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

The causes of megaloblastic anemia were studied in a survey of patients admitted to six Israeli hospitals over a period of 15 yr. Among the 203 patients identified, 69% had pernicious anemia, 12% had gastrointestinal disease, 9% had primary nutritional deficiency of whom only 1% were associated with pregnancy, and 7% had selective vitamin B12 malabsorption with albuminuria. Comparison with previously published surveys showed, that in contrast with earlier studies where primary nutritional deficiency was the cause of megaloblastic anemia in about 70% of cases and pernicious anemia in only 20%, in more recent studies the proportion of cases with primary nutritional anemia in general and those associated with pregnancy in particular was much lower. This is most probably the result of improved standards of living and a national program of preventive folate supplementation at maternity clinics. A potential hazard of such preventive programs is the aggravation of neurological complications in patients with undiagnosed vitamin B12 deficiency. Early recognition of pernicious anemia and other forms of selective B12 malabsorption is a new challenge created by the changing pattern of megaloblastic anemias.
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PMID:The changing pattern of megaloblastic anemia: megaloblastic anemia in Israel. 684 25

A review of 295 patients with autoimmune Addison's disease which occurred as part of a polyglandular autoimmune syndrome is presented. Information of 41 cases was obtained from our clinics and from the examination of medical records, while 254 cases were culled from the literature. We report that autoimmune Addison's disease in association with other autoimmune diseases occurs in at least two distinct types. Addison's disease occurring in Type I polyglandular autoimmune disease (PGA) is associated with chronic mucocutaneous candidiasis and/or acquired hypoparathyroidism. The age of onset is predominately in childhood or in the early adult years. Type I PGA syndrome is also frequently associated with chronic active hepatitis, malabsorption, juvenile onset pernicious anemia, alopecia and primary hypogonadism. Insulin requiring diabetes and/or autoimmune thyroid disease are infrequent. In contrast, Addison's disease in Type II PGA is associated with insulin requiring diabetes and/or autoimmune thyroid disease(s). Although the age of onset of Addison's disease in Type II PGA syndrome is not confined to any age group or any specific sex, it occurs predominately in the middle years of life in females. The associated autoimmune diseases found in Type I disease, such as chronic active hepatitis, etc. (see table II) are rare in Type II PGA disease except for a low frequency of gonadal failure. We provide evidence to support the concept that the Addison's diseases in Type I and II PGA syndromes have different genetic bases, as related to HLA haplotypes, and possibly have different underlying pathogeneses.
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PMID:Two types of autoimmune Addison's disease associated with different polyglandular autoimmune (PGA) syndromes. 702 19

Classic pernicious anemia with abnormal Schilling test results developed in a previously described vegan patient who had coexisting subtle cobalamin malabsorption (demonstrable by abnormal ovalbumin-cobalamin absorption test results but normal Schilling test results). This suggests that the ovalbumin-cobalamin absorption test or a modified version may serve as a prodromal phenomenon to identify patients at risk for developing pernicious anemia. The patient's transformation was also accompanied by the appearance of serum anti-intrinsic factor antibody. A modified assay retrospectively detected this antibody a year earlier than did the standard assay, indicating that such modification enhances the sensitivity of this useful test.
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PMID:Subtle cobalamin malabsorption in a vegan patient: evolution into classic pernicious anemia with anti-intrinsic factor antibody. 713 69

To evaluate the dual-isotope Schilling test for the diagnosis of pernicious anemia or malabsorption syndrome, 65 studies were selected for clinical correlation. Criteria for pernicious anemia included mean corpuscular volume greater than 100 cu micrometer, serum B12 greater than 100 ng/l, megaloblastic marrow, achlorhydria, reticulocytes greater than 5% on B12 therapy, atrophic gastritis, and elevated serum antibodies to parietal cells or intrinsic factor. Criteria for malabsorption syndrome included: decreased serum B12, folate, and carotene; increased fecal fat; abnormal D-xylose absorption; abnormal radiographic and biopsy findings. 58Co-cyanocobalamin and 57Co-cyanocobalamin bound to intrinsic factor were given orally to fasting patients; 1 mg of nonradioactive B12 was injected intramuscularly within two hours. Aliquots of 24-hour urine samples were counted. If the excretion of 58Co was less than 7% and the 57Co/58Co ratio was greater than 1.7, the test indicated pernicious anemia; a ratio less than 1.7 indicated malabsorption syndrome. Sensitivity, specificity, and accuracy of the dual-isotope Schilling test were 83%, 98%, and 94% for pernicious anemia, and 67%, 90%, and 86% for malabsorption syndrome, respectively.
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PMID:Reliability of the dual-isotope Schilling test for the diagnosis of pernicious anemia or malabsorption syndrome. 723 58

The megaloblastic anaemia observed in patients with chronic atrophic gastritis is usually due to malabsorption of vitamin B12. In some cases, the absence of intrinsic factor supports the diagnosis of pernicious anaemia but other factors, the importance of which varies from case to case, are also involved. They include proliferation of bacteria in the lumen of the gut, intestinal cell abnormalities resulting from lack of vitamin B12 and low hydrochloric acid output with subsequent reduction in the release of vitamin B12 from foodstuffs. With regard to treatment, it would seem justified to combine oral broad-spectrum antibiotics with parenteral administration of vitamin B12.
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PMID:[Vitamin B12 deficiency in chronic atrophic gastritis. 3 cases (author's transl)]. 726 28

