Hülya Uzunismail

Hyperhomocysteinemia in inflammatory bowel disease patients without past intestinal resections: correlations with cobalamin, pyridoxine, folate concentrations, acute phase reactants, disease activity, and prior thromboembolic complications.

Objective Homocysteine is a sulfur-containing amino acid formed during the demethylation of methionine and high levels of this amino acid is a known risk factor for both arterial and also venous thromboembolic complications. Deficiencies of cobalamin, folate, and pyridoxine may predispose subjects to hyperhomocysteinemia, a common phenomenon in inflammatory bowel disease (IBD) patients. The aim of this study was to identify the prevalence, risk factors of hyperhomocysteinemia and its correlation with prior thromboembolic events in an IBD cohort without past intestinal resections. Methods In this prospective study, we studied the concentrations of homocysteine, cobalamin, folate, and pyridoxine in 105 consecutive patients with IBD, of whom 11 had a prior history of thromboembolic complications. Data regarding smoking habits, medication use, disease location, and severity were gathered and patients with past intestinal resections were excluded. Age-matched and sex-matched 85 healthy volunteers served as controls and multivariate regression analysis was performed to find out independent predictors of hyperhomocysteinemia. Results The mean age (±SD) in the IBD cohort was 38.69±12.13 years, and 51% were male. The mean age in the control group was 37.61±10.05 years, and 52% were male. Homocysteine concentrations in patients were higher [16.35 μmol/L (range 6.82 to 48.15) vs. 9.60 μmol/L (range 4.97 to 17.39), P=0.000] and hyperhomocysteinemia had a higher prevalence in patients than in the controls (56.2% vs. 4.7%, χ2=56.179, P=0.000), thus IBD significantly increased the risk of hyperhomocysteinemia [odds ratio=25.973 (95% confidence interval: 8.861-76.128)]. Homocysteine concentrations in patients with a history of thrombosis were not higher than those without a history of thrombosis [16.29 μmol/L (range 8.45 to 34.75) vs. 16.36 μmol/L (range 6.82 to 48.15), not significant]. Hyperhomocysteinemia was found in 54.5% of patients with thrombosis and 56.4% of patients without thrombosis (not significant). On stepwise regression analysis, plasma cobalamin level, albumin concentration, erythrocyte sedimentation rate, and platelet count were found to be independent predictors of elevated homocysteine levels. Conclusions IBD patients have a higher prevalence of hyperhomocysteinemia than do healthy controls and elevated homocysteine levels are independently associated with lower serum cobalamin, albumin levels and elevated erythrocyte sedimentation rate, and platelet count. There is no correlation between hyperhomocysteinemia and a history of prior thromboembolic events.

Should we suppress the antigenic stimulus in IPSID for lifelong

jects in each study group. At histology, all subjects had mild-to-moderate chronic active superficial gastritis and mild-to-moderateH. pylori density with no major differences between groups. The 40 H. pylori strains tested for antimicrobial susceptibility were all sensitive to amoxicillin (minimal inhibitory concentration [MIC] , 4 mg/ml) and to tetracycline (MIC, 2 mg/ml). Nine (22.5%) strains were resistant to metronidazole (MIC. 8 mg/ml), five (12.5%) strains were resistant to clarithromycin (MIC . 2 mg/ml), and two (5%) strains were resistant to both metronidazole and clarithromycin. One patient in each group did not complete the study because of side effects. Susceptibility testing was associated with a higher eradication rate than nonsusceptibility testing (97.4%vs 79.5% and 95%vs 77.5%, in the PP and ITT analyses, respectively). Moreover, in the PP analysis, 1/39 (2.5%) subject in the susceptibility testing group and 8/39 (20.5%) sub jects in the nonsusceptibility testing group, failed to eradicate the infection ( p , 0.05 by Fisher exact test) (Table 1). In conclusion, pretreatment antimicrobial-susceptibility testing was associated with a higher eradication rate and a significantly lower rate of treatment failure in H. pyloriinfected dyspeptic patients. We postulate that because antimicrobial-resistantH. pylori strains are becoming increasingly prevalent (5), therapeutic regimens based on susceptibility testing may decrease the need for retreatment and prevent the emergence of secondary resistance and might, therefore, prove to be cost-effective.

Are Turkish Helicobacter pylori strains gaining resistance against clarithromycin

