Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00964 (EHDP)
 496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Women with long-lasting anorexia nervosa often display osteopenia. Furthermore, we have observed additional marked loss of bone mass under tube feeding in underweight anorexia patients. Such loss of bone substances can lead to spontaneous fractures. Therefore, we investigated in this study whether this undesirable effect of tube-feeding might be prevented by administration of bisphosphonates (Didronel), a substance that inhibits the activity of osteoclasts. Bone density was assessed by a high-precision, low dose, quantitative computed tomography of the distal radius and the distal tibia. A group of 6 anorexia patients (tube feeding with an initial underweight of 74.9 +/- 10.3% of ideal weight, mean +/- SD) treated with bisphosphonates showed only slight loss of trabecular bone (0.8 +/- 0.2%, mean +/- SEM) after 2 months of observation, whereas in 2 control groups a marked diminution of trabecular bone was observed (4.4 +/- 0.7% and 7.6 +/- 1.1% respectively, p less than 0.001 for each comparison). Cortical bone was unchanged throughout. Treatment with bisphosphonates provides effective prevention of bone loss observed in tube-feeding.
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PMID:[Loss of bone mass in patients with anorexia on tube feeding and its prevention with biphosphonates]. 156 19

Severe hypercalcemia is a medical emergency requiring urgent treatment. It most commonly is caused by malignant tumors, as in the case study, but can also be caused by advanced hyperparathyroidism or high serum levels of vitamin D. The patient described in the case study shows clinical evidence of volume contraction due to hypercalcemia-related anorexia and vomiting. His elevated serum concentrations of urea nitrogen and creatinine reflect intravascular volume depletion and hypercalcemia-induced reduction of renal perfusion. He is also likely to have irreversible renal damage as a result of nephrocalcinosis. His central nervous system depression is most likely a result of hypercalcemia, but other central nervous system disorders such as cerebral metastases should be considered. Appropriate treatment would include intravenous fluids to correct volume depletion, dilute extracellular fluid calcium, and promote renal calcium excretion. Before waiting for the effects of volume expansion, the first dose of an inhibitor of bone resorption should be given. The agent of choice now (this may change when second-generation bisphosphonates become available) is plicamycin. Etidronate is a reasonable second choice. Because both drugs require at least 48 hours before their hypocalcemic action is manifest, calcitonin could be used to accelerate the rate of decline of the serum calcium. As the patient becomes more alert, weight-bearing and ambulation should be encouraged. With this combination of therapeutic modalities, this patient's serum calcium level should be corrected within 3 to 5 days. Intermittent injections of mithramycin or etidronate could be given on an outpatient basis approximately once a week in order to maintain the serum calcium within the normal range. One of the most important aspects of treatment in hypercalcemic patients is eradication of the underlying disease, which usually calls for specific antitumor therapy, including chemotherapy, radiation therapy, or surgery. Most of the agents currently available for the correction of hypercalcemia have cumulative toxicities or are only transiently effective and, therefore, their use should be considered a temporizing measure until specific treatment directed at the primary disease takes effect.
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PMID:Management of severe hypercalcemia. 200 13