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

Hypolipidemias can be divided in primary, familial and hereditary forms and symptomatic forms which may accompany other diseases. The primary hypolipidemias (abetalipoproteinemia, hypobetalipoproteinemia and analphalipoproteinemia) are very rare. Severe hypolipidemia can be found in some peoples (e.g. the Masai). This article is chiefly devoted to secondary hypolipidemias such as those associated with malabsorption, malnutrition and maldigestion including protein-losing gastroenteropathy, with liver diseases, endocrine diseases (hyperthyroidism, hirsutism) and anemia. Finally, the hypolipidemias secondary to the formation of autoantibodies against HDL and LDL in M-gradient, carcinoma and rheumatoid arthritis are briefly reviewed.
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PMID:[Hypolipidemias]. 17 Jun 75

Malabsorption and diarrhea in hyperthyroidism has been attributed in part to an increased rate of gastrointestinal transit as measured with barium sulfate suspension. Data are unavailable on the effect of hyperthyroidism on gastric emptying rates of normal food and pancreatic enzyme secretion. These functions have been studied in 4 hyperthyroid patients and compared to results obtained when treatment achieved euthyroidism. Pancreatic trypsin secretion was half the euthyroid level in the hyperthyroid state. No significant change in bile salts occurred, although there was a tendency for a greater proportion of dihydroxy bile salts while hyperthyroid. Gastric emptying rates of a mixed fat, protein, and carbohydrate liquid meal were normal. Similarly the gastric emptying rate of a beef stew plus chicken liver meal was normal. We conclude that in hyperthyroidism gastric emptying rates of "physiologically active" food is normal. Pancreatic enzyme secretion is depressed in hyperthyroidism and may contribute to maldigestion.
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PMID:The effect of hyperthyroidism on gastric emptying rates and pancreatic exocrine and biliary secretion in man. 71 57

Experimental evidence is presented which suggests that age-induced changes in the collagenous matrix, the main constituent of the organic portion of bones, are at least partially responsible for age-induced physiological osteoporotic changes in the skeleton. In particular, there seems to be a labile fraction of recently synthesized collagen in bones, which loses its metabolic activity rapidly with advancing age. Experimental and clinical hormonal disorders and disturbances in calcium metabolism also cause changes in skeletal metabolism; these changes seem to be largely mediated through changes in the collagenous matrix. In experimental hyperthyroidism and hyperparathyroidism, the rate of degradation of the collagenous matrix appears to act as a moderator or "final messenger" in hormone-induced bone resorption. In conditions with altered calcium metabolism, such as malabsorption associated with hypocalcemia, altered bone metabolism may be due to osteomalacia or hypocalcemia-induced hyperparathyroidism. An increase in the rate of bone destruction in relation to the rate of bone formation is probably also the cause of postmenopausal osteoporosis. At present there is no optimal form of hormonal treatment for age-induced or post menopausal osteoporosis. Estrogen replacement therapy may be the best available treatment for postmenopausal osteoporosis, but slowing down the already low rate of bone catabolism in elderly subjects by estrogen or other therapeutic means requires long periods of treatment before pronounced increases in the total mass of bones take place and prophylactic administration of estrogen may produce better results.
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PMID:Relation to osteoporosis of age- and hormone-induced changes in the metabolism of collagen and bone. 97 17

