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

The prevalence of vitamin B-12 deficiency increases with age, probably resulting from malabsorption of food-bound B-12 secondary to gastric atrophy. On the basis of this assumption, the Institute of Medicine (IOM) recommends those aged >50 y consume crystalline vitamin B-12. There is limited information on the prevalence of gastric atrophy in the elderly and whether the IOM recommendation would be effective. The objective of this study was to assess predictors of vitamin B-12 status and their interactions in free-living elderly. Individuals (n = 57) with deficient plasma vitamin B-12 (p-B12 < 148 pmol/L) were compared with 68 individuals with marginal p-B12 (148-221 pmol/L) and 52 with normal p-B12 (>221 pmol/L) in a cross-sectional sample (n = 1546) of elderly (>60 y) Latinos in California. Associations were examined among p-B12 and serum gastrin, vitamin B-12 intake from food and crystalline sources, and medications that putatively affect vitamin B-12 absorption. Serum gastrin was elevated, indicating gastric atrophy, in 48% of participants with deficient p-B12, 23% with marginal p-B12 and 21% of normal p-B12 participants, and was a significant predictor of deficient p-B12 and high plasma homocysteine (p-tHcy). Median total vitamin B-12 intake exceeded recommendations and was similar among status groups. Crystalline vitamin B-12 intake in the normal p-B12 group was higher than in the deficient p-B12 group (P < 0.01), and tended to be higher than the marginal group (P = 0.07). When serum gastrin was elevated, p-B12 was predicted by crystalline vitamin B-12, but not by intake of vitamin B-12 from food. Elevated serum gastrin was highly prevalent and predicted vitamin B-12 depletion. Crystalline vitamin B-12 intake predicted p-B12 in individuals with elevated serum gastrin, supporting IOM recommendations to increase consumption of crystalline vitamin B-12.
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PMID:Plasma vitamin B-12 concentrations in an elderly latino population are predicted by serum gastrin concentrations and crystalline vitamin B-12 intake. 1294 63

Pernicious anemia (PA) is an autoimmune disorder associated with atrophic gastritis, presence of antibodies to gastric parietal cells and intrinsic factor (IF) and vitamin B2 malabsorption leading to megaloblastic anemia. It has a comparatively higher prevalence in people of North European origin, is uncommon in Arabs and usually affects the elderly. This report, the first from Bahrain, describes a rare case of PA in young female. The presenting symptoms, clinical and laboratory features were similar to those described in classical elderly Caucasian patients. No association with any other autoimmune disease was detected.
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PMID:Pernicious anemia in a young Bahraini female. 1502 26

There has been an increasing awareness recently of subtle, non-bleeding gastrointestinal conditions that may result in abnormal iron absorption leading to iron-deficiency anaemia (IDA) in the absence of gastrointestinal symptoms. Thus, the importance of coeliac disease as a possible cause of IDA refractory to oral iron treatment, without other manifestations of malabsorption syndrome, is increasingly being recognized. In addition, Helicobacter pylori has been implicated in several recent studies as a cause of IDA refractory to oral iron treatment, and the anaemia responds favourably to H. pylori eradication. Likewise, achlorhydric gastric atrophy or atrophic body gastritis (ABG), a condition associated with chronic idiopathic iron deficiency, has been shown to be responsible for refractory IDA in over 20% of patients with no evidence of gastrointestinal blood loss. It has also been suggested that H. pylori gastritis may represent an early phase of ABG in which infection may trigger an autoimmune process directed against gastric parietal cells by means of antigenic mimicry. In this review we examine in a critical manner the role of H. pylori gastritis in the causation of IDA, the role of ABG in the pathogenesis of iron malabsorption, the evidence supporting a possible cause-and-effect relationship between H. pylori gastritis and ABG, and the implications of these findings for the diagnostic work-up and management of IDA.
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PMID:Gastropathic sideropenia. 1573 96

Cobalamin deficiency is a common finding. In the elderly the prevalence is 10-20%, but only 5-10% of these are clinically symptomatic. Typical clinical symptoms include macrocytic anemia, neuropsychiatric symptoms and glossitis. In many cases this triad is lacking, however. The serum cobalamin assay is the best first line test, but the results must be carefully interpreted, since a normal level does not exclude deficiency. Markers of cobalamin activity, such as serum homocysteine or methylmalonic acid may be helpful in this situation. The main cause of cobalamin deficiency is atrophic gastritis. It is either caused by an autoimmune process which leads to achlorhydria and severe intrinsic factor deficiency ("classical pernicious anemia") or by atrophic gastritis from other causes, in particular helicobacter pylori infection. In the latter cases the lack of gastric acid does not allow separation of cobalamin from proteins, but intrinsic factor, although low, is sufficient for cobalamin protection (food cobalamin malabsorption). Helicobacter pylori eradication may cure some of these patients. While in food cobalamin malabsorption syndrome small doses of oral cobalamin are effective, parenteral therapy or high oral doses are required for treatment of pernicious anemia. While almost all patients respond hematologically, only half of the patients with neurological signs, and a small minority of psychiatric patients respond to treatment. Patients with pernicious anemia and atrophic gastritis have a greatly increased long-term risk for gastric carcinoids.
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PMID:[Vitamin B12 deficiency. New data on an old theme]. 1639 86

