Factors associated with bone mineral density in adults: a cross-sectional population-based study.

OBJECTIVE: This study aimed to analyze the association between lumbar spine, femoral neck, total hip bone mineral density (biophysical bone health assessment parameter), and sociodemographic, anthropometric, behavioral, and health condition factors in Brazilian adults. METHOD: This is a cross-sectional, population-based study performed with individuals of both genders, aged between 20 and 59 (n=701). The dependent variables were evaluated by Dual Energy X-ray Absorptiometry. The independent variables were evaluated through a questionnaire, anthropometric evaluation and blood collection. The association between bone mineral density and the independent variables was evaluated by linear regression analysis. All analyses were stratified by gender. RESULTS: Men presented higher bone mineral density than women. Bone mineral density was inversely associated with age range and directly associated with nutritional status in both genders and in the three bone sites analyzed. In addition, 25 Hydroxyvitamin D deficient status among men and contraceptive use among women were associated with lower bone mineral density, and a significant association was only found with lumbar spine bone mineral density in women. CONCLUSION: The factors associated with bone health among men were age, skin color, nutritional status, and vitamin D status. For women, the associated factors with bone health were age, skin color, nutritional status and contraceptive use.

Relación entre Nivel de 25 (OH) D Vitaminas y Deterioro Cognitivo en Enfermedad renal Crónica (ERC) en pacientes en diálisis y sin diálisis mediante el uso de la prueba B / Relationship between Level of 25 (OH) D Vitamins and Cognitive Impairment in Chronic Kidney Disease (CKD) in Dialysis and NonDialysis Patients Using Trial Making Test B

Deficiency in vitamin D and cognitive dysfunction commonly are associated together in patients suffering from chronic kidney disease (CKD) in both dialysis and non-dialysis patients, vitamin D develop new protective regulatory roles in the functions of CNS. Combination of low levels of vitamin D and CKD can be enrolled for devastating and lead to sever cognitive dysfunction. Patients with CKD mostly associated with Hypovitaminosisand moreover common in elderly patients and related with cognitive decline, one of the hypotheses that CKD patients commonly have a low level of vitamin D and have potential experience in accelerated cognitive decline which rarely link on this topic. Most of CKD patients particularly sensitive for developing in the deficiency of vitamin D. Reduce vitamin D intake, male absorption in compromised GIT patients, loosing of vitamin D binding protein with urine, and α-hydroxylase enzyme reduction in the kidney all are the risk factors included in the causes of 25(OH) D vitamin decrease production. Aim of study: assess cognitive function by using one validated score: trial making test B in patients with CKD in both dialysis and non-dialysis. Patients and methods: a total of 54 patients with CKD and 57 patients with ESRD on hemodialysis enrolled in this study, where CKD defined as GFR < 60 ml/min by MDRD study. Exclusion criteria include CVA, deaf and blind, and low education patients. Cognitive functions assessment done for patients who are on hemodialysis and non- dialysis by using trial B testing, this second assess spatial scanning concentration and executive function by time measuring that needed to connect the series of numbered that are sequentially and littered circles. Catastrophic shorter time completion with a maximum of 300 second indicates better performance. 25 (OH) D vitamins has assessed from each patients using direct immunoassay method, with assay at 4-110 ng/ml. Results: for patients on hemodialysis 27 (39.7%) has deficient 25(OH) D vitamin status 25 (36.7%) insufficient,20 (29.4%) had sufficient vitamin D levels, significant low level in patients on hemodialysis in comparison to those with non-hemodialysis. Trial making test B score was significantly lower in dialysis patients, significant correlation between cognitive function assessment (trial making test B) and low vitamin D level. Conclusions: the prevalence of deficiency in vitamin D in CKD especially hemodialysis patients associated with cognitive decline.

The relationship among vitamin D, TLR4 pathway and preeclampsia.

