Prevalence of 25-Hydroxyvitamin D Deficiency and its severity correlation with Acute Traumatic brain Injury in Indian Patients: A Perspective Observation Study

Author(s):  
Ajay Choudhary ◽  
Rajesh Sharma ◽  
Ashok Kumar ◽  
Kuldeep Kinja ◽  
Ravi Berwal ◽  
...  

Objective: To study the prevalence of 25-hydroxyvitamin D deficiency pattern during three year (2017-2020) and severity correlation among individuals with acute traumatic brain injury (TBI). Methodology: Subjects with acute TBI admitted from June 1st, 2017 through June 30th, 2020 were recruited. 280 out of 445 met inclusion criteria. The demographic injury related details, assessment of 25 OH vitamin D and Glasgow Comma (GCS) score were done at the time of admission. Results: The year wise enrolled subjects were young with mean age of 28.39±0.86 years with males (73.3%) and female (23.7%), in first year, 27.77±5.35 years with males (81.67%) and female (18.33%), in second year and 23.04±7.10 years with males (88.57%) and female (11.42%), in third years. Mean value of 25(OH) vitamin D in subjects during three years were 23.78±11.79ng/mL, 21.65±12.53 ng/mL and 25.18±18.58ng/mL. The vitamin D deficiency levels in this study were tabulated as: deficient (level <20 ng/mL), insufficient (level 20–29.9ng/mL), and sufficient (level ≥30ng/mL). Which were found during three years as: In First year, Deficient (64.44%), Sufficient (11.11%), insufficient (24.44%), in second years, Deficient (88.33%), Sufficient (2.66%), insufficient (10.00%) and in third year Deficient (88.57%), Sufficient (1.42%), insufficient (10.00%). In which sufficient level were found to be decreased statistically significant with years with P value= 0.0001. The severity assessment through GCS score were found to be statistically increased with deficient levels with P values=0.0447, but found no significance, when comparison were done between years wise GCS score and levels of vitamin D. Conclusion: The study found decreased prevalence of vitamin D deficiency levels with increased severity. Therefore it should be routinely screened and treated as indicated.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2139-2139
Author(s):  
Christine Duncan ◽  
Lynda Vrooman ◽  
Lori Bechard ◽  
Elly Barry ◽  
Leslie E. Lehmann

Abstract Children undergoing HSCT are at risk for vitamin D deficiency due to lack of sun exposure, the recommended use of sunscreen, dietary insufficiency, and the effects of medications such as glucocorticoids and calcineurin inhibitors. We assessed the prevalence of 25-hydroxyvitamin D (25-OH vitamin D) deficiency in pediatric post-HSCT patients in an outpatient oncology clinic during 4 weeks in May 2008. Patients found to have low 25-OH vitamin D levels were referred for dietary counseling and given supplementation or repletion as needed. 25-OH vitamin D and parathyroid hormone (PTH) levels were measured in 62 (88.6%) of 70 eligible patients. 83.8% of patients had a 25-OH vitamin D level less than the institutional lower limit of normal, 30 ng/mL. 29% of patients were 25-OH vitamin D insufficient with levels 20–29 ng/mL (range of 20–29). 54.8% of patients were 25-OH vitamin D deficient with levels &lt;20 ng/mL (range 5–19). The prevalence of insufficiency and deficiency was similar between male (87.8%; 57.6%) and female patients (57.6%; 55.2%).The mean duration of days following transplant was 532.6 days (median 251.5 days). The mean age at transplant was 3.7 years (median 3.5 years). 47% of patients were female. 75.8% were Caucasian. 90.3% received allogeneic transplants. The underlying diseases were as follows: ALL (27.4%), AML/MDS (24.2%), bone marrow failure (11.3%), nonmalignant hematologic diagnosis (8.1%), solid tumor (8.1%), immunodeficiency (6.5%), lymphoma (6.5%), and other diagnoses (8.1%). 8 patients regularly took either an over-the-counter multivitamin or vitamin D supplement and all 8 patients had 25-OH levels less than 30 ng/mL. There was a negative inverse correlation of (r= −0.3, p=0.029) between PTH and 25-OH vitamin D. There were no significant associations between 25-OH vitamin D level and any of the following: corticosteroid or calcineurin inhibitor use in the preceding year, time from transplant, age at transplant, current age, or graft-versus-host disease. 25-OH vitamin D insufficiency and deficiency are common following pediatric HSCT. We recommend vitamin D screening for all post-HSCT pediatric patients. Further investigation is needed to identify potential risk factors for vitamin D deficiency and the long-term effects of deficiency on bone health and development.


