Compensatory Hyperparathyroidism Research Articles

Association of Low Vitamin D and Intact Parathyroid Hormone (iPTH) in Nepalese Population: When Does iPTH Exactly Rise?

Vitamin D deficiency is a global public health concern that provokes bone demineralization and weakening. In response to the decreased vitamin D level, calcium stores wear out. The homeostatic effect of compensatory hyperparathyroidism in vitamin D deficiency incites variable discrepancies in different populations. This study intends to decipher the transition point of PTH in relation to levels of vitamin D in a Nepalese population. A cross-sectional study was carried out at Tribhuvan University Teaching Hospital, Nepal. Serum calcium, phosphorus, intact PTH, and 25-hydroxy vitamin D levels were assayed in an Abbott ARCHITECT Integrated System. A correlation plot of PTH and vitamin D was analyzed in Statistical Package for Social Sciences version 22.0. Using a locally weighted scatter plot smoothing method, the relation between these variables was presented graphically. Among 281 individuals, 30.2% had vitamin D levels below 20 ng/mL. There was an archetypical transition in the PTH levels in concert with the decrease in vitamin D level marked by 2 inflection points (ie, 18.5 and 42.0 ng/mL). Our findings suggest that to augment overall health and avert weakness due to vitamin D deficiency, the levels of vitamin D should be maintained above 42.0 ng/mL in our population.

Vitamin D Deficiency Reduces Postthyroidectomy Protracted Hypoparathyroidism Risk. Is Gland Preconditioning Possible?

Hypoparathyroidism is the most frequent complication after total thyroidectomy (PT-hypoPTH). After 1 year, most patients recover parathyroid function; however, the implicated physiologic dynamics remain unknown. Vitamin D deficiency (VDD) is the main cause of secondary hyperparathyroidism. Whether this compensatory hyperparathyroidism could influence parathyroid function recovery (PFR) in the setting of PT-hypoPTH has not been studied. This work aimed to evaluate the effect of preoperative VDD on PFR. A retrospective study was conducted with a prospectively maintained database including patients undergoing a total thyroidectomy between May 2014 and June 2019. Preoperative vitamin D (25(OH)D) less than 20 mg/mL was defined as VDD. Intact PTH less than 14 pg/mL on postoperative day 1 was defined as PT-hypoPTH. Transient PT-hypoPTH displayed PFR within the first year (early recovery: < 30 days; protracted recovery: > 30 days) whereas definite PT-hypoPTH did not. Survival analysis evaluated the effect of preoperative VDD on PFR, and a binary logistic regression model identified associated factors. A total of 397 patients were identified. The observed rates of transient, protracted, and definite PT-hypoPTH were 32.9%, 15.1%, and 5.2%, respectively. Rates of VDD were higher in the early-recovery PT-hypoPTH group (55.2% vs 31.5%; P = .01). Preoperative VDD was associated with faster PFR (19 vs 35 days; P = .03) and behaved as a protective factor for protracted PT-hypoPTH (odds ratio 0.47; 95% CI, 0.25-0.881; P = .016) in the multivariable analysis. Preoperative VDD could act as a preconditioning factor of the parathyroid glands prior to the surgical aggression exerted against them during surgery aiding PFR. Basic research studies and prospective clinical trials are needed to explain the underlying physiological mechanisms and to provide further evidence to improve clinical management.

Retraction: Does compensatory hyperparathyroidism predispose to ischemic stroke?

The editors of Neurology retract the article “Does compensatory hyperparathyroidism predispose to ischemic stroke?” by Sato et al.1

Reader response: Expression of Concern: Does compensatory hyperparathyroidism predispose to ischemic stroke? Decreased bone mass and increased bone turnover with valproate therapy in adults with epilepsy; An alternative to vitamin D supplementation to prevent fractures in patients with MS; High prevalence of vitamin D deficiency and reduced bone mass in Parkinson's disease.

