Who to screen and how to screen for celiac disease

Celiac disease (CeD) is a chronic gluten-induced enteropathy with plethoric manifestations. The typical manifestations of CeD such as chronic diarrhea and malabsorption are widely recognized, however, many patients have atypical manifestations like iron deficiency anemia, idiopathic short stature, hypertransaminesemia or infertility, etc. These patients often present to the primary care physicians and/or non-gastrointestinal specialties. However, due to a lack of awareness among the healthcare professionals about the various atypical manifestations, many patients are not screened for CeD. In this review, we have summarized the available literature about the prevalence of CeD in various gastrointestinal (chronic diarrhea) and non-gastrointestinal conditions (iron deficiency anemia, short stature, cryptogenic hypertransaminesemia, cryptogenic cirrhosis or idiopathic ataxia etc.) where the diagnosis of CeD should be con-sidered. In addition, we also discuss special scenarios where screening for CeD should be considered even in absence of symptoms such as patients with type 1 diabetes, Down’s syndrome, and first-degree relatives of patients with CeD. Further, we discuss the diagnostic performance and limitations of various screening tests for CeD such as IgA anti-tissue transglutaminase antibodies, anti-endomysial antibodies and anti-deamidated gliadin antibodies. Based on the current recommendations, we propose a diagnostic algorithm for patients with suspected CeD.     

Five cases of sprue-like enteropathy in patients treated by olmesartan

We describe five cases of sprue-like enteropathy during treatment with olmesartan, an angiotensin II receptor antagonist indicated for the treatment of hypertension. Patients presented severe diarrhoea, significant weight loss or dehydration, with or without intestinal villous atrophy. Clinical signs ceased upon drug discontinuation in all cases; olmesartan was reintroduced in two cases and rechallenge was positive in both. These add to the previously reported cases that led to a label change for olmesartan in the United States. However, all cases were observed in a small gastroenterology unit, which suggests that this adverse effect may not be rare. A preliminary search for the other angiotensin II receptor antagonists in the French pharmacovigilance system found severe diarrhoea and colitis, but no case with villous atrophy. Therefore, in the presence of severe diarrhoea, olmesartan or other angiotensin II receptor antagonists should be discontinued, even if the treatment has been taken for several months or years.     

Mechanisms underlying intestinal injury induced by anti-inflammatory COX inhibitors

By far the most attention has been paid to the deleterious actions of nonsteroidal anti-inflammatory drugs (NSAIDs), including isoform selective agents that inhibit cyclooxygenase (COX), on the upper gastrointestinal tract, particularly the gastric and duodenal mucosa. However, recent studies confirm a relatively high incidence of serious clinical events, especially with the more-established drugs of this class, involving the small intestine. Pathogenic factors that have been proposed from early studies in such enteropathy have included the enterohepatic circulation of the nonsteroidal anti-inflammatory drugs, inhibition of cyclooxygenase, surface epithelial changes and focal microvascular events. More recent work has concerned the role of infiltrating inflammatory cells, the relative roles of cyclooxygenase isoforms, COX-1 and COX-2 and the key involvement of inducible nitric oxide (NO) synthase and its product in combination with superoxide, peroxynitrite. In the present review, evidence for the underlying involvement of each these processes, and their sequential integration in the development of the intestinal injury and ulceration promoted by nonsteroidal anti-inflammatory drugs has been considered.     

The Role of Iron Deficiency in Protein‐losing Enteropathy Following the Fontan Procedure

We describe the case of an adult who developed protein‐losing enteropathy 21 years after having undergone a Fontan procedure. Investigations revealed iron deficiency anemia which was treated with intravenous iron sucrose leading to resolution of both the anemia as well as symptoms of protein‐losing enteropathy.