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

Local and systemic cellular immunity parameters of the blood and gastrointestinal mucosa were studied in 165 children suffering from chronic gastritis, duodenitis, celiac, secondary malabsorption syndrome, and phosphate diabetes by spontaneous E-RFC method with a number of loading tests in vitro. Thymalin, theophylline, cold incubation were used. Three types of T lymphocyte response were distinguished: the hypoergic, resistant, and hyperergic. To make the interpretation of the findings easier, coefficients were calculated for each type of response of the blood and gastrointestinal mucosa immunocompetent cells.
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PMID:[Evaluation of the state of systemic and local cellular immunity using loading tests]. 800 Jul 97

Two entities of considerable recent interest, Helicobacter pylori infection of the stomach and food-cobalamin malabsorption, are each intimately associated with gastric abnormalities. A possible connection between the two entities thus suggested itself and prompted us to study 98 subjects with low serum cobalamin levels but normal Schilling test results and 17 controls with normal cobalamin levels. Food-cobalamin absorption was measured with the egg yolk-cobalamin absorption test (EYCAT) and was abnormal in 56 of the 115 subjects. IgG antibody to H. pylori was found in 78% of the 27 patients with severe food-cobalamin malabsorption (EYCAT < 1.0% excretion), compared with only 45% of 29 subjects with mild malabsorption (EYCAT 1.0-1.99%) and 42% of 59 subjects with normal absorption (EYCAT > or = 2.0%) (chi 2 = 9.52, P < 0.01). Antibody-positive patients had lower EYCAT excretion values than those without antibody (2.03 +/- 1.83% vs 3.11 +/- 2.13%, t = 2.913, P = 0.005). While Hispanic patients tended to malabsorb food cobalamin more frequently than did white or black patients, and men were more often antibody-positive than women, race, sex, or age characteristics were not responsible for the significant association between serologic evidence of H. pylori infection and severe malabsorption of food cobalamin. The association that we describe suggests that gastritis induced by H. pylori predisposes to a more severe form of food-cobalamin malabsorption, among its other effects on gastric status.
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PMID:Helicobacter pylori infection and food-cobalamin malabsorption. 831 13

Over a 2.5-year period, 82 consecutive children complaining of recurrent abdominal pain underwent upper gastrointestinal endoscopy. Gastroscopy confirmed pathology in 48 of the children (58.5%). Four of the children, who also had undergone gastroscopy, had other diagnoses (lactose malabsorption, hydronephrosis, yersiniosis), and 30 of the children (36.6%) retained the initial diagnosis of recurrent abdominal pain syndrome. Gastritis was found in 48 of the children, 18 of whom (37.5%) had positive test results for Helicobacter pylori, based on histology and/or culture. Of 16 H. pylori-positive children tested, 12 (75%) also had an elevated concentration of IgG-class antibodies to H. pylori in their sera. Three of the children had duodenal ulcer disease, all of whom were H. pylori positive. Esophagitis was found in eight of the children with gastritis, all of whom were found to have gastroesophageal reflux. Our data suggest that among the children with recurrent abdominal pain syndrome, organic pathology is more common than was previously thought. Altogether 22% of the children with recurrent abdominal pain syndrome were infected with H. pylori.
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PMID:Upper gastrointestinal endoscopy in recurrent abdominal pain of childhood. 849 55

To investigate the prevalence and the significance of Helicobacter pylori duodenal colonization, endoscopic duodenal biopsies were performed in 168 children with chronic abdominal pain, gastroesophageal reflux, gastrointestinal bleeding, and malabsorption syndrome. Helicobacter pylori infection was detected in 68 children (40.4%): in 31 of them H. pylori was present in the gastric antrum, and in 37 in the duodenum also. Duodenitis was observed in 25 children with duodenal H. pylori; gastric metaplasia in 3. Scanning electron microscopy revealed the presence of the micro-organism in 3/13 cases; the bacteria were located in the intercellular spaces and alterations of the epithelial surface were found. In conclusion, H. pylori gastritis in children is often associated with duodenal colonization which can cause duodenitis, and also without gastric metaplasia, which indicates a possible role of the micro-organism in the pathogenesis of the lesions.
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PMID:Helicobacter pylori duodenal colonization in children. 917 19

