Correlation between 25-hydroxyvitamin D levels and latitude in Brazilian postmenopausal women: from the Arzoxifene Generations Trial.

SUMMARY: We investigated vitamin D status in Brazilian cities located at different latitudes. Insufficiency (<50 nmol/L) was common (17 %), even in those living in a tropical climate. Vitamin D insufficiency increased as a function of latitude. Mean 25-hydroxyvitamin D (25(OH)D) levels in each site and latitude correlation were very high (r = -0.88; p=0.02). [corrected]. INTRODUCTION: Inadequate vitamin D, determined by low levels of 25(OH)D, has become very common despite the availability of sunlight at some latitudes. National data from a country that spans a wide range of latitudes would help to determine to what extent latitude or other factors are responsible for vitamin D deficiency. We investigated vitamin D status in cities located at different latitudes in Brazil, a large continental country. METHODS: The source is the Brazilian database from the Generations Trial (1,933 osteopenic or osteoporotic postmenopausal women (60 to 85 years old) with 25(OH)D measurements). 25(OH)D below 25 nmol/L (10 ng/mL) was an exclusion criterion. Baseline values were between fall and winter. The sites included Recife, Salvador, Rio de Janeiro, São Paulo, Curitiba, and Porto Alegre. Mean and standard deviation of 25(OH)D, age, spine and femoral neck T-score, calcium, creatinine, and alkaline phosphatase were calculated for each city. Pearson correlation was used for 25(OH)D and latitude. RESULTS: Insufficiency (<50 or <20 ng/mL) was common (329 subjects, 17 %). Vitamin D insufficiency increased as a function of latitude, reaching 24.5 % in the southernmost city, Porto Alegre. The correlation between mean 25(OH)D levels in each site and latitude was very high (r = -0.88, p < 0.0001). CONCLUSION: There is a high percentage of individuals with vitamin D insufficiency in Brazil, even in cities near the equator, and this percentage progressively increases with more southern latitudes.

Androgens and bone.

Testosterone is the major gonadal sex steroid produced by the testes in men. Androgens induce male sexual differentiation before birth and sexual maturation during puberty; in adult men, they maintain the function of the male genital system, including spermatogenesis. Testosterone is also produced in smaller amounts by the ovaries in women. The adrenal glands produce the weaker androgens dehydroepiandrosterone, dehydroepiandrosterone sulfate, and androstenedione. Because testosterone can be metabolized to estradiol by the aromatase enzyme, there has been controversy as to which gonadal sex steroid has the greater skeletal effect. In this respect, there is increasing evidence that at least part of the effects of androgens in men can be explained by their aromatization into estrogens. The current evidence suggests that estradiol plays a greater role in maintenance of skeletal health than testosterone, but that androgens also have direct beneficial effects on bone.

Osteoporosis after solid organ transplantation.

Osteoporosis and high risk of fractures have emerged as frequent and devastating complications of organ solid transplantation process. Bone loss after organ transplant is related to adverse effects of immunosuppressive drugs on bone remodeling and bone quality. Many factors contribute to the pathogenesis of osteoporosis in transplanted patients. This review address the mechanisms of bone loss that occurs both in the early and late post-transplant periods including the contribution of the immunosuppressive agents as well as the specific features to bone loss after kidney, lung, liver and cardiac transplantation. Therapy for bone loss and prevention of fragility fracture in the transplant recipient will also be discussed.

Chronic obstructive pulmonary disease is associated with osteoporosis and low levels of vitamin D.

UNLABELLED: We did a cross-sectional analysis of chronic pulmonary obstructive disease (COPD) patients without chronic use of systemic glucocorticoids (CUG). Osteoporosis was found in 51% and bone mineral density (BMD) was correlated with severity of disease. Low levels of vitamin D were found in 94%. All COPD patients may benefit from vitamin D supplementation and screening for low BMD. INTRODUCTION: Patients with chronic pulmonary obstructive disease have low bone mineral density, caused by chronic use of systemic glucocorticoids and hypovitaminosis D. However, patients without CUG may also have low BMD. METHODS: We performed a cross-sectional analysis in 49 patients (21 men, 28 postmenopausal women), with COPD without CUG, from Brazil (25 degrees 25' S). Several markers of bone metabolism were measured, plus BMD. Osteoporosis risk factors and history of fractures were investigated. Respiratory function was assessed by venous gasometry, spirometry, and oximetry. BMD results were compared to those of 40 healthy non-smokers controls. RESULTS: COPD patients had lower BMD at all sites (p < 0.01). Osteoporosis was observed in 51%. BMD independently correlated with stage of disease (lumbar spine, R = 0.38, p = 0.01; total femur, R = 0.36, p = 0.01; femoral neck, R = 0.40, p < 0.01). Ninety-four percent had low levels of vitamin D (<30 ng/mL) and 67% had secondary hyperparathyroidism. Vitamin D was correlated with oxygen saturation (R = 0.36, p = 0.01), with lower levels in those with saturation <88% (p = 0.01). CONCLUSION: Patients with COPD without CUG have increased risk for osteoporosis. Such patients have hypovitaminosis D, which is correlated with the severity of disease. Screening for low BMD and vitamin D supplementation may be warranted to all COPD patients.

Bone turnover 18 months after a single intravenous dose of zoledronic acid.

Zoledronic acid inhibits bone resorption for up to 12 months. It is not known whether the duration of this antiresorptive effect extends beyond this period of time. The aim of this study was to evaluate the changes in bone turnover at 12 months (T12) and 18 months (T18) after a single injection of 4 mg of zoledronic acid. It is a prospective, longitudinal study, with a follow-up for 18 months. We studied male and female patients (60.5 +/- 11.0 years old), with low bone mineral density (BMD) coming from the outpatient clinic in a metabolic bone unit of a tertiary care hospital. All patients received a single intravenous dose of 4 mg of zoledronic acid, bone turnover markers [serum carboxyterminal telopeptide of type I collagen (CTX-I), bone-specific alkaline phosphatase (BSAP)] and BMD [lumbar spine (LS) and total hip (TH)] were measured at baseline, and after 12 months (T12) and 18 months (T18). Median serum CTX-I and BSAP levels were suppressed at T12 in comparison with baseline values: 0.183 to 0.039 ng/ml for CTX-I (p = 0.0002) and 16.95 to 13.96 U/l for BSAP (p = 0.005). At T18, both CTX-I and BSAP continued to be suppressed below baseline at 0.108 ng/ml and 12.23 U/l (p = 0.009 and p = 0.02, vs. T0). Significant increases in BMD at T18 as compared with T12 were observed in patients (median increase 6.1% for LS and 2.0% for TH). Zoledronic acid inhibits bone turnover effectively for 12 months, with evidence for continued suppression and gains in BMD even after 18 months.