Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case report of a young patient (born in 1980) with a 2-year history of chronic ulcerative proctocolitis was described. Checking colonoscopy 6 months from the beginning of disease showed multiple and even confluent polypoid lesions in transverse gut starting from hepatic flexure in addition to diffuse inflammatory rectosigmoideal changes. Biopsy found only colic mucosa without any tumorous structures. Five months later the patient's state got worse accompanied instantly by vomiting, weight loss and malabsorption symptoms. A duodenocolic fistula was supposed according to gastroduodenoscopy and biopsy. Because of progressive suffering of the patient colectomy with ileoduodenoanastomosis and ileosigmoidoanastomosis was performed. Polypous lesions were observed from the blind gut up to descendent colon and a transversoduodenal fistula was proved. The removed part of gut was completely changed into a dense network of elongated polypous lesions. In microscopy, bigger polyps showed an inner stromal part often with bands of smooth muscle cells covered by nearly normal gut mucosa. Smaller polyps were formed by hypertrophic gut mucosa only. At the base of polyps, a stagnation of gut contents was found as well as ulcerous defects of various depth. Macroscopy and microscopy of polypoid lesions formed by non-neoplastic gut mucosa were those of so called bizzare ("giant") inflammatory polyposis of the gut. Up to now the patient's clinical picture and local finding in the stump of resected gut have been typical for chronic ulcerous colitis and polypous lesions were not revealed by checking investigations.
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PMID:[A bizarre inflammatory polyposis of the colon in chronic ulcerative proctocolitis]. 962 28

Non-IgE-mediated gastrointestinal food-induced allergic disorders (non-IgE-GI-FAs) account for an unknown proportion of food allergies and include food protein-induced enterocolitis syndrome (FPIES), food protein-induced allergic proctocolitis (FPIAP), and food protein-induced enteropathy (FPE). Non-IgE-GI-FAs are separate clinical entities but have many overlapping clinical and histologic features among themselves and with eosinophilic gastroenteropathies. Over the past decade, FPIES has emerged as the most actively studied non-IgE-GI-FA, potentially because of acute and distinct clinical features. FPIAP remains among the common causes of rectal bleeding in infants, while classic infantile FPE is rarely diagnosed. The overall most common allergens are cow's milk and soy; in patients with FPIES, rice and oat are also common. The most prominent clinical features of FPIES are repetitive emesis, pallor, and lethargy; chronic FPIES can lead to failure to thrive. FPIAP manifests with bloody stools in well-appearing young breast-fed or formula-fed infants. Features of FPE are nonbloody diarrhea, malabsorption, protein-losing enteropathy, hypoalbuminemia, and failure to thrive. Non-IgE-GI-FAs have a favorable prognosis; the majority resolve by 1 year in patients with FPIAP, 1 to 3 years in patients with FPE, and 1 to 5 years in patients with FPIES, with significant differences regarding specific foods. There is an urgent need to better define the natural history of FPIES and the pathophysiology of non-IgE-GI-FAs to develop biomarkers and novel therapies.
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PMID:Non-IgE-mediated gastrointestinal food allergy. 2595 13

Food protein-induced enterocolitis (FPIES), allergic proctocolitis (FPIAP), and enteropathy (FPE) are among a number of immune-mediated reactions to food that are thought to occur primarily via non-IgE-mediated pathways. All three are typically present in infancy and are triggered most commonly by cow's milk protein. The usual presenting features are vomiting with lethargy and dehydration in FPIES; bloody and mucous stools in FPIAP; and diarrhea with malabsorption and failure to thrive in FPE. Diagnosis is based on convincing history and resolution of symptoms with food avoidance; confirmatory diagnostic testing other than food challenge is lacking. The mainstay of management is avoidance of the suspected inciting food, with interval challenge to assess for resolution, which usually occurs in the first years of life. Studies published in the past few years clarify common presenting features, report additional culprit foods, address potential biomarkers, and suggest new management strategies.
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PMID:Food Protein-Induced Enterocolitis Syndrome, Allergic Proctocolitis, and Enteropathy. 2617 34

Non-immunoglobulin E (IgE)-mediated food hypersensitivity includes a spectrum of disorders that predominantly affect the gastrointestinal tract. This review will focus on the following more common non-IgE-mediated food hypersensitivity syndromes: food protein-induced enterocolitis syndrome (FPIES), allergic proctocolitis (AP), food protein-induced enteropathy (FPE) and celiac disease. FPIES, AP and FPE typically present in infancy and are most commonly triggered by cow's milk protein or soy. The usual presenting features are profuse emesis and dehydration in FPIES; blood-streaked and mucousy stools in AP; and protracted diarrhea with malabsorption in FPE. Since there are no confirmatory noninvasive diagnostic tests for most of these disorders, the diagnosis is based on a convincing history and resolution of symptoms with food avoidance. The mainstay of management for FPIES, AP and FPE is avoidance of the suspected inciting food, with periodic oral food challenges to assess for resolution, which generally occurs in the first few years of life. Celiac disease is an immune-mediated injury caused by the ingestion of gluten that leads to villous atrophy in the small intestine in genetically susceptible individuals. Serologic tests and small intestinal biopsy are required to confirm the diagnosis of celiac disease, and management requires life-long adherence to a strict gluten-free diet.
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PMID:Non-IgE-mediated food hypersensitivity. 3027 46