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

Hyperparathyroidism is a disease characterized by hypercalcemia with hypophosphoremia resulting from increased secretion of parathyroid hormone (PTH). The disease may be divided into 3 forms: a) primary, b) secondary, c) tertiary (secondary refractory form). Primary hyperparathyroidism is rare in children; hyperplasia is more frequent during the early years of life (neonates and infants) and is difficult to distinguish from adenoma in children. The disease may be asymptomatic; elevated calcemia levels (>12 <13.5 mg/dl) are accompanied by anorexia, asthenia and persistent stipsis; severely elevated concentrations (>13.5 mg/dl) are accompanied by nausea, vomiting, polyuria due to osmosis, with dehydration and progressive onset of lethargy, stupor and coma. Osteopenia or osteitis fibrosa cystica may be present due to augmented bone resorption. Height and weight increases are altered due to anorexia and dehydration. Differential diagnosis includes iatrogenic causes of hypercalcemia (excessive vitamin D intake, prolonged immobilization, etc.) and idiopathic familial hypercalcemia. Emergency treatment is required in cases of extremely elevated hypercalcemia (Ca >13.5-14 mg/dl), due to risk of injury to the heart, the central nervous system, the gastrointestinal tract and the kidneys. The 4 cardinal points of treatment are: hydration, calciuresis, inhibition of bone calcium resorption, treatment of the cause underlying hyperparathyroidism. Secondary hyperparathyroidism is found in cases where chronic hypocalcemia is present, particularly in chronic renal failure, untreated deficiency rickets, chronic intestinal malabsorption, hepatobiliary disease, types I and II vitamin D-dependent rickets, tubular acidosis or Fanconi's syndrome. The tertiary form is distinguished by the autonomous nature of the parathyroid glands which have become hypertrophic/hyperplastic due to uncontrollable, chronic severe renal failure. It can also be of iatrogenic origin due to excessive intake of inorganic phosphates in familial hypophosphatemic rickets or chronic vitamin D deficiency.
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PMID:Hyperparathyroidism. 1524 24

Tropical sprue (TS) is a postinfective tropical malabsorption that occurs in tropical countries. TS is associated with a persisting colonization of the small-intestine lumen by enterotoxinogenic bacteria that cause subsequent enterocyte damage affecting all or part of the small-intestine. We report two cases of TS that occurred in inhabitants of Paris area returned from endemic areas. The first observation concerned a 76-year old woman admitted for anorexia, loss of 20 kg and anemia. The second observation concerned a 53-year old man referred for chronic diarrhea and loss of 40 kg within 4 years. In both cases, duodenal lesions consisted of subtotal and total villous atrophy with prominent infiltration of the damaged surface epithelium with lymphocytes and infiltrate of lymphocytes and plasma cells of the lamina propria. The two patients recovered under antibiotics, confirming the diagnosis of TS.
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PMID:[Tropical sprue: two cases in the Paris area]. 1552 31

Nutrition plays an important role in the pathogenesis, treatment, and morbidity of Crohn disease. Approximately two thirds to three fourths of hospitalized patients with active disease and one fourth of outpatients with Crohn disease are malnourished. Malnutrition, which can be present even when Crohn disease is in remission, can affect growth, cellular and humoral immunity, bone density, and wound healing. Decreased nutrient intake, malabsorption, drug-nutrient interactions, anorexia, and protein-losing enteropathy can all contribute to the protein-calorie malnutrition and other specific nutrient deficiencies seen in Crohn disease. Therefore, by preventing and correcting nutrient deficiencies, nutritional therapy is an important component in the overall management of patients with Crohn disease.
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PMID:Nutrition in Crohn disease. 1570 56

The health effects of long-term ingestion of rare earth elements (REEs) on the villagers living in high-REE-background areas in South Jangxi Province, China were studied. Major health complaints from the REE area population included indigestion, diarrhea, abdominal distension, anorexia, weakness, and fatigue, especially after high-fat or high-protein intake. Liver function tests were conducted for adult villagers. Among them, 45 live in a heavy rare earth (HREE) area, 62 in a light rare earth (LREE) area, and 49 in the control area. Test results showed that serum total protein and globulin from both HREE and LREE areas, as well as albumin from the LREE area, were significantly lower (p < 0.01 - 0.01) compared to the results from the control area, whereas albumin from the HREE area showed no significant variance (p > 0.05). The chi-square test showed that Serum-glutamic pyruvic transaminase (SGPT) in both areas were not significant (p > 0.05), whereas the IgM in the HREE area was significantly elevated. It is our conclusion that long-term ingestion of REE affected activities of some digestive enzymes, causing malabsorption and indigestion, and might further lead to a low-protein effect for the villagers in the LREE area. However, the damage to the liver was rather mild. The elevation of IgM was probably the result of stimulation induced by the formation of a large amount of granules as a result of direct binding of REEs to globulin or albumin (combination of REEs with globulin or albumin).
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PMID:Investigation on liver function among population in high background of rare earth area in South China. 1585 27

