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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case is reported of heat stroke associating dehydration, anuria, muscle disorders and early hypercalcemia. All disorders disappeared within 48 hours with rehydration. Early hypercalcemia differs from late hypercalcemia reported at resumption of diuresis. Early hypercalcemia might result from blood concentration with hyperproteinemia and release of bone calcium under the action of PTH. Its prognosis is good, which is not the case of late hypercalcemia.
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PMID:[Heat stroke with anuria, muscular disorders and early hypercalcemia]. 84 41

Several reports suggested an involvement of parathyroid function in blood pressure regulation in animals and humans: hyperparathyroid subjects frequently display an elevated systolic blood pressure and young mild hypertensive patients show enhanced serum PTH levels. Moreover, removal of parathyroid glands (PTX) in young rats attenuates and delays the development of mineralocorticoid and genetic hypertension. In addition, in vivo cardiovascular reactivity to norepinephrine in PTX rats from both spontaneously the hypertensive rat (SHR) and Lyon hypertensive rat (LH) strains is decreased, as is calcium content in aortic and heart fragments. Moreover, parathyroid grafts from SHR, stroke-prone SHR (SHR-SP), LH, or Milan hypertensive rats (MHS) into previously parathyroidectomized normotensive recipient rats have been shown to induce an increase in blood pressure. Recently, in essential hypertensive patients and in SHR, a circulating hypertensive factor has also been described. Produced by the PTX in SHR, this factor is inversely related to the amount of dietary calcium. It appears, therefore, that the PTX plays a major role in experimental and probably also in human hypertension.
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PMID:Ions, parathyroids, and genetic hypertension. 814 Nov 51

Intensive training in a humid and warm environment can cause exertional heat stroke (ExHS) and rhabdomolysis (RBD) in military recruits. To investigate the role of vitamin D and monomeric calcitonin (CT) on the calcium metabolism in ExHS with RBD and acute renal failure (ARF), we studied 21 recruits with ExHS (mean age 21.4 years), 7 of which had ARF. Another 11 age-matched recruits with heat exhaustion (HE) and 11 healthy subjects were selected as controls. Our results showed that in 14 ExHS patients without ARF, mean serum creatinine (Cr) levels were significantly higher (151.16 vs. 106.08 mumol/l, p < 0.01), whereas serum osteocalcin (OC) levels were significantly lower (2.22 vs. 4.65 micrograms/l, p < 0.01) than in healthy controls. In 7 patients with ExHS and ARF, the mean serum Cr (774.38 vs. 105.20 mumol/l, p < 0.01), phosphorus (P) (2.26 vs. 1.26 mmol/l, p < 0.05), creatine phosphokinase (CPK) 274,143.97 vs. 85.78 IU/l, p < 0.05), intact parathyroid hormone (I-PTH) (299.81 vs. 18.66 ng/l, p < 0.05) and CT (13.58 vs. 6.63 ng/l, p < 0.01) levels on admission were significantly higher while the mean ionized calcium (iCa) levels were significantly lower than the healthy controls (0.9 vs. 1.18 mmol/l, p < 0.01). The mean serum 25-hydroxyvitamin D [25(OH)D] levels were not significantly different from healthy controls. However, mean serum 1,25-dihydroxyvitamin D [1,25(OH)2D] levels and the ratio of 1,25(OH)2D to 25(OH)D were significantly lower than healthy controls throughout the whole course of ARF. None of the 7 patients with ExHS and ARF developed hypercalcemia during the diuretic phase. Their mean serum I-PTH levels decreased significantly from 299 to 18 ng/l during the recovery phase (p < 0.05). Our study seems to suggest that the abnormal calcium metabolism in this unique patient group is in part caused by persistently decreased renal production of 1,25(OH)2D, although increased monomeric CT levels were associated with hypocalcemia. However, whether or not a causal relationship exists merits further investigation.
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PMID:A prospective study of calcium metabolism in exertional heat stroke with rhabdomyolysis and acute renal failure. 858 23

