Abstract Vitamin D deficiency is a significant health issue, particularly among office workers. This literature review emphasizes the availability of evidence on vitamin D deficiency and its impacts on musculoskeletal health and immune functions, especially amongst office workers. A literature search of PubMed, Scopus, and Web of Science identified relevant studies on the relationship between vitamin D status and musculoskeletal health and infection risks, highlighting the prevalence of vitamin D deficiency in office workers due to limited sunlight exposure and sedentary lifestyles. The risks of osteoporosis, muscle weakness, and musculoskeletal pain, as well as impaired immune system function, are carefully examined. Potential intervention strategies include implementing work schedules allowing for outdoor breaks, providing access to vitamin D-fortified foods or supplements, and routine screening for vitamin D levels. Addressing the low level of vitamin D in office workers is essential for promoting musculoskeletal health, supporting immune functions, and enhancing workforce productivity. This review underscores the need for further research and the implementation of evidence-based interventions to mitigate the impact of vitamin D deficiency in this population.
Vitamin D deficiency ; office workers ; musculoskeletal ; Immunity

Introduction: Diabetic sensorimotor polyneuropathy (DSPN) is a common complication of long-standing diabetes mellitus marked by neuropathic pain and sensory deficits. Evidence supporting combination antioxidant and vitamin-based therapy remains limited, particularly in patients with chronic disease. This study aims to determine symptom improvement after 12 weeks of oral alpha-lipoic acid, vitamin B complex, and vitamin E (Bionerv E+) in chronic diabetic patients with symptomatic DSPN. Methodology: This single-centre, randomized, double-blind, placebocontrolled trial at HCTM enrolled 31 patients with symptomatic DSPN, assigned to Bionerv E+ (n = 16) or placebo (n = 15) for 12 weeks. Symptoms were assessed at baseline and post intervention using the Neuropathy Impairment Score–Lower Limb (NIS LL), Short Form McGill Pain Questionnaire (SF MPQ), Toronto Clinical Scoring System (TCSS), and nerve conduction studies (NCS). Results: A total of 31 participants were recruited; 18 completed the study (11 intervention, 7 placebo). The cohort was predominantly elderly (median age 68 ± 12 years), male (51.6%), with long-standing diabetes (mean duration of 18.6 ± 8.2 years), and a mean hemoglobin A1c of 7.3 ± 0.6%. A statistically significant reduction in TCSS score was observed in the intervention arm (5.5 ± 3.8 vs 3.3 ± 3.4; p = 0.002), indicating improvement in neuropathic symptom severity in this chronic population. The SF MPQ scores showed a downward trend in both arms, but were not statistically significant. Among intervention participants who completed sural NCS, three patients demonstrated normalization, and five showed partial amplitude gains, indicating directional improvement in nerve function. Four patients with normal baseline studies exhibited further amplitude gains. Otherwise, limited improvements were observed in those with abnormal conduction velocity parameters. Bionerv E+ was well tolerated, with only mild and self-limiting adverse events reported. Conclusion Short-term supplementation with Bionerv E+ showed improvement in neuropathic symptoms among longstanding diabetic patients. However, longer-term studies with larger cohorts are necessary to determine its effects on patients with DSPN.
Thioctic Acid ; Vitamin B Complex ; Polyneuropathies ; Vitamin E

Introduction: Vitamin D-dependent rickets type 2 (VDDR2) is traditionally defined by biallelic vitamin D receptor (VDR) mutations causing resistance to 1,25(OH)₂D. We describe a case of the classical VDDR2 phenotype with a single VDR mutation and an interesting physiological adaptation. Case: A female diagnosed with rickets at age three presented with a femoral fracture, severe short stature, hypocalcemia (2.1 mmol/L; NR 2.35–2.70), hypophosphatemia (0.8 mmol/L; NR 1.5–2.10), and evidence of renal phosphate wasting (TMP/GFR 0.5 mmol/L; NR 1.5–2.4). Biochemistry showed markedly elevated alkaline phosphatase (1,227 IU/L; NR 50–136) and secondary hyperparathyroidism (20.7 pmol/L; NR 0.8–7.8). Despite hypocalcemia, 1,25(OH)₂D was significantly elevated (>450 pmol/L; NR 60–150), consistent with VDDR2. There was no initial family history; however, subsequent evaluation of her mother—prompted by the patient’s diagnosis—revealed a similar biochemical profile, along with short stature (142 cm) and a history of multiple fractures. Genetic analysis in both individuals identified a heterozygous missense mutation in exon 10 of the VDR gene, affecting the ligand-binding domain, supporting a pattern of dominant inheritance. The patient was treated with cholecalciferol (1,200 IU daily), calcitriol (5–6 µg daily), and calcium carbonate (2,000 mg daily). Although biochemical responsiveness to therapy was evident, poor adherence resulted in suboptimal metabolic control throughout childhood and adolescence, including a second fracture at age 15 and a final adult height of 124 cm. Notably, calcium and phosphate levels progressively normalized after puberty, with sustained biochemical stability despite the patient omitting the treatment. Conclusion This case provides two important insights. First, it represents the fourth reported case worldwide demonstrating a dominant-negative effect of a VDR gene mutation, whereby a single mutant receptor interferes with wildtype VDR function. Second, it highlights postpubertal calcium adaptation, in which vitamin D–independent intestinal absorption may restore mineral homeostasis, and disease severity can attenuate over time through adaptive physiological mechanisms.
Calcium ; Mutation ; Vitamin D ; Rickets

