Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Treatment of osteoporosis with a complete reconstruction of the normal three dimensional architecture of trabecular bone is an unsolved problem. In addition to the well established fluoride therapy new concepts in the treatment of osteoporosis were developed. There is growing interest in the so called ADFR concept (activation, depression of resorption, formation, repeat the cycle) as a physiological stimulation of osteoblastic bone formation. The histological results following ADFR treatment in 8 patients are reported. After 12 months of treatment with parathyroid hormone [1-38)hPTH) (stimulation of the basic metabolic units) and the diphosphonate EHDP (depression of osteoclastic resorption) no change of remodelling processes at the trabecular bone surface could be observed. The results demonstrate many doubts in the importance of the ADFR concept for the treatment of osteoporosis.
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PMID:[Morphologic study of iliac crest spongiosa in patients with osteoporosis treated according to the ADFR (activation, depression of resorption, formation, repeat the cycle) with parathyroid hormone and diphosphonates (Hannover PTH I study)]. 213 78

The hemodynamic effects of the diphosphonate terminus of a new infarct-avid magnetic resonance (MR) imaging agent, gadolinium-DTPA (diethylenetriamine-pentaacetic acid) HPDP (1-hydroxo-3-aminopropane-1,1-diphosphonate), and HEDP (hydroxyethyl-1,1-diphosphonate) (a simple diphosphonate terminus model) have been evaluated at MR imaging doses in both isolated and intact rabbit hearts. Rapid injections of the sodium salt of the diphosphonates reversibly depressed left ventricular developed pressure and its first derivative (dP/dt) but did not affect the in vivo heart rate. Hemodynamic depression was prevented by the co-administration of two equivalents of calcium ion per diphosphonate terminus in the isolated heart and by either slow infusion or co-administration of one equivalent of calcium ion per diphosphonate terminus in the in vivo heart. Therefore, if these agents are to be used in MR imaging of acute myocardial infarction, appropriate measures should be taken to prevent negative inotropic effects.
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PMID:Gadolinium phosphonates as MR imaging contrast agents: physiologic effects in rabbit hearts. 828 Sep 69