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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intestinal immune responses are adapted to function at external mucosal surfaces. Specialized forms of antibody, secretory immunoglobulin A (IgA) and immunoglobulin M (IgM), provid humoral immunity but little is known of local cell mediated immune reactions. Antigens in the intestinal lumen gain preferential access via Peyer's patches in which sensitised lymphocytes proliferate before entering the lymphatic system. These lymphoblasts return to the intestinal mucosa via the bloodstream to provide predominantly IgA antibody responses. Secretory IgA antibody can neutralize viruses, bacteria and toxins, and appears to block the entry of some food antigens into the lamina propria. Disturbances of intestinal immunity may result in malabsorption. Immunodeficiency states are often associated with malabsorption due to Giardia lamblia infestation. In alpha chain disease there is a malignant expansion of plasma cells in the intestinal mucosa which secrete an abnormal heavy chain fragment of IgA. Arthus type hypersensitivity reactions to milk proteins and gluten may contribute to the mucosal injury in patients suffering from milk allergy and coeliac disease.
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PMID:An overview of intestinal immunity and malabsorption. 11 6

Described here is a patient with severe watery diarrhea associated with common variable immunodeficiency. Malabsorption for fat, bile acids, vitamin B12 and xylose was demonstrated, but the patient failed to respond to all the usual therapeutic maneuvers. The diarrhea responded only to high dose steroid therapy. Intestinal perfusion studies showed a hitherto undescribed, presumably acquired, glucose-stimulated water, sodium and chloride secretion in the jejunum and ileum, whereas normal fluid and electrolyte transport occurred from bicarbonate and mannitol solutions. Glucose absorption itself was normal and no hormonal, morphologic or biochemical defect was demonstrated to account for the phenomenon. The patient was also interesting when compared with other patients with common variable immunodeficiency in having normal plasma cells in the intestinal mucosa and an extensive family involvement.
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PMID:Immunodeficiency, malabsorption and secretory diarrhea. A new syndrome. 47 4

A model of digestion is proposed in which oligopeptides arriving at the small bowel epithelium are bound to secretory antibodies, which hold them in contact with proteases and thus facilitate their breakdown and utilization. "Immunity" and "digestion" are thus seen as two sides of the same coin. Absence of this pathway, predictably, would cause a degree of malabsorption, while partial deficiency (either quantitative or qualitative) would give rise to a coeliac-like illness. Breast-feeding with colostrum and then milk provides the infant gut with both immunity and "digestivity", and this could be adopted therapeutically for coeliac disease and other consequences of local immunodeficiency.
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PMID:Antibiody-facilitated digestion and its implications for infant nutrition. 55 18

A six-year old boy who had suffered from the age of two with chronic diarrhea has been found to be severely retarded in statural growth. Examinations discovered marked lymphopenia with a T lymphocyte defect accompanied by absent IgA and IgE. In contrast with other cases described in literature, in this case the immunodeficiency was not accompanied by bone or cartilage alterations. The only factor apparently responsible for his lack of growth was the malabsorption.
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PMID:Harmonic dwarfism, lymphopenia, deficit of IgA and IgE in a 6-year old boy. 61 Apr 13

In this review I have described the pathophysiology of allergic disorders of the gastrointestinal tract. Situations where the intestine cannot be a complete barrier to foreign allergens and antigens were discussed and etiological factors of gastrointestinal allergy were detailed. Clinical features of gastrointestinal allergy include diarrhea, vomiting, abdominal pain and colic, intestinal hemorrhage and malabsorption as well as symptoms and signs outside the gastrointestinal tract such as chronic rhinitis and asthma in the respiratory system, urticaria, angioedema and eczema as dermatological signs, headache, insomnia, hyperkinesis as central nervous system manifestations, failure to thrive and anaphylaxis as constitutional reactions. Milk allergy was discussed as an example of food allergy. Immunology of the gastrointestinal tract was presented, with examples of four types of hypersensitivity reactions, and gastrointestinal disturbances of immunodeficiency disorders and syndromes were named. Lastly, the autoimmune mechanism and the gut were described, with particular discussion of ulcerative colitis as an example of an autoimmune disease.
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PMID:The intestine in allergic diseases. 78 84

A young woman presented a mixed congenital and familial immunodeficiency syndrome consisting in an absence of IgA and lowered levels of IgG and IgM, with a defect in cellular immunity. She had a mild malabsorption syndrome with slight alterations of the jejunal mucosa. Non-caseating tuberculoid granulomata were found in skin lesions, in lymph nodes and in the spleen. At age 27 the patient died of a neurological disease of 4 months duration. Autopsy revealed a very widespread demyelinating process involving mainly the right cerebellar hemisphere but also most of the pons and left cerebellum, with the typical morphologic characters of PML. In the hemispheres lesions were limited to microscopical "microglial nodules" with discrete demyelination. A review of 86 published cases of PML revealed 9 other cases in which lesions showed a strong predilection for the subtentorial territories. This sampling allows for tha assumption that some 11% of the cases of PML have this particular lesion distribution. Other pertinent features of this case are briefly discussed.
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PMID:[Progressive multifocal leucoencephalopathy. Observation with predominant pontocerebellar lesions and association with congenital immune deficiency]. 87 53