Preeclampsia is a pregnancy-specific syndrome that has been the greatest cause of maternal and fetal morbidity and mortality. The impaired outcomes are related to maternal and the offspring healthy in the short and long-term. Although preeclampsia origins remain unclear, it is well known that there is impaired trophoblast invasion with culminant abnormal immune response. The early and late-onset preeclampsia have been studied, the subtypes have the same difference in the placentation and inflammatory features. Dietary compounds can stimulate or inhibit the activation of immune cells. Low vitamin D intake has been linked to impaired fetal development, intrauterine growth restriction, and preeclampsia. Vitamin D has been described as an anti-inflammatory effect. It can downregulate pro-inflammatory cytokines expression by the inhibition of the Nuclear Factor-ĸB pathway signaling cascade. High vitamin D levels could attenuate the immune response. On the other hand, vitamin D deficiency may contribute to increasing pro-inflammatory state. In preeclampsia, there is a reduced expression of vitamin D receptor and its metabolism is disrupted. In this review, we aimed to discuss the role of vitamin D as an anti-inflammatory agent in relation to the pro-inflammatory process of preeclampsia through the activation of the TLR4 pathway. Although there are limited studies showing the relation between vitamin D and lower risk of preeclampsia, the maternal status of vitamin D seems to influence the risk of PE development. Therefore, vitamin D supplementation in women may be a strategy to improve pregnancy outcomes.

Vitamin D-RAAS Connection: An Integrative Standpoint into Cardiovascular and Neuroinflammatory Disorders.

BACKGROUND: The neuroinflammatory process is associated with the pathogenesis of many cardiovascular disorders, particularly with hypertension. In this regard, the deficiency of vitamin D seems to increase the risk of cardiovascular pathologies related to neuroinflammation. Long-term lack of vitamin D leads to over-activation of the renin-angiotensin-aldosterone system (RAAS), one of the essential mechanisms of blood pressure regulation. PURPOSE OF REVIEW: This review summarizes the latest studies carried out to evaluate the primary mechanisms underlying the neuroprotective effect of vitamin D and its receptors (VDR) in the central nervous system. Besides, the present article condenses the evidence supporting the link between vitamin D and the RAAS in hypertension and neuroinflammation. Highlights Standpoints: Vitamin D deficiency is highly prevalent in the world, and the rising prevalence of neuroinflammatory diseases and associated pathologies such as hypertension around the world justifies the urgent need of searching new and more effective therapeutic methods that could be related to RAAS modulation and vitamin D levels management.

Vitamin D Deficient Older Adults Are More Prone to Have Metabolic Syndrome, but Not to a Greater Number of Metabolic Syndrome Parameters.

This study investigated the relationship between metabolic parameters and low serum 25-hydroxyvitamin D (25(OH)D) levels in older adults (n = 265). They were assessed for anthropometrics and metabolic measurements, including 25(OH)D, insulin, glucose, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) and other inflammatory markers. Vitamin D deficiency was defined as a 25(OH)D level below 50 nmol/L. Comparisons between groups were performed using Wilcoxon-Mann-Whitney or Pearson's Chi-squared test. A multivariate adjusted Poisson regression was used to model the number of metabolic parameters as a function of a set of explanatory variables. Subjects with 25(OH)D deficiency were predominantly females and presented higher body weight, body mass index, waist circumference, triglycerides and Tumor Necrosis Factor-α (TNF-α), and higher insulin resistance. Metabolic syndrome was also more prevalent among 25(OH)D-deficient subjects. In those without metabolic syndrome, 25(OH)D deficiency was related only to obesity and higher insulin resistance. Female sex, hypertension, higher waist circumference and higher levels of hemoglobin A1C (%), HDL-C, and TG were significantly associated with an increased number of metabolic syndrome parameters after adjusting for covariates, but 25(OH)D was not. The fact that serum 25(OH)D concentration was inversely associated with metabolic syndrome and insulin resistance not only reaffirms the relevance to consider serum 25(OH)D concentration as an influencing factor for insulin resistance, but also the need to actively screen for hypovitaminosis D in all patients with this condition.

Prevalence and factors associated with hypovitaminosis D in adolescents from a sunny country: Findings from the ERICA survey.

