Detection of anti-Saccharomyces cerevisiae antibodies in Crohn's disease: is it a reliable diagnostic and prognostic marker?

BACKGROUND: In the past few years, serologic markers have been proposed in inflammatory bowel disease. Anti-Saccharomyces cerevisiae antibodies showed high specificity for Crohn's disease. A prognostic role for serology has also been hypothesised. AIMS: To evaluate anti-Saccharomyces cerevisiae antibody distribution in an unselected Italian inflammatory bowel disease population. To analyse whether anti-Saccharomyces cerevisiae antibody status (positive/negative) and/or anti-Saccharomyces cerevisiae antibody titres are associated with clinical variables and outcome measures in Crohn's disease patients. PATIENTS AND METHODS: A series of 299 inflammatory bowel disease patients were evaluated; serum samples were taken and a short clinical history was recorded. anti-Saccharomyces cerevisiae antibodies IgG enzyme-linked immunosorbent assay Medilab (Milan, Italy) kit was used in order to determine anti-Saccharomyces cerevisiae antibody status. RESULTS: Sensitivity, specificity and likelihood ratio for positive test in the differential diagnosis of inflammatory bowel disease was 59%, 89%, 8.1, respectively. Clinical variables significantly associated with anti-Saccharomyces cerevisiae antibody status in logistic regression were found to be ileal location (p=0.01) and earlier age at diagnosis (p<0.01). Among ileal Crohn's disease patients, there was a trend in concordance between anti-Saccharomyces cerevisiae antibody titres and higher number of surgical procedures which was not statistically significant applying more complex statistics. CONCLUSIONS: In an Italian inflammatory bowel disease population, anti-Saccharomyces cerevisiae antibodies status showed characteristics similar to those previously reported. Anti-Saccharomyces cerevisiae antibody positivity is associated with ileal involvement and with earlier onset of Crohn's disease.

Serum interferon gamma in primary biliary cirrhosis: effect of ursodeoxycholic acid and prednisone therapy alone and in combination.

BACKGROUND: Interferon-gamma may have immunopathogenic importance in primary biliary cirrhosis, stimulating aberrant expression on biliary epithelium of class II major histocompatibility molecules and inter-cellular adhesion molecule-1. Liver transcripts for interferon-gamma are found in primary biliary cirrhosis. Its serum level is increased in pretransplantation stages and decreases after transplantation. OBJECTIVES: (1) To verify whether serum interferon-gamma levels are increased in non-cirrhotic stages of primary biliary cirrhosis. (2) To evaluate the effect of ursodeoxycholic acid and prednisone alone and in combination on serum levels of interferon-gamma and soluble inter-cellular adhesion molecule-1. METHODS: Nine non-cirrhotic, anicteric patients with primary biliary cirrhosis (patient test group), 14 healthy, negative controls and 14 positive controls, with chronic hepatitis related to hepatitis C virus were studied in basal condition. Primary biliary cirrhosis patients were treated with ursodeoxycholic acid, prednisone and the association of the two drugs for three 4-week periods, each period separated by a 4-week wash-out. Interferon-gamma and soluble inter-cellular adhesion molecule-1 were measured in serum by commercially available immuno-enzymatic kits. RESULTS: Median interferon-gamma levels were increased in patients with primary biliary cirrhosis compared with healthy controls (44 vs 19 pg/ml; P < 0.01) but similar to those in chronic hepatitis patients (47 pg/ml). Serum soluble inter-cellular adhesion molecule-1 was significantly reduced by ursodeoxycholic acid, and an even greater reduction was obtained on addition of prednisone. No treatment affected interferon-gamma levels. CONCLUSION: Serum interferon-gamma is increased in noncirrhotic patients with primary biliary cirrhosis, but this is not disease-specific. Neither ursodeoxycholic acid, nor prednisone, nor the combination of the two drugs influenced this immunological pathway of primary biliary cirrhosis.

Fecal pancreatic elastase 1 in the work up of patients with chronic diarrhea.

BACKGROUND: Quantitative determination of pancreatic elastase-1 (E1) in stools has been proposed as a novel, noninvasive test of pancreatic function. The aim of the study was to verify its role in the differential diagnosis of chronic diarrhea. METHODS: E1 was measured in spot stool samples of 50 patients with pancreatic disease (PD), 62 with inflammatory bowel disease (IBD), 45 with chronic diarrhea (CD), 34 with other gastroduodenal and liver disease (gastrointestinal; GI), and in 18 normal controls, by a commercial kit (Schebo-Tech., Wettemburg, Germany). RESULTS: In PD, patients with severe damage and diarrhea displayed E1 levels below 100 microg/g; normal values were found in mild-moderate disease. Abnormal values were detected in 4 CD and in 14 IBD patients, either in the presence of severe protein malnutrition or in patients with previous ileo-anal pouch anastomosis and pouchitis. In nine cases, values reverted to normal after adequate treatment. Diagnostic accuracy of E1 in discriminating diarrhea of pancreatic and nonpancreatic origin was: SS, 97%; SP, 84%; VP+, 66%; VP-, 100%. CONCLUSION: 1) The finding of a normal E1 value rules out a malabsorption of pancreatic origin. 2) in CD and IBD, decreased E1 might be owing to bacterial elastase degradation (pouchitis) or transient defective pancreatic enzyme secretion.

Amantadine hydrochloride decreases serum ALT activity without effects on serum HCV-RNA in chronic hepatitis C patients.

BACKGROUND AND AIMS: To investigate the effects and tolerance of amantadine in chronic hepatitis C patients. PATIENTS AND METHODS: Forty consecutive patients, with biopsy proven chronic active hepatitis, were treated with amantadine 200 mg daily in the morning for two months. Nineteen patients were previous non responders to alpha-interferon, nine patients experienced hepatitis relapse after interferon treatment, and twelve patients had never been treated with antiviral drugs. Complete blood count, liver and renal function tests were performed two months before, at baseline, end of therapy and two months after its completion. RESULTS: None of the patients experienced significant side effects. Twenty-four patients (60%) showed a reduction of serum aminotransferase levels (twelve patients > 30% and twelve patients < 30% of their basal levels). The analysis of variance showed a significant reduction in aminotransferase levels at the end of treatment (F = 11, p < 0.0001). In four patients, aminotransferases returned to normal, but none of them cleared HCV-RNA. After the end of treatment, serum ALT returned to baseline values in all patients. CONCLUSIONS: Amantadine is well tolerated in chronic hepatitis C patients. The time-relation between therapy and reduction of serum aminotransferase levels in 60% of patients suggests a potential anti-inflammatory activity of the drug without an effect on viraemia.