Despite frequent use of immunosuppressive drugs in patients with inflammatory bowel disease (IBD) and reports of cytomegalovirus (CMV) infection following post-transplant immunosuppression, data on the frequency and clinical significance of CMV in patients with IBD are scant. Sixty-three patients with IBD (61 ulcerative colitis and two Crohn's disease) were evaluated for CMV using serology (IgM antibody, ì-capture ELISA), PCR for CMV DNA in colonic biopsy and histological assessment of haematoxylin and eosin-stained colonic biopsy. Positive result in any test was considered as CMV infection. Various parameters associated with CMV infection were analysed using univariate and multivariate analysis. Ten of 63 (15 . 8 %) patients (age 36 . 0 AE 11 . 2 years, 31 female) were infected with CMV (DNA alone in four, IgM antibody alone in two and both in four, inclusion body in one). Patients with CMV infection were more often female (8/10 vs 23/53, P , 0 . 05), had pancolitis (10/10 vs 33/53, P , 0 . 05), histological activity (9/10 vs 17/53, P , 0 . 005) and used azathioprine (5/10 vs 7/53, P ¼ 0 . 04; Fisher exact test for all). On multivariate analysis, female gender, pancolitis and histological activity were the independent factors associated with infection. Patients with CMV infection more often required surgical treatment for IBD (4/10 vs 4/ 53, P ¼ 0 . 01) and had fatal outcome (3/10 vs 0/53, P ¼ 0 . 003). CMV infection in patients with IBD may be common and is associated with poor outcome. PCR of rectal biopsy was the most sensitive method of detection followed by IgM antibody for diagnosis. INTRODUCTIONInfection with cytomegalovirus (CMV) is an important cause of morbidity and mortality after solid organ (kidney and liver) transplantation, as these patients receive multiple immunosuppressive drugs (Patel & Paya, 1997; Wiesner et al., 1993). Patients with inflammatory bowel disease (IBD), particularly those with severe, corticosteroid-refractory and -dependent states are frequently treated with immunosuppressive agents including corticosteroids, cyclosporine, azathioprine and methotrexate, either alone or in combination (Kho et al., 2001). Therefore, patients with IBD [ulcerative colitis (UC) and Crohn's disease (CD)] are expected to be at an increased risk of infection with CMV. However, data on CMV infection in patients with IBD is still scant and most studies used only histology and/or serology for diagnosis of CMV infection (Powell et al., 1961;Cooper et al., 1977;Berk et al., 1985;Eyre-Brook & Dundas, 1986;Vega et al., 1999;Cottone et al., 2001). Although histology is quite specific, it is of low sensitivity (Beaugerie et al., 1997). PCR has emerged as the most sensitive method for diagnosis of viral infection including that with CMV (Storch et al., 1994). However, only a few studies used PCR for diagnosis of CMV infection in IBD. With blood and buffy coat preparation of leukocytes as specimens, PCR failed to detect CMV in blood of patients with IBD in some of these studies (Adani et al., 2001). Demonstrati...

Progress in the understanding of the pathophysiology of irritable bowel syndrome (IBS), once thought to be a purely psychosomatic disease, has advanced considerably and low-grade inflammation and changes in the gut microbiota now feature as potentially important. The human gut harbours a huge microbial ecosystem, which is equipped to perform a variety of functions such as digestion of food, metabolism of drugs, detoxification of toxic compounds, production of essential vitamins, prevention of attachment of pathogenic bacteria to the gut wall, and maintenance of homeostasis in the gastrointestinal tract. A subset of patients with IBS may have a quantitative increase in bacteria in the small bowel (small intestinal bacterial overgrowth). Qualitative changes in gut microbiota have also been associated with IBS. Targeting the gut microbiota using probiotics and antibiotics has emerged as a potentially effective approach to the treatment of this, hitherto enigmatic, functional bowel disorder. The gut microbiota in health, quantitative and qualitative microbiota changes, and therapeutic manipulations targeting the microbiota in patients with IBS are reviewed in this paper.

