The Italian journal of gastroenterology最新文献

Abnormalities in gastrointestinal motility have been reported in a substantial proportion of patients with functional dyspepsia, supporting the use of prokinetic drugs for treatment of dyspeptic symptoms. To evaluate efficacy and safety of levosulpiride in short-term treatment, 1298 patients were enrolled in a double-blind multicentric study carried out in 45 Italian Gastroenterology Departments. Patients were randomly assigned to either levosulpiride (25 mg tid), domperidone (10 mg tid), metoclopramide (10 mg tid) or placebo (1 tablet tid) for 4 weeks. Patients were selected on the basis of: a) occurrence in the last 4 weeks of at least 5/10 selected symptoms (anorexia, nausea, vomiting, upper abdominal pain, postprandial bloating, abdominal fullness, early satiety, belching, heartburn, regurgitation), severity of which should reach/exceed a total score of 8, as assessed by a specific scale ranging from 0 (absent) to 3 (severe); b) normal results of routine biochemical, ultrasound and endoscopic examinations. In addition, each patient subjectively evaluated efficacy of treatment by a visual analogue scale. Significant improvement was recorded for all symptoms at days 10 and 28 in all groups (p < 0.001), but levosulpiride was significantly (p < 0.01) superior to domperidone, metoclopramide and placebo both in the overall clinical improvement scale as well as in a subgroup of symptoms (postprandial bloating, epigastric pain, heartburn). Active treatments and placebo were comparable as far as concerns occurrence of side-effects (12-20%) including galactorrhoea, breast tenderness and menstrual changes.

In cirrhosis, Helicobacter pylori infection may be implicated, together with portal hypertension, bile reflux and alcohol abuse, in damage to gastric mucosa. Aim of this study was to define the influence of non-alcoholic liver disease on the incidence of Helicobacter pylori infection and on the diagnostic accuracy of specific serology. Enrolled in the study were 232 individuals, 105 also had cirrhosis. Infection by Helicobacter pylori, diagnosed by a positive concordance of quick urease test and histology, was detected in 97 (48 with cirrhosis) out of 184 patients. Severe gastritis was more frequent in patients with Helicobacter pylori infection than in patients without. Cirrhosis did not significantly affect the prevalence of Helicobacter pylori infection or the histological features of gastritis. Specific anti-Helicobacter pylori IgG and IgA assay (Bio-Rad GAP test) was used for serological diagnosis. Anti-Helicobacter pylori IgG showed a high sensitivity (85% in cirrhotics, 89% in non-cirrhotics) and low specificity being more evident in cirrhotics (38% vs 56% non-cirrhotics). Serum specific IgA showed low sensitivity (approximately 25% in both groups) and specificity of 79% in cirrhotics vs 84% in non-cirrhotics. In conclusion, non-alcoholic cirrhosis does not affect the incidence of Helicobacter pylori infection and the histological features of chronic gastritis but does decrease diagnostic efficiency of serological tests for Helicobacter pylori.

Cholesterol degradation to bile acids represents 50% of total elimination of cholesterol from the body each day. Cholesterol 7 alpha-hydroxylase and sterol 27-hydroxylase catalyze initial steps in the neutral and acidic pathways, respectively. Both enzymes were recently cloned and sequenced, and hence the molecular basis of their regulation could be studied. In the rat, cholesterol 7 alpha-hydroxylase is regulated by three classes of effector molecules: a) hydrophobic (but not hydrophilic) bile acids, b) cholesterol, and c) hormones (glucocorticoids plus thyroxine, glucagon and insulin). Most studies presented so far indicate that regulation of cholesterol 7 alpha-hydroxylase probably occurs at the level of gene transcription. Sterol 27-hydroxylase, a mitochondrial P-450 enzyme, appears to be regulated by hydrophobic bile acids, but to a lesser extent than cholesterol 7 alpha-hydroxylase. The contribution of this acidic pathway to total bile acid synthesis is not known but it appears to be more significant than previously thought.

Efficacy and safety of therapy with lymphoblastoid interferon-alpha alone or combined with deflazacort has been investigated in 38 HBsAg-HBeAg+ patients with biopsy-proven chronic hepatitis. Group I received 5 MU/m2 interferon thrice a week for 26 weeks; group II took interferon for 26 weeks simultaneously with a 6-week course of deflazacort. Follow-up was 18-72 months (median 42). After 12 months, responses were achieved in 3 (18%) out of 17 patients on interferon alone vs 5 (26%, p > 0.05) out of 19 on combined therapy. Blind histological assessment revealed no improvement in either group or in patients who responded to therapy within the first year of follow-up ("early responders"). "Delayed" responses were observed in 4 (29%) patients who took interferon alone vs 5 (36%, p > 0.05) who took the combined therapy. Serum HBV DNA levels decreased significantly during treatment and remained low up to 24 and 36 months of follow-up in both groups. One early responder developed hepatocellular carcinoma, another had exacerbation of liver disease in long-term follow-up. No non-responders developed liver failure or hepatocellular carcinoma. These results indicate that lymphoblastoid interferon-alpha inhibits HBV replication and corticosteroids have no synergistic effect in treatment of HBsAg-HBeAg+ chronic hepatitis.

