Normal Vitamin Research Articles

Seizure solver- pyridoxine dependent seizures

Pyridoxine dependency is a rare cause of seizures. Pyridoxine dependent seizures (PDS) occur despite normal vitamin B6 levels and is due to defective binding of pyridoxine to its apoenzyme, glutamate decarboxylase, which converts glutamic acid to gamma aminobutyric acid (GABA). Pyridoxine-dependent seizure is a rare autosomal recessive disorder that usually presents with neonatal intractable seizures. Parenteral pyridoxine injection test is a highly effective and reproducible test in confirming the diagnosis. Hunt, et al.(l) described the first case of PDS with autosomal recessive inheritance. Since then, several cases have been reported with onset of seizures after neonatal period (2-6). Pyridoxine-dependent epilepsy – ALDH7A1 (PDE-ALDH7A1) is characterized by seizures not well controlled with anti-seizure medication that are responsive clinically and electrographically to large daily supplements of pyridoxine (vitamin B6). This is true across a phenotypic spectrum that ranges from classic to atypical PDE-ALDH7A1. Intellectual disability is common, particularly in classic PDE-ALDH7A1.(7)

Post-Transplant Vitamin D Deficiency in Lung Transplant Recipients: Impact on Outcomes and Prognosis

Despite the recognized clinical significance of vitamin D deficiency in other solid organ transplant recipients, its specific relevance in lung transplantation remains to be fully understood. In this study, we performed a retrospective observational study on the impact of vitamin D deficiency on clinical outcomes and prognosis in 125 lung transplant recipients (LTRs) from October 2014 to March 2020 at a university hospital in Seoul, South Korea. Among 125 LTRs, 51 patients (40.8%) were vitamin D deficient. LTRs in the vitamin D-deficient group exhibited a higher incidence of post-transplant pneumonia and overall mortality than those with normal vitamin D levels during the follow-up period. This trend persisted when subjects were stratified into vitamin D tertiles. Furthermore, post-transplant vitamin D levels and C-reactive protein (CRP) significantly impacted pneumonia incidence and survival outcomes. Prognosis also varied based on cumulative vitamin D supplementation after transplantation, with patients receiving higher cumulative supplementation demonstrating improved prognosis. Our findings underscore the importance of assessing and maintaining optimal vitamin D levels post-transplantation, suggesting a potential avenue for improving outcomes in lung transplant recipients, especially in mitigating infection risk and enhancing long-term survival. Further research into optimal vitamin D levels and supplementation strategies in this population is warranted.

Exploring the Relationship between Vitamin D Deficiency and Disease Activity in Rheumatoid Arthritis Patients

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease marked by inflammation, pain, and joint damage. Vitamin D deficiency worsens inflammation and increases RA disease activity. Aim of the study: This study aimed to explore the relationship between Vitamin D deficiency and disease activity in rheumatoid arthritis patients. Methods: This cross-sectional study was conducted in the Department of Medicine, Mymensingh Medical College Hospital, Mymensingh, Bangladesh from January 2003 to December 2003. The study included 100 rheumatoid arthritis patients, divided into two groups- Group A: 50 patients with normal Vitamin D level and Group B: 50 patients with Vitamin D deficiency. Result: No significant difference was found between the groups in demographic characteristics. Group B exhibited significantly greater disease severity compared to Group A. The Disease Activity Score (DAS28) was higher in Group B (4.2 ± 1.3) than in Group A (2.8 ± 1.1), with a p-value < 0.001. CRP levels were also elevated in Group B (12.4 ± 3.5 mg/L vs. 5.3 ± 2.1 mg/L; p < 0.001). Group B had more swollen joints (6.2 vs. 3.5) and tender joints (7.3 vs. 4.1), with p < 0.001. ESR levels were higher in Group B (38.7 vs. 22.4 mm/h; p < 0.001). Negative correlations were found between Vitamin D levels and DAS28 (r = -0.48), CRP (r = -0.51), and ESR (r = -0.52). Conclusion: This study concludes that Vitamin D deficiency is significantly associated with increased disease activity, inflammation, and joint involvement in rheumatoid arthritis patients.

Associations between Circulating Biomarkers of One-Carbon Metabolism and Mitochondrial D-Loop Region Methylation Levels.

