Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Significant bone mass reduction occurs in stroke patients on the hemiplegic side compared with the intact side, correlating with the degree of paralysis and vitamin D deficiency. To evaluate the influence of long-standing immobilization on this osteopenia, we measured various serum markers of bone metabolism in 93 hemiplegic elderly patients with a long-standing stroke and in 37 controls. The bone mineral density (BMD) of the second metacarpal was determined bilaterally. The scoring of the stroke patients activity was based on the Barthel Index (BI). The serum ionized calcium was higher in the patients than in the controls, correlating negatively with the BI in the patients. The concentrations of parathyroid hormone (PTH), pyridinoline cross-linked carboxy-terminal telopeptide of type I collagen and bone Gla protein were normal or low. The serum 25-hydroxyvitamin D level was low in the patients, correlating positively with the BMD on both sides. The serum 1,25-dihydroxyvitamin D (1,25-[OH]2D) level was markedly reduced in the patients. Hemiplegia from a stroke can result in immobilization hypercalcemia which inhibits PTH secretion and 1,25-[OH]2D production. Bone remodelling may have almost reached an equilibrium, resulting in a steady rate of bone loss. This and the hypovitaminosis D appear to be the dominant causes of immobilization-induced osteopenia in elderly, long-standing hemiplegic stroke patients.
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PMID:Influence of immobilization on bone mass and bone metabolism in hemiplegic elderly patients with a long-standing stroke. 1022 20

A significant reduction in bone mineral density occurs in stroke patients on the hemiplegic side, correlating with the degree of paralysis and vitamin D deficiency due to malnutrition, sunlight deprivation, and immobilization-induced hypercalcemia, and increases the risk of hip fracture. We evaluated the effect of ipriflavone and 1alpha-hydroxyvitamin D3 [1alpha(OH)D3; vitamin D3] administration on bone mineral density preservation as compared with untreated controls. In a randomized and prospective study of 103 patients with hemiplegia after stroke (the mean duration of illness was 4.8 yr), 68 (34 patients in each group) were given 600 mg ipriflavone or 1 microg vitamin D3 daily for 12 mo, whereas the remaining 35 patients received no drug. Bone mineral density on the hemiplegic side decreased by 1.4% in the ipriflavone group, 3.8% in the vitamin D3 group, and 5.4% in the control group (P < .0001, ipriflavone v vitamin D3 and control). At baseline, all three groups of patients showed a 25-hydroxyvitamin D insufficiency, increased serum ionized calcium, and low levels of 1, 25-dihydroxyvitamin D, suggesting immobilization-induced hypercalcemia and inhibition of renal synthesis of 1, 25-dihydroxyvitamin D. After treatment, the serum 1, 25-dihydroxyvitamin D level increased by 139.9% in the ipriflavone group and by 26.9% in the vitamin D3 group. Significant decreases in the serum ionized calcium and pyridinoline cross-linked carboxyterminal telopeptide of type I collagen, and increases in parathyroid hormone and bone Gla protein were observed in the ipriflavone group, whereas no changes occurred in the other two groups. One patient in the untreated group suffered a hip fracture, compared with none in the ipriflavone and vitamin D3 groups. These results suggest that ipriflavone is more efficacious than vitamin D3 in the prevention of decreased bone mineral density in hemiplegic stroke patients because it decreases serum calcium levels through inhibition of bone resorption and cause a subsequent increase in 1, 25-dihydroxyvitamin D concentration.
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PMID:Effect of ipriflavone on bone in elderly hemiplegic stroke patients with hypovitaminosis D. 2935 Nov 3

Significant decreases in bone mineral density (BMD) occur on the hemiplegic side in chronic stroke patients, which correlate with the degree of paralysis and hypovitaminosis D. In this double-blind, randomized, and prospective study of 98 patients with hemiplegia involving both an upper and lower extremity (55 males and 53 females; mean age, 71.4 +/- 0.6 years) after an acute stroke, 49 were given etidronate for 56 weeks and 49 received a placebo. The BMD was measured by computed X-ray densitometry (CXD) of the second metacarpal bone bilaterally. Forty age-matched control subjects were followed for 56 weeks. At baseline, both groups had 25-hydroxyvitamin D [25(OH)D] insufficiency, increased serum ionized calcium and pyridinoline cross-linked carboxy-terminal telopeptide of type I collagen (ICTP), and low serum concentrations of parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25(OH)2D], suggesting immobilization-induced hypercalcemia and inhibition of renal synthesis of 1,25(OH)2D. The BMD on the hemiplegic side decreased by 2.3% and 4.8% in the etidronate and placebo groups, respectively (p = 0.0003). After treatment, the serum 1,25(OH)2D concentration increased by 62.2% in the etidronate group and decreased by 12.4% in the placebo group. The etidronate group had significant decreases in the serum ionized calcium and ICTP and increases in PTH and bone Gla protein (BGP), whereas the placebo group had higher serum calcium and ICTP concentrations but stable PTH. These results suggest that etidronate can prevent decreases in the BMD in hemiplegic stroke patients because it decreases the serum calcium through inhibition of bone resorption and causes a subsequent increase in the serum 1,25(OH)2D concentration.
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PMID:Beneficial effect of intermittent cyclical etidronate therapy in hemiplegic patients following an acute stroke. 2775 30

We report a 66-year-old Chinese man with chronic renal insufficiency (creatinine 1.7 mg/dL) and gout suffering from slurred speech and right hemiplegia for 3 days. Acute cerebral infarction was confirmed by computed tomography. Conscious disturbance occurred on the tenth hospital day without significant changes on imaging study when compared with a previous scan. Hypercalcemia (total calcium 14.1 mg/dL) and acute exacerbation of chronic renal failure (serum creatinine 2.5 mg/dL) were noticed. Hypercalciuria (FECa 3.2%), and low serum levels of intact parathyroid hormone and 1,25(OH)2D3 suggested nonparathyroidal hypercalcemia. An extensive workup failed to identify any etiology of hypercalcemia. Hypercalcemia and renal failure were temporarily ameliorated after aggressive volume expansion and loop diuretic treatment but recurred 2 weeks later. Immobilization hypercalcemia was considered after the exclusion of other discernible causes and was successfully treated with rehabilitative exercises and bisphosphonates without further recurrence during a 2-year follow-up. Clinical alertness to immobilization as a possible cause of hypercalcemia may avoid unnecessary and invasive examinations, life-threatening complications and annoying recurrences.
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PMID:An unrecognized cause of recurrent hypercalcemia: immobilization. 1663 46

THIS CASE REPORT EXPOSES A PHENOMENON WHICH, ALTHOUGH PROPOSED, HAS NOT BEEN DESCRIBED IN CLINICAL LITERATURE: transient postictal hemiplegia (Todd's paralysis) with concomitant electrocardiographic J-point deflection (Osborn waves). Although typically associated with hypothermia, a prominent J-wave on the electrocardiogram (ECG) results from a transmyocardial voltage gradient during ventricular repolarization. Rarely, the Osborn wave may be observed in a non-hypothermic setting such as hypercalcemia or cerebral hemorrhage. Transient postictal hemiplegia has been attributed to localized cerebral hypoperfusion resulting from motor cortex exhaustion following an epileptic seizure. The same central nervous system autonomic dysfunction has been theorized to produce subendocardial hypoperfusion with electrocardiographic change and cardiac troponin T elevation. This is the first described ECG evidence of a dynamically displaced J-point in the setting of postictal hemiplegia.
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PMID:Dynamic J-Point Elevation Associated with Epileptic Hemiplegia: The Osborn Wave of Todd's Paralysis. 2346 97