An Expression of Concern was issued about 4 publications.1 Initial investigations published last year about the work of this group included concerns on study recruitment rates, ethical oversight, lack of funding statements, and possible gift authorship.2 We have specific concerns about data integrity in the 3 observational studies. These reports contain both impossible and implausible data.

Editors' note: Expression of Concern: Does compensatory hyperparathyroidism predispose to ischemic stroke? Decreased bone mass and increased bone turnover with valproate therapy in adults with epilepsy; An alternative to vitamin D supplementation to prevent fractures in patients with MS; High prevalence of vitamin D deficiency and reduced bone mass in Parkinson's disease.

Bolland et al. raise specific concerns about data integrity in 3 observational studies published in Neurology ® by Sato et al. They found that the reports contain both impossible and implausible data. In 2 studies, mean values are incorrect. In 3 studies, reported p values are incorrect. In one study, the number of patients enrolled in the study seems implausible because of estimated prevalence of the disease studied. In another study, the average age at menopause of patients enrolled is implausibly higher than the reported median age in the general population, and 2 distinct subgroups within a cohort had markedly different means but equal SDs that are greater than the SD for the whole cohort. Finally, they found it implausible that among 107 controls of mean age 75 years, none had an abnormality detected on physical examination or extensive ancillary testing. Our attempts to contact the corresponding author of the observational studies for a response have so far been unsuccessful. In “Sex-specific stroke incidence over time in the Greater Cincinnati/Northern Kentucky Stroke Study,” Madsen et al. found that an overall reduction in stroke incidence over time is driven by a decrease in stroke in men. Commenting on the article, Dr. Kuller notes that the study includes only age-adjusted rates and it is important to provide age-specific rates by sex in order to interpret age-adjusted trends of stroke reported in the article.

Does compensatory hyperparathyroidism predispose to ischemic stroke? Decreased bone mass and increased bone turnover with valproate therapy in adults with epilepsy; An alternative to vitamin D supplementation to prevent fractures in patients with MS; High prevalence of vitamin D deficiency and reduced bone mass in Parkinson's disease

Because of known issues leading to several retractions of papers by Y. Sato et al., the editors of Neurology® have, as a matter of due diligence, researched other papers that this group published in Neurology. To ensure that the scientific literature is correct, the Editor chooses to publish an Expression of Concern regarding 3 observational studies and a Letter to the Editor published in Neurology prior to the retracted clinical trials.1–4

Vitamin D and atypical femoral fractures

Dear Editors, There have been recent reports of atypical femoral fractures occurring in patients treated with bisphosphonates [1]. While the primary hypothesis has centered on the oversuppression of bone turnover, there have been suggestions that vitamin D deficiency might also be an important risk factor [1, 2]. Thus far, only one series has examined the association between vitamin D levels and atypical femoral fractures [2]. In the study by Girgis et al., serum 25-hydroxyvitamin D (25OHD) of less than 16 ng/mL was associated with an increased the risk of atypical subtrochanteric fractures (OR03.2). While it is plausible that vitamin D deficiency may play a role in the pathogenesis of these fractures since it is associated with impaired calcium absorption, compensatory hyperparathyroidism, and increased bone resorption, it was not an evident risk factor in our clinical experience. In our case series, which was one of the first published series describing this phenomenon [3], there were 16 women, age 52 to 91 years and of Asian ethnicity, who had a serum 25OHD level ascertained at the time of presentation between May 2004 and March 2010. They were compared to age-, ethnicity-, and sex-matched controls with low-energy osteoporotic femoral neck or pertrochanteric fractures admitted during the same period of time. Vitamin D deficiency was defined as 25OHD <20 ng/mL. Baseline characteristics were similar between cases and controls. The median 25OHD was 26.2 ng/mL in cases vs 19.0 ng/mL in controls (p00.0127), consistent with a greater use of calcium (81.3 vs 37.5 %, p00.004) and vitamin D (68.8 vs 34.4 %, p0 0.024) supplementation in cases vs. controls. Only 3 out of 16 cases (18.75 %) were vitamin D deficient, while 17 out of 32 controls (53.13 %) were vitamin D deficient (p0 0.031). The odds ratio for vitamin D deficiency in cases vs controls was 0.20 (95 % CI 0.03, 0.97). The main limitation of this analysis was the measurement of 25OHD at the time of presentation rather than at the initiation of and during bisphosphonate therapy. Nevertheless, our study indicated that vitamin D status was significantly better in cases vs controls at the time of fracture, suggesting that vitamin D status might be a less important factor than previously thought in the development of bisphosphonate-associated atypical femoral fractures.

