Olaitan A. Adeniji

Durability of the diagnosis of irritable bowel syndrome based on clinical criteria

Our purpose was to evaluate the durability of the diagnosis of irritable bowel syndrome (IBS) based on clinical criteria. The study population consisted of a cohort of previously published study patients evaluated for IBS between 1989 and 1992, who met the International Congress of Gastroenterology criteria for IBS. Patients were reinterviewed for cardinal features of IBS, Rome I, Rome II, and Manning criteria 10–13 years after the initial diagnosis. During the observational follow-up period, there were 75 patients, 14 males and 61 females, with a mean age of 47.5 ± 11.3 years (SD; range, 20 to 75 years). Mean time of reinterview after initial diagnosis was 11.8 ± 0.9 years (range, 10 to 13 years). None of the 75 patients had an abdominal condition which could have been mistaken for IBS. Other abdominal conditions diagnosed during this period included diverticulitis (five), uterine fibromyoma (three), and gallbladder disease (three). Sixty-nine patients (92%) did not consider their symptoms as resolved. Thirty-five (46.7%) had repeat structural evaluation of the colon for similar symptoms without any new diagnoses made. Twenty-six (34.7%) and 32 (42.7%) presently meet the Rome II and Rome I criteria for IBS, respectively. Clinicians are advised to use clinical criteria for a specific and durable diagnosis of IBS.

Not one but two inflammatory bowel disease susceptibility loci map to chromosome 16

The association of NOD2 gene mutations with inflammatory bowel disease (IBD) has been reported by multiple research groups. In this high-density linkage experiment using 39 microsatellite markers, Hampe et al. observed a triple-peaked configuration of the linkage curve with peak logarithm of odds (lod) scores of 2.7, 3.2, and 3.1 on proximal 16p, proximal 16q, and central 16q, respectively. An exploratory association analysis yielded a strong lead at D16S3068 (p = 0.00028 for all IBD, 0.0079 for Crohns disease), and an IBD-associated haplotype consisting of three single nucleotide polymorphisms (p = 0.00027) was identified. After stratification for NOD2 genotype, the significance levels increased to p = 0.0001 for IBD phenotype; in subphenotype analysis, Crohns disease and ulcerative colitis significances peaked at p = 0.002 and 0.0076, respectively. Hampe et al. not only confirm the importance of NOD2, but also provide a clear evidence of a second NOD2-independent IBD susceptibility locus on chromosome 16.

Finally: changing the natural history of chronic hepatitis c!: Poynard T, McHutchison J, Davis GL, et al., Impact of Interferon Alfa-2b and Ribavirin on Progression of Liver Fibrosis in Patients With Chronic Hepatitis C, Hepatology 2000;32:1131–7

Previous studies have established the benefit of combined interferon and ribavirin therapy in achieving sustained virological clearance in chronic hepatitis C infection. Interferon has antifibrotic activity, but the added benefit of the combination regimen for the progression of liver fibrosis is unknown. The authors pooled individual data from three large, multicenter, randomized studies of combined interferon alfa-2b and ribavirin involving 1509 patients with pre- and posttreatment liver biopsies. Fibrosis was staged on a scale of 0 to 4: F0, no fibrosis; F1, portal fibrosis without septa; F2, few septa; F3, numerous septa without cirrhosis; and F4, cirrhosis. F2, F3, and F4 were considered significant fibrosis. Liver biopsies were done before and 1 yr after therapy, and the rates of progression or regression of fibrosis between the two biopsies were calculated. Ninety-six weeks after the initial biopsy, 68 ± 4% of patients were without significant fibrosis when treated with combination therapy for 48 wk, 64 ± 4% were without significant fibrosis with interferon alone for 48 wk, 42 ± 7% were without significant fibrosis with combination therapy for 24 wk (lower than both 48-wk therapies, p < 0.001), and 24 ± 9% were without significant fibrosis with interferon alone for 24 wk (lower than the combination therapy for 24 wk, p = 0.02). The patients with significant fibrosis at baseline, those who achieved a virological response, and those who received 48 wk of therapy had the most prominent results. The combination of interferon and ribavirin therapy significantly reduces the rate of progression of liver fibrosis in patients with chronic hepatitis C.

Finally: changing the natural history of chronic hepatitis c!

Previous studies have established the benefit of combined interferon and ribavirin therapy in achieving sustained virological clearance in chronic hepatitis C infection. Interferon has antifibrotic activity, but the added benefit of the combination regimen for the progression of liver fibrosis is unknown. The authors pooled individual data from three large, multicenter, randomized studies of combined interferon alfa-2b and ribavirin involving 1509 patients with pre- and posttreatment liver biopsies. Fibrosis was staged on a scale of 0 to 4: F0, no fibrosis; F1, portal fibrosis without septa; F2, few septa; F3, numerous septa without cirrhosis; and F4, cirrhosis. F2, F3, and F4 were considered significant fibrosis. Liver biopsies were done before and 1 yr after therapy, and the rates of progression or regression of fibrosis between the two biopsies were calculated. Ninety-six weeks after the initial biopsy, 68 ± 4% of patients were without significant fibrosis when treated with combination therapy for 48 wk, 64 ± 4% were without significant fibrosis with interferon alone for 48 wk, 42 ± 7% were without significant fibrosis with combination therapy for 24 wk (lower than both 48-wk therapies, p < 0.001), and 24 ± 9% were without significant fibrosis with interferon alone for 24 wk (lower than the combination therapy for 24 wk, p = 0.02). The patients with significant fibrosis at baseline, those who achieved a virological response, and those who received 48 wk of therapy had the most prominent results. The combination of interferon and ribavirin therapy significantly reduces the rate of progression of liver fibrosis in patients with chronic hepatitis C.