Symptom classification in irritable bowel syndrome as a guide to treatment.

OBJECTIVE: The treatment of irritable bowel syndrome (IBS) remains unsatisfactory. There are no objective markers for diagnosis, and classification (currently based on symptoms) provides little insight into potential causes or optimal therapy. The aim of this study was to determine whether a Swedish classification of IBS based on cluster analysis of patients' symptoms might provide a guide to successful treatment. MATERIAL AND METHODS: Patients in a research clinic for IBS were classified according to criteria published by Ragnarsson & Bodemar (R&B) and also assessed independently by a clinician. Patients fulfilling the R&B criteria for subgroups 1 and 2 received specific treatments, either bulk laxatives or dietary treatment to reduce colonic fermentation, respectively. Patients who did not fit into these categories were given "best treatment" targeted at their predominant symptoms, but not limited in any way. Results before and after follow-up were assessed using a validated symptom-scoring scale. RESULTS: Seventy-one successive patients were recruited, and the numbers falling into R&B subgroups 1 and 2 were 15 (21%), and 28 (39%), respectively, leaving 28 (39%) unclassified. Receiver operating characteristic plots showed that the criteria for separation into subgroups 1 and 2 correlated well with the clinician's assessment. After treatment, symptom scores for the whole group showed a significant improvement (p<0.0001), but results were significantly better in subgroups 1 and 2 than in those unclassified, even when allowance was made for a potential therapeutic placebo effect of 40%. CONCLUSION: The R&B classification provides a helpful guide to treatment in many cases of IBS.

Rheumatoid arthritis is associated with increased aortic pulse-wave velocity, which is reduced by anti-tumor necrosis factor-alpha therapy.

BACKGROUND: Rheumatoid arthritis (RA) is associated with increased cardiovascular risk, which is not explained by traditional cardiovascular risk factors but may be due in part to increased aortic stiffness, an independent predictor of cardiovascular mortality. In the present study, our aim was to establish whether aortic stiffness is increased in RA and to investigate the relationship between inflammation and aortic stiffness. In addition, we tested the hypothesis that aortic stiffness could be reduced with anti-tumor necrosis factor-alpha (TNF-alpha) therapy. METHODS AND RESULTS: Aortic pulse-wave velocity (PWV), augmentation index, and blood pressure were measured in 77 patients with RA and in 142 healthy individuals. Both acute and chronic inflammatory measures and disease activity were determined. The effect of anti-TNF-alpha therapy on PWV and endothelial function was measured in 9 RA patients at 0, 4, and 12 weeks. Median (interquartile range) aortic PWV was significantly higher in subjects with RA than in control subjects (8.35 [7.14 to 10.24] versus 7.52 [6.56 to 9.18] m/s, respectively; P = 0.005). In multiple regression analyses, aortic PWV correlated independently with age, mean arterial pressure, and log-transformed C-reactive protein (R2 = 0.701; P < 0.0001). Aortic PWV was reduced significantly by anti-TNF-alpha therapy (8.82+/-2.04 versus 7.94+/-1.86 versus 7.68+/-1.56 m/s at weeks 0, 4, and 12, respectively; P < 0.001); concomitantly, endothelial function improved. CONCLUSIONS: RA is associated with increased aortic stiffness, which correlates with current but not historical measures of inflammation, suggesting that increased aortic stiffness may be reversible. Indeed, anti-TNF-alpha therapy reduced aortic stiffness to a level comparable to that of healthy individuals. Therefore, effective control of inflammation may be of benefit in reducing cardiovascular risk in patients with RA.