One-carbon metabolism is a critical pathway for epigenetic mechanisms. Circulating biomarkers of one-carbon metabolism have been associated with changes in nuclear DNA methylation levels in individuals affected by age-related diseases. More and more studies are showing that even mitochondrial DNA (mtDNA) could be methylated. In particular, methylation of the mitochondrial displacement (D-loop) region modulates the gene expression and replication of mtDNA and, when altered, can contribute to the development of human illnesses. However, no study until now has demonstrated an association between circulating biomarkers of one-carbon metabolism and D-loop methylation levels. In the study presented herein, we searched for associations between circulating one-carbon metabolism biomarkers, including folate, homocysteine, and vitamin B12, and the methylation levels of the D-loop region in DNA obtained from the peripheral blood of 94 elderly voluntary subjects. We observed a positive correlation between D-loop methylation and vitamin B12 (r = 0.21; p = 0.03), while no significant correlation was observed with folate (r = 0.02; p = 0.80) or homocysteine levels (r = 0.02; p = 0.82). Moreover, D-loop methylation was increased in individuals with high vitamin B12 levels compared to those with normal vitamin B12 levels (p = 0.04). This is the first study suggesting an association between vitamin B12 circulating levels and mtDNA methylation in human subjects. Given the potential implications of altered one-carbon metabolism and mitochondrial epigenetics in human diseases, a deeper understanding of their interaction could inspire novel interventions with beneficial effects for human health.

8106 An Uncommon Cause Of Hyperparathyroidism: A Case Report

Abstract Disclosure: A. Calderon: None. M.C. Aguilera: None. A. Kansara: None. Introduction: Parathyroid adenomas are the most common cause of primary hyperparathyroidism. Imaging techniques to locate parathyroid adenomas and hyperplasia include U/S (Sensitivity: 72%-89%), Sestamibi Tc-99 (Sensitivity of 68-95%), and 4D CT scan (Sensitivity of 80%). Combined imaging modalities increase sensitivity to 95%. We describe a case of symptomatic primary hyperparathyroidism with rapid development of hypercalcemia, and conflicting imaging findings. The final diagnosis was made after surgery and pathology review. Case presentation: A 76-year-old man with a history of hypertension, Parkinson’s disease, and prostate cancer was admitted due to a calcium level of 13 mg/dL (8.0 - 10.2 mg/dl) on routine blood tests. He had complained of progressive fatigue and constipation, attributed to Parkinson’s Disease. Five months prior his calcium was 9.7 mg/dL. Hydrochlorothiazide was discontinued due to hypotension after two months. Blood tests in the hospital showed a corrected calcium of 12.5 mg/dL, phosphorus of 1.7 (2.4 - 4.5 mg/dl), PTH of 195 (15 - 65 pg/ml), with normal vitamin D and undetectable PTHrP. A U/S of the neck showed a 0.4 x 0.5 cm cystic mass in the right-inferior pole of the thyroid. A 4D CT scan of the neck showed a non-enhancing 0.9 x 7 x 1 mm mass in the same location, and a 7 x 4.7 x 4.8 mm mildly enhancing mass in the left lower pole of the thyroid. A parathyroid nuclear scan did not identify a parathyroid adenoma. He underwent minimally invasive parathyroidectomy and was found to have a 3.2 cm enlarged and cystic right inferior parathyroid gland weighing 792 mg. Frozen section showed hypercellular parathyroid with cystic and fibrotic changes. The PTH level dropped 59% after removal of the right cystic mass. The left inferior mass identified on CT scan was identified as normal thyroid tissue. Conclusions: Parathyroid cysts are uncommon neck masses and represent less than 5% of causes of all neck masses. They can be divided into functional and non-functional. Large retrospective studies have shown that about 5% of patients manifest as classic hyperparathyroidism, whereas the most common presentation was neck mass (40%). Identification of parathyroid cysts through imaging can be challenging. In our case, the patient presented with symptomatic and rapidly progressive primary hyperparathyroidism, and imaging findings that were discordant among ultrasound, 4DCT scan and Sestamibi Tc-99 scan. The final surgical and pathology reports identified a large parathyroid cyst. This case emphasizes the variable clinical and imaging behavior of parathyroid cysts, imposing a puzzling medical challenge. Presentation: 6/3/2024