Disabled elderly stroke patients occasionally have very low serum 25-hydroxyvitamin D (25-OHD), which may be due to sunlight deprivation and malnutrition. Many of such patients have very low level of serum 1, 25-dihydroxyvitamin D (1, 25-[OH]2D; calcitriol), and immobilization-induced hypercalcemia may be responsible for inhibition of renal synthesis of calcitriol. To elucidate determinants of serum 1, 25-[OH]2D levels in elderly poststroke patients, we measured serum indices of bone and calcium metabolism and metacarpal bone mineral density (BMD). Patients whose serum 1, 25-[OH]2D concentration was below the mean-3 SD of normal control subjects were defined as the low 1, 25-[OH]2D group and the rest of the patients were designated as the normal group. Mean illness duration was 59 months in the normal group and 20 months in the low group. The Barthel index (BI), which predicts the degree of immobilization, was significantly lower in the low group than in the normal group. Mean serum 1, 25-[OH]2D and 25-OHD concentrations in the normal group were 36.7 pg/ml and 4.4 ng/ml, respectively; and those in the low group were 14.2 pg/ml and 1.8 ng/ml, respectively. Multiple regression analysis identified illness duration and calcium level as independent determinants of 1, 25-[OH]2D in both groups, and PTH in the normal group and 25-OHD in the low group were additional independent determinants. BMD in stroke patients was significantly lower than that in controls, and BMD in the normal group was lower as compared to the low group. BMD correlated negatively with 1, 25-[OH]2D and PTH in the normal group, and hyperparathyroidism may contribute to reduced BMD. These results suggest that treatment of decreased bone mass in stroke patients has to be individualized according to vitamin D status and calcium homeostasis.
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PMID:Abnormal calcium homeostasis in disabled stroke patients with low 25-hydroxyvitamin D. 3071 Oct 55

Cardiovacular disease is the main cause of morbidity and mortality in hemodialysis (HD) patients. However, there are no reliable data neither on the prevalence of cardiovacular disease nor its risk factors in Spain. The Morbidity and mortality Anemia Renal study (MAR) is a two-year multicenter, open-label, prospective cohorts study. Its main objective is to assess the general morbidity and mortality, particularly of a cardiovascular cause, and its relationship with the degree of anemia. Secondary objectives are: a/ the description of current clinical practices in anemia, dialysis, vascular access, and CV risk factor management; and b/ the description of hospitalization and mortality causes. This paper describes the prevalence of cardiovascular disease and risk factors of the HD population in Spain. A total of 1.710 patients were included (60% male, aged 64.4 years, 16.2 months on HD). The mean co-morbidity Charlson index was 6.5 +/- 2.3. Cardiovascular disease was the most prevalent comorbidity, 16.7% had a coronary disease, and 13.9% had different degrees of heart failure, while 11.6% had arrhythmia, 1.7% stroke and 5.5% peripheral artery disease. The prevalence of hypertension was 75.8%, 74.4% of patients received antihypertensive drugs, and still 40% of patients had an inadequate blood pressure control. The investigators considered as dyslipidemic 34.1% of patients, and prescribed treatment to 69.5% of them, while the remaining 30.5% (10.4% of the total) had hyperlipidemia with no drug therapy. Eleven percent was active smoker, and 26.6% former smoker. There was 47.4% of patients with a corporal mass index above 25. Secondary hyperparathyroidism with PTH above of 300 pg/ml was present in 22.2% of patients. Despite the EBPG and K-DOQI recommendations, only 68.8% of prevalent hemodialysis patients attained a hemoglobin (Hb) above 11 g/dl, 89.4% ferritin levels above 100 ng/ml, 66.5 degrees/a a transferrin saturation index (TSI) above 20%, and 61.1% met all three objectives. In summary, this first cross-sectional analysis has allowed us to know in detail the standard practice in multiple aspects of management of HD population in Spain. It has also established clear differences in the prevalence of cardiovascular disease and risk factors from the US registries. Last but not least we have identified therapeutic opportunities to improve the course and prognosis of our patients.
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PMID:[Cardiovascular risk in hemodialysis in Spain: prevalence, management and target results (MAR study)]. 1605 11

