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Background/Objectives: In older people, small bowel bacterial overgrowth syndrome may be a common, but under-diagnosed, cause of diarrhoea and nutrient malabsorption. We aim to determine which clinical features and baseline laboratory investigations indicate a high likelihood of small bowel bacterial overgrowth as defined by a positive glucose breath test. Methods: A retrospective analysis of records for all patients referred for glucose breath test over a 6-year period to a teaching hospital. Results: Out of 197 referrals, 168 patient records were located and analysed (62 male, 106 female; median age 65). Patient characteristics predictive of a positive glucose breath test were: increasing age (p < 0.01), low serum vitamin B12 (p = 0.02), low serum albumin (p = 0.03), previous partial gastrectomy (p < 0.01), previous right hemi-colectomy (p < 0.01), presence of small bowel diverticulae (p = 0.01) and concurrent use of a proton pump inhibitor (p < 0.01). 52.5% (n = 21/40) of patients studied who were over 75 years old versus 21.8% (n = 28/128) of those under 75 years old had a positive glucose breath test (p < 0.01). The median time to diagnosis, from first hospital visit to positive glucose breath test, was 39 weeks. Conclusions: There is often a significant delay in diagnosis of small bowel bacterial overgrowth. We suggest that this diagnosis should be considered earlier in the investigative algorithm in older patients with indicative symptoms and a predisposing factor (including previous partial gastrectomy, previous right hemi-colectomy, small bowel diverticulae or use of a proton pump inhibitor) or concurring laboratory indices (low vitamin B12 or albumin). Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Introduction Up to 40% of patients with inflammatory bowel disease (IBD) also suffer with osteoporosis. Receptor activator of NF-kB ligand (RANKL) promotes the formation of bone resorbing osteoclasts and is linked to osteoporosis. RANKL is controlled by decoy receptors, osteoprotegerin (OPG) and TNF-stimulated gene-6 (TSG6) that bind to it and block osteoclast bone resorption. We have shown increased serum levels of RANKL in a mouse model of colitis and bone disease. RANKL may also increase the lifespan and activity of dendritic cells (DCs), which accumulate in the colon in colitis. We hypothesise that the RANKL pathway links the development of colitis with bone disease and aimed to determine the mechanism of action of RANKL, OPG and TSG6 on DC function. Methods We used the validated , mouse whipworm induced model of colitis. After infection, wildtype C57BL/6 mice develop a resolving colitis while IL10-KO (knockout) mice develop a chronic colitis. Colitis was assessed histologically and expression of RANKL family members by immunofluorescence and quantitative real time PCR (qRT-PCR). Additionally, the effects of RANKL family members were assessed in cultured bone marrow derived DCs. Results The colitis was severe in the IL10-KO mice, with statistically significant increases in colitis scores and crypt length from a mean of 80 to 147 μm, p<0.001 between uninfected and infected IL10-KO mice but not wildtype controls with resolving colitis. qRT-PCR of RANKL, OPG and TSG6 mRNA in colonic snips showed increased expression over the course of infection in wildtype mice but decreased expression in IL10-KO mice. Immunofluorescence staining of colonic sections showed expression of OPG and TSG6 in macrophages and epithelial cells. Finally, in vitro functional assays on bone marrow DCs from wildtype naïve mice surprisingly showed that RANKL had little effect on the expression of DC maturation markers (CD80, CD86, MHCII). In contrast, OPG and TSG6 promoted MHCII and CD86 expression but not CD80. Conclusion The results suggest that increased expression of RANKL, OPG and TSG6 may be important in the resolution of colitis, in contrast to their decreased expression in persistent colitis. This finding supports our hypothesis that molecules which control bone homeostasis are involved in controlling colitis. The direct effects of RANKL members on DCs is unclear as the decoy receptors may partially activate DC function or promote activation of specific DC subsets. [ABSTRACT FROM PUBLISHER]

The aim of this study was to evaluate the role of cervicovaginal fibronectin as a screening test in a low-risk population. Swabs were taken from the posterior fornix at 28 weeks gestation and foetal fibronectin levels were assayed using enzyme immunoassay. Eighteen patients (7.7%) delivered at less than 37 weeks of gestation, and 6 (2.4%) at less than 34 weeks of gestation. Five patients (2.1%) had a positive fibronectin test result. The sensitivity, specificity, positive predictive value and negative predictive value in the prediction of delivery less than 37 weeks of gestation were 16.7%, 99.1%, 60.0% and 93.4%, respectively. The sensitivity of foetal fibronectin in the prediction of delivery less than 34 weeks of gestation was higher (50%) compared with the prediction of delivery less than 37 weeks of gestation (16.7%). The low sensitivity of this test suggests a limited role for cervicovaginal fibronectin in the low-risk population. Further studies need to be carried out to assess whether multiple testing of cervicovaginal fibronectin at different gestational ages will further increase the sensitivity.

Suppressor cell function was assessed in 13 patients with chronic renal failure not on dialysis, 10 patients on regular hemodialysis and 11 renal transplant patients by means of the Concanavalin A inducible Suppressor Cell Assay. The mean Suppression Index (S.I.) in the undialysed patients (0.76 +/- 0.39) and those of the dialysed patients (0.72 +/- 0.18) were not significantly different from the 25 healthy controls (0.68 +/- 0.22). However the S.I. in the renal transplant patients (1.11 +/- 0.41) was significantly different from the normal controls as well as the undialysed and dialysed patients. Although there was no correlation between S.I. and age, post transplant follow up period, serum creatinine concentration, prednisolone or azathioprine dosage it is likely that the cause of the impaired suppressor cell function was due to the immunosuppressive agents used.

Newly diagnosed NPC patients were found to have impaired general T-cell functions, as determined in vivo by the Mantoux test and in vitro by the PHA response assay. Treated remission patients were as hyporesponsiveness as newly diagnosed patients. PHA hyporesponsiveness was associated with the HLA profile of A2-B Sin 2 and with high antibody titres to EBV-related antigens, in particular to the early antigen. Impaired responses in the Mantoux or PHA tests were associated with poor survival. The impaired response could be partially or totally restored by in vitro treatment of the hyporesponsive lymphocytes with levamisole.

Using the method of concanavalin A (Con a) inducible suppressor activity the peripheral mononuclear cells (PMC) of 17 patients with Mesangial IgA nephritis, 13 patients with idiopathic mesangial proliferative glomerulonephritis but with no IgA deposits on immunofluorescence (Non-IgA nephritis) and 18 healthy subjects were studied. DNA synthesis was measured by incorporation of 3H Thymidine. The mean suppression index (S.I.) of 0.94 +/- 0.08 (SEM) in the IgA nephritic patients was significantly different from that of the non-IgA nephritic patients (0.67 +/- 0.05) (P less than 0.01) as well as the group of normal healthy controls (0.64 +/- 0.05) (P less than 0.0025). The data show that patients with IgA nephritis have abnormal suppressor cell function and suggest an autoimmune basis in the pathogenesis of IgA nephritis.