Unusual case of duodenobiliary fistula complicating Crohn's disease successfully treated with Adalimumab

Crohn's disease [CD] is characterized by transmural inflammation of the gastrointestinal tract, which predisposes to the formation of fistula. Duodenal involvement occurs in less than 5% of cases and often leads to clinically relevant strictures. However, fistula formation in the duodenum is exceptional. Herein, we report an unusual case of duodenobiliary fistula due to CD occurring in a 65-year-old patient who was successfully treated by anti-tumor necrosis factor [TNF] agents. This case report highlights the efficacy of anti-TNF alpha agents in the treatment of a bilioenteric fistula because it increases the probability of clinical remission and mucosal healing and therefore reduces the need for surgical treatment which may be associated morbidity

[Prevalence of helicobacter pylori infection and gastroscopic finding in diabetic patients: case control study]

Current data on the prevalence of Helicobacter pylori infection in dyspeptic diabetic patients are contradictory in the literature. The aim was to assess the prevalence of Helicobacter pylori infection, gastroscopic lesions, and gastric histopathological lesions, in dyspeptic diabetic patients. It was a case-control study collecting 394 dyspeptic patients [194 diabetic and 200 nondiabetic patients]. The average age of patients was 47 years. 144 patients [47%] were male and 150 patients [53%] were female. The two patient groups were matched for age and sex. The prevalence of Helicobacter pylori infection was comparable between the two groups of patients [85% in diabetics versus 90% in the controls]. The frequency of gastroscopic lesions was 50% in diabetics and 55% in controls with no significant difference between the two groups. At histology, the prevalence of chronic gastritis, intestinal metaplasia, and gastric atrophy was 85%, 13% and 39% respectively in the group of diabetic patients. These results were comparable to those found in patients without diabetes. Our work shows no difference between diabetics and non-diabetics on the prevalence of Helicobacter pylori infection, gastroscopic, and gastric histopathological lesions

[Hepatic steatosis in chronic hepatitis B: Prevalence, risk factors, and impact on fibrosis and therapeutic response]

Steatosis is a common injury in chronic hepatitis C, but this association has not been sufficiently studied in chronic hepatitis B. To evaluate the prevalence of hepatic steatosis in chronic hepatitis B and determine its association with various histologic, biochemical, virological, and metabolic diseases, and its effect on fibrosis and therapeutic response. Our study was compiled 133 patients with chronic hepatitis B who received no antiviral therapy and who had a liver biopsy. Our patients were divided into 2 groups: 51 patients [38.3%] had steatosis [Group I], while 82 [61.7%] had no steatosis [Group II]. In group l, the average age, BMI, cholesterol, triglycerides, and glucose were significantly higher than the group without steatosis in univariate study [P <0.05]. In multivariate analysis, only high BMI and hypertriglyceridemia were included. No significant difference between the two groups was observed in the rate of transaminases, HBeAg status, viral load [P> 0.05]. Steatosis doesn't influence fibrosis stage and therapeutic response. During chronic hepatitis B, steatosis appears to be the result of metabolic factors of the host rather than the effect of the virus. Hepatic steatosis does not seem to influence the progression of liver fibrosis, or therapeutic response, however, the role of steatosis should be better studied by prospective longitudinal clinical studies on large populations of patients

[ natural history of hepatitis B virus cirrhosis after the first hepatic decompensation in Tunisia]

To define the natural long term course of viral B cirrhosis after the onset of hepatic decompensation and to determine the predictive factors of death. Retrospective longitudinal study including 77 cases of viral B cirrhosis among 192 consecutive patients with cirrhosis, hospitalized between 1997 and 2005 for the first hepatic decompensation. All those patients were followed- up until death or until December 2006. The probability of survival after the first hepatic decompensation was calculated using the Kaplan Meier method. The predictive factors of death were determined through univariate and multivariate analyses with the Cox regression model. Fifty four men and 23 women with an average age of 54 +/- 14.9 years were hospitalized for the first decompensation of the viral B cirrhosis. The 77 patients had been under observation for an average period of 24.2 +/- 21.1 months. During that time 64% among them died. The probability of survival after decompensation was 47% in 2 years and 22% in 5 years. During follow- up, ascites was the most frequent decompensation [85%] followed by hepatic encephalopathy [38%], variceal hemorrhage [34%], jaundice [30%], hepato renal syndrome [27%], hepatocellular carcinoma [21%], and spontaneous bacterial peritonitis [14%]. At univariate analysis four factors were predictive of death: Child Pugh C score [p=0.009], hepatocellular carcinoma [p=0.01], rate of serum gammaglobulin superior to18g / l [p=0.008] and prothrombin time inferior to 50% [p=0.02]. According to the multivariate analysis only the rate of serum gammaglobulin superior to 18g /l was an independent predictive factor of mortality [p=0,001] with IC [95%] [1.623 - 5.88]. In Tunisia, the prognosis of viral B cirrhosis after the first decompensation is bad, because a patient on 5 only was able to survive beyond 5 years. Ascites is the most frequent decompensation. Only the rate of serum gammaglobulin superior to 18g / l is an independent predictive factor of mortality