7508 Primary Hyperparathyroidism Caused By A CDC73-related Atypical Parathyroid Tumor

Abstract Disclosure: R. Cardenas: None. S. Tariq: None. R. Habibi: None. N. Ebrahimi: None. E. Astiazaran-Symonds: None. Background: Primary hyperparathyroidism (PHPT) is a common endocrine disease, causes include: parathyroid adenomas (80-85%), parathyroid hyperplasia (10-15%), atypical parathyroid adenomas (APA) (1.2 %) and parathyroid carcinomas (PC) (1%). APA share many anatomic and histopathologic features with PC making the distinction between the two challenging. Although most are sporadic, some APA are caused by germline mutations in the CDC73 gene, which is associated with hyperparathyroidism-jaw tumor (HPT-JT) syndrome PC and familial isolated PHPT with APA. Clinical Case: A 42-year-old female presented to the clinic for evaluation of recurrent PHPT. She was diagnosed at age 22 when she experienced fatigue, polydipsia with hypercalcemia (12.9mg/dl). She underwent superior bilateral parathyroidectomy with pathology consistent with parathyroid adenoma. Twenty years later, symptoms recurred and tests showed hypercalcemia (13.0 mg/dl), elevated PTH (252 pg/dl), kidney function preserved (GFR: 82.5 ml/min), normal vitamin D 25 OH (31 ng/dl). Patient denied history of nephrolithiasis or fractures. Family history was positive for kidney stones in father and siblings, also history of a jaw tumor in niece. Sestamibi scan showed a left inferior parathyroid adenoma. Patient underwent resection of the adenoma; pathology revealed a left parathyroid adenoma with atypical parathyroid tumor, >95% cellularity with cytologic features concerning for malignancy, prominent macronucleoli, necrosis, elevated mitotic activity and Ki67 with 15% tumor cells without vascular invasion. Post-op Calcium and PTH normalized (9.6 mg/dl and 10.8 pg/ml, respectively). Genetic testing via multi-gene panel identified a whole gene deletion of CDC73, consistent with hyperparathyroidism-jaw tumor syndrome. Panoramic jaw x-rays did not show jaw tumors. Genetic testing for family members is underway. Conclusion: Although somatic mutations in CDC73 are frequently found in sporadic APA and PC, germline mutations are a rare cause of PHPT associated with these tumors. Histopathological examination is necessary to confirm the diagnosis of APA and to differentiate it from PC, which has a recurrence rate >50%. APA should be treated as a “tumor of uncertain malignant potential” and needs to be carefully and periodically followed up with measurement of Ca, PTH and vitamin D. Confirmation of a CDC73 mutation by genetic testing helped identify the increased risk for other associated tumors in jaw, kidneys and uterus prompting initiation of surveillance with panoramic jaw x-rays with neck shielding, renal US and pelvis US. Genetic testing of family members will allow timely detection and treatment of individuals at risk. Presentation: 6/3/2024

8290 Hypervitaminosis A Induced Severe Hypercalcemia In A Patient With Cirrhosis

Abstract Disclosure: N. Vennelaganti: None. S. Vennelaganti: None. R.L. Fitzgerald: None. K.C. McCowen: None. Introduction The liver stores vitamin A in hepatic stellate cells and regulates its absorption through bile production and distribution via retinol-binding protein 4 and transthyretin synthesis. Cirrhosis compromises these functions, resulting in vitamin A deficiency, which is inversely linked to the severity of nonalcoholic steatohepatitis. Addressing this deficiency in chronic liver diseases, particularly cirrhosis, is challenging due to the risk of vitamin A toxicity. This case describes a cirrhotic patient who developed hypervitaminosis A, leading to severe hypercalcemia. Clinical Case A 54-year-old male with alcoholic cirrhosis was diagnosed with hypovitaminosis A. He was prescribed 10,000 IU of vitamin A due to a low serum retinol level of less than 0.06 mg/L (reference range: 0.3-1.2 mg/L ). Two months later, he presented to the hospital with an erythematous patchy, scaling facial rash. His serum calcium corrected for albumin was high at 15.6 mg/dL. The rash and hypercalcemia, alongside vitamin A supplementation, raised suspicion of vitamin A toxicity. The patient, however, exhibited no hypercalcemia symptoms. He also had an acute kidney injury. His lab results revealed a PTH level of 10 pg/mL (normal range 15-65 pg/ml) and a normal myeloma screen, as well as normal vitamin D and TSH levels. An elevated PTHrP level of 5.2 pmol/l (normal range 0-2.3) was noted, which was attributed to the kidney injury(Cr 2.55 mg/l, eGFR 23 ml/min). Malignancy was excluded after a pan scan. Hypervitaminosis A is a clinical diagnosis, as serum vitamin A levels correlate poorly with toxicity. His serum retinol was normal at 0.83 mg/l, but his retinyl palmitate was high at 0.38 mg/L(reference range 0-0.10 mg/l), which supported our diagnosis. He received continuous IV 0.9% saline and subcutaneous calcitonin at 4 units/kg twice, and had a reduction in corrected calcium to 11 mg/dL over a week. The vitamin A-induced contact dermatitis improved with topical steroids. He was discharged; two months later, he remained asymptomatic with a corrected calcium of 11.1 mg/dL. He was not interested in further management as he was asymptomatic and serum calcium levels were improving. Labs were, however, notable for worsening renal function of unclear etiology. We will be trending his labs for improvement in serum calcium as the Vitamin A clears from his system. Clinical Lesson Vitamin A supplementation in cirrhotic patients is necessary in those with deficiency but carries a risk of toxicity. There are no definitive hepatology guidelines on the replacement of Vitamin A in patients with cirrhosis. This case emphasizes the importance of awareness of hypervitaminosis A-induced hypercalcemia in this population. Clinicians must carefully monitor and manage Vitamin A levels to avoid toxicity. Further research is essential for the management of this condition in cirrhotic patients. Presentation: 6/2/2024