Variceal bleeding and hepatocellular carcinoma are two severe complications of cirrhosis. One of our patients who bled from oesophageal varices was found to have a malignant hepatic nodule. As the patient refused liver transplantation, a transjugular intrahepatic portosystemic stent was carried out for portal hypertension, and transcatheter arterial chemoembolization for cancer. Both procedures were successful and one year later liver function has not deteriorated. This case shows that intrahepatic stent placement and selective arterial chemoembolization can be safely performed in cirrhotic patients with a solitary hepatocarcinoma nodule and a good liver function reserve.

Patients with primary biliary cirrhosis have a higher prevalence of gallstone disease. Aim of this study was to determine whether gallbladder bile of these patients is lithogenic. We studied 11 patients with early stage primary biliary cirrhosis, and compared them with 16 control subjects. We combined a cholescintigraphic method with nasoduodenal bile sampling to measure the mass of lipids within the gallbladder. Cholesterol saturation index, as measured by standard techniques, was similar in patients with primary biliary cirrhosis and controls (medians: 0.85 vs 0.90). Primary biliary cirrhosis patients showed a significant reduction in the masses of cholesterol, phospholipids and bile acids, as well as in percent biliary deoxycholic acid, as measured by high pressure liquid chromatography (medians 8.6% vs 17.4% in controls; p < 0.05). Percent deoxycholic acid directly correlated with cholesterol mass in all subjects (r = 0.48; p < 0.05). Biliary lipid coupling were similar in the two groups. We conclude that, in patients with early stage primary biliary cirrhosis, gallbladder bile is not lithogenic and biliary lipid coupling is normal, due to a parallel reduction in the masses of cholesterol, phospholipids and bile acids. The significant reduction in percent deoxycholic acid, characteristic of cholestasis, may help explain this biliary lipid mass pattern, that differs from that of cholesterol gallstone patients.

Functional dyspepsia (FD) includes a heterogeneous group of patients suffering from a variety of different conditions. The Dyspepsia Project has been implemented in 14 GI Units since 1984, in order to epidemiologically test the discriminating power of the Working Teams definitions and of standardized questionnaires. Five per cent of admitted subjects were subclassified as sphincter of Oddi dysfunction or biliary dyspepsia (BD), defined as biliary pain associated or not to bilirubin or alkaline phosphatase elevation, in the abscence of ultrasonographic evidence of gallstone disease or bile duct dilatation. The more useful symptoms in favour of the diagnosis of biliary dyspepsia were found to be pain in the right hypochondrium, radiating to the shoulder, or to the back, initiated by food, and eventually associated with constipation, or epigastric postprandial discomfort. Interestingly, symptoms suggesting biliary dyspepsia are partially shared by dysmotility-like dyspepsia. The placebo response in functional dyspepsia is variable, between 6 and 80% of patients, reflecting variations in the kind and severity of the diseases in different studies. That represents a considerable difficulty in evaluating drug efficacy, even in the case of biliary dyspepsia. A therapeutic double-blind trial in functional dyspepsia using tauro-ursodeoxycholic acid is discussed.

Variceal and portal pressure measurements are currently the most widely used invasive techniques for the haemodynamic evaluation of portal hypertension in cirrhotic patients. Variceal pressure can be measured during endoscopy either directly by variceal puncture or indirectly by using a pressure sensitive gauge. More recently, an indirect technique which uses a plastic balloon attached to the end of the endoscope has been described. Variceal pressure appears to be an important risk factor for the occurrence of variceal haemorrhage as most studies concluded that variceal pressure tends to be higher in patients with previous bleeding than those without. Hepatic venous catheterization with measurements of the wedged and free hepatic pressures has become the method of choice in the estimation of portal pressure as it is a simple, fast and safe procedure, less invasive and more reproducible than the other techniques. Information obtained from hepatic vein catheterization gives a significant prognostic value in predicting survival. Despite the lack of a linear relationship between portal pressure and risk of variceal bleeding most prospective studies have concluded that the height of portal pressure is an important and independent predictive factor for bleeding. Hepatic venous catheterization is currently the best method of assessing the haemodynamic response to drug treatment and prediction of therapeutic response for the prevention of bleeding.

Meckel's diverticulum is the most common congenital anomaly of the gastrointestinal tract occurring in approximately 2% of the population. In our retrospective study, we analyzed 58 surgical specimens of Meckel's diverticulum operated on in our hospital. Heterotopic gastric mucosa was found in ten. Aim of this study was to establish the aetiopathogenesis of inflammation and consequent haemorrhage in Meckel's diverticulum with heterotopic gastric mucosa. Some studies showed that Helicobacter-like bacteria could play an important role in determining local phlogosis in heterotopic gastric mucosa of Meckel's diverticulum, however, none were found in our biopsy specimens. Analyzing patients with acute intestinal haemorrhage (4 out of 10 with heterotopic gastric mucosa) in Meckel's diverticulum a history of previous oral administration of NSAID's was positive in 3 of them. Although in the recent literature there were few case reports on the use of NSAID's and bleeding from Meckel's diverticulum, our results suggest that even short-term use, in small quantities, of NSAID's can play an important role in determining acute bleeding from Meckel's diverticulum with heterotopic gastric mucosa.