A retrospective study was undertaken to audit physician's management of patients with a low serum level of vitamin B12 who were admitted to a university-affiliated teaching hospital during 1 year. Among the 34 patients 13 were proved to have pernicious anemia or vitamin B12 malabsorption, but for 12 of them there were unnecessary delays (several days or weeks) before initiation of investigation and therapy. An additional six patients, who had low serum levels of vitamin B12 and macrocytosis, most likely had true vitamin B12 deficiency, but proper investigation was not done and they did not receive any vitamin B12 or folic acid therapy. In another nine cases unexplained low serum levels of vitamin B12 were not properly investigated, and the patients either did not receive any vitamin B12 therapy or received it without proper documentation of a deficiency. Suggestions for facilitating early detection, investigation and treatment of megaloblastic anemia or vitamin B12 deficiency are given.
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PMID:Physician's management of suspected vitamin B12 deficiency. 745 53

The clinical and laboratory data from 75 patients with altered vitamin B 12 absorption were reviewed. In 36 cases the diagnosis of pernicious anaemia had been established. Of these, 14 patients showed malabsorption of radiolabelled vitamin B 12, but the absorption of vitamin B 12 bound to the intrinsic factor (IF) was normal (Group A). The other 22 patients with pernicious anaemia showed altered free and IF-bound vitamin B 12 absorption (Group B). Laboratory and clinical data and the absorption tests (xylose and fat excretion) were more abnormal in group B than in group A. Finally, 39 patients (Group C) with general malabsorption showed alternation of the absorption of free and IF-bound vitamin B 12 (Group C). The clinical nd biological data were different in these patients from that found in groups A and B. It is possible that in patients with pernicious anaemia who are untreated an alteration of the intestinal mucosa may produce a malabsorption of vitamin B 12 even in the presence of intrinsic factor.
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PMID:Clinical evaluation of simultaneously administered 58Co labelled vitamin B12 and 57Co labelled vitamin B12 bound to intrinsic factor in patients with pernicious anaemia. 747 Jun 41

The high incidence of megaloblastic anemia observed at our institution (2.1% of hospital admissions) prompted us to analyze the causes of cobalamin and/or folate deficiency in 30 patients admitted during the period 1983-1991 to the Medical Department of Locarno District Hospital. The study population includes 19 women and 11 men with a mean age of 69 years (range 28-91 years). All patients had severe macrocytic anemia (mean hemoglobin 74 +/- 23 g/l, MCV 121 +/- 12 fl), striking megaloblastic changes in aspirated marrow, and an elevated serum level of LDH (2170 +/- 2150 U/l). 19 patients had associated thrombocytopenia, 12 leukopenia and 11 both thrombocytopenia and leukopenia. Treatment led to prompt reticulocytosis and correction of megaloblastic changes in all patients, as well as to nearly complete resolution of the neurologic disorder in a patient with severe spastic ataxia. In 15 patients, megaloblastic anemia was caused by folate deficiency related to alcoholism (n = 6, mean age 55 years) and old age or poverty (n = 9, mean age 73 years). Cobalamin deficiency was present in 9 patients (mean age 69 years); it was due to pernicious anemia in 6 patients and to malabsorption in 2, while the cause remained unexplained in 1. The last patients (mean age 76 years) had deficiency of both cobalamin and folate, related to alcoholism (n = 3) or poverty (n = 3).
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PMID:[Megaloblastic anemia: 30 cases in a district hospital]. 787 99

A 21-year-old female with autoimmune polyglandular failure (APG) manifested by insulin-dependent diabetes mellitus (IDDM), hypothyroidism and pernicious anaemia developed severe malabsorption due to exocrine pancreatic insufficiency. Supplemental pancreatic enzymes resulted in marked improvement of steatorrhea. There was also an incidental finding of gastric carcinoid tumour. We identified only 13 other patients in our institution with either type 2 or 3 APG, one of which had significant steatorrhoea. Another patient with IDDM, hypothyroidism and pernicious anaemia had an asymptomatic gastric carcinoid tumour. The possible mechanisms for malabsorption in APG are discussed.
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PMID:Autoimmune polyglandular failure associated with malabsorption and gastric carcinoid tumour. 825 57

Food-cobalamin malabsorption is marked by the inability to release cobalamin from food, which therefore cannot be taken up by intrinsic factor for absorption. The defect is not detectable by classical clinical tests like the Schilling test which are all based on the absorption of free, crystalline cobalamin. Tests of food-cobalamin absorption have been devised, the most popular ones using cobalamin bound to eggs or to chicken serum. The disparity between the abnormal results of these tests and the normal results with the Schilling test defines the disorder of food-cobalamin malabsorption. Release of cobalamin from food requires acid and pepsin, and most food-cobalamin malabsorptive states can be traced to gastric defects. However, other mechanisms may also play a role. The malabsorption is limited to food cobalamin and any free cobalamin, presumably including recycled biliary cobalamin, will be absorbed normally, which may explain its frequently insidious nature. The effect on cobalamin status covers a broad spectrum. At one extreme, some individuals, perhaps in the earliest stages, have normal cobalamin status, while at the other extreme may be found deficiency every bit as severe as in the most florid case of pernicious anaemia. Most often, however, the deficiency is mild, frequently marked by only a low serum cobalamin level, mild evidence of metabolic insufficiency and, sometimes, minimal clinical sequelae. Moreover, in some cases the gastric defect progresses and intrinsic factor secretion is affected, thus transforming into classical pernicious anaemia; this is not inevitable, however, and probably occurs in only a minority of patients. The course of food-cobalamin malabsorption is therefore a varied one. Nevertheless, it may be the most common cause of subtle or mild cobalamin deficiency and it is also sometimes associated with severe deficiency. Its identification and treatment need to be considered more widely in the clinical setting.
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PMID:Malabsorption of food cobalamin. 853 65


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