Vitamin D plays a role in bone and metabolic health in life long, however hypovitaminosis D is common in different settings. The aim of this study was to describe vitamin D status among adolescents from a large sunny country and analyze associated factors. This was a multicenter, cross-sectional, school-based study. A total of 1152 adolescents age 12-17 from four Brazilian cities, Rio de Janeiro, Fortaleza, Brasília, and Porto Alegre, were included. Anthropometric variables, diet, type of school, race and season of data collection were evaluated. Serum concentrations of 25-hydroxyvitamin D [25(OH)D] were measured and categorized into three levels: ≤ 20 ng/mL, 21-29 ng/mL and ≥ 30 ng/mL. Ordered logistic regression models were used to explore the factors associated with hypovitaminosis D. The prevalence of vitamin D levels below 20 ng/mL, between 21 and 29 ng/mL and above 30 ng/mL was 21 % (95 %CI: 19 %-24 %), 42 % (95 %CI: 39 %-46 %) and 37 % (95 %CI: 33 %-40 %), respectively. In the final adjusted model, hypovitaminosis D was positively associated with gender, center (latitudes), data collected in winter or spring, non-whites, and private school students. A higher proportional odds ratio (POR) for hypovitaminosis D was found among obese boys (POR = 2.2, 95 %CI: 1.1-4.5), but not girls. Adequate dietary intake of vitamin D was a protective factor (POR = 0.4, 95 %CI: 0.2-0.6) against hypovitaminosis D. In conclusion, there is a high prevalence of Brazilian adolescents at risk of hypovitaminosis D, independent of region. Due to their potential benefits, lifestyle changes should be stimulated, including healthier food choices and spending more time outdoors (with sun protection).

Vitamin D deficiency contributes to vascular damage in sustained ischemic acute kidney injury.

Reductions in renal microvasculature density and increased lymphocyte activity may play critical roles in the progression of chronic kidney disease (CKD) following acute kidney injury (AKI) induced by ischemia/reperfusion injury (IRI). Vitamin D deficiency is associated with tubulointerstitial damage and fibrosis progression following IRI-AKI We evaluated the effect of vitamin D deficiency in sustained IRI-AKI, hypothesizing that such deficiency contributes to the early reduction in renal capillary density or alters the lymphocyte response to IRI Wistar rats were fed vitamin D-free or standard diets for 35 days. On day 28, rats were randomized into four groups: control, vitamin D deficient (VDD), bilateral IRI, and VDD+IRI Indices of renal injury and recovery were evaluated for up to 7 days following the surgical procedures. VDD rats showed reduced capillary density (by cablin staining), even in the absence of renal I/R. In comparison with VDD and IRI rats, VDD+IRI rats manifested a significant exacerbation of capillary rarefaction as well as higher urinary volume, kidney weight/body weight ratio, tissue injury scores, fibroblast-specific protein-1, and alpha-smooth muscle actin. VDD+IRI rats also had higher numbers of infiltrating activated CD4(+) and CD8(+) cells staining for interferon gamma and interleukin-17, with a significant elevation in the Th17/T-regulatory cell ratio. These data suggest that vitamin D deficiency impairs renal repair responses to I/R injury, exacerbates changes in renal capillary density, as well as promoting fibrosis and inflammation, which may contribute to the transition from AKI to CKD.

Adverse effects of vitamin D deficiency on the Pi3k/Akt pathway and pancreatic islet morphology in diet-induced obese mice.

SCOPE: To investigate the impact of vitamin D deficiency on insulin resistance and abnormal glucose homeostasis in obesity. METHODS AND RESULTS: Sixty male C57BL/6 mice (3 months old) were fed a control diet (C-10% energy as fat) or a high-fat diet (HF-50% energy as fat), with or without vitamin D, for 8 weeks. There was no difference in body mass between the HF and HF/VitD- groups. Vitamin D deficiency (VitD) in the diet-induced obese mice increased hyperinsulinemia (p = 0.04), hyperleptinemia (p = 0.0002), insulin resistance (HOMA-IR, p = 0.04), and islet changes, including alpha and beta cell disarray. In the insulin signaling pathway, insulin receptor substrate 2 expression was upregulated in the C/VitD- group (p = 0.001) and downregulated in the HF/VitD- group (p = 0.009). Interestingly, forkhead box protein O1 expression was higher in the HF/VitD- group than in the HF group (p = 0.03), and pancreatic and duodenal homeobox 1 expression was lower in the HF/VitD-group than in the HF group (p = 0.025), indicating that the HF diet and vitamin D deficiency influenced the downregulation of the expression of these proteins (two-way ANOVA, p < 0.0001). CONCLUSION: Vitamin D deficiency exacerbated the adverse structural and physiological remodeling of pancreatic islets due to obesity, contributing to abnormal glucose homeostasis.