Benign paroxysmal positional vertigo（BPPV）is a common peripheral vestibular disorder，and at present，otolith shedding and displacement is highly recognized as the main pathological mechanism of BPPV. An increasing amount of evidence has shown that otolith particle shedding is closely associated with vitamin D，and 25-（OH）D is expected to become a potential biomarker for BPPV and an important target for the treatment of BPPV and residual symptoms after successful repositioning. This article reviews the pathophysiological mechanism of vitamin D in BPPV and residual dizziness and summarizes the association of vitamin D with BPPV and residual symptoms based on the treatment methods for vitamin D regulation.
Vitamin D

OBJECTIVE: Attention Deficit Hyperactivity Disorder (ADHD) is a common mental disorder in children. It is unclear how nutrition and dietary components relate to ADHD. Some studies suggest that children with ADHD have lower serum levels of vitamin D than healthy controls. In the current study, the effects of Vitamin D supplementation on ADHD were reviewed and analyzed using available literature. MATERIALS AND METHODS: A meta-analysis and systematic review were performed. Children less than 18 years old diagnosed with ADHD given Vitamin D supplementation or placebo were included. A search was performed in PubMed/MEDLINE, EMBASE, Scopus, Cochrane, and Google Scholar databases from inception to August 2024 using the MeSH keywords: "Vitamin D" AND (ADHD OR Attention Deficit Hyperactivity Disorder) AND (children OR pediatric OR adolescents) AND randomized controlled trial. Standardized Mean Difference (SMD) was used as an effect measure and pooled using random effects meta-analysis. RESULTS: The pooled SMS showed significantly lower ADHD scores (SMD=-0.59, 95%CI=-1.06 to -0.11, p=0.01), lower inattentive scores (SMD=-0.61, 95%CI=-1.00 to -0.23, p=0.002), and lower hyperactivity scores (SMD=-0.64, 95%CI=-1.08 to -0.20, p=0.004) in children given Vitamin D supplementation. The adverse events reported were minor only and did not vary significantly between intervention and control groups. CONCLUSION Vitamin D treatment as an adjuvant to methylphenidate alleviated ADHD symptoms without significant adverse effects, correlating with enhanced vitamin D levels. Given the robust evidence and well-structured randomized controlled trials, we strongly advocate for the integration of vitamin D supplementation with ADHD treatment.
Human ; Male,Female ; Adolescent: 13-18 yrs old ; Child Preschool: 2-5 yrs old ; Child: 6-12 yrs old ; Vitamin D ; meta-analysis ; systematic review

INTRODUCTION

Despite advancements in surgical techniques aimed at preserving parathyroid function, postoperative hypocalcemia (PoH) remains a challenge following elective total thyroidectomy. Management typically involves postoperative calcium supplementation; however, some studies suggest preoperative calcium and/or vitamin D supplementation may prevent PoH. This paper analyzed existing studies to determine efficacy of preoperative calcium, with or without vitamin D, in preventing hypocalcemia in total thyroidectomy patients. Level of Evidence: Meta-analysis, Level IV.

A systematic review and meta-analysis was conducted with PROSPERO Registration No. CRD42024426410. Searches were performed on PubMED, PubMED Central, Embase, Cochrane Library, and HERDIN without date or language restrictions. Relevant studies underwent multiple screenings, with accepted individual studies assessed for bias or quality. Meta-analysis was performed using SPSS version 24.