An eight-month-old Border collie was presented with anorexia, cachexia, failure to thrive and stupor. Laboratory tests demonstrated a mild anaemia, neutropenia, proteinuria and hyperammonaemia. Serum bile acid concentrations were normal, but an ammonia tolerance test (ATT) was abnormal. The dog responded to symptomatic therapy for hepatoencephalopathy. When a low serum cobalamin (vitamin B12) concentration and methylmalonic aciduria were noted, the dog was given a supplement of parenteral cobalamin. Two weeks later, a repeat ATT was normal. Cobalamin supplementation was continued every two weeks, and all clinical signs, except for proteinuria, resolved despite withdrawing all therapy for hepatoencephalopathy. A presumptive diagnosis of hereditary selective cobalamin malabsorption was made, based on the young age, Border collie breed, low serum cobalamin concentration and methylmalonic aciduria. Although hereditary selective cobalamin malabsorption in Border collies, giant schnauzers, Australian shepherd dogs and beagles has previously been reported in North America, to the authors' knowledge this is the first report of the condition in the UK and the first to document an abnormal ATT in a cobalamin-deficient dog.
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PMID:Hyperammonaemic encephalopathy secondary to selective cobalamin deficiency in a juvenile Border collie. 1603 51

Pellagra is a systemic disturbance caused by a cellular deficiency of niacin, resulting from inadequate dietary nicotinic acid and/or its precursors, the essential amino-acid tryptophan. In Europe and North America cases of pellagra are rarely encountered, but in some developing countries this disease is frequent, and is the most frequent clinical feature of nutritional deficiency of adult. The principal causes of pellagra are: nutritional niacin deficiency; chronic alcoholism; gastro-intestinal malabsorption; some medications (5-fluoro-uracil, isoniazid, pyrazinamide ehtionamide, 6-mercaptopurine, hydantoins, phenobarbital and chloramphenicol). The diagnosis of pellagra is based on the patient's history and the presence of "3 D syndrome": dermatitis, diarrhea, and dementia. The dermatitis caused by pellagra is a bilaterally symmetrical erythema at the sites of solar exposure. The dermatitis begins in the form of an erythema with acute or intermittent onset gradually changing to an exsudative eruption on the dorsa of the hand, face, neck, and chest with pruritus and burning. Acute dermatitis of pellagra resembles sunburn in the first stages, sometimes with vesicles and bullae. The gastro-intestinal disturbances are: anorexia, nausea, epigastric discomfort and chronic or recurrent diarrhea. Anorexia and malabsorbative diarrhea lead to a state of malnutrition and cachexia. Stools are typically watery, but occasionally can be bloody and mucoid. Neuropsychologic manifestation included photophobia, asthenia, depression, hallucinations, confusions, memory loss and psychosis. As pellagra advances, patient become disoriented, confused and delirious; then stuporous and finally die. Pathological changes in the skin is non-specific, there are no chemical tests available to definitively diagnose pellagra. However low levels of urinary excretion of N-methylnicotinamide and pyridone indicates niacin deficiency. The treatment of pellagra consisted to exogenous administration of niacin or nicotinamide cures. Topical management of skin lesions with emollients may reduce discomfort. The therapy should also include other B vitamins, zinc and magnesium as well as a diet rich in calories. The prevention is based in the nutritional education (food sources of niacin: eggs, bran, peanuts, meat, poultry, fish, red meat, legumes and seeds), and the eviction of alcohol.
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PMID:[Pellagra]. 1620 85

