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Query: UMLS:C0038454 (stroke)
 147,016 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

To assess bone changes in hemiplegic stroke patients, vitamin D status and bone density on hemiplegic and intact sides of sunlight deprived stroke patients were evaluated. Sera were collected from 88 hemiplegic stroke patients and 34 controls. The sera were assayed for 25-hydroxyvitamin D (25-OHD) and 1, 25 dihydroxyvitamin D (1, 25-[OH]2D). Bone density was measured bilaterally from radiographs of the hands using computed X-ray densitometry (CXD) and the Z-score of bone mineral density was calculated. Serum 25-OHD and 1, 25-[OH]2D concentrations were significantly lower in patients (11.5 +/- 5.4 ng/mL, 23.1 +/- 10.3 pg/mL) than in controls (21.6 +/- 3.1 ng/mL, 49.6 +/- 9.2 pg/mL) (P < .0001). The patients' Z-scores for osteopenia were lower on the hemiplegic side than on the nonhemiplegic side. Even on the intact side, the Z-scores were significantly lower as compared to controls. In addition to the strong positive correlation between the Z-scores on the hemiplegic side and degree of hemiplegia, the Z-scores on both sides in patients correlated positively with the serum 25-OHD concentration. These results suggest that vitamin D deficiency and disuse can cause osteopenia on the hemiplegic side and may increase the risk of hip fracture. In addition, it was demonstrated that hypovitaminosis D decreased bone mass on the nonhemiplegic side. This hypovitaminosis D might be corrected readily by the routine use of vitamin D supplements.
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PMID:Vitamin D status and nonhemiplegic bone mass in patients following stroke. 978 96

The significant bone-mass reduction that occurs on the hemiplegic side of stroke patients due to disuse and vitamin D deficiency may explain the increased post-stroke incidence of hip fractures. To further evaluate this osteopenia, the Z-score of bone mineral density (BMD) in both second metacarpals was assessed in 54 stroke patients and 27 control subjects. Serum concentrations of intact parathyroid hormone (PTH), osteocalcin (OC), tartrate-resistant acid phosphatase (TRAP) and 25-hydroxyvitamin D (25-OHD) were also determined. The patients' Z-scores were lower on the hemiplegic side than on the nonhemiplegic side. Serum concentrations of PTH, OC and TRAP exceeded those in control subjects. Serum 25-OHD was reduced in patients and correlated negatively with the Z-score on the hemiplegic side. Serum PTH was elevated markedly in 17% of the patients and correlated positively with the levels of OC, but not with TRAP, 25-OHD or the Z-scores on both sides. The results indicate that skeletal remodeling is accelerated in patients with hemiplegia and suggest that vitamin D deficiency and insufficient compensatory hyperparathyroidism stimulating skeletal turnover is an important cause of osteopenia in immobilized stroke patients.
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PMID:Role of the parathyroid gland on bone mass and metabolism in immobilized stroke patients. 978 97

Bone mineral density is reduced in stroke patients on the hemiplegic and contralateral sides, reflecting a degree of paralysis and vitamin D deficiency. Because the deficiency of vitamin K, a factor essential for site-specific carboxylation of bone Gla protein, is also associated with reduced bone mineral density, an additional contribution of vitamin K to bone changes was assessed in 168 elderly patients with long-standing post-stroke hemiplegia and hypovitaminosis D. Sera were analyzed to relate vitamin K1 concentrations to bone-related biochemical indexes and bone mineral density measured by radiodensitometry of the second metacarpal. Bone mineral density was lower on both sides in patients than in the 56 controls (P < 0.02). Serum vitamin K1 concentrations, which correlated positively with bone Gla protein concentrations (P < 0.0001), were lower in patients (0.48 +/- 0.47 nmol/L) than controls (1.33 +/- 0.49; P < 0.0001). Serum bone Gla protein and 25-hydroxyvitamin D concentrations were lower in patients than controls (P < 0.0001), whereas ionized Ca concentrations were higher in patients (1.277 +/- 0.041 mmol/L) than controls (1.210 +/- 0.049; P < 0.0001), correlating with the Barthel index. Multivariate linear regression identified vitamin K1, bone Gla protein, 25-hydroxyvitamin D, ionized calcium, and the Barthel index as independent bone mineral density determinants on the hemiplegic side and 25-hydroxyvitamin D, calcium, and the Barthel index on the intact side. Immobilization and vitamin K deficiency had stronger osteopenic effects on the hemiplegic side than contralaterally.
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PMID:Vitamin K deficiency and osteopenia in disuse-affected limbs of vitamin D-deficient elderly stroke patients. 3176 25

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

A significant bone-mass reduction occurs on the hemiplegic side of stroke patients because of disuse and vitamin D deficiency. This may explain why hip fractures in poststroke patients occur almost exclusively on the hemiplegic side. To further evaluate this osteopenia, bone mineral density (BMD) in both second metacarpals was assessed in 61 patients and 28 control subjects. Serum concentrations of intact parathyroid hormone (PTH), osteocalcin (OC), tartrate-resistant acid phosphatase (TRAP), 25-hydroxyvitamin D (25-OHD), and calcium also were determined. The patients' BMD values were higher on the hemiplegic side than on the nonhemiplegic side. BMD on the hemiplegic side correlated positively with serum concentrations of PTH, OC and TRAP, which exceeded those in control subjects. Serum 25-OHD was low in patients, correlating negatively with BMD on the hemiplegic side. Serum PTH correlate positively with the levels of OC and TRAP and negatively with 25-OHD concentrations. The results indicate that skeletal remodeling is accelerated in patients with hemiplegia, with resorption predominating. We concluded that vitamin D deficiency and compensatory secondary hyperparathyroidism stimulating skeletal turnover is an important cause of osteopenia in the hemiplegic limbs of stroke patients. This osteopenia might be corrected by administration of etidronate to inhibit osteoclastic bone resorption together with a vitamin D supplement.
J Stroke Cerebrovasc Dis
PMID:Accelerated bone remodeling in patients with poststroke hemiplegia. 3178 24