The aim of this work was to review the literature concerning cobalamin deficiency in elderly patients. Articles were identified through searches of PubMed-MEDLINE (January 1990 to June 2006), restricted to: English and French language, human subjects, elderly patients (>65 years), clinical trial, review and guidelines. Additional unpublished data from our cohort with cobalamin deficiency at the University Hospital of Strasbourg, France, were also considered. All of the papers and abstracts were reviewed by at least two senior researchers who selected the data used in the study. In elderly people, the main causes of cobalamin deficiency are pernicious anemia and food-cobalamin malabsorption. The recently identified food-cobalamin malabsorption syndrome is a disorder characterized by the inability to release cobalamin from food or from its binding proteins. This syndrome is usually the consequence of atrophic gastritis, related or not to Helicobacter pylori infection, and of the long-term ingestion of antacids and biguanides (in around 60% of the patients). Management of cobalamin deficiency has been well established with the use of cobalamin injections. However, new routes of cobalamin administration (oral and nasal) are currently being developed, especially the use of oral cobalamin therapy to treat food-cobalamin malabsorption.
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PMID:Clinical aspects of cobalamin deficiency in elderly patients. Epidemiology, causes, clinical manifestations, and treatment with special focus on oral cobalamin therapy. 1782 56

Norwegian Lundehunds are often affected by gastrointestinal disease, the most common clinical signs of which are intermittent diarrhea, vomiting, weight loss, lethargy, ascites, and subcutaneous edema of the hind legs. The most frequent laboratory changes include hypoalbuminemia (with or without hypoglobulinemia), hypocalcemia, a decrease in the serum cobalamin concentration, and an increase or decrease in the serum folate concentration, reflecting microbial synthesis or malabsorption, respectively. Histopathologic abnormalities can include chronic atrophic gastritis, intestinal lymphangiectasia, and lymphoplasmacytic enteritis. Because the underlying cause of gastroenteropathy in Norwegian Lundehunds has not been identified, treatment is symptomatic.
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PMID:Gastroenteropathy in Norwegian Lundehunds. 1784

Sodium levothyroxine is one of the most prescribed drugs all over the world. Oral thyroxine treatment is often used lifelong and the search for optimal daily dose may be a challenge for the physician. Patient age and compliance to prescribed regimen are in fact relevant features to achieve therapeutic goal. Also, the absorption of thyroxine is not a linear function of the ingested dose being sensitive to several interferences. Inaccurate administration modality, thyroxine interaction with different drugs, pregnancy, and malabsorption are all possible causes of increased need for thyroxine. Important and simple evidences are now available to improve the accuracy of drug administration and optimize the treatment. In fact, recent evidence pointed out the role of gastric acid secretion on the subsequent intestinal absorption of thyroxine in relation with the timing of food ingestion as well as with pH impairment associated to frequent gastric disorders like Helicobacter pylori infection and gastric atrophy.
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PMID:[Oral thyroxine treatment: towards an individually tailored dose]. 1790 70

Anemia is often observed in digestive diseases such as gastroduodenal ulcers, esophageal varices, atrophic gastritis, malignant neoplasms, inflammatory bowel diseases, gastrectomy, malabsorption syndrome, and liver diseases. Anemia in these digestive diseases is caused by bleeding, iron deficiency, vitamin B12 deficiency including pernicious anemia, chronic inflammation (anemia of chronic disorders), malnutrition, hypersplenism. Especially in case of gastrointestinal bleeding, double balloon enteroscopy has been recently introduced to contribute to the diagnosis and treatment as well as gastroendoscopy and colonoscopy. In the treatment of digestive disease with anemia, it is important to treat digestive diseases appropriately. In treatment of patients with anemia of unknown origin, examinations about digestive diseases should be considered.
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PMID:[Digestive disease with anemia]. 1832 21

This review describes current knowledge of the main causes of vitamin B12 and folate deficiency. The most common explanations for poor vitamin B12 status are a low dietary intake of the vitamin (i.e., a low intake of animal-source foods) and malabsorption. Although it has long been known that strict vegetarians (vegans) are at risk for vitamin B12 deficiency, evidence now indicates that low intakes of animal-source foods, such as occur in some lacto-ovo vegetarians and many less-industrialized countries, cause vitamin B12 depletion. Malabsorption of the vitamin is most commonly observed as food-bound cobalamin malabsorption due to gastric atrophy in the elderly, and probably as a result of Helicobacter pylori infection. There is growing evidence that gene polymorphisms in transcobalamins affect plasma vitamin B12 concentrations. The primary cause of folate deficiency is low intake of sources rich in the vitamin, such as legumes and green leafy vegetables, and the consumption of these foods may explain why folate status can be adequate in relatively poor populations. Other situations in which the risk of folate deficiency increases include lactation and alcoholism.
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PMID:Causes of vitamin B12 and folate deficiency. 1870 79

Cobalamin (vitamin B12) deficiency is particularly common in the elderly (>65 years of age), but is often unrecognized because of its subtle clinical manifestations; although they can be potentially serious, particularly from a neuropsychiatric and hematological perspective. In the general population, the main causes of cobalamin deficiency are pernicious anemia and food-cobalamin malabsorption. Food-cobalamin malabsorption syndrome, which has only recently been identified, is a disorder characterized by the inability to release cobalamin from food or its binding proteins. This syndrome is usually caused by atrophic gastritis, related or unrelated to Helicobacter pylori infection, and long-term ingestion of antacids and biguanides. Besides these syndromes, mutations in genes encoding endocytic receptors involved in the ileal absorption and cellular uptake of cobalamin have been recently uncovered and explain, at least in part, the hereditary component of megaloblastic anemia. Management of cobalamin deficiency with cobalamin injections is currently well codified, but new routes of cobalamin administration (oral and nasal) are being studied, especially oral cobalamin therapy for food-cobalamin malabsorption.
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PMID:An update on cobalamin deficiency in adults. 1899 Jul 19


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