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

Three persons in a kindred of 43 had variable expression of a syndrome consisting of immunoglobulin A deficiency, diabetes mellitus, malabsorption, and a common HLA haplotype. Findings from the proband included life-threatening malabsorption; idiopathic intestinal mucosal atrophy with infalmmation; IgA deficiency and antibodies to multiple endocrine organs; insulin-dependent diabetes mellitus; and the major histocomptability antigens HLA-A2, B8, and DW3. In addition to the described syndrome other conditions present in the family include Graves' disease, vitiligo, hypocomplementemia, rheumatic fever, multiple sclerosis, and a high frequency of antibodies to endocrine tissue. Since Graves' disease, diabetes mellitus, and idiopathic Addison's disease have all been described in association with HLS-B8 and DW3, we believe that the occurrence of these diseases in this family suggests that a single immune response gene or gene complex is linked with HLA-B8 and DW3.
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PMID:A syndrome of immunoglobulin A deficiency, diabetes mellitus, malabsorption, a common HLA haplotype. Immunologic and genetic studies of forty-three family members. 57 75

Ten patients with untreated Graves' disease underwent tests to determine lactose absorption, liquid gastric emptying, and oral cecal transit time. To determine the influence of thyroid hormone status on lactose absorption, eight of these same patients had repeat studies when rendered euthyroid. Two of these eight patients also underwent studies while transiently hypothyroid. Motility studies were also evaluated in a group of 11 control subjects. Lactose malabsorption occurred in nine patients with Graves' disease. In seven patients who repeated these studies, lactose malabsorption normalized in three, symptoms induced by lactose improved in two and were unchanged in two. However, these latter two patients appeared to have improved symptoms in the transient hypothyroid state. Liquid gastric emptying was significantly faster in untreated patients than controls and treated self-same patients. Transit time was significantly faster in untreated patients than when they were rendered euthyroid. There may be a relationship between altered lactose absorption states and changes in intestinal motility in patients with Graves' disease.
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PMID:Reversible lactose malabsorption and intolerance in Graves' disease. 189 49

A 40-year-old man developed dyspepsia, watery diarrhea, and weight loss. A clinical diagnosis of hyperthyroidism due to Graves' disease was confirmed [free thyroxine, 87 pmol/L (normal range, 8.6-27 pmol/L)]. Bile acid malabsorption was demonstrated by a low 23-selena-25-homocholyltauric acid retention of 7.1% (normal, > 15%). Antithyroid treatment (carbimazole and propranolol) was instituted, and his diarrhea subsided with the control of hyperthyroidism (free thyroxine, 15 pmol/L) along with an improvement of bile acid absorption (Se-HCAT retention, 14.7%). This case very strongly suggests the existence of bile acid malabsorption in hyperthyroidism. The temporal association suggests that the diarrhea may have been due at least in part to bile acid malabsorption, raising the possibility that the latter may be an etiological factor in thyrotoxic diarrhea. We believe this is the first such report.
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PMID:Bile acid malabsorption associated with Graves' disease. 793 Apr 35

The effects of endocrine disease on bone mass continue to attract attention. Investigations include the effects on the skeleton of thyroid disease, primary hyperparathyroidism, and their treatment. The effect of growth hormone replacement in adults with panhypopituitarism has also been investigated; children with treated growth hormone deficiency appear to reach adulthood with low bone mass. The indications for surgery in asymptomatic primary hyperparathyroidism have recently been reviewed. The associations between autoimmune thyroid disease and connective tissue disease have been investigated. Although patients with Graves' disease are frequently positive for antinuclear antibodies, there appears to be no increased risk of systemic autoimmune disease. The possible pathogenesis of diabetic bone disease via calcium malabsorption, hypercalciuria, reduced bone formation, and collagen abnormalities has been reviewed. A long-term study has clarified the links among diabetic control, limited joint mobility, nephropathy, and retinopathy. The possible mechanisms by which pregnancy may induce remission in rheumatoid arthritis have been discussed.
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PMID:Endocrine disease. 843 94

We treated a patient who was hyperthyroid due to Graves' disease and strongly resistant to methimazole (MMI): in spite of good compliance, she needed 150 mg of MMI daily to control her hyperthyroidism. To elucidate the reasons of resistance to MMI, her serum and intrathyroidal MMI concentrations were determined by high pressure liquid chromatography (HPLC). After taking a 30 mg dose of MMI, she had a similar serum MMI concentration-time curve to that of a normal subject: drug malabsorption and rapid drug metabolism were not evident when studied after surgical treatment. After her serum containing MMI was incubated with Protein G, the MMI concentration of the fraction not bound to Protein G did not change significantly from that of untreated serum: the possibility of anti-MMI IgG antibody production was considered unlikely. Furthermore, the intrathyroidal concentration of MMI in a surgically obtained tissue specimen was 3 micrograms/g wet tissue and appeared to be comparable with those of other Graves' tissues reported. Considering that the patient had been taking 150 mg per day of MMI by the time of thyroidectomy, her intrathyroidal MMI concentration was relatively low, suggesting possible impairment of intrathyroidal MMI accumulation. The possibilities of impaired intrathyroidal actions and the severity of hyperthyroidism, especially high T3 levels, also remained as possible causes. In conclusion, here was a severely hyperthyroid patient who was poorly responsive to conventional doses of MMI, and impairment of thyroid uptake of MMI or of pathways after uptake were considered as possible mechanisms.
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PMID:A hyperthyroid patient with Graves' disease who was strongly resistant to methimazole: investigation on possible mechanisms of the resistance. 857 95

