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

In a consecutive study of 228 patients with folate deficiency originating from various gastrointestinal and haematological disorders, the clinical value of the folic acid absorption (TRIFA) test is assessed. It is concluded that the test is a simple, rapid, and reliable index for folic acid malabsorption of importance as well as a research tool as in daily practice.
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PMID:Folic acid absorption in various gastrointestinal disorders. 127 9

A 30 year old woman with recurrent anaemia due to folate deficiency had evidence of sarcoid granuloma on small bowel biopsy but was presumed to have Crohn's disease. The diagnosis of small bowel sarcoidosis was not seriously considered until she developed systemic manifestations of sarcoidosis (cutaneous and pulmonary lesions) over the following 20 years. Sarcoidosis of the gastrointestinal tract, particularly the small bowel, is rare and this case is unusual because bowel pathology preceded more generalised lesions. As far as is known it is also the first case to be described presenting with malabsorption of folic acid.
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PMID:Sarcoidosis: association with small bowel disease and folate deficiency. 140 Dec 18

The case of a young woman from Guadeloupe developing severe megaloblastic anemia is reported. She presented with fever and hemolysis (she had heterozygotic beta-thalassemia) after a six month history of diarrhea. She was shown to have folate deficiency, steatorrhea, vitamin K and B12 malabsorption. She responded well to intravenous folinic acid and tetracyclines. Diagnosis was based on the following criteria: a) no other cause of malabsorption was found despite a comprehensive inquiry, b) the pattern of the illness corresponded to the definition of disease. Three particular aspects are outlined: the acute onset, malabsorption of vitamin B12 requiring prolonged and combined treatment, and the unusual place in which the disease was contracted.
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PMID:[Tropical sprue revealed by severe anemia in a woman from Guadeloupe]. 158 43

Nutritional deficiencies are eminent at all socioeconomic levels of the world population and have created a critical need for a reevaluation of the nutritional quality of the food supply. A particular group of vitamers, collectively referred to as folates, has received a great deal of attention due to their significance in human metabolism, their prevalent deficiency worldwide, as well as their complexity of analysis. Severe folate deficiency may result in megaloblastic anemia and is generally attributed to low dietary intake, although it may also result from malabsorption. Such concerns have instigated increased interest in food-fortification programs. In order to ensure appropriate levels of nutrient fortification and optimization of food processes for maximum folate retention, it is of great importance to have a basic understanding of the kinetic behavior of individual vitamers with respect to processing parameters and various environmental conditions. This article reviews kinetic stability of folates as affected by processing conditions, discusses problems associated with current methodology for folate analyses, and integrates this information with the nutritional aspects of folates.
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PMID:Folates in foods: reactivity, stability during processing, and nutritional implications. 269 10

The aim of the present work was to perform a prospective analysis of the significance of macrocytic red cells through the study of all patients with MCV higher than 105 fl (those treated with cytotoxic or immunosuppressing drugs were excluded). Conventional clinical, haematologic and biochemical studies were carried out on every patient, along with B12 and folate levels, bone marrow examination and bone marrow karyotype and, whenever B12 deficiency was present, complete Schilling's test. Special attention was paid to the aetiological inquiry and post-therapeutical course. A series of 109 patients was collected. Decreased serum B12 rates with abnormal Schilling's test and response to parenteral therapy were present in 26 cases (24%). Of them, 22 fulfilled the diagnostic criteria for Biermer's anaemia, while in the remaining 4 there was impaired intestinal absorption. Serum or red-cell folate deficiency was found in 34 other cases (31%). Alcoholism was present in 20 of them, abnormal diet in 10, malabsorption syndrome in 2, and excessive demands in 2 others. Hence, vitamin deficiency underlay macrocytosis in 60/109 cases (55%). In the remaining 49 cases (45%) macrocytosis was not accompanying folate or B12 deficiency. Of these, severe liver disease was found in 16 patients (alcoholic in 15 and post-hepatitis in 1 case), with increased serum B12 in 10 cases and increased serum or erythrocytic folate in 3 others. Nineteen patients within this group had primary myelodysplastic syndromes (RA, 8; SRA, 4; RAEB, 7), and the remaining 14 cases had several haematological (AIHA, 4; CLL, 1, T-cell lymphoma 1, M-6, 1, and myelofibrosis with myeloid metaplasia, 2) or non-haematological diseases (heart insufficiency, 2; COPD,3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hematologic significance of erythrocytic macrocytosis: prospective analysis of 109 successively studied cases]. 271 Dec 82

138 Indian patients with megaloblastic haemopoiesis were studied. All were lifelong vegetarians. The diagnosis was nutritional cobalamin deficiency in 95 and pernicious anaemia in 20; only 4 patients had folate deficiency. A third had intestinal malabsorption, 20 had features of osteomalacia, and 87 were iron deficient. Tuberculosis was diagnosed in 17. Cobalamin deficiency may have contributed to these complications via intestinal malabsorption and impaired bacterial killing of phagocytosed bacilli by cobalamin-deficient macrophages. The frequency of pernicious anaemia was the same in Indian subjects as in Caucasians.
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PMID:Megaloblastic anaemia in a vegetarian Hindu community. 286 24