Insulin resistance is characterized by the systemic impairment of insulin action and is usually the result of aging, obesity, chronic inflammation, or another factor that may contribute to the inhibition of the insulin signaling pathway. Insulin resistance is accompanied by defects in lipid metabolism and blood coagulation, hypertension, obesity, and vascular inflammation in a syndrome called syndrome X or metabolic syndrome. Metabolic syndrome is involved in the development of atherosclerosis with consequent cardiovascular complications including acute myocardial infarction, stroke, and vascular disease. Recent data have shown that vitamin D acts as a negative regulator of the renin gene and that vitamin D deficiency is followed by increased renin-angiotensin II expression. The link between the insulin signaling pathway/insulin resistance and the renin-angiotensin system has been well documented in previous studies. The present review focuses on disorders characterized by a reduction in vitamin D concentration or its receptor function and the development of insulin resistance or metabolic syndrome, and discusses also possible therapeutic interventions.
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PMID:Vitamin D, the renin-angiotensin system, and insulin resistance. 1819 90

The accomplishments of John Snow (1813-1858), physician-epidemiologist, inventor and anaesthetist to Queen Victoria, are well documented, but the causes of his untimely death at age 45 remain conjectural. Snow suffered a paralysing stroke while working on his magnum opus, On Chloroform and Other Anaesthetics, and died a few days later on 16 June 1858. Snow had a history of renal problems associated with tuberculosis. He also experimented on himself with ether, chloroform and other agents over several years, but whether this prolonged self-experimentation contributed to his early death is uncertain. A photograph of Snow taken in 1857 shows that the fingers of his right hand were swollen. Could this be a clue to the cause of his death? The "modern" view is that Snow's early tuberculosis and associated renal disease led to hypertension, chronic renal failure and stroke. The tuberculosis and renal involvement may have been worsened by vegetarianism and perhaps resulting vitamin D deficiency. However, the renal damage caused by tuberculosis is unlikely to have been progressive. Based on current evidence of renal toxicity associated with exposure to anaesthetic agents, it is perhaps more likely that extensive and prolonged self-experimentation with anaesthetics over a 9-year period led to Snow's renal failure, swollen fingers and early death from stroke.
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PMID:The hands of John Snow: clue to his untimely death? 1922 82

It is the purpose of this comprehensive report to outline a revolutionary strategy to prevent vitamin D deficiency in our nation. Vitamin D is a unique vitamin. Its metabolic product, calcitriol, is a profound secosteroid hormone that has impact on over 1000 genes in the human body. Recent clinical research has implicated vitamin D deficiency as a major factor in the etiology of rickets, a wide variety of cancers, as well as hypertension, stroke, heart attack, diabetes, bone fractures, periodontal disease, and even multiple sclerosis. There are two forms of vitamin D utilized in the human body: D2 and D3. Measurement of 25(OH)D is the most reliable method of detecting vitamin D deficiency. Several methods, including high-performance liquid chromatography (HPLC), chemoluminescence, and radioimmunoassay (RIA), have been developed for the measurement of total 25(OH)D levels. Prevention and treatment of vitamin D deficiency is accomplished by regulated sun exposure as well as vitamin D, supplementation. This information describing our plan to prevent vitamin D deficiency in the patients and employees of Legacy Health System is a landmark accomplishment that should be replicated in every healthcare setting in our country to prevent vitamin D deficiency.
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PMID:Modern concepts in the diagnosis and treatment of vitamin D deficiency and its clinical consequences. 1939 50

Cardiovascular disease (CVD) is a major cause of morbidity and mortality worldwide. Recently vitamin D deficiency has been identified as a potential risk factor for many diseases not traditionally associated with vitamin D, such as cancer and CVD. This review discusses the evidence suggesting an association between low 25-hydroxyvitamin D levels and CVD and the possible mechanisms mediating it. Vitamin D deficiency has been associated with CVD risk factors such as hypertension and diabetes mellitus, with markers of subclinical atherosclerosis such as intima-media thickness and coronary calcification as well as with cardiovascular events such as myocardial infarction and stroke as well as congestive heart failure. It could be suggested that vitamin D deficiency contributes to the development of CVD through its association with risk factors, such as diabetes and hypertension. However, direct effects of vitamin D on the cardiovascular system may also be involved. Vitamin D receptors are expressed in a variety of tissues, including cardiomyocytes, vascular smooth muscle cells and endothelial cells and vitamin D has been shown to affect inflammation and cell proliferation and differentiation. While much evidence supports a potential antiatherosclerotic effect of vitamin D, prospective, placebo-controlled randomized as well as mechanistic studies are needed to confirm this association. Since vitamin D deficiency is easy to screen for and treat, the confirmation of such an association could have important implications for both, patient care and health policy.
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PMID:Vitamin D and cardiovascular disease. 1960 65


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