Primary hyperparathyroidism is seldom associated with other autoimmune disorders. The presence of normocalcemia in primary hyperparathyroidism should prompt the physician to look for vitamin D deficiency. This observation concerns a 34-year-old vegetarian woman with combined primary hyperparathyroidism, Graves' disease, and celiac disease. The patient presented with severe bone deformities; she was unable to walk, and had severe muscular weakness and weight loss. Biochemical findings revealed severe hyperparathyroidism with normocalcemia, hypophosphatemia, very low urinary calcium, and low 25-hydroxy vitamin D level. Thyroid tests showed hyperthyroidism with positive thyroid receptor antibodies, confirming the presence of Graves' disease. Positive antigliadin and antireticulin antibodies and complete villous atrophy on duodenal biopsy established the presence of celiac disease. The patient underwent a near-total thyroidectomy, with the removal of a parathyroid adenoma. To our knowledge, this observation is the first finding of an association between celiac disease, Graves' disease, and primary hyperparathyroidism. It emphasizes the need to rule out intestinal malabsorption in the case of normocalcemic hyperparathyroidism.
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PMID:Osteomalacia secondary to celiac disease, primary hyperparathyroidism, and Graves' disease. 947 14

Patients with an underlying autoimmune endocrine disorder are at an increased risk of developing other autoimmune diseases. We describe a patient with idiopathic autoimmune hypoparathyroidism who developed hyperthyroidism due to Graves disease and subsequently was diagnosed with celiac disease. Malabsorption of L-thyroxine was the only clue regarding the presence of celiac disease. This particular association of these three autoimmune disorders occurring in the same patient has not, to our knowledge, been previously reported. The presentation, investigations performed, and treatment provided are discussed and the literature pertaining to similar cases is reviewed.
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PMID:Celiac disease occurring in a patient with hypoparathyroidism and autoimmune thyroid disease. 1655 6

Many causes of thyroxine malabsorption are described in the literature, but the most common cause of failure of thyroxine therapy is poor patient compliance, or pseudomalabsorption. We describe the case of a female patient who underwent total thyroidectomy for Basedow-Graves disease. Post-operatively, several treatment regimens were employed to achieve euthyroidism, but only injectable thyroxine was found to be effective. To exclude levothyroxine malabsorption, the patient was hospitalized in a hypothyroid state while a single oral test dose of levothyroxine (1000 microg) was administered. Within 4 hours a decrease of TSH level (from 59.7 to 55.6 microUI/ml) and a significant increase in free T4 levels (from 0.8 to 15.5 pg/ml) was observed, eliminating a malabsorption problem. The cause of resistance to thyroid hormone therapy was poor patient compliance, leading to the designation of this as a case of pseudomalabsorption.
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PMID:Pseudomalabsorption of thyroid hormones: case report and review of the literature. 1798 45

Iron deficiency anemia as a hematologic complication of the antithyroid medication (ATS) that has not been already described in the literature. We report on two exceptional cases: the first case concerns a 24 years old man admitted for an anemic syndrome. He was treated with carbimazole for Graves' disease. The blood count showed a non-regenerative microcytic anemia. Serum ferritin was severely decreased. The etiologic searching for bleeding, hemolysis, malabsorption or iron deficiency was negative. Treatment with iron salts was introduced without any real improvement. Given this situation, and given the negativity of the etiologic investigations, the decision to stop carbimazole was taken. Since that, the clinical and biological evolutions have been favorable. The second observation is much more original and concerns a 35 years old woman. The clinical, laboratory, etiological and treatment data are similar to those of the first observation. The evolution after withdrawal of carbimazole was favorable. The originality of this observation is that a reintroduction test of carbimazole was performed and allowed to reproduce the same haematological effects. These findings led us to hold the diagnosis of anaemia due to carbimazole. In this occasion, and in the light of the data in the literature, we underline the exceptional character of these two cases and we raise the possibility of an etiopathogenic link between administration of ATS and the occurrence of anaemia by iron deficiency.
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PMID:[Carbimazole can be the cause of iron deficiency anemia?]. 2211 33

The thyrogastric autoimmune syndrome (TAS) was described in patients in whom the serum cross-reacted both with gastric parietal cells antigens and thyroid antigens. We report two cases illustrating the spectrum of pathogical features of TAS. The first case associates Hashimoto's thyroiditis and anemia perniciosa,and develops a gastric neuroendocrine tumor during follow up. The second case presents with a Graves' disease and an autoimmune reversible gastritis, secondary to Helicobacter pylori. Whereas type III autoimmune polyendocrinopathy is rare, TAS is frequent in our experience. Some 13% (32/240) of patients that we have prospectively followed affected with thyroiditis have also autoimmune gastritis. Helicobacter pylori is clearly implicated in 16% of autoimmune gastritis cases. Infection, malabsorption and gastritis are potentially reversible after bacterial eradication treatment. In the other 84% of gastritis patients, no histological or serological proof of Helicobacter pylori is found. Gastric autoimmunity is then irreversible, leading to gastric severe atrophy, hypochlorhydria and hypergastrinemia. Hypergastrinemia stimulates enterochromaffin cell hyperplasia, possibly progressing to neuroendocrine tumors. We propose a diagnostic approach to improve the characterization of TAS. We review the literature on the subject and discuss some interesting animal models of infectious gastric autoimmunity.
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PMID:[The thyrogastric syndrome: its effects on micronutriments and gastric tumorigenesis]. 2439 72


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