Cobalamin (vitamin B12) deficiency is more common in the elderly than in younger patients. This is because of the increased prevalence of cobalamin malabsorption in this age group, which is mainly caused by (autoimmune) atrophic body gastritis. Cobalamin supplementation is affordable and nontoxic, and it may prevent irreversible neurological damage if started early. Elderly individuals with cobalamin deficiency may present with neuropsychiatric or metabolic deficiencies, without frank macrocytic anaemia. An investigation of symptoms and/or signs includes the diagnosis of deficiency as well as any underlying cause. Deficiency states can still exist even when serum cobalamin levels are higher than the traditional lower reference limit. Cobalamin-responsive elevations of serum methylmalonic acid (MMA) and homocysteine are helpful laboratory tools for the diagnosis. The health-related reference ranges for homocysteine and MMA appear to vary with age and gender. Atrophic body gastritis is indirectly diagnosed by measuring serum levels of gastrin and pepsinogens, and it may cause dietary cobalamin malabsorption despite a normal traditional Schilling's test. The use of gastroscopy may also be considered to diagnose dysplasia, bacterial overgrowth and intestinal villous atrophy in healthy patients with atrophic body gastritis or concomitant iron or folic acid deficiency. Elderly patients respond to cobalamin treatment as fully as younger patients, with complete haematological recovery and complete or good partial resolution of neurological deficits. Chronic dementia responds poorly but should, nevertheless, be treated if there is a metabolic deficiency (as indicated by elevated homocysteine and/or MMA levels). Patients who are at risk from cobalamin deficiency include those with a gastrointestinal predisposition (e.g. atrophic body gastritis or previous partial gastrectomy), autoimmune disorders [type 1 (insulin-dependent) diabetes mellitus and thyroid disorders], those receiving long term therapy with gastric acid inhibitors or biguanides, and those undergoing nitrous oxide anaesthesia. To date, inadequate cobalamin intake has not proven to be a major risk factor. Intervention trials of cobalamin, folic acid and pyridoxine (vitamin B6) in unselected elderly populations are currently under way.
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PMID:Age-related changes in cobalamin (vitamin B12) handling. Implications for therapy. 957 92

Antacids containing aluminum and magnesium hydroxide are widely used nonprescription agents for treatment of gastritis and peptic ulcer disease. One of the side effects of these antacids is that they bind phosphate in the gut, resulting in its malabsorption. Short-term use, consistent with the directions on the manufacturer's label, is safe and effective for most patients. Heavy chronic use, even when within label, can cause serious skeletal impairment. This report concerns the case of a 39-year-old pharmacist who self-mediated for peptic ulcer disease with high doses of a potent antacid containing aluminum and magnesium hydroxide. The patient consumed over 18 kg of elemental aluminum and 15 kg of elemental magnesium over 8 years of antacid use. This treatment resulted in the clinical syndrome of severe osteomalacia due to profound phosphate depletion. Bone biopsy revealed stainable aluminum deposits along 27.6% of the total bone surface, which is a unique observation in a patient with normal renal function. Treatment included withdrawing the antacid and supplementation with phosphate, calcium, and vitamin D. She experienced marked subjective and objective improvement with this regimen. This included a striking increase in her bone mineral density occurring over the 2-year follow-up period. This case documents that long-term antacid therapy, even when used by patients with normal renal function and within the manufacturer's label recommendations, can lead to severe phosphate depletion, osteomalacia, and toxic accumulation of aluminum and magnesium. This clinical syndrome was readily treated by withdrawal of the antacid and with calcium and phosphate supplementation. Physicians recommending treatment with these compounds or learning of their patient's self-medication with them should inform the patient of the potential serious side effects these agents can cause when used chronically at maximally recommended doses.
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PMID:An interesting case of osteomalacia due to antacid use associated with stainable bone aluminum in a patient with normal renal function. 962 11

