No abstract

This is a prospective study, carried out in patients with portal hypertension and bleeding oesophageal varices secondary to Symmers (Schistosomal) periportal fibroses, to determine the efficacy of sclerotherapy, the number of sessions needed to achieve full sclerosis, the complications associated with sclerotherapy and the incidence and risk factors for rebleeding. In total, 85 patients were studied with a mean age of 38 years, 76.5% were males. All underwent upper gastrointestinal endoscopy, had different grades of oesophageal varices and underwent intravariceal injection with 5% ethanolamine oleate until they achieved full sclerosis or were referred to surgery. Complications of sclerotherapy included oesophageal strictures, deep oesophageal ulcers, pleural effusion and ascites. Following obliteration of oesophageal varices, 3.5% and 20% developed new gastric varices and portal gastropathy, respectively. Rebleeding occurred in 32% - the only significant predictive risk factor for which was patients with GIII varices following the first sclerotherapy session. Varices recurred in 6% of patients after a mean follow-up period of one year. In total, 93% of our patients achieved full sclerosis after an average of four sessions, and 3.5% were referred for surgery. Three patients (3.5%) died, all from massive rebleeding. In conclusion, sclerotherapy is a safe effective method for treating patients with oesophageal varices due to periportal fibroses.

Epidemiological studies have demonstrated a variety of potential environmental factors that may alter susceptibility to chronic pancreatitis (CP) through oxidative/xenobiotic stress; however, a direct causal and mechanistic role has not been established. We aimed (1) to determine the prevalence of functional genetic polymorphisms in the antioxidant enzymes, glutathione S-transferase GSTM-1, GSTP-1, and GSTT-1, manganese superoxide dismutase, and catalase in CP and (2) to reveal evidence of oxidative stress in patients with CP by measuring whole-blood glutathione redox status. In total, 122 patients with CP (75 alcohol-induced [A1CP], 33 idiopathic [ICP], and 13 hereditary) and 245 age- and sex-matched controls were recruited. The prevalence of the functional GSTT-1 genotype (GSTT-1*A) was significantly higher in CP (88.5%) compared to healthy controls (76%; chi2 = 7.26, P = 0.007). Stratification to disease etiology demonstrated that the GSTT-1*A genotype was also significantly more prevalent among patients with ICP (94%; P = 0.02; 95% CI, 0.04-9.16) but not in those with A1CP. In 22 patients with stable CP, the whole-blood glutathione concentration (median [IQR]: 72 micromol/L [21-181 micromol/L]) and the glutathione redox ratio (GSH/GSSG) (median [IQR]: 9 (3-77]) were significantly reduced compared to those in 20 healthy volunteers (median [IQR]: 815 micromol/L [679-1148 micromol/L], P < 0.001, and 96 [52-347], P = 0.005, respectively). We conclude that the GSTT-1 functional genotype is associated with ICP. Evidence of altered glutathione redox status suggests that this disease modification may be a consequence of oxidative stress or the bioactivation of xenobiotics.

In this study we compared the results of measurement of duodenogastric reflux using 24-hour intragastric pH monitoring and nasogastric aspiration with analysis of bile acid and alpha amylase concentrations. Eight patients were studied at least 5 months after biliary and/or gastric surgery. The correlation coefficient of pH and bile acid concentration was 0.36 (p less than 0.001) and of pH and amylase concentration was 0.48 (p less than 0.001). If a pH greater than 4.0 was taken to indicate duodenogastric reflux this had a sensitivity of 84% compared with either high bile acid or amylase concentration. Bile acid concentration has been the "standard" method of measuring duodenogastric reflux. pH monitoring is relatively simple to perform, causes little patient distress, and can measure episodes of duodenogastric reflux over a continuous 24-hour period.