Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium metabolism was studied in a 12-year-old girl preseting with idiopathic juvenile osteoporosis. Absorption of orally administered 47-Ca was high. Serum calcium and phosphorus, serum immunoreactive PTH and CT and tubular phosphate reabsorption were found to be within normal limits. The data suggest that calcium malabsorption, nutritional calcium deficiency, hyperparathyroidism, a dysfunction related to sex hormones, and Cushing's syndrome cannot be implicated in the aetiology of the osteoporosis in this case who recovered spontaneously with sexual maturation.
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PMID:A case-report of idiopathic juvenile osteoporosis with particular reference to 47-calcium absorption. 89 71

This paper is intended to give a review of the etiology and symptoms of potassium deficiency in man, as an introduction to the section on potassium and cardiac arrhythmias of this symposium. A review is given of different conditions where hypokalemia and/or total potassium deficiency is or might be part of the clinical picture, such as conditions with insufficient dietary intake, gastrointestinal potassium losses (e.g. vomiting, fistulas, malabsorption, abuse of laxatives and diarrhea), and renal potassium losses (e.g. primary and secondary hyperaldosteronism, Cushing's syndrome, intake of licorice, diabetic coma, renal disease, diuretic treatment and l-dopa treatment). Common symptoms of hypokalemia and/or potassium deficiency are reviewed as well, such as general and unspecific symptoms (e.g. tiredness, lack of concentration, lack of appetite and vomiting), and symptoms from the heart, kidneys and skeletal muscle.
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PMID:Hypokalemia--clinical spectrum and etiology. 702 Mar 49

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

The negative effect on bone due to the glucocorticoid excess is mediated by the direct action of cortisol in reducing bone apposition and increasing bone resorption, and by indirect mechanisms such as the calcium malabsorption, hypercalciuria and hypogonadism. The condition of overt hypercortisolism, also called Cushing's syndrome, leads to osteoporosis and fractures in up to the 70% of cases, even in the presence of normal gonadal status and in males. The recovery from Cushing's syndrome leads to a normalization of bone mineral density only after several years, even if some data show that the risk of fractures normalizes after one year from the cure. Alendronate has been demonstrated to be useful to accelerate the restoration of normal bone mass after the cure of Cushing's syndrome Several studies, even not all, have been demonstrated that also the condition of asymptomatic or "subclinical" hypercortisolism (often associated to adrenal adenoma) is associated to a reduction of bone mineral density and increased prevalence of fracture even in the presence of eugonadal status and in males. Unfortunately, data regarding the effect of the normalization of cortisol secretion on bone mass and risk of fractures are lacking. On the other hand, it is known that osteoporotic fractures may be the clinical presentation of an otherwise asymptomatic hypercortisolism. In a recent study we have demonstrated that in a population of outpatients with established osteoporosis and without known or clinically evident secondary causes, the prevalence of subclinical hypercortisolism is about 10%. This finding suggests that the presence of subclinical hypercortisolism has to be taken in to account when evaluating patients with unexplainable established osteoporosis.
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PMID:[Role of cortisol hypersecretion in the pathogenesis of osteoporosis]. 1871 63

Despite many recent advances, the management of patients with Cushing's disease continues to be challenging. Cushing's syndrome is a complex metabolic disorder that is a result of excess glucocorticoids. Excluding the exogenous causes, adrenocorticotropic hormone-secreting pituitary adenomas account for nearly 70% of all cases of Cushing's syndrome. The suspicion, diagnosis, and differential diagnosis require a logical systematic approach with attention paid to key details at each investigational step. A diagnosis of endogenous Cushing's syndrome is usually suspected in patients with clinical symptoms and confirmed by using multiple biochemical tests. Each of the biochemical tests used to establish the diagnosis has limitations that need to be considered for proper interpretation. Although some tests determine the total daily urinary excretion of cortisol, many others rely on measurements of serum cortisol at baseline and after stimulation (e.g., after corticotropin-releasing hormone) or suppression (e.g., dexamethasone) with agents that influence the hypothalamic-pituitary-adrenal axis. Other tests (e.g., measurements of late-night salivary cortisol concentration) rely on alterations in the diurnal rhythm of cortisol secretion. Because more than 90% of the cortisol in the circulation is protein bound, any alteration in the binding proteins (transcortin and albumin) will automatically influence the measured level and confound the interpretation of stimulation and suppression data, which are the basis for establishing the diagnosis of Cushing's syndrome. Although measuring late-night salivary cortisol seems to be an excellent initial test for hypercortisolism, it may be confounded by poor sampling methods and contamination. Measurements of 24-hour urinary free-cortisol excretion could be misleading in the presence of some pathological and physiological conditions. Dexamethasone suppression tests can be affected by illnesses that alter the absorption of the drug (e.g., malabsorption, celiac disease) and by the concurrent use of medications that interfere with its metabolism (e.g., inducers and inhibitors of the P450 enzyme system). In this review, the authors aim to review the pitfalls commonly encountered in the workup of patients suspected to have hypercortisolism. The optimal diagnosis and therapy for patients with Cushing's disease require the thorough and close coordination and involvement of all members of the management team.
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PMID:Pitfalls in the diagnosis and management of Cushing's syndrome. 2563 22

In spite of the presence of definitive diagnostic criteria to diagnose Cushing syndrome diagnosis may become challenging. We report a young female with mild clinical features of Cushing syndrome, who had nonsuppressible oral dexamethasone suppression tests; also she had a suspicious pituitary lesion. She underwent pituitary surgery and a pituitary microadenoma (non-ACTH staining) was removed. Now she had come to us with similar complaints to those before. Again she had nonsuppressible oral dexamethasone suppression tests. As the diurnal variation of serum and salivary cortisol was maintained and urinary free cortisol was normal, further evaluation with IV dexamethasone suppression test was performed which clearly ruled out Cushing syndrome. The patient was not on any medicines known to alter dexamethasone metabolism. Fat malabsorption was also ruled out using appropriate tests. The reason for this discrepancy is thought to be altered (increased) metabolism of dexamethasone in this patient as it is widely variable in the general population.
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PMID:Nonsuppressible Oral Dexamethasone Suppression Tests but Not Cushing Syndrome. 2709 81