Vitamin D Deficiency-Induced Vertebral Fractures May Cause Stooped Posture in Parkinson Disease

To determine the pathogenesis of the stooped posture in Parkinson disease (PD), we prospectively studied fractures in a cohort of patients with Parkinson disease for 5 yrs. At baseline, we recorded the dietary intake of vitamin D and serum concentrations of parathyroid hormone and 25-hydroxyvitamin D. Bone mineral density and lateral thoracic and lumbar spine radiographs were obtained at baseline and every year for 5 yrs. During the 5-yr study period, stooped posture developed in 34 patients; the rest of the 58 patients did not show stooped posture. At baseline, mean serum 25-hydroxyvitamin D and parathyroid hormone levels were 10.9 ng/ml and 73.1 pg/ml, respectively, in the stooped group and 18.6 ng/ml and 56.4 pg/ml, respectively, in the nonstooped group. Bone mineral density in the stooped group was significantly lower than in the nonstooped group. Dietary intake of vitamin D in the stooped group was significantly lower than in the nonstooped group. During the study period, 19 (22%) patients in the nonstooped group developed new vertebral fracture, compared with 23 (100%) patients in the stooped group. The mean ± SD percentage changes in bone mineral density were -6.5 ± 0.6 in the stooped group and -3.8 ± 0.8 in the nonstooped group. Mean serum levels of 25-hydroxyvitamin D after 5 yrs were 7.0 ng/ml in the stooped group and 14.1 ng/ml in the nonstooped group. Stooped posture in Parkinson disease may be caused by vertebral fractures resulting from vitamin D deficiency with compensatory hyperparathyroidism. Vitamin D supplementation may reduce stooped posture in patients with Parkinson disease.

RETRACTED: Amelioration of osteoporosis and hypovitaminosis D by sunlight exposure in Parkinson’s disease

A high incidence of fractures, particularly of the hip, represents an important problem in patients with Parkinson's disease (PD), who are prone to falls and have osteoporosis. We previously showed that 25-hydroxyvitamin D (25-OHD) deficiency due to sunlight deprivation with compensatory hyperparathyroidism causes reduced bone mineral density (BMD) in elderly patients with PD. The present study was undertaken to address the possibility that sunlight exposure may maintain BMD and reduce the incidence of hip fracture in elderly patients with PD. In a prospective study, PD patients were assigned to regular sunlight exposure (n=162) or usual lifestyle (n=162), and followed for 2 years. BMD of the second metacarpal bone was measured using a computed X-ray densitometer. Incidence of hip fracture in the two patient groups during the 2 year follow-up period was assessed. At baseline, patients of both groups showed vitamin D deficiency due to sunlight deprivation with compensatory hyperparathyroidism. The exposed group patients were exposed to sunlight (3231 min/year). BMD increased by 3.8% in the sunlight-exposed group and decreased by 2.6% in the usual lifestyle group (p<.0001). Serum 25-OHD level increased from 27 nmol/L to 52 nmol/L in the sunlight-exposed group. Eleven patients sustained hip fracture in the normal lifestyle group, and 3 fractures occurred among the sunlight-exposed group (p=.03; odds ratio=2.4). Sunlight exposure can increase the BMD of vitamin D deficient bone by increasing 25-OHD concentration and leads to the prevention of hip fracture.

The prevention of hip fracture with menatetrenone and risedronate plus calcium supplementation in elderly patients with Alzheimer disease: a randomized controlled trial.