A total of 345 studies were initially identified. Following deduplication, exclusion, and quality appraisal, 8 studies were included for analysis. Random effects model was utilized for all analysis due to heterogeneity in data. Results indicate that preoperative calcium, with or without vitamin D supplementation, correlated with higher postoperative calcium levels (z = 3.09, p < 0.001), reduced incidence of laboratory (z= 2.05, p = 0.03) and clinical hypocalcemia (z= 2.94, p < 0.001), and shorter hospital stay (z= 2.32, p = 0.01).

Results from the conducted meta-analysis support the proposed practice of providing calcium with or without vitamin D supplementation among patients who are to undergo total thyroidectomy procedures to prevent postoperative hypocalcemia.

Multiple myeloma (MM) is a common hematologic malignancy that originates from precursor conditions such as monoclonal gammopathy of undetermined significance (MGUS) and smoldering multiple myeloma (SMM). Identifying its risk factors is crucial for early intervention. The etiology of MM is multifactorial, involving race, familial clustering, gender, age, obesity, cytogenetic abnormalities, and environmental exposures. Among these, cytogenetic abnormalities and modifiable factors play pivotal roles in MM pathogenesis and progression. 1) cytogenetic abnormalities. Primary abnormalities [e.g., hyperdiploidy, t(11;14), t(14;16)] emerge at the MGUS stage, while secondary abnormalities [e.g., 1q+, del(17p)] drive disease progression. The accumulation of 1q+ promotes clonal evolution, and del(17p) is associated with significantly reduced survival. 2) modifiable risk factors. Obesity promotes MM via the acetyl-CoA synthetase 2 (ACSS2)-interferon regulatory factor 4 (IRF4) pathway. Vitamin D deficiency weakens immune surveillance. Exposure to herbicides such as Agent Orange and glyphosate increases MGUS incidence. Insufficient UV exposure, by reducing vitamin D synthesis, elevates MM risk. Gut microbiota dysbiosis (enrichment of nitrogen-cycle bacteria and depletion of short-chain fatty acids producers) induces chromosomal instability through the ammonium ion-solute carrier family 12 member 22 (SLC12A2)-NEK2 axis. Therefore, risk-based screening among high-risk populations (e.g., those who are obese, elderly, or chemically exposed), along with early interventions targeting cytogenetic abnormalities [e.g., B cell lymphoma 2 (Bcl-2) inhibitors for t(11;14), ferroptosis inducers for t(4;14)] and modifiable factors (e.g., vitamin D supplementation, gut microbiota modulation), may effectively delay disease progression and improve prognosis.
Humans ; Multiple Myeloma/epidemiology* ; Risk Factors ; Obesity/complications* ; Chromosome Aberrations ; Monoclonal Gammopathy of Undetermined Significance/etiology* ; Gastrointestinal Microbiome ; Vitamin D Deficiency/complications* ; Precancerous Conditions/genetics*

Objective:To observe and analyze the levels of vitamin D（VD） and their influencing factors in children undergoing adenoidectomy and/or tonsillectomy. Methods:A total of 147 children who received adenoidectomy and/or tonsillectomy in our hospital from November 2018 to March 2019 were selected as the experimental groups, gender and age matched 147 healthy children of the same period were selected as the control group. The differences of VD levels between the two groups were compared, the factors affecting VD levels were investigated, and patients with VD deficiency/insufficiency in the experimental groups were followed up postoperatively. Results:The VD levels of the experimental groups were（19.6±6.6） ng/mL and those of the control groups were （22.5±6.5）ng/mL, which was significantly different （P<0.01）. The experimental groups were divided into inflammation groups and Sleeping disorder breathing（SDB）groups. The VD levels of the two groups were （19.1±6.7）ng/mL and （21.9±6.4）ng/mL, which was significantly different （P<0.05）. Regression analysis showed that VD levels were negatively correlated with age, body mass index （BMI）, adenoid hypertrophy, tonsil hypertrophy and Anti-streptolysin O（ASO）levels （P<0.05）. VD values were remeasured one year postoperatively in 23 of 72 children in the VD deficiency/deficiency groups, and there was a statistically significant difference between preoperative and postoperative VD values[（14.3±3.9）ng/mL and （17.1±5.5） ng/mL, respectively, P<0.05]. There was a significant difference in postoperative VD value between the inflammation groups and the SDB groups[ （15.6±5.9） ng/mL and （20.5±2.1） ng/mL, respectively, P<0.05]. Conclusion:Children who underwent adenoidectomy and/or tonsillectomy had lower VD levels than healthy children.VD levels decreased with increasing age,BMI and ASO values,and associated with the size of adenoid and tonsil. Preoperative VD levels were lower in the inflammation groups, adenoidectomy and/or tonsillectomy improved VD deficiency/insufficiency status, and postoperative elevation of VD levels was more pronounced in the SDB groups.
Humans ; Tonsillectomy ; Adenoidectomy ; Vitamin D/blood* ; Vitamin D Deficiency ; Male ; Female ; Postoperative Period ; Child ; Case-Control Studies ; Child, Preschool

