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)

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

A 76-year-old woman was treated with oral bisphosphonate, alendronate, for osteoporosis in an outpatient clinic. Routine blood tests 4 months after alendronate prescription surprisingly revealed severe hypophosphataemia. The patient was hospitalised and treated with intravenous and oral phosphate supplements. Alendronate was later reintroduced as treatment for osteoporosis and the patient once again presented with severe hypophosphataemia in subsequent routine blood tests. The patient had only presented with lower extremity pain, muscle weakness and difficulty walking. Blood tests in the emergency department both times reconfirmed severe hypophosphataemia. Plasma (p-)ionised calcium levels were normal or slightly elevated and p-parathyroid hormone levels were normal or slightly suppressed. The p-25-hydroxyvitamin-D and p-creatine were in the normal range. Critical illness, malabsorption, nutritional issues and genetics were reviewed as potential causes but considered unlikely. Phosphate levels were quickly restored each time on replacement therapy and the case was interpreted as bisphosphonate-induced severe hypophosphataemia.
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PMID:Severe hypophosphataemia following oral bisphosphonate treatment in a patient with osteoporosis. 3303 1