Celiac disease is a gastrointestinal disorder characterized by inflammation, leading to injury to the mucosal lining of the small intestine. The inflammation occurs when gliadin, a protein found in such gluten-containing foods as wheat, rye, and barley, is ingested by genetically susceptible individuals. The mucosal damage and subsequent malabsorption of nutrients leads to various complications. Researchers estimate that more than 2 million people in the United States have celiac disease-a prevalence that is greater than was previously believed. Approximately 60,000 Americans are diagnosed annually with celiac disease. Until recently, diagnosis has been complicated by the fact that the indicators of celiac disease are nonspecific. However, because of the development of new, easy-to-administer serology tests, diagnosis has become much less complicated. After conducting a review of the literature, the authors recommend a serologic testing sequence for diagnosis of celiac disease and urge that adults and children with an assortment of symptoms be tested for this disease. Common signs and symptoms of celiac disease include anemia, arthralgia, fatigue, infertility, neuropathy, and weight loss, in addition to such gastrointestinal symptomatology as abdominal pain, anorexia, bloating, constipation, and diarrhea. The only treatment for patients with celiac disease remains a gluten-free diet.
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PMID:New strategies for diagnosis and management of celiac disease. 1658 82

Celiac disease, or gluten-sensitive enteropathy, is an immune-mediated disease of the small bowel that results in malabsorption. It classically presents with gastrointestinal symptoms including chronic diarrhea, weight loss, abdominal bloating and anorexia. It is becoming more frequently identified in asymptomatic patients with a diagnosis of deficiencies related to malabsorption of iron, folic acid, vitamin B12 and vitamin D. It is increasingly identified as a cause for early or refractory osteoporosis. Occasionally, celiac disease presents with cutaneous manifestations alone. Dermatitis herpetiformis is a well-recognized cutaneous manifestation of celiac disease. Other cutaneous manifestations include alopecia, angular stomatitis and aphthous ulcerations. Described here is a case of a 24-year-old woman who presented with intermittent urticaria and gastrointestinal complaints. She was found to have celiac disease on small-bowel biopsy. Both her gastrointestinal symptoms and urticaria resolved when she was put on a gluten-free diet, suggesting that her urticaria was a cutaneous manifestation of celiac disease.
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PMID:Chronic urticaria: a cutaneous manifestation of celiac disease. 1660 61

The synergistic association between malnutrition and infection remains today the most worrisome public health problem in the world. Although the high level of mortality among children in developing countries is mainly due to infectious and parasitic diseases, more than half of these children die in a state of overt undernourishment. Energy and nutrient deficiencies adversely affect various aspects of immunocompetence, thus malnourished people are particularly sensitive to many opportunistic infections. These, in turn, induce anorexia, various metabolic changes and malabsorption, which affect nutritional reserves, and lead to malnutrition if prolonged. In the absence of efficient measures to break this vicious cycle, malnutrition and morbidity lead to high levels of mortality. Experience from developing countries suggests that to improve the prevention and treatment of infectious diseases in such a context of poverty, one need to take into account simultaneously the basic environment of underprivileged groups and their dietary intake as well as their level of access to health care services.
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PMID:[The "malnutrition-infection" complex, the most widespread public health problem in underprivileged populations.]. 1729 2

Gastrointestinal (GI) problems at high altitude are commonplace. The manifestations differ considerably in short-term visitors, long-term residents and native highlanders. Ethnic food habits and social norms also play a role in causing GI dysfuntion. Symptoms like nausea and vomiting are common manifestations of acute mountain sickness and are seen in 81.4% short-term visitors like mountaineers. Anorexia is almost universal and has a mutifactorial causation including effect of hormones like leptin and cholecystokinin and also due to hypoxia itself. Dyspepsia and flatulence are other common symptoms. Diarrhoea, often related to poor hygiene and sanitation is also frequently seen especially among the short-term visitors. Peptic ulceration and upper gastro-intestinal haemorrhage are reported to be common in native highlanders in the' Peruvian Andes (9.6/10000 population per year) and also from Ladakh in India. A hig h incidence o f gastriccarcinoma is also reported, especially from Bolivia (138.2 cases per 10000 population per year). Megacolon and sigmoid volvulus are common lower GI disorders at high altitude. The latter accounted for 79% of all intestinal obstructions at a Bolivian hospital. Thrombosis of the portosystemic vascultature and splenic hematomas has been reported from India. Malnutrition is multifactorial and mainly due to hypoxia. Fat malabsorption is probably significant only at altitudes > 5000m. Neonatal hyperbilirubinemia was found to be four times more common in babies born at high altitude in Colorado than at sea level. Gall stones disease is common in Peruvian highlands. A high seroprevalence of antibodies to H pylori (95%) has been found in Ladakh but its correlation to the prevalence of upper gastro-intestinal disease has not been proven.
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PMID:Gastrointestinal problems at high altitude. 1754 91


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