetes were treated with insulin. Of the 75 patients with type 2 diabetes, 22 received insulin injections and 53 were on oral hypoglycaemic agents or special diet. Hepatitis B surface antigen (HBsAg) and immunoglobulin G antibody to hepatitis B core antigen (anti-HBc) were detected using enzyme-linked immunosorbent assays (ELISA) (Institut Pasteur, Paris, France). HCV antibody (anti-HCV) was detected by second-generation ELISA (Abbott Laboratories) and the positive results were confirmed by recombinant immunoblot assay (RIBA 11) (Ortho Diagnostic). The results were compared using the chi-squared test with Yate’s

Budd-Chiari syndrome: analysis of 30 cases.

The authors report their experience with 30 adult patients with Budd-Chiari syndrome (BCS), which is a rare and serious disorder, characterized by hepatic outflow obstruction caused by many different conditions. The diagnosis was based on the clinical data, ultrasonography (US), vena cavography and hepatic venography, computed tomography (CT), and liver bi opsy. Behçets disease (BD) was found in 10 patients with BCS as an underlying disease. Two patients used oral contraceptive drugs, 2 had liver tumor hepato cellular carcinoma and liver lymphoma, and 1 patient had chronic lymphocytic leukemia. Despite full investigation, the authors could not find any obvious un derlying cause in the other 15 patients. The results suggest that (1) BCS must be considered as a possible complica tion in patients with Behçets disease when they have hepatomegaly even if there were no cardinal manifestations of the disease at the time of admission, and BD is the most common etiologic factor in BCS (33%) in Turkey, where the inci dence of Behçets disease is relatively high. (2) Anti-aggregant treatment seems to be effective in many instances. (3) There were space-occupying lesion-like appearances in the liver of 7 cases by CT and US examination in the acute stage, and these disappeared on the follow-up CT and US in 5 patients but continued in 2. BCS should thus be differentiated from other liver lesions. (4) There were other great-vessel involvements in 43% of the cases, mostly venous, but only 1 pulmonary arterial occlusion.

The use of deferoxamine infusions to enhance the response rate to interferon-α treatment of chronic viral hepatitis B

Summary An individuals iron status may affect the response rate achieved with the use of interferon (IFN) as therapy for chronic viral hepatitis. A total of 27 patients with chronic hepatitis B viral infection, who had elevated serum ferritin levels, were randomized to receive either IFN 5 MU, three times weekly by subcutaneous injection alone (n= 14) or in combination with cycles of deferoxamine at a dose of 80 mg kg‐1 per cycle (n= 13) administered over 3 consecutive days, to reduce their iron and maintain a serum ferritin level less than 250 ng ml‐1. All deferoxamine‐treated patients were on a low iron‐containing diet. An IFN response was defined as a normalization of the serum alanine aminotransferase (ALT) level and seroconversion from hepatitis B e antigen (HBeAg) positivity to hepatitis B e antibody (HBeAb) positivity. The deferoxamine‐treated group experienced a reduction in their serum ferritin level to 226 ± 73 ng ml‐1 as a result of the deferoxamine treatment. Six of the 13 (46%) deferoxamine‐treated patients and two of the 14 (14%) control patients normalized their ALT levels. Seven of the 13 (54%) deferoxamine but only 14% of the IFN‐treated group seroconverted to HBeAb positivity. A greater rate of histological improvement and loss of hepatitis B virus (HBV) DNA was seen in the deferoxamine‐treated group. Two of the deferoxamine‐treated patients were treated only once, two were treated twice, seven were treated three times and two were treated four times to achieve a ferritin level below 250 ng ml‐1.

Relationship between the serum alanine aminotransferase level at the end of interferon treatment and histologic changes in wild‐type and precore mutant hepatitis B virus infections

Summary Unravelling the role of interferon (IFN) in the treatment of chronic hepatitis B is complicated by many factors. Several mutant forms of hepatitis B virus (HBV) have recently been discovered; the most common of these is the precore mutant, characterized by hepatitis Be antigen (HBeAg) negativity and hepatitis Be antibody (HBeAb) positivity in an individual with an active HBV infection. The aim of this study was to compare the response rate to IFN therapy in patients with wild‐type HBV infection and in individuals infected with the precore mutant. A second aim was to evaluate the role of an increased serum ferritin in terms of the IFN response rate in these two different types of HBV infection.

Interleukin-1β in chronic hepatitis C virus infection

cillin, 500 mg/8 hr + ciprofloxacin, 200 mg/12 hr), so that, at the fifth day the patient began to eat a normal diet. Coproculture (obtained at admission) was positive for Salmonella sp. The following day, however, the patient complained of right upper abdominal pain, and fever persisted. The Murphy sign was positive. Laboratory evaluation at this time revealed 21,300 leukocytes/mm, ASAT 24 units/ liter, ALAT 26 units/liter, alkaline phosphatase, 336 units/liter, and GGT 44 units/liter. An ultrasound scan revealed a moderately dilated gallbladder without stones and a thickened wall. A gallbladder nuclear scan showed nonvisualization of the gallbladder, consistent with acute cholecystitis. The clinical picture slowly improved during the following days until hospital discharge on the fourteenth day after admission. The patient remains doing well on further ambulatory control. Although acute cholecystitis is a frequent complication of typhoid fever and other Salmonella infections, it almost always occurs in the presence of morphological anomalies of the biliary tract and/or gallbladder stones (5). As in the case described by Avalos et al, our patient presented with complaints attributable to acute gastroenteritis, and signs and symptoms derived from biliary disease appeared a few days later. The few reported cases of acute acalculous cholecystitis due to Salmonella precludes the existence of a standard therapy for them. For chronic carriers without stones, a six-week course of oral antibiotherapy has been recommended (6, 7); the patient of Avalos et al was treated with an l 1-day ampicillin course; other cases have been subjected to cholecystectomy (2); our patient completed a 25-day course of ciprofloxacin, remaining asymptomatic afterwards. In summary, the present report adds a new case to the short number of patients affected by this entity. P. GARRIDO-BENEDICTO E. GONZALEZ-REIMERS F. SANTOLARIA-FERNANDEZ F. RODRfGUEZ-MORENO Dpt. de Medicina Interna Hospital Universitario de Canarias La Laguna, Tenerife, Canary Islands, Spain