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Hypovitaminosis D (hypovitaminosis + d)

Distribution by Scientific Domains

Medical Sciences	92%

Selected Abstracts

The prevalence of vitamin D abnormalities in South Asians with type 2 diabetes mellitus in the UK

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 3 2010
A. A. Tahrani
Summary Background:, The high prevalence of both hypovitaminosis D and type 2 diabetes (T2DM) in the Asian community is well recognised, but the impact of diabetes on vitamin D status and vice versa, has not been well reported. Aims:, To determine the prevalence of hypovitaminosis D in Asian patients with T2DM and its impact on glycaemic control. Methods:, A cross-sectional study was conducted in a tertiary referral centre in the UK. Two hundred and ten Asian patients aged more than 40 years were included (170 with and 40 without T2DM). Each had a standard bone profile (serum calcium, phosphate and alkaline phosphatase), serum parathyroid hormone and 25-hydroxycholecalciferol. Results:, The prevalence of low serum 25-hydroxyvitamin D (< 50 nmol/l) was high in the group as a whole (> 80%) and more common in diabetics compared with controls (83% vs. 70%; p = 0.07). This was particularly so in men (82.5% vs. 57.9%; p = 0.02). HbA1c was higher in women with vitamin D deficiency (< 12.5 nmol/l) (8.11 ± 1.11% vs. 7.33 ± 1.32%, p = 0.046). In logistic regression analysis, T2DM was an independent predictor of hypovitaminosis D. In linear regression analysis, vitamin D deficiency was independently related to HbA1c in women with T2DM. Conclusions:, Hypovitaminosis D remains a major public health issue in the Asian population and is exaggerated in patients with T2DM. The fact that vitamin D deficient women had higher HbA1c levels raises the possibility that vitamin D replacement may improve glycaemic control. [source]

A high prevalence of hypovitaminosis D in Finnish medical in- and outpatients

JOURNAL OF INTERNAL MEDICINE, Issue 6 2001
R. Kauppinen-Mäkelin
Abstract.,Kauppinen-Mäkelin R, Tähtelä R, Löyttyniemi E, Kärkkäinen J, Välimäki MJ (Peijas Hospital, Vantaa; United Laboratories, Leiras Research, and Division of Endocrinology; Helsinki University Central Hospital, Helsinki, Finland). A high prevalence of hypovitaminosis D in Finnish medical in- and outpatients. J Intern Med 2001; 249: 559,563. Objective.,To study the prevalence of hypovitaminosis D [serum 25(OH)D , 37 nmol L,1)] in Finnish medical in- and outpatients in a cross-sectional study. Methods.,The subjects were 106 consecutive medical inpatients (57 females, 49 males with mean ages of 65 and 58 years) from the Peijas Hospital, Vantaa, Finland, and 99 ambulatory patients (48 females, 51 males with mean ages of 42 and 46 years) contacting a private outpatient centre in Helsinki, Finland. Serum 25(OH)D, vitamin D binding protein (DBP), free vitamin D index (FDI), intact PTH (iPTH), and albumin-corrected calcium were measured. Results.,Serum 25-hydroxyvitamin D [25(OH)D] was 37 nmol L,1 or less in 70% of female and in 61% of male inpatients and in 44% of female and in 37% of male outpatients. In the whole population, a statistically significant inverse association (P < 0.0001) was detected between iPTH and 25(OH)D levels; the iPTH concentration appeared to start increasing when 25(OH)D concentration was 50 nmol L,1 or less. The association remained the same (P < 0.0001) when FDI was used instead of 25(OH)D in the calculations. When the sexes were analysed separately, the statistically significant association was found only in females (P < 0.0001 for iPTH versus 25(OH)D; P < 0.0001 for iPTH versus FDI) but not in males. Conclusion.,Hypovitaminosis D is very common amongst Finnish in- and outpatients in both sexes, causing secondary hyperparathyroidism in females. More extensive studies are warranted to elucidate the vitamin D status of the Finnish population. [source]