A high incidence of fractures, particularly of the hip, represents an important problem in patients with Alzheimer disease (AD), who are prone to falls and have osteoporosis. We previously found that vitamin K deficiency and low 25-hydroxyvitamin D (25-OHD) with compensatory hyperparathyroidism cause reduced bone mineral density (BMD) in female patients with AD. This may modifiable by intervention with menatetrenone (vitamin K2) and risedronate sodium; we address the possibility that treatment with menatetrenone, risedronate and calcium may reduce the incidence of nonvertebral fractures in elderly patients with AD. A total of 231 elderly patients with AD were randomly assigned to daily treatment with 45 mg of menatetrenone or a placebo combined with once weekly risedronate sodium, and followed up for 12 months. At baseline, patients of both groups showed high undercarboxylated osteocalcin (ucOC) and low 25-OHD insufficiency with compensatory hyperparathyroidism. During the study period, BMD in the treatment group increased by 5.7% and increased by 2.1% in the control group. Nonvertebral fractures occurred in 15 patients (10 hip fractures) in the control group and 5 patients (2 hip fractures) in the treatment group. The relative risk in the treatment group compared with the control group was 0.31 (95% confidence interval, 0.12-0.81). Elderly AD patients with hypovitaminosis K and D are at increased risk for hip fracture. The study medications were well tolerated with relatively few adverse events and effective in reducing the risk of a fracture in elderly patients with AD.

RETRACTED ARTICLE: Prevention of hip fractures by exposure to sunlight and pharmacotherapy in patients with Alzheimer’s disease

Hypovitaminosis D and K due to malnutrition or sunlight deprivation, compensatory hyperparathyroidism, increased bone resorption, low bone mineral density (BMD), and an increased risk of falls may contribute to an increased risk of hip fractures in patients with Alzheimer's disease. The purpose of the present study was to clarify the efficacy of interventions against hip fractures in patients with Alzheimer's disease. With respect to randomized controlled trials (RCTs) regarding Alzheimer's disease and hip fractures, the literature was searched with PubMed. Three RCTs were identified, and the relative risk (RR) and 95% confidence interval (CI) were calculated for individual RCTs. Exposure to sunlight with calcium supplementation, menatetrenone (vitamin K2) plus calcium and vitamin D supplementation, and risedronate plus calcium and vitamin D supplementation improved hypovitaminosis D and hyperparathyroidism, contributing to a reduction in bone resorption. Risedronate itself strongly decreased bone resorption. Menatetrenone also decreased the serum level of undercarboxylated osteocalcin. The three interventions increased metacarpal BMD and reduced the incidence of hip fractures. The respective RRs (95% CI) were 0.22 (0.049-0.999), 0.13 (0.031-0.554), and 0.26 (0.100- 0.690). The present study clarified the efficacy of three interventions, including exposure to sunlight, menatetrenone, and risedronate with calcium and/or vitamin D supplementation against hip fractures in patients with Alzheimer's disease.

Changes in serum seromucoid following compensatory hyperparathyroidism: A sequel to chronic fluoride ingestion.

This study was conducted to find out the possible underlying mechanism of various manifestation of fluorosis, a disease caused by excess ingestion of fluoride. For this the fluoride belt of Jaipur district was selected. The parameters selected were serum Parathyroid hormone, the levels of which are directly affected by fluoride intake. The levels of serum seromucoid, serum and leucocyte ascorbic acid, serum sialic acid (SSA) reflects ground substance metabolism. The study was conducted on two hundred children, selected from four areas (50 from each area) consuming water containing 2.4, 4.6, 5.6 and 13.6 mg/l of fluoride. Drinking water fluoride and serum fluoride were measured by Ion selective electrode method. Serum parathyroid by RIA and all other parameters were measured spectrophotometrically. The results revealed an increase in levels of fluoride, parathyroid hormone and seromucoid in serum with increasing water fluoride concentrations. Serum Calcium and serum ascorbic acid were found in normal range, how ever leucocyte ascorbic acid were decreased. A high positive correlation among fluoride concentration in drinking water and serum parathyroid hormone (r=0.967), and, serum parathyroid hormone and serum seromucoid concentration (r=0.935) was also observed The results indicated that secondary hyperparathyroidism due to hypocalcemic stress caused by excess fluoride ingestion disturbs normal metabolism of ground substance in calcified tissues of the body reflected as altered levels of the components of ground substance in the serum.