7633 Novel CASR Gene Mutation in a patient with Familial Hypocalciuric Hypercalcemia and Papillary Thyroid Cancer

Abstract Disclosure: A. Parihar: None. E.S. Nylen: None. S.M. Gandhi: None. Familial Hypocalciuric Hypercalcemia (FHH) is predominantly caused by loss-of-function mutations in the calcium-sensing receptor (CaSR) characterized by a benign elevation in calcium and PTH which can be mistaken for primary hyperparathyroidism (PHPT). Missense mutations in the CaSR gene causing FHH have been documented but not much is known regarding their clinical significance. We describe a patient with FHH found to have a novel variant mutation. A 37-year-old male with hypogonadism and fatty liver was incidentally found to have hypercalcemia suggestive of PHPT with elevated PTH (102-114 pg/ml), normal vitamin D, and Fractional Excretion of Calcium (FECa) of 0.014. His father also had hypercalcemia and had undergone parathyroid surgery. The patient denied kidney stones and had a normal bone density. Subsequent Sestamibi and 4D CT scan suggested parathyroid adenoma on the left mid-lower pole of the thyroid. Neck ultrasound also showed a left 1.2 x 1 x 1 cm thyroid nodule as well as a left neck mass with calcifications. Fine needle aspiration was positive for metastatic Papillary thyroid cancer(PTC) in the left neck mass and patient underwent total thyroidectomy along with subtotal parathyroidectomy and lateral neck dissection. Thyroid pathology confirmed multifocal PTC with lymph node involvement that were BRAF V600 positive. Parathyroid pathology was benign hyperplasia. The PTH level decreased appropriately intraoperatively (69%), but postoperatively a rise was noted with levels remaining 70-90 pg/ml with normal calcium levels. Repeat FECa was 0.007, supporting the diagnosis of FHH. Given patient’s father also had hypercalcemia, genetic testing was pursued. This revealed CaSR gene missense mutation (c.1382T>C p.Leu461Pro, heterozygous). This variation is not present in population databases and has been classified as a variant of uncertain significance. It can be difficult to distinguish PHPT from FHH based on FECa as in this case. The patient also had PTC which is not known to be associated with FHH. Due to uncertain significance of this novel CaSR missense mutation, long term follow-up and further familial genetic testing will help better understand clinical implications. Presentation: 6/2/2024

8472 A Little Too Much Of Tums: A Unique Presentation Of Milk Alkali Syndrome

Abstract Disclosure: Z. Al-Hiti: None. A. Misbah: None. Milk-Alkali Syndrome is characterized by a triad of hypercalcemia, metabolic alkalosis, and renal dysfunction. Historically associated with the excessive consumption of milk and alkali-containing antacids, it has re-emerged in recent years due to the widespread use of calcium and vitamin D supplements. It primarily results from an imbalance between calcium intake and renal excretion, leading to elevated calcium levels in the bloodstream. We present a case of milk-alkali syndrome with persistent renal dysfunction after normalizing calcium levels. We present the case of a 65-year-old male who presented to the emergency department with generalized weakness, poor oral intake, and confusion for 3 days. He was noted to have been more adherent with taking his prescribed medications over the last 2 weeks, which include calcitriol 0.5 mcg BID, calcium acetate 667 mg TID, and calcium carbonate 800 mg TID. On admission, he was afebrile and hemodynamically stable. . On examination, he had dry mucous membranes. He had no focal neurological deficits but he was confused and lethargic, and was only oriented to self. Other examination was noncontributory. Complete blood count and urinalysis were largely unremarkable. Chemistry demonstrated an elevated calcium level of 16.0 (8.3-10.6 mg/dL), ionized calcium of 7.3 (4.6-5.3 mg/dL), sodium of 134 (135-145 mmol/L), potassium of 5.4 (3.5-5.1 mmol/L), high phosphorus of 5.3 (2.4-5.1 mg/dL), and bicarbonate of 36 (20-31 mEq/L). Creatinine was elevated at 2.9 (0.6-1.1 mg/dL) from baseline of 1.3 to 1.4 mg/dL, and he had a BUN of 40(9-23 mg/dL). Venous blood gas showed a pH of 7.54( 7.32-7.42), pCO2 of 56 (40-52 mm Hg), and bicarbonate of 38 (23-28 mEq/L), indicating metabolic alkalosis. TSH was elevated at 36.15 (0.55- 4.78 uIU/mL) with a level of 140 two weeks back. Chest X-ray, renal ultrasound and CT head all showed no acute disease. Further work-up revealed a low PTH level of 6.3 (18.4-80 pg/mL), normal PTHrP level and 25-OH Vitamin D. There was no monoclonal gammopathy. Management included aggressive IV fluid resuscitation and IV calcitonin. However, no zoledronic acid was given due to a history of parathyroidectomy and risk of hypocalcemia. His serum calcium improved and eventually normalized. His confusion resolved. However, his creatinine and BUN increased to 3.4 mg/dL and 77, respectively, and did not improve to his baseline. This case highlights the importance of recognizing Milk-Alkali Syndrome as a potential consequence of over-the-counter calcium supplementation and highlights the potential for acute kidney injury which could be irreversible. Healthcare providers should be vigilant in identifying patients at risk, which includes older patients and patients with chronic kidney disease. Early recognition and appropriate management are crucial to prevent further renal deterioration and improve outcomes in individuals with Milk-Alkali Syndrome. Presentation: 6/2/2024

