SLC11A1 promoter gene polymorphisms and fibrosis progression in chronic hepatitis C.

BACKGROUND AND AIMS: The solute carrier family 11 member 1 (SLC11A1) gene (formerly Nramp1) encodes for the protein solute carrier family 11, member 1. It affects susceptibility and clinical outcome of autoimmune and infectious diseases. We investigated the possible role of the functional polymorphism located in the promoter region of SLC11A1 and tumour necrosis factor (TNF) genes in the progression of fibrosis in chronic hepatitis C. METHODS: A total of 242 Caucasian Spanish patients with biopsy proven chronic hepatitis C and 194 healthy control subjects were genotyped for SLC11A1 and TNF promoter polymorphisms. RESULTS: No significant differences in the distribution of frequencies among patient and control groups were observed. The SCL11A1 homozygous 2/2 genotype was rarely detected among patients showing advanced fibrosis (2/82; 2.4%) but was highly represented in those with mild fibrosis (29/160; 18.1%; odds ratio (OR) 8.85 (95% confidence interval (CI) 1.9-55.2, p(c) = 0.002). In patients carrying allele 3 of SLC11A1, the presence of -238 TNF A/G was associated with advanced fibrosis (14/26 (53.8%) v 68/216 (31.4%); OR 2.53 (95% CI 1.03-6.23); p = 0.02). CONCLUSIONS: SLC11A1 gene promoter polymorphism could influence fibrosis progression in chronic hepatitis C in that the homozygous genotype 2/2 exerts a protective effect against cirrhosis development. Also, the combination of TNF -238 A/G and the presence of allele 3 is conducive to progression to pre-cirrhotic or cirrhotic stages of the disease.

Intravenous eradication therapy for bleeding gastroduodenal ulcer associated with Helicobacter pylori infection.

OBJECTIVE: To evaluate the efficacy of an ultrashort intravenous triple therapy against Helicobacter pylori infection in patients with bleeding peptic ulcer. METHODS: Thirty patients with bleeding peptic ulcer were studied prospectively. At endoscopy, two corpus and antrum biopsies were obtained for urease testing and culture. If H. pylori infection was found (positive urease test), the patient was treated with omeprazole 40 mg bid, metronidazole 500 mg tid and ampicillin 2000 mg fid for three days and then with ranitidine 150 mg bid for 2 months until eradication. In all patients a [13C]urea breath test was done at 2-month intervals, and in patients with gastric ulcer an endoscopy was also done and biopsies for culture and urease testing were obtained. RESULTS: Eradication efficacy (intention-to-treat) was 86.6% (26 out of 30). All schedules were administered in full and no patient had any adverse reactions. No patients had rebleeding. CONCLUSIONS: Ultrashort three-day triple therapy can achieve an eradication rate greater than 80%, with good acceptance and compliance, and without adverse events.

[Anti-Sp100 and anti-Gp210 in the diagnosis of primary biliary cirrhosis in patients with autoimmune cholangitis]. / Anti-Sp100 y anti-Gp210 en el diagnóstico de cirrosis biliar primaria en pacientes con colangitis autoinmune.

We describe 2 women with features of autoimmune cholangitis. Serum biochemical studies showed cholestasis and increased immunoglobulin M with negative antimitochondrial antibodies. Markers of hepatitis B and C viruses were absent. Both had positive antinuclear antibodies. One had a speckled pattern (multiple nuclear dots) and the other a perinuclear pattern (pore nuclear). In the first case anti-Sp100 was positive by EIA and in the second anti-Gp210 was detected by immunoblot. Diagnosis of primary biliary cirrhosis was made and the patients were treated with UDCA. Current knowledge indicates that determination of anti-Sp100 and anti-Gp210 substantially improves diagnosis of primary biliary cirrhosis as these ANA are highly specific for this disease. These autoantibodies may lead to the classification of different groups of patient included in autoimmune cholangitis. All patients with autoimmune cholangitis should be tested for anti-Sp100 and anti-Gp210.