The pathogenesis of irritable bowel syndrome (IBS), once thought to be largely psychogenic in origin, is now understood to be multifactorial. One of the reasons for this paradigm shift is the realization that gut dysbiosis, including small intestinal bacterial overgrowth (SIBO), causes IBS symptoms. Between 4% and 78% of patients with IBS and 1% and 40% of controls have SIBO; such wide variations in prevalence might result from population differences, IBS diagnostic criteria, and, most importantly, methods to diagnose SIBO. Although quantitative jejunal aspirate culture is considered the gold standard for the diagnosis of SIBO, noninvasive hydrogen breath tests have been popular. Although the glucose hydrogen breath test is highly specific, its sensitivity is low; in contrast, the early-peak criteria in the lactulose hydrogen breath test are highly nonspecific. Female gender, older age, diarrhea-predominant IBS, bloating and flatulence, proton pump inhibitor and narcotic intake, and low hemoglobin are associated with SIBO among IBS patients. Several therapeutic trials targeting gut microbes using antibiotics and probiotics have further demonstrated that not all symptoms in patients with IBS originate in the brain but rather in the gut, providing support for the micro-organic basis of IBS. A recent proof-of-concept study showing the high frequency of symptom improvement in patients with IBS with SIBO further supports this hypothesis.

Differentiating intestinal tuberculosis from Crohn's disease (CD) is an important clinical challenge of considerable therapeutic significance. The problem is of greatest magnitude in countries where tuberculosis continues to be highly prevalent, and where the incidence of CD is increasing. The final clinical diagnosis is based on a combination of the clinical history with endoscopic studies, culture and polymerase chain reaction for Mycobacterium tuberculosis, biopsy pathology, radiological investigations and response to therapy. In a subset of patients, surgery is required and intraoperative findings with pathological study of the resected bowel provide a definitive diagnosis. Awareness of the parameters useful in distinguishing these two disorders in each of the different diagnostic modalities is crucial to accurate decision making. Newer techniques, such as capsule endoscopy, small bowel enteroscopy and immunological assays for Mycobacterium tuberculosis, have a role to play in the differentiation of intestinal tuberculosis and CD. This review presents currently available evidence regarding the usefulness and limitations of all these different modalities available for the evaluation of these two disorders.

Background and Aim Because acute infectious gastroenteritis may cause post‐infection irritable bowel syndrome and functional dyspepsia and the severe acute respiratory syndrome coronavirus‐2 affects gastrointestinal (GI) tract, coronavirus disease‐19 (COVID‐19) may cause post‐infection‐functional GI disorders (FGIDs). We prospectively studied the frequency and spectrum of post‐infection‐FGIDs among COVID‐19 and historical healthy controls and the risk factors for its development. Methods Two hundred eighty patients with COVID‐19 and 264 historical healthy controls were followed up at 1 and 3 months using translated validated Rome Questionnaires for the development of chronic bowel dysfunction (CBD), dyspeptic symptoms, and their overlap and at 6‐month for IBS, uninvestigated dyspepsia (UD) and their overlap. Psychological comorbidity was studied using Rome III Psychosocial Alarm Questionnaire. Results At 1 and 3 months, 16 (5.7%), 16 (5.7%), 11 (3.9%), and 24 (8.6%), 6 (2.1%), 9 (3.2%) of COVID‐19 patients developed CBD, dyspeptic symptoms, and their overlap, respectively; among healthy controls, none developed dyspeptic symptoms and one developed CBD at 3 months ( P < 0.05). At 6 months, 15 (5.3%), 6 (2.1%), and 5 (1.8%) of the 280 COVID‐19 patients developed IBS, UD, and IBS‐UD overlap, respectively, and one healthy control developed IBS at 6 months ( P < 0.05 for all except IBS‐UD overlap). The risk factors for post‐COVID‐19 FGIDs at 6 months included symptoms (particularly GI), anosmia, ageusia, and presence of CBD, dyspeptic symptoms, or their overlap at 1 and 3 months and the psychological comorbidity. Conclusions This is the first study showing COVID‐19 led to post‐COVID‐19 FGIDs. Post‐COVID‐19 FGIDs may pose a significant economic, social, and healthcare burden to the world.

On the basis of culture, 19% patients with IBS had SIBO. The specificity of GHBT was 100%, but the sensitivity of this test and the diagnostic performances of LHBT and breath methane were all very poor. SIBO was more common in IBS patients with diarrhea than in patients with other bowel habits.

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Fecal microbiota was different among IBS than HC, and different sub-types were associated with different microbiota. P. aeruginosa was more frequent and higher in number among IBS patients.