The Relationship of Vitamin A and Neonatal Respiratory Diseases: A Meta-Analysis.

This study systematically analyzes the relationship of vitamin A on the neonatal respiratory diseases. An extensive literature search for relevant studies was conducted on PubMed, Web of Science, and so on. After screening in strict accordance with the inclusion and exclusion criteria, 12 articles on vitamin A deficiency and 12 articles on vitamin A supplementation were included. Stata 17.0 software was used to perform meta-analysis, heterogeneity test, and sensitivity analysis, and the corresponding mathematical model was used to merge the data. The meta-analysis results of the relationship between vitamin A deficiency and neonatal respiratory diseases indicated that compared with the neonates with normal vitamin A, the neonates with vitamin A deficiency had adverse health outcomes of neonatal respiratory diseases (OR = 4.86, 95% CI: 2.68-8.84), of which neonatal respiratory distress syndrome (NRDS) (OR = 4.10, 95% CI: 2.32-7.23) and neonatal pneumonia (OR = 3.22, 95% CI: 2.18-4.77) were analyzed by subgroup analysis. The meta-analysis of the relationship between vitamin A supplementation therapy and neonatal respiratory diseases showed that vitamin A supplementation was an effective therapeutic measure for neonatal respiratory diseases (RR = 1.06, 95% CI: 1.04-1.07): NRDS (RR = 1.03, 95% CI: 1.02-1.05) and NBPD (RR = 1.08, 95% CI: 1.01-1.15). The funnel chart method results show that there was publication bias in studies on vitamin A deficiency induced to and vitamin A supplementation therapy for neonatal respiratory diseases. The sensitivity analysis results showed that excluding some special article had some effect on the final pooled effect. But generally speaking, the result of meta-analysis was stable. There is a statistical correlation of vitamin A on the neonatal respiratory diseases from two aspects of etiological exploration and effect evaluation of treatment.

Is vitamin D deficiency a risk factor in the occurrence and recurrence of febrile convulsions in children?

Background: Febrile seizure (FS) is the commonest childhood seizure. Our aim was to evaluate low Serum 25(OH) vitamin D level (vitamin D) as a risk factor for FS and whether vitamin D supplementation reduces its recurrence. Methods: A prospective cohort of children aged 6-60 months with FS (cases) and children with fever ≤3 days without seizures (controls) were recruited over a 2-year period. Vitamin D level was measured; those with low levels (<20 ng/ml) were treated with vitamin D for 3 months. Telephonic follow up was done upto 3 months regarding compliance, thereafter, upto 24 months for seizure recurrence. Results: 259 children (125 cases,134 controls) were recruited. Overall, 90 children (34.7%) had low vitamin D level. There was no difference between cases and controls with low vitamin D levels (p=0.37). 22 (17.6%) children had seizure recurrence. Of this serum vitamin D level was low in 2 (9.1%) while 20 (90.9%) had sufficient levels (p=0.021). The odds ratio for FS recurrence was 5.8 times higher among cases with normal vitamin D level (>20 ng/ml). Conclusions: There was no difference in mean vitamin D levels between cases and controls. However, there was significantly lower seizure recurrence in children who had low vitamin D level at presentation and had received vitamin D therapy. We postulate that treatment with vitamin D may reduce risk of FS recurrence even in those with serum vitamin D level in the “sufficient” range as per the recommended guidelines. Larger RCTs are needed to confirm these findings.