Because of the large liver stores (about 5 mg), low turnover rate (0.143%) and small daily requirement (3 micrograms), vitamin B12 deficiency does not occur under normal circumstances. This is not the case in individuals with chronic inflammatory or trophic changes at vitamin B12 absorption sites. Without supplementation, vitamin B12 deficiency can be expected within 5 years of gastrectomy. Characteristic features of type A gastritis are hyposecretion and mucosal atrophy in the fundus and body of the stomach, with absent intrinsic factor. In the small intestine, active and/or passive absorption is impaired by extensive ileal resection, exocrine pancreatic insufficiency and chronic inflammatory disorders such as Crohn's disease. Definitive plasma concentrations cannot be quoted for vitamin B12 deficiency. Dietary habits, subjective symptoms, hematological laboratory results, function tests and gastrointestinal endoscopic and histological findings must all be taken into account in the diagnosis. Modern diagnostic parameters, such as methylmalonic acid and homocysteine serum assays, are useful for achieving early diagnosis and hence optimal treatment. With their assured availability, parenteral vitamin B12 preparations remain the treatment of choice. Results from vitamin B12 bioavailability studies in healthy subjects suggest that > 300 micrograms probably suffices as an oral maintenance dose after parenteral loading. Further well-documented cases are needed in order to establish whether these doses are adequate in malabsorption syndromes and gastrointestinal diseases. Various case reports indicate the value of prophylactic and therapeutic oral vitamin B12 administration, especially in disorders of homocysteine metabolism, a substance postulated as a further important risk factor for atherosclerosis.
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PMID:Studies on vitamin B12 status in the elderly--prophylactic and therapeutic consequences. 1038 32

Elevated plasma homocystein (tHcy) is a marker for functional deficiency of folate and/or cobalamin. Malabsorption of these vitamins occurs in various gastroenterologic diseases. A frequent mutation (C677T) in the gene coding for the enzyme methyltetrahydrofolate reductase (MTHFR) is often associated with elevated values of tHcy. We have investigated 24 patients with tHcy > 40 mumol/l for gastrointestinal disease that can contribute to such elevation. Of these, 19 were homozygous for mutated MTHFR, four were heterozygous and one was normal. We found two cases of probable celiac disease, one case of Crohn's disease and one case of ulcerative colitis. These four were homozygous for the C667T mutation. Furthermore, we found eight persons who were anacidic; four homozygous, three heterozygous and one normal. All had gastritis histologically, six had serum gastrin > 50 pmol/l, and four were already on treatment with cobalamin injections. Helicobacter pylori-infection was found in nine out of 22 persons. Gastrointestinal disease occurs frequently in patients with tHcy > 40 mumol/l, but with the exception of conditions resulting in serious deficiency of cobalamin, these diseases alone do not seem sufficient to cause such high levels. We suggest that a reasonable approach to patients with homocystein values above 40 mumol/l is to exclude cobalamin deficiency, and that further investigations should be based upon thorough anamnesis and symptoms.
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PMID:[Gastrointestinal disease with elevated plasma homocysteine level]. 1056 75

Regardless of the type and dose of beverage involved, alcohol facilitates the development of gastroesophageal reflux disease by reducing the pressure of the lower esophageal sphincter and esophageal motility. Fermented and nondistilled alcoholic beverages increase gastrin levels and acid secretion. Succinic and maleic acid contained in certain alcoholic drinks also stimulate acid secretion. Low alcohol doses accelerate gastric emptying, whereas high doses delay emptying and slow bowel motility. Alcohol facilitates the development of superficial gastritis and chronic atrophic gastritis--though it has not been shown to cause peptic ulcer. Alcoholic beverages, fundamentally wine, have important bactericidal effects upon Helicobacter pylori and enteropathogenic bacteria. The main alcohol-related intestinal alterations are diarrhea and malabsorption, with recovery after restoring a normal diet. Alcohol facilitates the development of oropharyngeal, esophageal, gastric, and colon cancer. Initial research suggests that wine may be comparatively less carcinogenic.
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PMID:The effects of alcohol consumption upon the gastrointestinal tract. 1115 64

Atrophic chronic gastritis and Helicobacter pylori infection are considered possible causes of iron deficiency anemia, and sideropenic anemia is also frequent after subtotal gastrectomy. In this study, thirty-three patients who underwent subtotal gastrectomy for primary adenocarcinoma of stomach were follow-up for at least 3 years, and included in this analysis. The presence of atrophic gastritis and H. pylori infection were detected by biopsy sampling and endoscopy every year after surgery. The iron status was evaluated by the assay of serum ferritin, serum iron and hemoglobin level. Statistical analysis revealed that atrophic gastritis was associated with lower iron serum levels, and gastric stump H. pylori infection was related to lower serum ferritin levels; on the contrary, no correlation of these factors with sex, age, malabsorption symptoms and stage of tumor was found. Atrophic chronic gastritis and Helicobacter pylori infection seem to play an important role as possible causes of post gastrectomy anaemia.
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PMID:[Correlation between chronic gastritis of the gastric stump, Helicobacter pylori infections and iron deficiency after gastrectomy for gastric cancer]. 1242 77


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