OBJECTIVES: To investigate the changes in blood levels of calcium and bone metabolism biochemical markers in patients with primary osteoporosis receiving treatment with denosumab. METHODS: Seventy-three patients with primary osteoporosis treated in our Department between December, 2021 and December 2023 were enrolled. All the patients were treated with calcium supplements, vitamin D and calcitriol in addition to regular denosumab treatment every 6 months. Blood calcium, parathyroid hormone (PTH), osteocalcin (OC), type I procollagen amino-terminal propeptide (PINP), and type I collagen carboxy-terminal telopeptide β special sequence (β‑CTX) data before and at 3, 6, 9, and 12 months after the first treatment were collected from each patient. RESULTS: Three months after the first denosumab treatment, the bone turnover markers (BTMs) OC, PINP, and β-CTX were significantly decreased compared to their baseline levels by 39.5% (P<0.001), 56.2% (P<0.001), and 81.8% (P<0.001), respectively. At 6, 9, and 12 months of treatment, OC, PINP, and β-CTX remained significantly lower than their baseline levels (P<0.001). Blood calcium level was decreased (P<0.05) and PTH level increased (P<0.05) significantly in these patients at months of denosumab treatment, but their levels were comparable to the baseline levels at 6, 9, and 12 months of the treatment (P>0.05). CONCLUSIONS Denosumab can suppress BTMs and has a good therapeutic effect in patients with primary osteoporosis, but reduction of blood calcium and elevation of PTH levels can occur during the first 3 months in spite of calcium supplementation. Blood calcium and PTH levels can recover the baseline levels as the treatment extended, suggesting the importance of monitoring blood calcium and PTH levels during denosumab treatment.
Humans ; Denosumab/therapeutic use* ; Calcium/blood* ; Parathyroid Hormone/blood* ; Biomarkers/blood* ; Osteoporosis/blood* ; Osteocalcin/blood* ; Procollagen/blood* ; Female ; Collagen Type I/blood* ; Peptide Fragments/blood* ; Bone Density Conservation Agents/therapeutic use* ; Bone and Bones/metabolism* ; Male ; Middle Aged ; Vitamin D ; Peptides/blood* ; Aged

OBJECTIVES: To prepare a stable mouse model of chronic liver fibrosis induced by dietary vitamin A (VA) deficiency combined with CCl₄ injections. METHODS: A total of 126 Balb/c mice were randomized into 3 groups for feeding with a normal VA diet or a VA-deficient diet containing 500 or 200 IU/kg VA. After 4 weeks of feeding, half of the mice in each group were given intraperitoneal injections of 5% CCl₄ (10 mL/kg, twice a week) for 8 weeks. Serum retinol, ALT/AST and liver index of the mice were examined, liver tissue pathologies were observed with HE and Masson staining, and liver fibrosis score and oxidative stress level were evaluated. RESULTS: Four weeks of VA-deficient feeding, especially at 200 IU/kg, significantly lowered serum retinol level of the mice. CCl₄ injections for 8 weeks obviously increased liver index and ALT/AST and caused obvious liver fibrosis in all the mice, but liver pathologies were more severe in the 2 VA-deficient groups; severe liver necrosis with inflammatory cell infiltration was observed in 200 IU/kg VA group, where 2 mice died. After discontinuation of CCl₄, the mice with normal dietary VA showed gradual recovery of the liver index, ALT/AST, liver cord structure and liver fibrosis; the mice with VA deficiency, however, showed no significant improvements in these parameters, and the mice with 200 IU/kg VA still had serious abdominal adhesion, false lobules and massive inflammatory cell infiltration with a fibrosis stage score of 3. The oxidative damage index 8-OHdG was significantly higher in 500 IU/kg VA group than in normal VA group after CCl₄ modeling. CONCLUSIONS Feeding with diet containing 500 IU/kg VA for 4 weeks and 10 mL/kg CCl₄ injections for 8 weeks can result in stable moderate to severe liver fibrosis in mice without spontaneous reversal at 8 weeks of drug withdrawal.
Animals ; Mice ; Mice, Inbred BALB C ; Disease Models, Animal ; Carbon Tetrachloride ; Vitamin A Deficiency/complications* ; Male ; Liver Cirrhosis/etiology* ; Oxidative Stress ; Vitamin A/blood*