Iron deficiency is a common medical problem that may present in a variety of ways to the general practitioner or the specialist. An understanding of iron physiology is relevant to diagnosis and treatment of iron deficiency. Human iron metabolism is a system based on conservation. For this reason, the most common cause of iron deficiency is loss of the normal conservation of iron and this usually means blood loss. The important implication is that the search for the cause of iron deficiency will usually focus on the gastrointestinal tract in males and non-pregnant, non-menstruating females. Iron deficiency is commonly misdiagnosed. The usual error is misinterpretation of the laboratory features of the anaemia of chronic disease. The serum iron is low, but the iron binding capacity is normal and ferritin is normal or high. There are problems and exceptions involved in interpretation of iron indices. Treatment of iron deficiency requires an understanding of iron absorption and the ability of the marrow to respond. In most circumstances, iron deficiency will respond to adequate doses of oral iron; however, there are a few situations when oral iron is unsuitable and parenteral iron is required. An inadequate response to iron may indicate inadequate supply of iron to the bone marrow (e.g. malabsorption, non-compliance) or failure of the marrow to respond (e.g. concomitant folate deficiency). Pregnancy is a special situation in which conservation of iron is overcome by fetal iron requirements and in which application of the knowledge of iron physiology should be applied to prevent and treat iron deficiency.
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PMID:Iron deficiency. Misunderstood, misdiagnosed and mistreated. 310 99

Preferential depletion of corrinoids on transcobalamin II (i.e., sharply reduced holo transcobalamin II (TC II)) occurs early in vitamin B12 deficiency. We measured corrinoids (Cor) and cobalamins (Cbl) on transcobalamins I and III (TC I + III) and on TC II. We also measured the unsaturated B12 binding capacities of transcobalamin I and III and TC II in serum from patients with B12 deficiency (N = 5) (with or without concurrent folate deficiency), with pernicious anemia in remission (N = 7) (1 month after therapy), and in several control groups including healthy volunteers (N = 6), hematologically normal elderly hospitalized patients (N = 5), and non-B12 nonfolate deficient anemic elderly hospitalized volunteers (N = 5). In B12 deficient patients, Cor = 177 +/- 92 pg/ml, Cbl = 56 +/- 20 pg/ml, TC II Cor = 1.0 +/- 2.2 pg/ml, and TC II Cbl = 4.4 +/- 4.9 pg/ml in contrast to pooled controls with Cor = 730 +/- 229, Cbl = 523 +/- 198, TC II Cor = 100 +/- 84, and TC II Cbl = 88 +/- 70 (all values expressed in picograms/milliliters). In pernicious anemia in remission, Cor = 505 +/- 138, Cbl = 294 +/- 77, TC II Cor = 80 +/- 31 and TC II Cbl = 37 +/- 36. TC II unsaturated B12 binding capacity was significantly higher in B12 deficient patients than in pooled controls. These data support that: (a) holo TC II is sharply depleted in untreated B12 deficiency; (b) normally, the only Cor on TC II are cobalamins; (c) in treated pernicious anemia, TC II appears to also bind non-cobalamin corrinoids; (d) continued malabsorption of vitamin B12 may result in reduced B12 on TC II within a month after the last parenteral therapy with 1000 micrograms of cyanocobalamin, and (e) TC II UBBC rises as B12 deficiency is developing. Further investigation is required for definitive delineation of whether sharply reduced Cor on TC II in untreated B12 deficiency can diagnose "true" B12 deficiency, in view of false positive or false negative results which occur in all serum B12 assays.
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PMID:Depletion of serum holotranscobalamin II. An early sign of negative vitamin B12 balance. 334 9

Nutritional status of 86 patients with dermatitis herpetiformis (DH) was defined by anthropometric measurements and hematological and biochemical laboratory tests to establish prevalence of malabsorption and malnutrition. Anthropometric measurements in DH patients were comparable to normal control patients. Four individuals were of short stature; two had had diarrhea and failed to thrive in childhood. Abnormalities attributable to nutritional deficiency were detected in only 6 of the 86, whereas drug-associated hematological or biochemical changes were present in 36 of 55 subjects treated with dapsone or sulfapyridine. Twenty patients had hemolytic anemia or macrocytosis related to drug therapy. Only two had anemias attributable to malabsorption; one was iron deficient, the other folate deficient. Two other patients were mildly Fe deficient and two had slight folate deficiency; they lacked other stigmata of malabsorption. Drug-induced hematological and biochemical abnormalities were more common than changes that suggest nutritional disease, even though most DH patients had an enteropathy at presentation.
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PMID:Nutritional status in patients with dermatitis herpetiformis. 340 14

Patients with phenylalanine hydroxylase deficiency show increased concentrations of biopterins and neopterins, and reduced concentrations of serotonin and catecholamines, when phenylalanine concentrations are raised. The pterin rise reflects increased synthesis of dihydroneopterin and tetrahydrobiopterin, and the amine fall a reduction in amine synthesis due to inhibition by phenylalanine of tyrosine and tryptophan transport into neurones. The pterin and amine changes appear to be independent of each other and are present in the central nervous system as well as the periphery; they disappear when phenylalanine concentrations are reduced to normal. Patients with arginase deficiency show a similar amine disturbance but have normal pterin levels. The amine changes probably contribute neurological symptoms but pterin disturbance is not known to affect brain function. Patients with defective biopterin metabolism exhibit severely impaired amine synthesis due to tetrahydrobiopterin deficiency. Pterin concentrations vary with the site of the defect. Symptoms include profound hypokinesis and other features of basal ganglia disease. Neither symptoms nor amine changes are relieved by controlling phenylalanine concentrations. Patients with dihydropteridine reductase (DHPR) deficiency accumulate dihydrobiopterins and develop secondary folate deficiency which resembles that occurring in patients with defective 5,10-methylene tetrahydrofolate reductase activity. The latter disorder is also associated with Parkinsonism and defective amine and pterin turnover in the central nervous system, and a demyelinating illness occurs in both disorders. In DHPR deficiency cerebral calcification may develop in a similar distribution to that seen in congenital folate malabsorption and methotrexate toxicity. Symptoms are ameliorated by therapy with 5-formyltetrahydrofolate but exacerbated by folic acid.
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PMID:Pteridines and mono-amines: relevance to neurological damage. 354 Sep 26


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