Assessing vitamin D in the central nervous system

ACTA NEUROLOGICA SCANDINAVICA, Issue 2010
T. Holmøy
Holmøy T, Moen SM. Assessing vitamin D in the central nervous system. Acta Neurol Scand: 2010: 122 (Suppl. 190): 88,92. © 2010 John Wiley & Sons A/S. Epidemiological and experimental evidence suggest that vitamin D deficiency is a risk factor for multiple sclerosis and other autoimmune diseases. The activated form of vitamin D exerts several immunomodulating properties in vitro and in vivo, that could contribute to explain the association with multiple sclerosis. Hypovitaminosis D is also associated with several other neurological diseases that is less likely mediated by dysregulated immune responses, including Parkinson's disease and Alzheimer's disease, schizophrenia and affective disorders, suggesting a more diverse role for vitamin D in the maintenance of brain health. Accordingly, both the vitamin D receptor and the enzymes necessary to synthesize bioactive 1,25-dihydroxyvitamin D are expressed in the brain, and hypovitaminosis D is associated with abnormal development and function of the brain. We here review current knowledge on the intrathecal vitamin D homeostasis in heath and disease, highlighting the need to assess vitamin D in the intrathecal compartment. [source]

Vitamin D and calcium deficits predispose for multiple chronic diseases

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 5 2005
M. Peterlik
Abstract There is evidence from both observational studies and clinical trials that calcium malnutrition and hypovitaminosis D are predisposing conditions for various common chronic diseases. In addition to skeletal disorders, calcium and vitamin D deficits increase the risk of malignancies, particularly of colon, breast and prostate gland, of chronic inflammatory and autoimmune diseases (e.g. insulin-dependent diabetes mellitus, inflammatory bowel disease, multiple sclerosis), as well as of metabolic disorders (metabolic syndrome, hypertension). The aim of the present review was to provide improved understanding of the molecular and cellular processes by which deficits in calcium and vitamin D cause specific changes in cell and organ functions and thereby increase the risk for chronic diseases of different aetiology. 1,25-dihydroxyvitamin D3 and extracellular Ca++ are both key regulators of proliferation, differentiation and function at the cellular level. However, the efficiency of vitamin D receptor-mediated intracellular signalling is limited by the negative effects of hypovitaminosis D on extrarenal 25-hydroxyvitamin D-1,-hydroxylase activity and thus on the production of 1,25-dihydroxyvitamin D3. Calcium malnutrition eventually causes a decrease in calcium concentration in extracellular fluid compartments, resulting in organ-specific modulation of calcium-sensing receptor activity. Hence, attenuation of signal transduction from the ligand-activated vitamin D receptor and calcium-sensing receptor seems to be the prime mechanism by which calcium and vitamin D insufficiencies cause perturbation of cellular functions in bone, kidney, intestine, mammary and prostate glands, endocrine pancreas, vascular endothelium, and, importantly, in the immune system. The wide range of diseases associated with deficits in calcium and vitamin D in combination with the high prevalence of these conditions represents a special challenge for preventive medicine. [source]

Report on the vitamin D status of adult and pediatric patients with inflammatory bowel disease and its significance for bone health and disease

INFLAMMATORY BOWEL DISEASES, Issue 12 2006
Helen M. Pappa MD
Abstract Vitamin D is a hormone responsible for calcium homeostasis and essential for bone mineralization throughout the lifespan. Recent studies revealed a high prevalence of hypovitaminosis D among healthy adults and children, especially in the northern hemisphere, and a link between this condition and suboptimal bone health. Moreover, maintenance of what are today considered optimal vitamin D stores has not been achieved throughout the year with currently recommended daily intake for vitamin D. The prevalence of hypovitaminosis D is even higher among adults with inflammatory bowel disease (IBD), a situation that may be caused by malabsorption and gastrointestinal losses through an inflamed intestine, among other factors. In children with IBD, existing reports of vitamin D status are scarce. The relationship between vitamin D status and bone health, although well-established in healthy adults and children, has been controversial among adults and children with IBD, and the reasons for this have not been investigated to date. Studies in animal models of colitis and in vitro human studies support a role of vitamin D in the regulation of the immune system of the gut and the potential of vitamin D and its derivatives as therapeutic adjuncts in the treatment of IBD. This role of vitamin D has not been investigated with translational studies to date. Currently, there are no guidelines for monitoring vitamin D status, treating hypovitaminosis D, and maintaining optimal vitamin D stores in patients with IBD. These tasks may prove particularly difficult because of malabsorption and gastrointestinal losses that are associated with IBD. [source]

