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)

The corn protein gluten causes the gluten-sensitive enteropathy in susceptible persons (HLA-antigens). The diagnosis is made on the basis of the morphological criteria of villous atrophy of the jejunal mucosa and the clinical observation that the malabsorption can be healed by a gluten-free diet. The disease, which occurs in children and adults, is a distinct entity. Life-long adherence to a gluten-free diet is difficult. Intentional or unintentional reintroduction of gluten often causes masked disease states. These are best classified on the basis of electron-microscopy study of the jejunal biopsy. We propose a new classification of the phases of remission. A group of diseases exist which are closely related to gluten-sensitive enteropathy. Frequently villous atrophy is detectable. However, the disease does not respond to a gluten-free diet. The pathophysiology of these diseases is at present unclear. Diseases involving autoimmune processes also appear to be associated with gluten-sensitive enteropathy. The common factor is probably an immuno-genetic defect. This is supported by the existence of common HLA-antigen constellations. Gluten has been characterised in vitro as a lectin with oligomannose specificity. This provides a new pathomechanism for the gluten induced enterocytic destruction.
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PMID:[Gluten-sensitive enteropathy--in the light of new clinical and pathogenetic aspects]. 635 Jun 94

Plant lectins or carbohydrate binding proteins interact with membrane receptors on cellular surfaces but their antinutritional effects are poorly defined. Studies were conducted to determine the effects of phytohemagglutinin, a lectin derived from raw red kidney bean (Phaseolus vulgaris), on small intestinal absorptive function and morphology, and on the intestinal microflora. Phytohemagglutinin was isolated in purified form by thyroglobulin-sepharose 4B affinity chromatography. Red kidney bean and phytohemagglutinin (6% and 0.5%, respectively, of dietary protein) were fed in a purified casein diet to weanling rats for up to 21 days. Weight loss, associated with malabsorption of lipid, nitrogen, and vitamin B12, developed in comparison with animals pair-fed isonitrogenous casein diets. Antinutritional effects of red kidney bean were reversible on reinstitution of a purified casein diet. An increase in bacterial colonization of the jejunum and ileum occurred in red kidney bean- and phytohemagglutin-fed animals. When antibiotics were included in the diet, malabsorption of [3H]triolein and 57Co-vitamin B12 in red kidney bean-fed animals was partially reversed and, in germ-free animals, purified phytohemagglutinin had no demonstrable antinutritional effect. Mucosal disaccharidase activity was reduced in red kidney bean- and phytohemagglutinin-fed animals, but intestinal mucosal morphology was unchanged. Dietary administration of phytohemagglutinin, alone or as a component of red kidney bean, caused intestinal dysfunction, which was associated with, and dependent upon, small intestinal bacterial overgrowth. Adherence of enteric bacteria to the mucosal surface was enhanced by phytohemagglutinin which may have facilitated small intestinal bacterial overgrowth.
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PMID:Phytohemagglutinin derived from red kidney bean (Phaseolus vulgaris): a cause for intestinal malabsorption associated with bacterial overgrowth in the rat. 682 24

Cryptosporidium parvum is a coccidian parasite originally described a century ago and, until recently, not considered to be a human pathogen. It has a complex life cycle, including both sexual and asexual reproduction, an auto-infectious cycle, and the ability to complete its development within a single host. The transmission form is a robust, environmentally resistant oocyst, excreted in the stool, which can exist for long periods of time in the environment. Because animals, in particular domesticated livestock, are its primary host, human infection is usually zoonotic. Oocysts often find their way into water supplies, and it resists chlorination and is incompletely filtered from processed drinking water supplies, even when filtration is working optimally. Transmission via ingestion of fecally contaminated swimming pool water, food, fomites, and sexual activities facilitating fecal-oral inoculation have been demonstrated. The major target of C. parvum in the host is the intestinal epithelial cell, resulting in diarrhea, sometimes profuse and persistent, although it may also infect other organs such as the gall bladder and lungs. Pathogenesis involves attachment, probably via a sporozoite lectin, invasion, probably involving apical organelles, replication within a parasitophorous vacuole with the host cell membrane, causing cellular dysfunction. Diagnosis is generally made by visualization of the oocyst form in stool by staining methods, the best of which appears to be auramine and fluorescence microscopy. Those at greatest risk are immunocompromised adults and children, especially those with AIDS, children in day care, travelers to endemic regions, dairy or cattle farm workers of their families or contacts, household contacts of cases or carriers, and possibly owners of infected dogs or cats or their neighbors. There is no specific therapy available, however in the immunocompetent host the illness is self-limited, lasting from a few days to 3 weeks, and long term carriage is uncommon. In the immunocompromised host, infection is prolonged, sometimes asymptomatic, but may result in chronic debilitating diarrhea with dehydration, malabsorption and wasting. Public health measures to reduce contamination of water supplies and vigilant surveillance will reduce the risk to populations. Reducing behaviors favoring fecal-oral transmission, such as certain sexual activities, and scrupulous hygiene in the day care setting would also reduce the likelihood of transmission but not eliminate it. Given our lack of knowledge about Cryptosporidium biology and pathogenesis, high priority should be given to research designed to increase our understanding of the organism and improve the chance of developing useful therapeutic or preventative drugs or strategies.
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PMID:Cryptosporidia--who is at risk? 777 Jul 51

Giardiasis is the most common small intestinal protozoal infection and is found worldwide. The mechanisms by which Giardia duodenalis (= G. lamblia) produces chronic diarrhoea and malabsorption have still not been clearly defined. Many infections are associated with mild to moderate mucosal damage which, in animal models of infection, have functional correlates. Possible mechanisms include direct physical injury, release of parasite products such as proteinases or lectin, and mucosal inflammation associated with T cell activation and cytokine release. Other possible mechanisms of malabsorption include associated bacterial overgrowth and bile salt deconjugation, bile salt uptake by the parasite with depletion of intraluminal bile salts, and inhibition of pancreatic hydrolytic enzymes. Thus, there is no single mechanism to explain the diarrhoea and malabsorption caused by Giardia, which currently should be regarded as a multifactorial process.
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PMID:Diarrhoeal disease: current concepts and future challenges. Pathogenesis of giardiasis. 810 43

Giardia intestinalis (syn. G. lamblia, G. duodenalis) is a flagellated unicellular eukaryotic microorganism that commonly causes diarrheal disease throughout the world. In humans, the clinical effects of Giardia infection range from the asymptomatic carrier state to a severe malabsorption syndrome possibly due to different virulence of the Giardia strain, the number of cysts ingested, the age of the host, and the state of the host immune system at the time of infection. The question about how G. intestinalis is controlled by the organism remains unanswered. Here, we investigated the role of the complement system and in particular, the lectin pathway during Giardia infections. We present the first evidence that G. intestinalis activate the complement lectin pathway and in doing so participate in eradication of the parasite. We detected rapid binding of mannan-binding lectin, H-ficolin and L-ficolin to the surface of G. intestinalis trophozoites and normal human serum depleted of these molecules failed to kill the parasites. Our finding provides insight into the role of lectin pathway in the control of G. intestinalis and about the nature of surface components of parasite.
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PMID:Involvement of lectin pathway activation in the complement killing of Giardia intestinalis. 2038 17