In this review, benefits and side-effects of current and emerging therapies to treat and prevent pathological bone loss are described. Bisphosphonates are the antiresorptive compounds most widely used in the treatment of bone-loss associated diseases. They are generally well-tolerated although have recently been associated with osteonecrosis of the jaw and other complications. Therapies modulating estrogen receptor activation are indicated in the prevention and treatment of either breast cancer or osteoporosis in postmenopausal women. Thus, hormone replacement therapy is effective in prevention of osteoporosis, but its long-term use can increase the risk of breast cancer, stroke and embolism. Tamoxifen benefits all stages of breast cancer, but its use may lead to uterine cancer and thromboembolism. Raloxifene is approved in prevention of breast cancer and treatment of postmenopausal osteoporosis, but its use can increase the risk of fatal stroke. Aromatase inhibitors are superior to tamoxifen at advanced stages of disease and as adjuvants, but their use increase fracture incidence. Fulvestrant is as effective as aromatase inhibitors in the treatment of advanced breast cancer and does not cause bone fractures. Another antiresorptive available for the treatment of postmenopausal osteoporosis, Paget's disease and hypercalcemia is calcitonin, which also exhibits analgesic effects. A promising antiresorptive agent currently in clinical trials is denosumab. Aditional therapies for osteoporosis that decrease fracture risk consist of PTH-like anabolic agents and the dual action bone agent strontium ranelate. Antiseptics and antibiotics are used extensively in periodontal disease intervention to target bacterial biofilm, although host-directed therapies are also being developed.
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PMID:Pharmacotherapies to manage bone loss-associated diseases: a quest for the perfect benefit-to-risk ratio. 1828 84

Recent studies have indicated a link between bone metabolism and cardiovascular events in patients with chronic kidney disease (CKD). CKD is a major health problem worldwide. This study evaluates the role of noninvasive markers of bone metabolism in predicting cardiovascular morbidity (coronary artery disease, peripheral vascular disease, stroke) and mortality in patients with mild to severe forms of CKD. In a prospective cohort study, 627 patients with CKD were screened. To focus on bone metabolism, traditional risk factors for cardiovascular events were excluded, and 135 patients with CKD stages 1-5 were followed for 4 yr. Glomerular filtration rate was calculated by the Modification of Diet in Renal Disease formula. PTH (measured by four different assays), vitamin D 25 and 1,25, bone-specific alkaline phosphatase (BSALP), TRACP-5b, osteocalcin, serum collagen cross-link molecules, RANKL, and osteoprotegerin were determined. Predictors of cardiovascular events were evaluated by multivariable logistic regression, Kaplan-Meier survival, and Cox regression analysis. There were a total of 45 cardiovascular events (33%). Event rates were 5.6%, 29.1%, 45.2%, and 45.0% in CKD stages 1-2, 3, 4, and 5, respectively. In logistic regression, cardiovascular events were predicted only by (1) CKD stage (independent of age or sex; p < 0.001); (2) BSALP (p = 0.03); and (3) TRACP-5b (p = 0.04). Markers of bone formation (BSALP) and resorption (TRACP-5b) can serve as predictors of cardiovascular morbidity and mortality in CKD.
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PMID:Bone markers predict cardiovascular events in chronic kidney disease. 1859 36

Extrarenal calcifications, particularly affecting the cardiovascular system, are common observations which can be a source of serious complications in patients with chronic renal disease, especially those on dialysis. In these patients, cardiovascular disease - myocardial infarction, arrhythmia, calcified valvulopathy, stroke, peripheral ischemic arteriopathy, calciphylaxy, etc. - is the leading cause of death (more than 50%). These complications are closely related to the presence of vascular calcifications (VC) which are much more frequent, severe, and progressive than in the general population. Previously, these calcifications were considered to arise via a passive process within the context of comorbid conditions without specific signs of gravity: high blood pressure, atherosclerosis, aging, diabetes, smoking, dyslipidemia, chronic micro-inflammation, hyperhomocysteinemia, disorders of calcium-phosphorus metabolism. It is now established that VC arise via a complex, probably regulated, active process analogous to the processes leading to bone formation and/or remodeling. New insight provided by a large body of work designed to ascertain the mechanisms underlying the onset of VC has enabled the development of new diagnostic and therapeutic approaches. It is now possible to identify factors clearly favoring the formation of VC: TNF-alpha (which stimulates cell necrosis/apoptosis), CRP, oxidized lipids, AGEs, leptin, inorganic phosphate, high calcium-phosphorus product (CaxPO(4)), calcium, 1,25-OH(2)D(3) and Vitamin D(3), PTHrP (via an intracrine pathway), cyclic AMP, TGF-beta, bone morphogenic protein 2 (BMP2) and factors protective against the formation of VC: magnesium, HDL, inorganic pyrophosphate, albumin, ahsg/fetuin A, osteopontin (OPN), osteoprotegerin (OPG), osteonectin (ON), bone morphogenic protein 7 (BMP7), klotho, PTHrP (via a paracrine pathway), matrix gla protein (MGP), PTH (via Msx2) and vitamin K. In conclusion, until recently, neglected disorders of calcium-phosphorus metabolism are currently recognized as the main actors in the process leading to vascular mediacalcosis in patients with chronic kidney failure.
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PMID:[Origin of the mediacalcosis in kidney failure]. 1934 26

