Association of Glucocorticoid Use and Low 25-Hydroxyvitamin D Levels: Results from the National Health and Nutrition Examination Survey (NHANES): 2001-2006
Division of Pediatric Nephrology, Albert Einstein College of Medicine, The Children's Hospital at Montefiore, Bronx, New York 10467, USA. The Journal of Clinical Endocrinology and Metabolism
(Impact Factor: 6.21).
09/2011; 96(12):3838-45. DOI: 10.1210/jc.2011-1600
In many disorders requiring steroid therapy, there is substantial decrease in bone mineral density. The association between steroid use and 25-hydroxyvitamin D [25(OH)D] deficiency has not been confirmed in large population-based studies, and currently there are no specific vitamin D recommendations for steroid users.
The aim of the study was to evaluate the association of serum 25(OH)D deficiency [defined as 25(OH)D <10 ng/ml] with oral steroid use.
Cross-sectional analysis was performed using NHANES 2001-2006.
We analyzed a nationally representative sample of U.S. children and adults.
The study sample consisted of children, adolescents, and adults from NHANES 2001-2006 (n = 22,650), representative of 286 million U.S. residents, with serum 25(OH)D levels and data on other potential confounders.
We measured serum 25(OH)D levels below 10 ng/ml.
A total of 181 individuals (0.9% of the population) used steroids within the past 30 d. Overall, 5% of the population had 25(OH)D levels below 10 ng/ml. Among steroid users, 11% had 25(OH)D levels below 10 ng/ml, compared to 5% among steroid nonusers (P = 0.009). The odds of having 25(OH)D deficiency were 2-fold higher in those who reported steroid use compared to those without steroid use [odds ratio (OR), 2.36; 95% confidence interval (CI), 1.25, 4.45]. This association remained after multivariable adjustment (OR, 2.21; 95% CI, 1.01, 4.85) and in a multivariable model using NHANES III data (OR, 1.88; 95% CI, 1.01, 3.48).
Steroid use is independently associated with 25(OH)D deficiency in this nationally representative cohort limited by cross-sectional data. It suggests the need for screening and repletion in patients on chronic steroids.
Available from: Hiroshi Kaji
- "Our previous study revealed that femoral neck BMD was negatively related to percent LBM in postmenopausal women with glucocorticoid treatment, although the influence of body composition on vertebral fracture risk seemed to differ depending on age. Moreover, glucocorticoid use was independently related to 25(OH)D deficiency in a large, nationally representative sample of children and adults, although vitamin D deficiency affects both muscle and bone. "
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ABSTRACT: The clinical significance of sarcopenia and osteoporosis has increased with the increase in the population of older people. Sarcopenia is defined by decreased muscle mass and impaired muscle function, which is related to osteoporosis independently and dependently. Numerous lines of clinical evidence suggest that lean body mass is positively related to bone mass, which leads to reduced fracture risk. Genetic, endocrine and mechanical factors affect both muscle and bone simultaneously. Vitamin D, the growth hormone/insulin-like growth factor I axis and testosterone are physiologically and pathologically important as endocrine factors. These findings suggest the presence of interactions between muscle and bone, which might be very important for understanding the physiology and pathophysiology of sarcopenia and osteoporosis. Muscle/bone relationships include two factors: local control of muscle to bone and systemic humoral interactions between muscle and bone. As a putative local inducer of muscle ossification, we found Tmem119, a parathyroid hormone-responsive osteoblast differentiation factor. Moreover, osteoglycin might be one of the muscle-derived humoral bone anabolic factors. This issue may be important for the development of novel drugs and biomarkers for osteoporosis and sarcopenia. Further research will be necessary to clarify the details of the linkage of muscle and bone.
Available from: John Lally
- "Neither was there an effect due to treatment with antipsychotics observed. No patients were treated with corticosteroids at the time of the study, which can also be associated with vitamin D deficiency (Skversky et al., 2011). There are difficulties inherent to the measurement and interpretation of vitamin D levels (Harvey and Cooper, 2012; Rosen, 2011) with a lack of unanimity on the best tests or range of tests to use. "
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ABSTRACT: Vitamin D deficiency is seen in a high proportion of people with established psychotic disorders, but it is not known if this is present at onset of the illness. We set out to examine vitamin D levels in people with their first episode of psychosis (FEP).
We conducted a matched case-control study to examine vitamin D levels and rates of vitamin D deficiency in sixty nine patients presenting with their FEP and sixty nine controls matched for age, sex and ethnicity. Differences between groups were tested using student's-t tests, paired t-tests and odds ratios for further analysis.
Vitamin D levels were significantly lower in cases than in controls (p<0.001). The odds ratio of being vitamin D deficient was 2.99 in the FEP group relative to the control group. There was no correlation between vitamin D levels and length of hospitalisation in the patient group (r=-0.027, p=0.827).
We found higher rates of vitamin D deficiency in people with FEP compared to matched controls. Given that vitamin D is neuroprotective; that developmental vitamin D deficiency may be a risk factor for psychosis, and that incipient psychosis may affect lifestyle factors and diet, future studies are required to examine this association further. In the meantime, there is a need for more widespread testing of vitamin D levels in FEP and for the development of appropriate management strategies.
Available from: PubMed Central
- "Haglin et al.  hypothesize that the mechanism that cause hypophosphatemia in relation to obesity is an overconsumption of a diet with low nutrient density or phosphate depletion due to low protein intake and in animal experiments, hypophosphatemia is associated with glucose uptake  and hypophosphatemia is related to reduced glucose tolerance . Lastly, we did not find any association between phosphate levels and steroid use, in contrast with the study by Skversky et al., which found an inverse association between steroid use and vitamin D levels . "
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ABSTRACT: Hyperphosphatemia, serum phosphorus >=4.4mg/dL, is associated with increased risk for chronic kidney disease and cardiovascular disease. Previous studies have shown a weak association between dietary phosphorus intake and serum phosphorus concentrations. While much less common in the general population, hypophosphatemia (<2.5mg/dL) may be associated with metabolic syndrome and obesity.
Using three cycles from the National Health and Nutrition Examination Survey (NHANES) (2005--2010), this study evaluated independent risk factors for hyperphosphatemia and hypophosphatemia.
Risk factors for hyperphosphatemia included higher adjusted calcium (OR 2.90, 95%CI 2.43-3.45), increasing cholesterol (OR 1.003, 95%CI 1.001-1.005), female gender (OR 1.61, 95%CI 1.39-1.87) and low hemoglobin (OR 1.52, 95%CI 1.17-1.98). Advanced age was protective (OR 0.98, 95%CI 0.977-0.987). Models that included fasting serum glucose found lower body mass index (BMI) to be protective (OR 0.97, 95%CI 0.96-0.99) and adjusting for serum vitamin D and parathyroid hormone removed the association with low hemoglobin and BMI. Risk factors for hypophosphatemia included the following protective factors: higher albumin (OR 0.56, 95%CI 0.35-0.93), higher BUN (OR 0.90, 95%CI 0.86, 0.95), corrected calcium (OR 0.38, 95%CI 0.23-0.63) and female gender (OR 0.47, 95% 0.24-0.94). In men, higher fasting glucose levels increased risk (OR 1.01, 95%CI 1.0004-1.01).
This study is the first to show an association between low hemoglobin levels and increased risk for hyperphosphatemia among individuals without chronic kidney disease. We did not find any association between diabetes mellitus, increasing BMI or fasting glucose levels and hypophosphatemia.
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