formed stool. Colonoscopy performed 4 wk later showed that inflammation was remarkably improved, scoring 2 on Haring’s criteria (Fig. 1B). No adverse events were observed during the treatment, and she has not experienced relapsing to date. Even though there is not control group, rebamipide enema had obviously a beneficial effect, clinically and endoscopically, on proctitis-type ulcerative colitis. Rebamipide (2-(4chlorobenzoylamino)-3-[2-(1H)-quinolinon-4-yl]-propionic acid), an antiulcer agent, has been reported to reduce gastric mucosal injury induced by several mechanisms, particularly that induced by oxidative stress. On the other hand, it is proposed that the anti-inflammatory effects of this drug on tissue are through enhancement of the production of mucus and mucosal protective prostaglandins (2), inhibition of the production of superoxides (released by neutrophils) and lipid peroxidation, preservation of intracellular glutathione and activity of antioxidant enzymes such as Cu,Zn-SOD (3) in colonocytes, and scavenging reactive oxygen species (hydroxyl radicals). Anti-cytokine (4) actions (inhibition of IL-8, IL-1b, TNF-a) have been also suggested. Considering that inflammation is the most important event in the pathophysiology of IBD, these effects considerably attracted our attention to the putative anti-inflammatory effects of this agent on IBD. In 1996, we reported the beneficial effect of rebamipide on experimental TNBS-induced colitis in rats, especially, preserving antioxidant enzymes and glutathione (3). Kishimotoet al. also reported that rebamipide reduced plasma levels and colonic tissue concentrations of substance P in DSS-induced colitis rats, suppressing colonic inflammation (5). As reactive oxygen metabolites may play a role in IBD, these results aimed us to look at rebamipide as a novel therapeutic alternative for UC. Rebamipide was administered by enema to exert its protective effect directly on colonic mucosa. It clearly showed its effectiveness, suggesting that rebamipide enema may be a new therapeutic approach for treating UC. It is also possible that rebamipide enema will be effective not only for proctitis-type but also for left-sided colitis. To clarify the mechanism of protection and clinical usefulness of rebamipide, further studies are warranted.

Mast cells: do they really have a role in disturbed bowel habits of IBS patients?

b.i.d., slowly swallowed but not inhaled, as used by Faubion et al. (5). At posttherapy endoscopy, only one (dysphagia dating back 3 decades) significantly improved. At each of his previous endoscopies, moving from 38 F dilator to just 40 F or 42 F (14 mm) always inflicted classic long deep mucosal separations. Postfluticasone, rescoping after eac h 2 F (2/3rd mm) dilator increment, I reached 48 F (16 mm) before diffuse tightness precluded larger dilators (eosinophilia-mediated deeper fibrosis?). But without any visible trauma! One other patient manifested a minor, a probably insignificant increase—trauma now at 45 F, rather than 42 F (1 mm). In the other three (including the “denovo” CRE), mucosal separations were apparent at sizes identical to prior endoscopies. Postfluticasone, biopsies in all confirmed dramatic improvement in intramucosal eosinophilia—now absent or nearly absent. I am aware of one mature adult CRE (personal communication, Dr. Peter Bonis, 2000) initially with “sheets of eosinophils” remaining dramatically better on chronic low doses after a similar fluticasone loading. Recently, an 8-yrold boy (8) (no mention of dilations or postdilatory trauma) resolved both symptoms and corrugations over 3 months on a soy-free/cows milk-free diet. Major allergies in most adult CREs are historical—decades ago. In fully developed adult CRE, my still limited corticosteroid experience seems pessimistic—only one of five! Even that “responder’s” esophagus is fibrotic, still far smaller than usual adult esophagi. My 11 CREs usually avoid impactions by chewing till liquified and occasional in-office Maloney dilations to sizes below significant trauma. (I suspect their numerous long thin vertical scars at endoscopy are from postdilatory and transient food impaction trauma.) CRE challenges quality of life! Since IEE responds to allergy interventions, could CRE be prevented by aggressively diagnosing and treating IEE (requiring increased awareness and biopsies of often endoscopically normal dysphagics) at, hopefully, a still reversible pre-CRE stage?

PPIs and Food Allergy

make the environment of the small intestine similar to that of the colon, thereby making it more susceptible to overgrowth with C. diffi cile . According to Kralovich et al. ( 2 ), the ileocecal valve inhibits the colonization of the small bowel with C. diffi cile with its peristaltic action; therefore, patients who undergo intestinal resections that include the ileocecal valve may be predisposed to develop C. diffi cile enteritis. Other studies have shown that the neoterminal ileum aft er ileocolonic resection is colonized heavily by colonic-type bacterial fl ora ( 1 ). Th e long duration between the primary intestinal operation and C. diffi cile enteritis may support the hypothesis that phenotypic changes may occur in the epithelium of the small intestine, which alter the normal anatomy or fecal fl ow ( 1,2,11,12 ). Th e mortality rate for C. diffi cile enteritis is quite high (60 – 80 % ). Factors having a role include probably the high permeability of the small-bowel mucosa ( 2 ), host factors, and delayed diagnosis secondary to the rarity of this illness. More cases of C. diffi cile enteritis have come to light in the past few years. Only 14 case reports were documented in the literature from 1980 to 2006. Seven more cases have been reported in the past 2 years, including six case series from the Department of Surgery, Medical College of Wisconsin. We can see the changing trend of C. diffi cile infections and one should therefore have a high clinical suspicion of C. diffi cile enteritis in patients with a history of IBD, at least in patients who have undergone colectomy. CONFLICT OF INTEREST Th e authors declare no confl ict of interest.

Dört olgu nedeniyle değişken immün yetersizlik sendromu

Common variable immunodeficiency is a syndrome of immune disorders that may occur spontaneously, usually in the second or third decade of life, in both males and females. These patients usually have very low serum levels of immunoglobulin classes, with normal or slightly reduced numbers of B cells. T cells are also not fully functional in a proportion of patients. Patients with this disorder are susceptible to frequent bacterial infections, particularly of the chest, ears and sinuses. Infection of the gut, particularly with Giardia lamblia is also a significant problem. There is a high incidence of gut cancer and lymphoma and noncaseating granulomas in multiple organs can also occur. In this report four cases with common variable immunodeficiency who presented with chronic diarrhea are discussed in the light of the relevant literature.