The prevalence of vitamin D abnormalities in South Asians with type 2 diabetes mellitus in the UK

Heterogeneity in Serum 25-Hydroxy-Vitamin D Response to Cholecalciferol in Elderly Women with Secondary Hyperparathyroidism and Vitamin D Deficiency

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 8 2010
Andrea Giusti MD
OBJECTIVES: To compare the effects on parathyroid hormone (PTH) and 25-hydroxy-vitamin D (25(OH)D) of two dosing regimens of cholecalciferol in women with secondary hyperparathyroidism (sHPTH) and hypovitaminosis D and to investigate variables affecting 25(OH)D response to cholecalciferol. DESIGN: Randomized-controlled trial with 6-month follow-up. SETTING: Two osteoporosis centers in northern Italy. PARTICIPANTS: Sixty community-dwelling women aged 65 and older with sHPTH and hypovitaminosis D, creatinine clearance greater than 65 mL/min and without diseases or drugs known to influence bone and vitamin D metabolism. INTERVENTION: Cholecalciferol 300,000 IU every 3 months, once at baseline and once at 3 months (intermittent D3 group) or cholecalciferol 1,000 IU/day (daily D3 group). MEASUREMENTS: Serum PTH, 25(OH)D, calcium, bone-specific alkaline phosphatase, ,-C-terminal telopeptide of type I collagen, phosphate, 24-hour urinary calcium excretion. RESULTS: The two groups had similar baseline characteristics. All participants had vitamin D deficiency [25(OH)D<20 ng/mL)], and 36 subjects (60%) had severe deficiency (<10 ng/mL), with no difference between the groups (severe deficiency: intermittent D3 group, n=18; daily D3 group, n=18). After 3 and 6 months, both groups had a significant increase in 25(OH)D and a reduction in PTH. Mean absolute increase±standard deviation of 25(OH)D at 6 months was higher in the intermittent D3 group (22.7±11.8 ng/mL) than in the daily D3 group (13.7±6.7 ng/mL, P<.001), with a higher proportion of participants in the intermittent D3 group reaching desirable serum concentration of 25(OH)D , 30 ng/mL (55% in the intermittent D3 group vs 20% in the daily D3 group, P<.001). Mean percentage decrease of PTH in the two groups was comparable, and at 6 months, a similar proportion of participants reached normal PTH values. 25(OH)D response to cholecalciferol showed a wide variability. In a logistic regression analysis, body mass index and type of treatment appeared to be significantly associated with normalization of 25(OH)D values. CONCLUSION: Cholecalciferol 300,000 IU every 3 months was more effective than 1,000 IU daily in correcting vitamin D deficiency, although the two groups achieved similar effects on PTH at 6 months. Only 55% of the higher-dose intermittent group reached desirable concentrations of 25(OH)D, suggesting that yet-higher doses will be required for adequate vitamin D repletion. [source]

Review: Energy regulation and neuroendocrine,immune control in chronic inflammatory diseases

JOURNAL OF INTERNAL MEDICINE, Issue 6 2010
R. H. Straub
Abstract., Straub RH, Cutolo M, Buttgereit F, Pongratz G (University Hospital Regensburg, Regensburg, Germany; University of Genova, Genova, Italy; and Charité University Medicine Berlin, Berlin, Germany). Energy regulation and neuroendocrine,immune control in chronic inflammatory diseases (Review). J Intern Med 2010; 267:543,560. Energy regulation (EnR) is most important for homoeostatic regulation of physiological processes. Neuroendocrine pathways are involved in EnR. We can separate factors that provide energy-rich fuels to stores [parasympathetic nervous system (PSNS), insulin, insulin-like growth factor-1, oestrogens, androgens and osteocalcin] and those that provide energy-rich substrates to consumers [sympathetic nervous system (SNS), hypothalamic,pituitary,adrenal axis, thyroid hormones, glucagon and growth hormone]. In chronic inflammatory diseases (CIDs), balanced energy-rich fuel allocation to stores and consumers, normally aligned with circadian rhythms, is largely disturbed due to the vast fuel consumption of an activated immune system (up to 2000 kJ day,1). Proinflammatory cytokines such as tumour necrosis factor or interleukins 1, and 6, circulating activated immune cells and sensory nerve fibres signal immune activation to the rest of the body. This signal is an appeal for energy-rich fuels as regulators are switched on to supply energy-rich fuels (,energy appeal reaction'). During evolution, adequate EnR evolved to cope with nonlife-threatening diseases, not with CIDs (huge negative selection pressure and reduced reproduction). Thus, EnR is inadequate in CIDs leading to many abnormalities, including sickness behaviour, anorexia, hypovitaminosis D, cachexia, cachectic obesity, insulin resistance, hyperinsulinaemia, dyslipidaemia, fat deposits near inflamed tissue, hypoandrogenaemia, mild hypercortisolaemia, activation of the SNS (hypertension), CID-related anaemia and osteopenia. Many of these conditions can contribute to the metabolic syndrome. These signs and symptoms become comprehensible in the context of an exaggerated call for energy-rich fuels by the immune system. We propose that the presented pathophysiological framework may lead to new therapeutical approaches and to a better understanding of CID sequence. [source]