Antibodies to digitalis glycosides have been elicited in experimental animals and have been utilized in the development of rapid, sensitive, specific and convenient radioimmunoassay methods for the clinical measurement of digoxin and other cardiac glycosides in man. The use of these assay methods has supplemented earlier studies with radiolabeled digitalis preparations and has made it possible to obtain much new information concerning factors which may contribute to the well known patient to patient variability in digitalis dosage requirements and in sensitivity to the toxic effects of cardiac glycosides. In some patients with a poor clinical response to digitalis, the finding of a serum concentration which is relatively low for the dose prescribed may suggest that true digitalis resistance is not present and may raise questions of poor patient compliance, tablet inadequacies, intestinal malabsorption, increased metabolic degradation or hyperthyroidism; if the cause of the low serum level cannot be identified or corrected, serial serum measurements should enable safe and rational upward adjustment of dosage. In some patients with digitalis toxicity, the finding of a serum level which is relativity high for the dose prescribed may suggest that the patient is not sensitive to digitalis but rather is excreting it slowly; in such instances in elderly patients (with decreased glomerular filtration rates) and in patients with renal disease, serial digitalis measurements are useful adjuncts to clinical observation in determining optimal digitalis dosage schedules. A knowledge of serum digitalis concentrations should enable us to develop sound principles for a more rational approach to the clinical administration of cardiac glycosides, especially in patients with unusually high dosage requirements or with unusual sensitivity to relatively small doses of digitalis.
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PMID:Serum digitalis measurements in the assessment of digitalis resistance and sensitivity. 109 61

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Diarrhea and malabsorption are common manifestations of hyperthyroidism, whereas constipation or obstipation frequently occur in hypothyroidism. Abnormalities of gastrointestinal motility have been proposed as the primary cause of these complaints, but documentation has been conflicting and largely limited to observations of the transit time of a barium meal. We studied gastrointestinal transit time in fasting patients with thyroid dysfunction using the pulmonary excretion of H2 after the ingestion of a nonabsorbable carbohydrate, lactulose, as an indicator of the rate of transit to the colon. Mean transit time of 10 hyperthyroid patients (29 +/- 4.0 min) was significantly less than that of 42 healthy controls (72 +/- 3.7 min, p less than 0.001), and of 6 hyperthyroid patients when they became hypothyroid after treatment (80 +/- 11.0 min, p less than 0.05). Transit time decreased significantly when hypothyroid patients were given thyroid replacement (p less than 0.01). These findings support the hypothesis that abnormal gut motility may be the primary cause of the diarrhea and malabsorption of hyperthyroidism, and the constipation and obstipation commonly seen in hypothyroidism.
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PMID:Gastrointestinal transit in thyroid disease. 670 68

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

Secondary osteoporosis may be associated with a number of endocrine dysfunctions and metabolic disorders. In this paper, osteoporosis in patients with Cushing's syndrome, hyperthyroidism, primary hyperparathyroidism, acromegaly, hypogonadism and some metabolic disorders such as diabetes mellitus, chronic renal failure and malabsorption syndrome are described. While the major manifestation of bone in these conditions is a reduction of bone mass and may be somewhat different from bone loss in primary osteoporosis histologically or radiologically, it is considered to be the same bone loss as primary osteoporosis in the present paper. In some conditions, for example, Cushing's syndrome, diabetes mellitus etc, factors responsible for bone loss are demonstrated.
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PMID:[Osteoporosis associated with endocrine dysfunctions or metabolic disorders]. 796 90

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

The occurrence of chronic diarrhea in infants younger than three months suggests disaccharidase deficiency, cow's milk or soy protein intolerance, cystic fibrosis or an immunodeficiency state, while chronic diarrhea in children three to 18 years of age suggests celiac disease, late-onset primary lactose deficiency and inflammatory bowel disease. Gastrointestinal infection is the most common cause of chronic diarrhea in children of all ages. Diarrhea that develops after the introduction of cow's milk, cereals and fruits suggests an enzyme deficiency or protein intolerance. Watery, explosive stools suggest sugar intolerance, and foul-smelling, greasy, bulky stools suggest fat malabsorption. Marked weight loss suggests malabsorption, inflammatory bowel disease, hyperthyroidism or malignancy. The presence of neutrophils or red blood cells in the stool indicates bacterial gastroenteritis or inflammatory bowel disease, while the presence of eosinophils suggests protein intolerance or parasitic infestation. A toddler who is thriving and cheerful despite having diarrhea may have chronic nonspecific diarrhea of childhood.
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PMID:Evaluating the child with chronic diarrhea. 862 43


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