2011 ◽  
Vol 4 ◽  
pp. CMED.S7116 ◽  
Author(s):  
Evgenia Korytnaya ◽  
Nagashree Gundu Rao ◽  
Jane V. Mayrin

Objective To present a case of hypercalcemia associated with thyrotoxicosis in a patient with vitamin D deficiency and review biochemical changes during the course of treatment. Methods We report a case, describe the changes in serum calcium, phosphorus, parathyroid hormone in Graves’ disease and concomitant Vitamin D deficiency. We compare our findings to those reported in literature. Results Our patient had hypercalcemia secondary to thyrotoxicosis alone, which was confirmed by low parathyroid hormone level and resolution of hypercalcemia with treatment of thyrotoxicosis. The case was complicated by a concomitant vitamin D deficiency. Serum calcium elevation in patients with thyrotoxicosis occurs secondary to hyperthyroidism alone or due to concurrent hyperparathyroidism. Hypercalcemia from thyrotoxicosis is usually asymptomatic and is related to bone resorption. Vitamin D deficiency can be seen in patients with thyrotoxicosis because of accelerated metabolism, poor intestinal absorption and increased demand during bone restoration phase. Coexistence of hypercalcemia and Vitamin D deficiency in patients with thyrotoxicosis is rare, but possible, and 25-hydroxyvitamin D levels should be checked. The definite treatment for hypercalcemia in thyrotoxicosis is correction of thyroid function. Conclusion Hypercalcemia in thyrotoxicosis should be distinguished from concomitant hyperparathyroidism and confirmed by resolution of hypercalcemia with control of thyrotoxicosis. Patients with hypercalcemia and thyrotoxicosis may also have vitamin D deficiency and 25-OH Vitamin D levels should be checked.


2019 ◽  
Vol 16 (4) ◽  
pp. 340-347
Author(s):  
Yuge Wang ◽  
Yanqiang Wang ◽  
Bingjun Zhang ◽  
Yinyao Lin ◽  
Sha Tan ◽  
...  

Background and Objective: Vitamin D deficiency is internationally recognized among the potentially modifiable risk factors for ischemic cardio-cerebrovascular diseases. However, the association between vitamin D deficiency and stroke morbidity or mortality remains insufficiently known. Our aim is to investigate their relevance to 25-hydroxyvitamin D [25(OH) D] levels and clinical severity and outcome after 3 months in first-ever ischemic stroke. Methods: Retrospective analysis of 356 consecutive patients in first-ever ischemic stroke between 2013 and 2015. Serum 25(OH) D levels were measured at baseline. Stroke severity was assessed at admission using the National Institutes of Health Stroke Scale (NIHSS) score. Functional outcome after 3 months of onset was evaluated using the modified Rankin scale (mRS). Results: Among the 356 enrolled patients, HbA1c was higher in insufficiency/deficiency group than that in the sufficiency group (6.3 ± 1.7 vs. 5.9 ± 1.1, p =0.015). The hospital stay was longer in insufficiency/deficiency group than that in the sufficiency group (11 (8-17) vs. 9.5 (7-13), p = 0.035). There was a significant inversed trend between serum 25(OH) D levels and hospital stay (OR 0.960, P = 0.031), using logistic regression. Conclusions: 25(OH)D levels are associated with glucose homeostasis, 25(OH) D contributes to increase the length of hospital stay. Low serum 25-OHD level is an independent predictor for hospital stay in first-ever ischemic stroke. Vitamin D deficiency did not predict functional outcome in the span of 3 months.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jing Xiao ◽  
Jingyi Lv ◽  
Shiyu Wang ◽  
Yang Zhou ◽  
Lunwen Chen ◽  
...  

Abstract Background Vitamin D deficiency has been associated with type 2 diabetes (T2D) and metabolic syndrome (MS) and its components. However, it is unclear whether a low concentration of vitamin D is the cause or consequence of these health conditions. Thus, this study aimed to evaluate the association of vitamin D concentrations and its genetic risk scores (GRSs) with MS and its component diseases, such as T2D, in middle-aged and elderly participants from rural eastern China. Methods A subset of 2393 middle-aged and elderly individuals were selected from 70,458 participants of the Nantong Chronic Diseases Study of 2017–2018 in China. We used two 25-hydroxyvitamin D (25[OH]D) synthesis single-nucleotide polymorphisms (SNPs) (DHCR7-rs12785878 and CYP2R1-rs10741657) and two 25(OH) D metabolism SNPs (GC-rs2282679 and CYP24A1-rs6013897) for creating GRSs, which were used as instrumental variables to assess the effect of genetically lowered 25(OH) D concentrations on MS and T2D based on the Wald ratio. F statistics were used to validate that the four SNPs genetically determined 25(OH) D concentrations. Results Compared to vitamin D sufficient individuals, individuals with vitamin D insufficiency had an odds ratio (OR [95% confidence interval {CI}]) of MS of 1.30 (1.06–1.61) and of T2D of 1.32 (1.08–1.64), individuals with vitamin D deficiency had an ORs (95% CI) of MS of 1.50 (1.24–1.79) and of T2D of 1.47 (1.12–1.80), and those with vitamin D severe deficiency had an ORs (95% CI) of MS of 1.52 (1.29–1.85) and of T2D of 1.54 (1.27–1.85). Mendelian randomization analysis showed a 25-nmol/L decrease in genetically instrumented serum 25(OH) D concentrations using the two synthesis SNPs (DHCR7 and CYP2R1 genes) associated with the risk of T2D and abnormal diastolic blood pressure (DBP) with ORs of 1.10 (95%CI: 1.02–1.45) for T2D and 1.14 (95%CI: 1.03–1.43) for DBP. Conclusions This one sample Mendelian randomization analysis shows genetic evidence for a causal role of lower 25(OH) D concentrations in promoting of T2D and abnormal DBP in middle-aged and elderly participants from rural China.