[VITAMIN D AND ITS RELATION WITH THE ANATOMICAL LOCATION OF HIP FRACTURE IN CHILEAN OLDER ADULTS HOSPITALIZED]. / VITAMINA D Y SU RELACIÓN CON LA UBICACIÓN ANATÓMICA DE LA FRACTURA DE CADERA EN ADULTOS MAYORES CHILENOS HOSPITALIZADOS.

INTRODUCTION: in older adults, deficit of Vitamin D and hip fractures are common. There exists relationships between both conditions, and it have been shown that supplementation of Vitamin D improve prognosis of hip fractures. In the case of Chile, information about relationship between Vitamin D and hip fractures is scarce. OBJECTIVE: quantify plasma levels of vitamin D and relate them to the anatomical location of hip fracture. METHODS: cross-sectional study. 222 Chilean adults ≥60 years, hospitalized for hip fracture between June, 2014 and June, 2015. We use data of medical records about gender, age, seasonality and anatomical location of hip fracture (intra and extracapsular). We measure plasmatic levels of Vitamin D (PLVD) and glomerular filtration rate (GFR) (MDRD-6). Kolmogorov-Smirnov test and non-parametric test were used. For determine relations between PLVD and anatomical location we use linear regression. RESULTS: there was a predominance of women (80.6%). The average age was 80.7 years (SD=7.8). Intracapsular hip fractures were 43.2%. 80% of the sample presents Vitamin D in deficitary levels (n = 180). PLVD average was 13.3 ng/cc (SD=6.7), in subjects with intracapsular fractures were significantly lower (p<0.001). CONCLUSIONS: PLVD in subjects with hip fracture should be monitored, as there are differences according to anatomical location of the fracture. This precedent could favor the treatment and recovery of subjects presenting for the first time hip fracture.

Introducción: en los adultos mayores son frecuentes el deficit de vitamina D y las fracturas de cadera (FC). Existe relacion entre ambas condiciones, demostrandose que la suplementacion de vitamina D mejora el pronostico de las FC. En el caso de Chile, existe escasa informacion sobre la relacion entre vitamina D y FC. Objetivo: cuantificar los niveles plasmaticos de vitamina D (NPVD) y relacionarlos con la ubicacion anatomica de la FC. Métodos: estudio transversal. 222 adultos mayores chilenos ≥60 anos hospitalizados por FC entre junio de 2014 y junio de 2015. Se utilizaron los datos de ficha clinica de genero, edad, estacionalidad y ubicacion anatomica (FIC = intra, FEC = extracapsular) de la FC. Se midio NPVD y velocidad de filtrado glomerular (VFG) (MDRD- 6). Se utilizaron la prueba de Kolmogorov-Smirnov y pruebas no parametricas. Para determinar la relacion entre NPVD y el tipo de fractura se uso regresion lineal. Resultados: hubo predominio de mujeres (80,6%), la edad promedio fue 80,7 anos (DE=7,8) y se encontro 43,2% de FIC. Los NPVD promedio fueron 13,3 ng/cc (DE=6,7); los sujetos con FIC tienen 4,52 ng/cc menos de vitamina D que aquellos con FEC (p.

Cerebrovascular correlates of vitamin D deficiency in older adults living near the Equator: results from the Atahualpa Project.