25(OH)D Serum Levels Decline With Age Earlier in Women Than in Men and Less Efficiently Prevent Compensatory Hyperparathyroidism in Older Adults

Although a host of factors are known to influence 25-hydroxyvitamin D [25(OH)D] serum levels, few studies addressed the distinctive sex-specific influence of aging, and the age-specific relationship of parathyroid hormone (PTH) with 25(OH)D. The aims of this research were to evaluate changes of 25(OH)D and PTH levels with age in a large population-based sample of men and women and to test the hypothesis that 25(OH)D serum concentrations needed to offset age-associated hyperparathyroidism are significantly higher in older than in younger persons. In 1107 participants of the InCHIANTI (Invecchiare in Chianti, i.e., Aging in the Chianti area) study, we collected information on dietary intake, daylight exposure, and disability, and measured renal function and serum 25(OH)D and PTH. In women, the age-related decline of 25(OH)D was already evident shortly after age 50, whereas in men it started only after age 70 and was substantially less steep. Age, daylight exposure, winter season, and disability were independent predictors of low 25(OH)D levels. For any given level of 25(OH)D, PTH levels were progressively and consistently higher in older than in younger participants. These findings suggest that the age-associated fall of serum 25(OH)D starts earlier in women than in men and that higher levels of 25(OH)D are required in older compared to younger persons to avoid the age-associated compensatory hyperparathyroidism.

The Prevention of Hip Fracture With Risedronate and Ergocalciferol Plus Calcium Supplementation in Elderly Women With Alzheimer Disease

A high incidence of fractures, particularly of the hip, represents an important problem in patients with Alzheimer disease (AD), who are prone to falls and have osteoporosis. We previously found that deficiency of 25-hydroxyvitamin D and compensatory hyperparathyroidism cause reduced bone mineral density in female patients with AD. We address the possibility that treatment with risedronate sodium and ergocalciferol plus calcium supplementation may reduce the incidence of nonvertebral fractures in elderly women with AD. A total of 500 elderly women with AD were randomly assigned to daily treatment with 2.5 mg of risedronate sodium or a placebo, combined with 1000 IU of ergocalciferol and 1200 mg of elementary calcium, and followed up for 18 months. At baseline, patients of both groups showed 25-hydroxyvitamin D deficiency with compensatory hyperparathyroidism. During the study period, bone mineral density in the risedronate group increased by 4.1% and decreased by 0.9% in the control group. Vertebral fractures occurred in 29 patients (24 hip fractures) in the control group and 8 patients (5 hip fractures) in the risedronate group. The relative risk in the risedronate group compared with the control group was 0.28 (95% confidence interval, 0.13-0.59). Elderly patients with AD hypovitaminosis D are at increased risk for hip fracture. Treatment with risedronate and ergocalciferol may be safe and effective in reducing the risk of a fracture in elderly patients with AD.

Impetigo herpetiformis with hyperparathyroidism

Impetigo herpetiformis, first described by Hebra, is a rare pustular disorder that primarily affects pregnant women and it is often complicated by an increased risk of spontaneous abortion. A commonly associated hypocalcemia often appears with hypoparathyroidism. Here we report a case of complicated impetigo herpetiformis without hypocalcemia paired with a compensatory hyperparathyroidism.