Vitamin A deficiency disturbs Ret expression and induces urinary tract developmental abnormalities in mice.

Moderate vitamin A levels during pregnancy are strongly related to normal embryonic development in both animal models and population studies. Abnormal development of urinary tract system is linked to either an excess or a shortage of vitamin A. The relationships among maternal vitamin A deficiency prior to conception, moderate vitamin A supplementation during pregnancy, and abnormal urinary system development in offspring are unclear. By creating preconception and preconception + pregnancy vitamin A insufficiency mouse models, we investigated whether moderate vitamin A treatment during pregnancy may reduce the prevalence of CAKUT and increase distant vitamin A levels in offspring, as well as any potential pathways involved. We effectively established a prepregnancy vitamin A-deficient mouse model by providing a particular diet with or without vitamin A for four weeks. The offspring of the hypovitaminosis A model group presented a greater proportion of neonatal urinary tract developmental malformations. Abnormalities in ureteral bud emergence and key molecules during renal development, such as p-Plcγ and Ret, may be the primary causes of offspring development of CAKUT as a result of mothers' hypovitaminosis A. Normal vitamin A diets, on the other hand, may help mitigate the teratogenic consequences of prepregnancy hypovitaminosis A, as well as defects produced by ureteral budding and major molecular changes. In contrast, the administration of normal vitamin A feeds during pregnancy may ameliorate the teratogenic effects of prepregnancy hypovitaminosis A to a certain extent and may also ameliorate the abnormalities associated with ureteral budding and key molecular changes.

Effect of vitamin-D and other factors on the presence and severity of urinary incontinence and overactive bladder in elderly individuals

Objective: This study aimed to investigate the effect of serum vitamin D levels on urinary incontinence and overactive bladder in elderly individuals. Methods: The study included 106 elderly individuals who had their serum vitamin D levels measured in the past year. Sociodemographic characteristics, habits, medical histories, medications used, height, and weight data were collected. The ICIQ-UI short form and Overactive Bladder-V8 form were adminis-tered. Participants were grouped based on their vitamin D levels. Results: Among participants, 17.9% had severe vitamin D deficiency, 28.3% had vitamin D deficiency, 18.9% had vitamin D insufficiency, and 34.9% had normal vitamin D levels. No significant association was found between vitamin D levels and the presence of urinary incontinence and overactive bladder. When participants were grouped by vitamin D levels, there was no significant difference in the presence of urinary incontinence and overactive bladder among the groups. However, a significant difference was found in the severity of overactive bladder. Individuals with normal vitamin D levels had significantly higher rates of urinary incontinence and overactive bladder compared to those with lower levels. Conclusion: Urinary incontinence increases with age and may be associated with aging-related comor-bidities. Although reports in the literature suggest a relationship between vitamin D deficiency and urinary incontinence and overactive bladder, this relationship was not confirmed in our study. This discrepancy may be due to differences in the characteristics of the populations studied in the literature.

The Relationship between Vitamin D, Inflammatory Markers, and Insulin Resistance in Children.

In this study, we investigated 25-hydroxyvitamin D (25(OH)D, vitamin D), inflammatory hematologic ratios such as neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), monocyte/HDL-C ratio (MHR) and plasma atherogenic index (PAI) and possible relationships with insulin resistance (IR) in children. A total of 210 individuals, including 96 children with IR and 114 children without IR, aged 6-18 years, who were admitted to the Pediatric Endocrinology Outpatient Clinic at Medicine Hospital, Istanbul Atlas University were included in our study. Compared to patients without IR, NLR, PLR, SII, and MHR were significantly higher in patients with IR. Fasting insulin, PAI, homeostasis model assessment of insulin resistance (HOMA-IR), and HOMA-β were significantly higher and quantitative insulin sensitivity check index (QUICKI) was considerably lower in patients with IR compared to those without IR. NLR, SII, and MHR were lower in normal vitamin D groups than the others (p < 0.001). PLR was lower in the group with normal vitamin D levels than the groups with insufficient or deficient levels of vitamin D (D < 21). We found that vitamin D deficiency in childhood is related to increased levels of circulating inflammatory markers (NLR, PLR, MHR, PAI), IR, and decreased insulin sensitivity. According to our results, supplementation of vitamin D may be beneficial in averting IR and enhanced systemic inflammation.