All studies attempting to find an association between vitamin D deficiency and cerebrovascular diseases have been conducted at latitudes far away from the Equator, where living conditions, cardiovascular risk factors, and sunshine exposure are different from tropical regions. We aimed to assess cerebrovascular correlates of vitamin D deficiency in community-dwelling older adults living in Atahualpa, a village located in rural coastal Ecuador. Out of 267 individuals enrolled in the neuroimaging substudy of the Atahualpa Project, 220 (82%) signed the informed consent. Mean age of participants was 70·9 ± 7·8 years, and 126 (57%) were women. Fifty-four (25%) persons have vitamin D levels <20 ng/ml, 47 (21%) had ischemic strokes, and 53 (24%) had moderate-to-severe white matter hyperintensities of presumed vascular origin. Exposure effect models constructed with vitamin D deficiency as the exposure, white matter hyperintensities and ischemic stroke as the outcomes, and confounders--age, gender, body mass index, physical activity, blood pressure, fasting glucose, total cholesterol, ionized calcium, phosphorus, intact parathormone, and serum creatinine--as independent variables revealed a significant association of vitamin D deficiency with white matter hyperintensities (P = 0·006) but not with ischemic strokes (P = 0·359). This study shows an association of vitamin D deficiency with diffuse subcortical brain damage in older adults living in a tropical region. Lack of awareness of the importance of vitamin D deficiency might be one of the factors influencing the high prevalence of white matter hyperintensities of presumed vascular origin in underserved Latin American populations.

Vitamin D-mediated immune regulation in multiple sclerosis.

Although Vitamin D is best known as a modulator of calcium homeostasis, it also has immune modulating potential. A protective effect of Vitamin D on Multiple Sclerosis (MS) is supported by the reduced risk associated with sun exposure and use of Vitamin D supplements. Moreover, high circulating levels of Vitamin D have been associated with lower risk of MS. To gain more insight into putative regulatory mechanisms of Vitamin D in MS pathogenesis, we studied 132 Hispanic patients with clinically definite MS, 58 with relapsing remitting MS (RR MS) during remission, 34 RR MS patients during relapse, and 40 primary progressive MS cases (PP MS). Sixty healthy individuals matched with respect to place of residence, race/ethnicity, age and gender served as controls. Levels of 25(OH) Vitamin D and 1,25(OH)(2) Vitamin D, measured by ELISA were significantly lower in RR MS patients than in controls. In addition, levels in patients suffering relapses were lower than during remissions. By contrast, PP MS patients showed similar values to controls. Proliferation of both freshly isolated CD4+ T cells and MBP-specific T cells was significantly inhibited by 1,25(OH)(2) Vitamin D. Moreover, activated Vitamin D enhanced the development of IL-10 producing cells, and reduced the number of IL-6 and IL-17 secreting cells. Notably, VDR expression was induced by 1,25(OH)(2) Vitamin D in both activated and resting cells. Interestingly, T cells were able to metabolize 25(OH) Vitamin D into biologically active 1,25(OH)(2) Vitamin D, since T cells express 1α-hydroxylase constitutively. Finally, 1,25(OH)(2) Vitamin D also increased the expression and biological activity of IDO, triggering significant increase in the number of CD4+CD25+ T regulatory cells. Collectively, these findings suggest that 1,25(OH)(2) VitaminD plays an important role in T cell homeostasis during the course of MS, suggesting correction of its deficiency may be useful during treatment of the disease.

Hypovitaminosis D is associated with systemic inflammation and concentric myocardial geometric pattern in hemodialysis patients with low iPTH levels.

BACKGROUND: Vitamin D [25(OH)D] deficiency is a cardiovascular risk factor in the hemodialysis (HD) population. The aim of this study was to identify hypovitaminosis D in HD patients without signs of hyperparathyroidism and to analyze its association to inflammation and echocardiographic alterations. METHODS: Patients on HD with iPTH <300 pg/ml not receiving vitamin D therapy were recruited. Hypovitaminosis D was defined as 25(OH)D <30 ng/ml. High-sensitivity C-reactive protein, interleukin-6 and serum albumin were used as inflammation markers. Echocardiograms were performed in an interdialytic mid-week day. RESULTS: Sixty-one patients (mean age of 56 ± 15 years, 52% males, 93% Caucasians, 31% diabetic) were included, and 75% presented hypovitaminosis D. Inflammation was more prevalent among those with hypovitaminosis D, and these patients presented higher relative wall thickness (0.48 ± 0.11 vs. 0.42 ± 0.10 mm; p = 0.05) and lower left ventricular diastolic (49.8 ± 6.2 vs. 54.7 ± 5.8 mm; p = 0.013) and systolic (31.9 ± 5.7 vs. 36.8 ± 7.2 mm; p = 0.012) diameters. CONCLUSIONS: Hypovitaminosis D is associated with inflammation and concentric geometric pattern of the left ventricle, even in the absence of high iPTH levels. Vitamin D repletion (aiming to reduce cardiovascular complications) should also be considered in HD patients with normal or low iPTH levels.