To evaluate whether there is a relationship between admission serum leptin concentrations and peri-operative myocardial injury, 238 consecutive older patients (mean age 81.9+/-7.9 years; 172 women) with low-trauma hip fracture were assessed. Myocardial injury as defined by elevated serum cardiac troponin I was associated with lower leptin levels analyzed as continuous or categorical variables. Patients with serum leptin concentrations <12ng/ml (medium value) had a two-fold greater increased risk for such complications compared with those with higher leptin levels (odd ratio 2.13, 95% confidence interval 1.06-4.28; p=0.033). This association remained significant after adjustments for age, gender, clinical (history of coronary artery disease [CAD], stroke, hypertension, diabetes, dementia), hematological (red, white, and lymphocyte count, hemoglobin, hematocrit), metabolic (parathyroid hormone [PTH], albumin), renal(creatinine, urea, glomerular filtration rate [GFR]), and inflammatory (C-reactive protein [CRP], ferritin) factors. The predictive value of lower leptin levels increased significantly when used in combination with traditional risk factors for myocardial injury.
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PMID:Serum leptin levels in older patients with hip fracture--impact on peri-operative myocardial injury. 1974 42

To determine whether serum 25(OH)D and/or PTH levels in older patients with hip fracture (HF) could predict short-term clinical outcomes, we conducted a prospective observational study of 287 consecutive HF patients (mean age 81.9 + or - 7.5 [SD] years, 72% females). The prevalence of vitamin D inadequacy (25[OH]D < 80 nmol/l) was 97.1%, that of vitamin D deficiency (25[OH]D < 50 nmol/l) was 79.8%, and that of elevated PTH level (>6.8 pmol/l) was 35.5%. After adjustment for age and sex, PTH was significantly associated with in-hospital mortality (OR = 1.12, 95% CI 10.5-1.20, P < 0.001), myocardial injury (OR = 1.05, 95% CI 1.03-1.15, P = 0.002), prolonged length of stay (LOS > or = 20 days; OR = 1.05, 95% CI 1.01-1.06, P = 0.044), and being discharged to institutional care (OR = 1.07, 95% CI 1.01-1.18, P = 0.48). Secondary hyperparathyroidism (SHPT), but not vitamin D deficiency, was associated with older age, a higher prevalence of trochanteric fracture, coronary artery disease, hypertension, previous stroke, renal impairment, increased levels of serum osteocalcin, bone-specific alkaline phosphatase, and adiponectin as well as a significantly higher in-hospital mortality (11.8 vs. 0.54%, P = 0.001), perioperative myocardial injury (32.7 vs. 22.5%, P = 0.043), LOS > or = 20 days (40.2 vs. 26.9%, P = 0.017), and being discharged to institutional care (29.5 vs. 14.6%, P = 0.019). In multivariate regression analyses, SHPT was strongly associated with in-hospital mortality and LOS > or = 20 days. We conclude that elevated PTH (but not vitamin D deficiency per se) is a strong independent predictor of poor outcomes in older patients.
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PMID:Elevated serum PTH is independently associated with poor outcomes in older patients with hip fracture and vitamin D inadequacy. 1976 73


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