Evaluation of the natural killer cell subsets and their relationship with serum interferon gamma and vitamin D levels in women with stages III and IV endometriosis: A case-control study.

Natural killer (NK) cells play a critical role in the pathogenesis of endometriosis. Moreover, a normal vitamin D level is remarkably associated with an optimal immune response. So, there may be a probable relationship between these factors and the endometriotic women. This study aimed to evaluate the percentage of NK cells and their subsets and their relationship with serum levels of vitamin D and interferon-gamma (IFN-γ) in women with endometriosis. In this case-control study, 29 women with stage III-IV endometriosis and 30 healthy controls were enrolled. The study was conducted in the Immunology Department of Isfahan University of Medical Sciences, Isfahan, Iran between November 2021 and June 2022. The percentage of NK cells and their subsets, including CD56 CD16 , CD56 CD16 and CD56 CD16 were measured in the peripheral blood samples using flow cytometry. Serum levels of vitamin D and IFN-γ were also measured using the enzyme-linked immunosorbent assay. The mean percentage of NK cells in women with endometriosis increased significantly compared to the control group (p = 0.03). The percentage of CD56 CD16 (p = 0.007) and CD56 CD16 (p = 0.043) increased significantly in women with endometriosis in comparison with the control group, but the percentage of CD56 CD16 subset was not significantly different. No relationship was observed between NK cells and their subsets with vitamin D and IFN-γ in the studied groups. The study of NK cell subsets and their related factors can be useful in assessing and treating women suffering from endometriosis. However, more comprehensive studies are required to draw definitive conclusions about these observations.

Features of supply and approaches to the use of vitamin D in children in the post-COVID period

Vitamin D is an important component of immune function, and deficiency in childhood is associated with an increased risk of acute respiratory viral infections. Purpose. To assess the dynamics of vitamin D supply in children after a new coronavirus infection with the use of cholecalciferol. Material and methods. We examined 55 children aged 0–17 years (10.0 [9.2; 10.6] years), 52.7 % boys with COVID-19, who received cholecalciferol in a dose of 1000 to 3000 IU for 30 days in depending on the concentration of 25(OH)D. After 30 days of taking vitamin D3, the levels of total vitamin D in the blood serum were re-determined. Results. The median 25(OH)D level in children with COVID-19 was 24.5 [23.9; 26.7] ng/ml. 34.5 % of children had vitamin D deficiency status (≤ 20 ng/ml), 32.7 % had insufficiency (21–30 ng/ml), a third of patients had normal vitamin D status (≥ 30 ng/ml). As a result of treatment with cholecalciferol, the number of children with hypovitaminosis D decreased by 2 times (35.4 %, p &lt; 0.05), with an adequate level — doubled (65.5 %, p &lt; 0.05). Depending on the level of 25(OH)D, no statistically significant differences were found in the severity of coronavirus infection (χ² = 0.872, p = 0.929). Conclusion. In 2/3 of cases, children infected with SARS-CoV-2 had hypovitaminosis D. Children under 6 years of age were more likely to have vitamin D insufficiency, while patients 7–17 years of age had a deficiency. The distribution of vitamin D levels did not differ depending on the severity of coronavirus infection. Doses of cholecalciferol taken for 30 days were sufficient to increase the concentration of vitamin D in the blood serum of children with deficiency but did not reach standard values in patients with vitamin D deficiency.

Effect of Deficiency of Vitamin D on Depression and Premenstrual Syndrome.

Vitamin D, otherwise called the daylight vitamin, is critical for the control of calcium and phosphorus assimilation. Defienceny of it is also associated with many medical problems like multiple sclerosis, cancer,cardiovascular disease and can also lead to psycho somatic issues. The study was conducted on 80 subjects who were further divided into 2 groups of 40 each. Group A with normal Vitamin D levels and group B was formed of people suffering from hypovitaminosis D, 20 females were tested on Premenstrual Syndrome as well. Hamilton Depression Rating Scale was used to measure level of depression. It was hypothesized that hypovitaminosis D would be positively related to depression, and premenstruation syndrome

Prevalence of low vitamin D status in an urban district in Sri Lanka: a population-based study