A high prevalence of hypovitaminosis D in Finnish medical in- and outpatients

Vitamin D status of chronically ill or disabled children in Victoria

JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 7 2003
A Greenway
Objective: To establish the percentage prevalence of hypovitaminosis D in chronically ill or disabled children in Melbourne, Australia. Methodology: A group of inpatients at the Royal Children's Hospital, Melbourne, Victoria, as identified by the primary unit, were sampled to measure serum vitamin D and parameters of bone turnover. A second group of disabled children (outpatients) were also measured to establish vitamin D status. Results: Of the total population, 54.9% were found to have low serum 25 hydroxy (25OH) vitamin D levels. Of the inpatient group, 25.4% were vitamin D deficient (<30 nmol/L), and 27.1% were vitamin D insufficient (30,50 nmol/L). The mean 25OH vitamin D was 52.1 nmol/L. Of the outpatient group, 15.4% were vitamin D deficient, whilst 42.3% were found to be insufficient. The mean vitamin D level was 41.2 nmol/L. No difference attributable to intellectual versus physical disability was found. Anticonvulsant use and ambulatory status was not predictive of vitamin D status in the children examined. Of the total population, 0.05% were found to have secondary hyperparathyroidism. The mean 25OH vitamin D level of this subgroup was 30.6 nmol/L. Dark skin tone was found to be significantly associated with hypovitaminosis D (P = 0.001), where all five children with dark skin tone were found to have serum 25OH vitamin D levels <50 nmol/L. Of the seven disabled children (outpatients) found to be iron deficient, four had coexistent hypovitaminosis D. Conclusion: The percentage prevalence of hypovitaminosis D is high in both chronically ill, and physically/intellectually disabled children in Melbourne, Australia. Increased vigilance and recognition of this deficiency state is needed as an important health prevention strategy. [source]

Developmental vitamin D deficiency alters brain protein expression in the adult rat: Implications for neuropsychiatric disorders

PROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 5 2007
Lionel Almeras
Abstract An increased risk for multiple sclerosis and schizophrenia is observed at increasing latitude and in patients born in winter or spring. To explore a possible link between maternal vitamin D deficiency and these brain disorders, we examined the impact of prenatal hypovitaminosis D on protein expression in the adult rat brain. Vitamin D-deficient female rats were mated with vitamin D normal males. Pregnant females were kept vitamin D-deficient until birth whereupon they were returned to a control diet. At week 10, protein expression in the progeny's prefrontal cortex and hippocampus was compared with control animals using silver staining 2-D gels associated with MS and newly devised data mining software. Developmental vitamin D (DVD) deficiency caused a dysregulation of 36 brain proteins involved in several biological pathways including oxidative phosphorylation, redox balance, cytoskeleton maintenance, calcium homeostasis, chaperoning, PTMs, synaptic plasticity and neurotransmission. A computational analysis of these data revealed that (i) nearly half of the molecules dysregulated in our animal model have also been shown to be misexpressed in either schizophrenia and/or multiple sclerosis and (ii) an impaired synaptic network may be a consequence of mitochondrial dysfunction. [source]