Amelioration of Osteoporosis and Hypovitaminosis D by Sunlight Exposure in Hospitalized, Elderly Women With Alzheimer's Disease: A Randomized Controlled Trial

In a random and prospective study, Alzheimer's disease (AD) patients were assigned to regular sunlight exposure (n = 132) or sunlight deprivation (n = 132) and followed for 1 year. Serum 25-OHD level increased by 2.2-fold in the sunlight-exposed group. Eleven patients sustained fractures in the sunlight-deprived group, and three fractures occurred among the sunlight-exposed group (p = 0.0362; odds ratio = 3.7). A high incidence of fractures, particularly of the hip, represents an important problem in patients with Alzheimer's disease (AD), who are prone to falls and have osteoporosis. We previously showed that 25-hydroxyvitamin D (25-OHD) deficiency caused by sunlight deprivation with compensatory hyperparathyroidism causes reduced BMD in elderly women with AD. This study was undertaken to address the possibility that sunlight exposure with calcium supplementation may maintain BMD and reduce the incidence of nonvertebral fractures in elderly women with AD. In a random and prospective study, AD patients were assigned to regular sunlight exposure (n = 132) or sunlight deprivation (n = 132) and followed for 1 year. BMD of the second metacarpal bone was measured using a computed X-ray densitometer (CXD). The CXD method measures BMD and cortical thickness at the middle of the second metacarpal bone on a radiogram of the hand and an aluminum step wedge as a standard (20 steps; 1 mm/step). Incidence of nonvertebral fractures in the two patient groups during the 1-year follow-up period was assessed. At baseline, average hospitalization period was 1.7 years in both groups, and activity of daily living (ADL) was decreased. Patients of both groups showed vitamin D deficiency caused by sunlight deprivation and decreased dietary intake of vitamin D with compensatory hyperparathyroidism. The exposed group patients were exposed to sunlight (3615 minutes/year). BMD increased by 2.7% in the sunlight-exposed group and decreased by 5.6% in the sunlight-deprived group (p < 0.0001). Serum 25-OHD level increased from 24.0 to 52.2 nM in the sunlight-exposed group. Eleven patients sustained fractures in the sunlight-deprived group, and three fractures occurred among the sunlight-exposed group (p = 0.0362; odds ratio = 3.7). Sunlight exposure can increase the BMD of vitamin D-deficient bone by increasing 25-OHD concentration and lead to the prevention of nonvertebral fractures.

RETRACTED: Risk factors for hip fracture among elderly patients with Alzheimer's disease

Incidence of hip fracture among patients with Alzheimer's disease (AD), especially in elderly patients, is high. To analyze risk factors of hip fracture, we prospectively studied a cohort of elderly female patients with AD. Subjects studied were 225 female patients with AD, and the average age was 76 years old. At baseline, we recorded body mass index (BMI), a score of Mini-Mental State Examination (MMSE) and bone mineral density (BMD), and measured serum concentrations of ionized calcium, intact parathyroid hormone (PTH), pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP), intact bone Gla protein (BGP), 25-hydroxyvitamin (25-OHD) and 1, 25-dihydroxyvitamin D (1, 25-[OH] 2D). The patients were followed for 2 years. During the 2-year study, hip fractures occurred in 29 patients. We compared baseline variables between the 29 patients with and 176 patients without hip fracture. AD patients with lower BMD, low concentrations of serum ionized calcium and 25-OHD (mean 3.0 ng/ml) with compensatory hyperparathyroidism were found to have an increased risk of hip fracture. Also, concentrations of serum ICTP and BGP were higher in the fracture group than in the nonfracture group. Elderly female AD patients with low BMD and serum 25-OHD concentrations <5 ng/ml with secondary hyperparathyroidism have a high risk of hip fracture, and the risk may be reduced by vitamin D supplementation.