2021 ◽  
Vol 53 (02) ◽  
pp. 105-111
Author(s):  
Dongdong Zhang ◽  
Cheng Cheng ◽  
Yan Wang ◽  
Yuan Xue ◽  
Yiming Liu ◽  
...  

AbstractThere is a paucity of data on the relation between serum 25-hydroxyvitamin D [25(OH)D] concentration and cardiometabolic biomarkers in the Chinese population. To comprehensively and quantitatively examine the association of 25(OH)D and cardiometabolic traits, we conducted a cross-sectional study in the Chinese rural population. Serum 25(OH)D and eight cardiometabolic biomarkers were measured in 1714 individuals from Henan province, China. Scatter plot was used to visualize the distribution and correlation of 25(OH)D and cardiometabolic indicators. Moreover, multivariate linear regressions and restricted cubic spline (RCS) functions were performed to examine the quantitative association between the serum 25(OH)D and cardiometabolic parameters. The median serum 25(OH)D level was 19.94 ng/ml in all participants, with an estimated 50.12% presenting vitamin D deficiency. Serum 25(OH)D level showed significantly modest association with cardiometabolic parameters (p<0.05) except for diastolic blood pressure (r=0.03, p=0.22). Multiple linear regression models showed that 25(OH)D concentration was positively associated with high-density lipoprotein cholesterol (HDL-C) and negatively associated with low-density lipoprotein cholesterol (LDL-C) and fasting serum glucose (GLU). The results of restricted cubic spline models indicated a positively linear association of 25(OH)D with HDL-C (p for overall<0.001, p for nonlinearity=0.191) and a negatively linear association with GLU (p for overall=0.024, p for nonlinearity=0.095). Overall, vitamin D deficiency was very common among Chinese rural population living near the 34 degrees north latitude. Besides, there were significant association between 25(OH)D concentrations and cardiometabolic biomarkers including HDL-C and GLU levels. Future longitudinal studies and randomized trials are warranted to clarify the causal relationship.


Thorax ◽  
2018 ◽  
Vol 74 (2) ◽  
pp. 200-202 ◽  
Author(s):  
Hooman Mirzakhani ◽  
Amal A Al-Garawi ◽  
Vincent J Carey ◽  
Weiliang Qiu ◽  
Augusto A Litonjua ◽  
...  

Cord blood 25-hydroxyvitamin D (25OHD) has been reported in association with risk of early life recurrent wheeze. In a subset of infants who participated in the Vitamin D Antenatal Asthma Reduction Trial, we demonstrated that higher cord blood 25OHD at birth (>31 ng/mL) was associated with a reduced risk of recurrent wheeze in the first year of life. We then identified a module of co-expressed genes associated with cord blood 25OHD levels >31 ng/mL. Genes in this module are involved in biological and immune pathways related to development and progression of asthma pathogenesis including the Notch1 and transforming growth factor-beta signalling pathways.


2005 ◽  
Vol 34 (1) ◽  
pp. 237-245 ◽  
Author(s):  
I Hendrix ◽  
P H Anderson ◽  
J L Omdahl ◽  
B K May ◽  
H A Morris

The enzyme 25-hydroxyvitamin D 1α-hydroxylase, or CYP27B1, is the key enzyme in the two-step activation process of vitamin D to 1,25-dihydroxyvitamin D (1,25D). While a number of regulators of the renal CYP27B1 enzyme activity have been recognized for some years, their underlying molecular mechanisms remain largely unknown, and the DNA regions involved in the in vivo regulation of gene expression by these factors have not been delineated. We have generated a transgenic mouse line that expresses 1501 bp of 5′ flanking region together with 44 bp of 5′ untranslated region of the human CYP27B1 gene fused to the firefly luciferase reporter gene. Animals expressing the luciferase gene demonstrated that both luciferase protein and mRNA for CYP27B1 were localized to proximal convoluted tubule cells of the kidney. In 2-week-old animals, the expression of the transgene and the endogenous CYP27B1 mRNA levels in the kidney were highest and fell with increasing age. Both reporter gene expression and CYP27B1 mRNA levels were downregulated in response to increasing amounts of dietary calcium in a dose-dependent manner. Vitamin D deficiency resulted in an increase in both the reporter gene and CYP27B1 expression. Interestingly, the increase in CYP27B1 mRNA levels was substantially higher than the increase in reporter gene expression, suggesting either that there is a post-transcriptional mechanism that increases the amount of CYP27B1 mRNA or that other regulatory elements are required to maximize the effect of vitamin D deficiency. These findings demonstrate that the 1501 bp 5′ flanking region of the CYP27B1 gene directs expression to the proximal convoluted tubules of the kidney and is responsible for increasing transcriptional activity when dietary calcium and vitamin D levels are depleted. It also responds in the kidney to the physiological regulators of development and ageing.


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