Gastrointestinal (GI) disease is frequently encountered in patients with defective defense mechanisms. The incidence of GI disease and the structure and function of the GI tract have been studied systematically in 41 patients with immunodeficiency syndromes (IDS) and in 9 patients with chronic granulomatous diesase (CGD). Giardia lamblia was a major cause of GI disease in patients with IDS. Eradication of the parasite resulted in disappearance of symptoms and malabsorption, and normalization of the villus architecture. Six of 9 patients with CGD had either GI symptoms or malabsorption or both. Typical histologic changes were found in the small intestinal and rectal mucosa of all patients biopsied.
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PMID:Structure and function of the gastrointestinal tract in primary immunodeficiency syndromes (IDS) and in granulocyte dysfunction. 114 81

Three horses suffering from malabsorption were shown to have alimentary lymphosarcoma predominantly affecting the small intestine and the associated lymph nodes. The diffuse cellular infiltration in two of the case produced marked changes in the villous architecture reducing the available mucosal surface area, and, with lowered or barely detectable disaccharidase activities, contributed to the impairment of digestive-absorptive processes. One of the horses maintained a voracious appetite and was not diarrhoeic, but failed to gain weight, indicating differences in the production and utilisation of energy sources absorbed from the small and the large intestines. A large proportion of plasma cells in the infiltrate, and the resulting morphological changes in two of the cases bore a striking resemblance to features of alpha chain disease, an immunodeficiency disease of man, although immunological studies were not conducted on these horses.
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PMID:Malabsorption in the horse associated with alimentary lymphosarcoma. 117

49 gay men confirmed to be infected with the human immunodeficiency virus (HIV) and 9 HIV seronegative gay men participated in a pilot study comparing clinical status and enteric parasite load with gastrointestinal structure, function and symptomatology. Cases included 16/49 (33%) men who were CDC stage II, 7/49 (14%) who were CDC stage III, and 26/49 (53%) who were CDC stage IV. The mean CD4-lymphocyte count was 476 +/- 199 (SD)/microliter. The prevalence of enteric parasitic flora was similar in HIV seropositive patients and controls. Seven cases had enteric infection with pathogenic agents including 3 patients with Entamoeba histolytica, and 4 patients with Giardia lamblia, one of whom also had cryptosporidiosis. Other cases were most frequently colonized with Blastocystis hominis (44%) and Endolimax nana (41%) regardless of the HIV clinical status. HIV seropositive patients with enteric parasitic colonization tended to have lower mean levels of serum IgA than cases without parasites. Duodenal morphometric mucosal changes demonstrated a significant decrease in the mean villous height (p < 0.01) with no elongation of the crypt depth in HIV-infected patients with and without diarrhea compared to controls. Despite gastrointestinal symptoms including diarrhea and weight loss being more prevalent in HIV infected individuals than controls, no correlations were found between the presence of particular enteric parasites, gastrointestinal symptomatology, the clinical HIV status of the CD4-lymphocyte count, the malabsorption of D-xylose or morphometric changes in the duodenum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Absence of an association between enteric parasites in the manifestations and pathogenesis of HIV enteropathy in gay men. The GI/HIV Study Group. 136 Dec 41

AIDS-associated gastric secretory failure has been characterized by decreased secretion of acid, pepsin, and gastric juice volume. To determine whether decreased intrinsic factor secretion and vitamin B12 malabsorption occur in this entity, we performed prospective measurements of maximal acid output, intrinsic factor output, vitamin B12 absorption, serum vitamin B12, and holotranscobalamin II in 10 consecutive AIDS patients. Four of 10 patients had low maximal acid output, i.e., < or = 1.5 mEq/h (control = 12.8 +/- 9.0, range 2.5-25 mEq/h). Four patients had low intrinsic factor output, i.e., < or = 1.1 microgram/h (control = 8.2 +/- 6.9, range 3.1-19.4 micrograms/h). One patient with low intrinsic factor output had low serum vitamin B12 and a Schilling test consistent with pernicious anemia. A second patient with very low intrinsic factor output (0.16 micrograms/h) had low parts I and II Schilling tests; malabsorption most likely resulted from both low intrinsic factor secretion and ileal disease. One of three vitamin B12 malabsorbing patients, with normal serum vitamin B12, had low holotranscobalamin II, 25 pg/ml (control holotranscobalamin II = 76 +/- 44, range 44-152 pg/ml). Maximal acid output and intrinsic factor output did not correlate in AIDS (r = 0.36, p = 0.30) in contrast to the expected correlation in controls (r = 0.91, p = 0.03). We conclude that low intrinsic factor secretion is common in AIDS and contributes to vitamin B12 malabsorption. Decreased parietal cell secretion of intrinsic factor and acid may occur independently in human immunodeficiency virus-associated gastric secretory failure. Low holotranscobalamin II, an early manifestation of vitamin B12 malabsorption, results in decreased delivery to vitamin B12-dependent tissues prior to depletion of serum vitamin B12. Regular supplementation with vitamin B12 may therefore be warranted in patients with advanced HIV infection.
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PMID:Decreased intrinsic factor secretion in AIDS: relation to parietal cell acid secretory capacity and vitamin B12 malabsorption. 144 41


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