RETRACTED: Risk factors for hip fracture among elderly patients with Parkinson's disease

Incidence of hip fracture among patients with Parkinson's disease (PD) is high, especially in elderly women. To determine the effects of various factors on hip fracture risk, we prospectively studied fractures in a group of 115 elderly patients of both genders with PD (46 men, 69 women; mean age, 71.9 years) for 1 year. At baseline, we recorded body mass index (BMI), Hoehn and Yahr stage, and postmenopausal interval, and also measured bone mineral density (BMD) and serum concentrations of ionized calcium, intact parathyroid hormone (PTH), pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP; a bone resorption marker), and 25-hydroxyvitamin D (25-OHD). During the year, hip fractures occurred in 18 patients (2 male and 16 female). We compared baseline variables between patients with and without hip fracture. PD patients with decreased BMI, lower BMD, and low concentrations of serum ionized calcium, and 25-OHD (mean 4.0 ng/ml) with compensatory hyperparathyroidism had increased risk of hip fracture. Female PD patients with long postmenopausal intervals also had increased hip fracture risk. BMI, illness duration, postmenopausal intervals, Hoehn and Yahr stage, 25-OHD, PTH, calcium and ICTP were determinants of BMD in patients with fracture. Elderly PD patients with low BMI, low BMD and serum 25-OHD concentrations ≤5 ng/ml with secondary hyperparathyroidism have increased risk of hip fracture, as do female PD patients with long postmenopausal intervals.

A duality in the roles of reactive oxygen species with respect to bone metabolism

Background: Rampant production in skeletal abnormalities can lead to hyperoxidant stress though the production of “reactive oxygen species” (ROS) by osteoclasts, which assist in bone remodeling under physiological conditions. Methods: Thirty cases each of post-menopausal osteoporosis, renal osteodystrophy and bone fractures constituted the test groups. Thirty healthy subjects made up the control group. Serum total alkaline phosphatase served as an index of osteoblastic activity. Serum calcium and phosphorous indicated bone remodeling status. Serum superoxide dismutase, glutathione peroxidase and glutathione reductase represented the enzymatic antioxidants. Results: Mean values for malondialdehyde were significantly elevated ( P<0.001) in test groups, indicating enhanced osteoclastic activity. Significantly depressed ( P<0.001) activities of superoxide dismutase and glutathione peroxidase reinforced hyperoxidant stress. Mean values of glutathione reductase remained unaltered. Diminished osteoblastic activity in post-menopausal osteoporosis was indicated by depressed alkaline phosphatase ( P<0.001). Increased serum calcium ( P<0.001) and decreased serum phosphorous ( P<0.001) in renal osteodystrophy indicated compensatory hyperparathyroidism. Conclusions: The findings indicate that ROS have a major role to play in bone metabolism.

RETRACTED: Abnormal bone and calcium metabolism in patients after stroke

To review how mineral stores and endocrine factors affect bone mass in poststroke patients immobilized by hemiparesis. Computer databases and published indexes. Case-control studies of hemiparetic poststroke patients examined regarding bone metabolism. References were obtained from MEDLINE; all data concerning the objective were used. Bone loss occurs in affected extremities after stroke. Immobilization from hemiplegia causes hypercalcemia. Insufficiency or deficiency of 25-hydroxyvitamin D (25-OHD) is very common in stroke patients and may be caused by poor dietary intake, decreased sunlight exposure, or both. Compensatory hyperparathyroidism may not occur because hypercalcemia inhibits the parathyroid glands even when 25-OHD is in the insufficient range. However, hyperparathyroidism does occur when 25-OHD is in the deficient range, in which case the parathyroid response to hypovitaminosis D overrides effects of hypercalcemia. Increased bone resorption was observed during the first year after stroke, declining to normal during the second year. During the first year, determinants of bone mineral density (BMD) in hands affected by hemiplegia were age, severity of hemiplegia, duration of paralysis, serum calcium concentration, and 25-OHD concentration. In the second year, BMD determinants on the hemiplegic side were severity of hemiplegia and 25-OHD concentration, whereas 25-OHD concentration was the only BMD determinant on the intact side. Administering 1alpha-hydroxyvitamin D3, vitamin K2, or ipriflavone ameliorated osteopenia on both sides and decreased the frequency of hip fracture on the hemiplegic side. Bone remodeling and determinants of bone mass for the affected and unaffected sides after stroke differ between the first and subsequent years.