BackgroundVitamin D deficiency (VDD) is conventionally associated with inadequate sunlight exposure. Ironically, recent evidence suggests a rising prevalence in urban areas of tropical regions like Sri Lanka, where comprehensive data are unavailable. This study aimed to estimate the prevalence of low vitamin D status in urban adults and its impact on serum calcium.MethodsA population-based cross-sectional study was conducted among 1260 adults aged 35–74 years, living in Colombo, the most urban district in Sri Lanka. They were recruited from 63 administrative divisions, using multi-stage, probability-proportionate-to-size, cluster sampling. Non-fasting venous blood was collected without tourniquet. Low vitamin D (< 30.0 ng/mL), VDD (< 20 ng/mL) and vitamin D insufficiency (20.0–29.9 ng/mL) were determined using chemiluminescence assay method, and serum calcium using Calcium Gen2 reagent.ResultsAmong the population (53.3% females; mean age = 51.8 years), the prevalence of low vitamin D was 93.9% (95% CI: 92.5–95.2). This was primarily due to VDD (67.5%; 95% CI: 64.9.0–70.1%), with some insufficiency (26.4%; 95% CI: 24.0–28.9%). Most VDD cases (53.9.0%) were 'mild' (10.0- < 20.0 ng/mL) in severity, with fewer 'moderate' (12.8%) and 'severe' (0.8%) cases. Prevalence of VDD was highest in females, aged 35–44-years, living in 'highly urban' areas and of Tamil ethnicity. Further, VDD showed a decreasing trend with older age groups, while it was significantly more prevalent in females than males (72.6% vs. 61.7%; p < 0.01), across all age groups. Low serum calcium levels were observed in 9.8% of adults with low vitamin D, compared to 22.4% with normal vitamin D, implying that there could be factors other than vitamin D in maintaining serum calcium levels.ConclusionsColombo District, representing urban settings in Sri Lanka faces a high prevalence of low vitamin D, primarily VDD, with higher rates in females, younger individuals and highly urban areas. These findings challenge assumptions about tropical regions being guaranteed of optimal vitamin D levels; and underscore the need for national vitamin D supplementation and food fortification programs, especially in high-risk urban settings in South Asian countries like Sri Lanka.

Is vitamin D associated with disease activity in patients with axial or peripheral spondyloarthritis? A real-life study.

Vitamin D plays important role in inflammatory rheumatic diseases, which in turn rose an interest for investigating association of its deficiency with disease activity. In this research we aimed to evaluate this matter in the context of spondyloarthritis (SpA), together with treatment modalities and bone density in people diagnosed with axial or peripheral SpA in real-life setting. In our study we enrolled 99 patients with diagnosis of SpA treated at the tertiary level rheumatology department. Serum 25(OH)D levels, treatment modality (NSAIR or DMARDs), disease activity, tobacco smoking habits, mineral density of bone, supplementation and seasonal variations were assessed. We used standardized questionnaires such as ASDAS-CRP, BASFI and joint count, among many others, to evaluate some of the mentioned parameters. Sixty-five percent of patients had vitamin D deficiency. We found marginaly higher activity of disease in subjects with low vitamin D. In cases of peripheral SpA, there was a significant association of higher number of swollen joints and lower vitamin D levels. Additionally, the significant correlation was seen between normal serum vitamin D and supplementation. In our real-life study of patients with SpA we found a significant percentage of vitamin D deficit, with a tendency of slightly higher disease activity in those patients.In order to clarify the impact of the vitamin on disease activity in SpA and the supplementation recommendations for patients with these conditions, the conduction of further studies is required.

Somatic Structure and Ultrasound Parameters of the Calcaneus Bone in Combat Sports Athletes in Relation to Vitamin D3 Levels.

Background/Objectives: Physical activity is widely recognized for its beneficial effects on bone density during adolescence, which could lead to enhanced bone density in later life, thus acting as a health-promoting activity with long-lasting implications. However, not all studies are conclusive regarding the type, intensity, duration, and frequency of the most effective physical activities. This study focuses on combat sports athletes and examines the relationship between their somatic build and heel bone parameters using ultrasound (USG) and their vitamin D3 levels. Methods: The study included 40 male athletes specializing in various combat sports. The measurements of body height, body mass, skinfold thickness, and bone widths at multiple sites were performed to estimate the somatic build. The USG parameters of the heel bone and the blood levels of vitamin D3 were also recorded. Statistical significance was determined using one-way ANOVA, with differences among sports disciplines also examined. Results: The study found significant differences in the body composition and USG bone parameters among athletes from different combat sports (p ≤ 0.05). The calcaneus stiffness index (SI) and speed of sound (SOS) were significantly higher in athletes with normal vitamin D3 levels compared to those with below-normal levels (p = 0.0015 and p = 0.001, respectively). These findings suggest that vitamin D3 may influence bone stiffness and density. Conclusions: The study underscores the importance of maintaining adequate vitamin D3 levels to support bone mineralization in athletes, particularly those training indoors with limited exposure to sunlight. It also highlights the potential of using USG as a non-invasive method to assess bone health, aiding in the optimization of training programs to prevent injuries and improve performance.