Low bone mass in juvenile onset sclerosis systemic: the possible role for 25-hydroxyvitamin D insufficiency.

Juvenile onset systemic sclerosis (JoSSc) is a rare disease, and there are no studies focusing in bone mineral density and biochemical bone parameters. Ten consecutive patients with JoSSc and 10 controls gender, age, menarche age, and physical activity matched were selected. Clinical data were obtained at the medical visit and chart review. Laboratorial analysis included autoantibodies, 25-hydroxyvitamin D (25OHD), intact parathyroid hormone, calcium, phosphorus, alkaline phosphatase and albumin sera levels. Bone mineral density was analyzed by dual-energy X-ray absorptiometry, and bone mineral apparent density (BMAD) was calculated. A lower BMAD in femoral neck (0.294 ± 0.060 vs. 0.395 ± 0.048 g/cm(3), P = 0.001) and total femur (0.134 ± 0.021 vs. 0.171 ± 0.022 g/cm(3), P = 0.002) was observed in JoSSc compared to controls. Likewise, a trend to lower BMAD in lumbar spine (0.117 ± 0.013 vs. 0.119 ± 0.012 g/cm(3), P = 0.06) was also found in these patients. Serum levels of 25OHD were significantly lower in JoSSc compared to controls (18.1 ± 6.4 vs. 25.1 ± 6.6 ng/mL, P = 0.04), and all patients had vitamin D insufficiency (<20 ng/mL) compared to 40% of controls (P = 0.01). All other biochemical parameters were within normal range and alike in both groups. BMAD in femoral neck and total femur was correlated with 25OHD levels in JoSSc (r = 0.82, P = 0.004; r = 0.707, P = 0.02; respectively). We have identified a remarkable high prevalence of 25OHD insufficiency in JoSSc. Its correlation with hip BMAD suggests a causal effect and reinforces the need to incorporate this hormone evaluation in this disease management.

From mild to severe primary hyperparathyroidism: The Brazilian experience.

Primary hyperparathyroidism often presents as an asymptomatic disorder. In our institution, routine serum calcium measurements have now been used as part of medical examination for 23 years. Out of 124 patients consecutively seen at our institution, 47% presented with no symptoms related to the disease, while 25% presented with severe skeletal involvement and osteitis fibrosa cystica, 25% with renal stone disease without overt bone involvement, and 2% with the typical neuropsychiatric syndrome. This same pattern is seen in the city of São Paulo. In severe disease pathological fractures are frequently seen, especially in long bones of the lower extremities, and also loss of lamina dura of the teeth and salt-and-pepper appearance of the skull. Bone mineral density is extremely low in these patients but usually show remarkable recovery following surgical cure. Serum PTH and bone markers are considerable higher in severely affected patients, who also have a high rate of vitamin D deficiency, and the parathyroid lesion is easier located compared with asymptomatic patients. From pathological specimens 87% had histological confirmation of a single adenoma, 6.4% multiple gland hyperplasia and 3.8% carcinoma.

From mild to severe primary hyperparathyroidism: the Brazilian experience / Do hiperparatiroidismo primário leve ao severo: a experiência brasileira

Primary hyperparathyroidism often presents as an asymptomatic disorder. In our institution, routine serum calcium measurements have now been used as part of medical examination for 23 years. Out of 124 patients consecutively seen at our institution, 47 percent presented with no symptoms related to the disease, while 25 percent presented with severe skeletal involvement and osteitis fibrosa cystica, 25 percent with renal stone disease without overt bone involvement, and 2 percent with the typical neuropsychiatric syndrome. This same pattern is seen in the city of São Paulo. In severe disease pathological fractures are frequently seen, especially in long bones of the lower extremities, and also loss of lamina dura of the teeth and salt-and-pepper appearance of the skull. Bone mineral density is extremely low in these patients but usually show remarkable recovery following surgical cure. Serum PTH and bone markers are considerable higher in severely affected patients, who also have a high rate of vitamin D deficiency, and the parathyroid lesion is easier located compared with asymptomatic patients. From pathological specimens 87 percent had histological confirmation of a single adenoma, 6.4 percent multiple gland hyperplasia and 3.8 percent carcinoma.

Na maioria dos relatos da literatura recente, o hiperparatiroidismo primário apresenta-se, com freqüência, na forma assintomática. Em nossa instituição utilizamos a determinação rotineira do cálcio sérico há 23 anos. Em nossa série de 124 casos consecutivos, 45 por cento não apresentavam sintomas relacionados com a doença, 25 por cento tinham envolvimento esquelético intenso com osteíte fibrosa cística, 25 por cento tinham nefrolitíase sem envolvimento ósseo severo, e 2 por cento apresentavam a síndrome neuro-psiquiátrica típica. Esse mesmo padrão tem sido observado na cidade de São Paulo. Na doença severa são freqüentes as fraturas patológicas, especialmente nos ossos longos dos membros inferiores, como também a reabsorção da lâmina dura dos dentes e o aspecto em "sal e pimenta" nas radiografias do crânio. A densidade mineral óssea mostra-se extremamente reduzida nesses pacientes, mas em geral exibe melhora marcante após a cura cirúrgica. O PTH no soro e os marcadores bioquímicos da remodelação óssea estão significativamente mais altos nos pacientes com doença severa, os quais freqüentemente apresentam deficiência de vitamina D e localização mais fácil da lesão paratiroideana, quando comparados aos pacientes assintomáticos. Ao exame anátomo-patológico, 87 por cento tiveram confirmação de adenoma único, 6,4 por cento hiperplasia glandular difusa e 3,8 por cento carcinoma.

Vitamin D insufficiency reduces the protective effect of bisphosphonate on ovariectomy-induced bone loss in rats.

The present study was carried out to obtain an experimental model of vitamin D (vit D) insufficiency and established osteopenia (experiment 1) to then investigate whether vit D status, i.e. normal or insufficient, interferes with bone mass recovery resulting from bisphosphonate therapy (experiment 2). Rats (n = 40) underwent OVX (n = 32) or a sham operation (n = 8). The first 15 days post-surgery, all groups were kept under fluorescent tube lighting and fed a diet containing 200 IU% vit D (+D). They were then assigned during an additional 45 days to receive either +D or a diet lacking vit D (-D) and kept under 12 h light/dark cycles using fluorescent or red lighting. Serum 25HOD was significantly lower in -D rats (P < 0.0001). The type of lighting did not induce differences in 25OHD, calcium (sCa), phosphorus (sP), bone alkaline phosphatase (b-AL), CTX, bone density or histology. No osteoid was observed in undecalcified bone sections. Experiment 2 (105 days): rats were fed either +D or -D according to experiment 1 and were treated with either placebo or 16 mug olpadronate (OPD)/100 g rat/week during the last 45 days. Whereas 25HOD was significantly lower (P < 0.0001) in -D/OPD than in +D/OPD rats, no significant differences in sCa, sP, b-AL or CTX were observed. OPD prevented the loss of lumbar spine (LS) and proximal tibia (PT) BMD and the decrease in bone volume (BV/TV) (P < 0.05) and in the number of trabeculae observed in untreated rats. However, +D/OPD animals presented significantly higher values of LS BMD, PT BMD and BV/TV than -D/OPD rats (P < 0.05). No osteoid was observed in undecalcified sections of bone. In summary, this is the first experimental study to provide evidence that differences in vit D status may affect the anticatabolic response to bisphosphonate treatment. However, the molecular mechanism through which vit D insufficiency reduces the effect of the aminobisphosphonate remains to be defined.