25-OH Vit Research Articles

Serum 25-Hydroxy Vitamin D Level Does Not Reflect The Severity of Wart: A Cross-Sectional Study

Objective: Verruca vulgaris is a benign epithelial proliferative disease caused by human papilloma viruses. Topical and intralesional vitamin D applications are effective methods in the treatment of warts. However, the relationship between the disease and serum vitamin D levels is unclear. The correlation between the severity of the disease and serum 25-hydroxy vitamin D (25-OH vit D) levels have not been previously investigated. This study aimed to determine the relationship between serum 25-OH vit D levels and disease severity in patients with verruca vulgaris.
 Material and Methods: Serum 25-OH vit D levels were evaluated in 40 patients with verruca vulgaris and 43 sex and age-matched healthy volunteers. Serum 25-OH vit D levels were compared by grouping the patients according to the severity and duration of verruca vulgaris disease Results: There was no significant difference in serum 25-OH vit D levels between verruca vulgaris patients and the control group (p=0.760). There was no significant difference between serum 25-OH vit D level, disease severity and disease duration in the verruca vulgaris group (p =0.102, p=0.257, respectively).
 Conclusion: Serum 25-OH vit D level was not associated with verruca vulgaris. Serum 25-OH vit D levels are not related to disease severity and duration. Our data do not support vitamin D supplementation for the prevention or treatment of verruca vulgaris.

MO095: Normocalcaemic Hyperparathyroidia Diagnosed by Calcium Load

Abstract BACKGROUND AND AIMS Calcium load is usually used in clinical practice to diagnose a normocalcaemic hyperparathyroidia in stone disease. However, the calcium load developed by Pak and colleagues has been described in very few patients. We aimed to provide data about calcium load in a bigger cohort of patients. METHOD We included retrospectively 115 patients who underwent a calcium load for stone disease or hypercalciuria with a basal increased PTH. At basal state, ionized calcium (iCa2+), PTH, phosphate urinary Calcium to creatinine ratio (UCa/creat), 25 OHvit D and 1–25 OHvit D were measured. Patients ingested 1g of calcium and iCa2+ PTH, phosphate and UCa/creat were measured after 2 h and 4. Calcium load was interpreted based on Pak's publications. Normocalcaemic hyperparathyroidia was defined by fasting urinary calcium/creatinine ratio >0.35 mmol/mmol associated with a non-adapted PTH to ionized calcium (iCa2+) after calcium load and absorptive hypercalciuria. Renal hypercalciuria is defined by fasting and absorptive hypercalciuria with an adapted decrease of PTH to iCa2+. RESULTS At a basal state, PTH was 88 (±19) ng/L, calcium was 2.36 (±0.14) mmol/L, iCa 1.23 (±0.08) mmol/L, calcium excretion fraction was 1.5 (0.85)% and phosphataemia was 0.88 (±0.14) mmol/L. The mean fasting Ca/creat ratio was 0.4 mmol/mmol. A total of 21% were hypercalcemic (iCa > 1.30 mmol/L). iCa2+ was 1.28 (±0.07) 2 h after calcium load (H2) and was 1.27 (±0.07) mmol/L 4 h after calcium load (H4). The mean decrease in PTH was 32% after H2 and 44% after H4. Urinary Ca/creat was 0.55 and 0.73 mmol/mmol after H2 and H4, respectively. A total of 27% of patients had a UCa/creat increase of >0.5 mmol/mmol after H2, and 47% after H4. A total of 72% had a calcium excretion fraction of >1%. Normocalcaemic hyperparathyroidia was diagnosed in 64% of these patients. In Normocalcaemic hyperparathyroidia, mean PTH was 91 (±21) ng/L, the mean decrease of PTH was 35% and 27% after H2 and H4, respectively. The mean iCa2+ increased from 1.24 (±0.07) to 1.28 (±0.07) mmol/L. UCa/creat increased from 0.45 (±1.26) to 0.71 (±1.26) and 0.81 (±1.26) after H2 and H4, respectively. The 1–25 OH vit D was 159 (±55) pmol/L. In renal hypercalciuria, mean PTH was 66 (±26) ng/L, 42 (±20) after H2 and 30 (±13) after H4. The mean decrease in PTH was 65% after H4. Mean iCa2+ increased from 1.24 (±0.07) to 1.27 (±0.07) mmol/L. UCa/creat increased from 0.33 (±0.19) to 0.37 (±0.25) and 0.68 (±0.44) mmol/mmol after H2 and H4, respectively. The 1–25 OH vit D was 130 (±67) pmol/L. Basal PTH is significantly higher in normocalcaemic hyperparathyroidia compared with renal hypercalciuria, but there is no difference in fasting UCa/creatinine ratio between both group. The 1–25 OHvit D level was significantly increased in normocalcaemic hyperparathyroidia. CONCLUSION Calcium load allows to discriminate patients with basal increased PTH between normocalcaemic hyperparathyroidia and renal hypercalciuria. We provide new data to help physicians in clinical practice.

Hypophosphatemia Associated with Tumor-Induced Osteomalacia Caused by A Third Primary Tumor: A Case Report

Tumor-induced osteomalacia (TIO) is a paraneoplastic condition in which a tumor, usually of mesenchymal origin, causes osteomalacia often by producing Fibroblast Growth Factor-23 (FGF-23). FGF-23 induces hypophosphatemia through its phosphaturic action. Case Presentation: A 65-year-old male patient presented with complaints of muscle weakness, difficulty walking and severe bone pain. His medical history included distal gastrectomy for a moderate-risk gastrointestinal stromal tumor (GIST) of 4 cm in diameter, Billroth II antecholic gastroenterostomy and subsequently total thyroidectomy for Stage 1 multicentric micropapillary carcinoma (CA). Widespread lesions detected on bone scintigraphy were considered as bone metastases of GIST. Laboratory investigations revealed the following results: calcium (Ca): 8.3 mg/dL; phosphate (P): 1.5 mg/dL; Parathormone (PTH): 75 pg/mL; 25-OH vit D3: 31 ng/mL; 1-25-(OH)2 vit D3: 36 pg/mL; creatinine: 0.75 mg/dL; alkaline phosphatase (ALP): 109 IU/L, urine phosphate: 2.54 g/day. His hypophosphatemia was considered to be most probably due to TIO induced by bone metastases of GIST. Since it was not possible to remove the metastases, the patient was started on oral phosphate and calcitriol therapy. However, despite an improvement in Ca levels after the initiation of the treatment, P levels persisted around 2 mg/dL. After one year of treatment, an ulcer developed on his right first toe, which was excised and identified as “extraskeletal myxoid chondrosarcoma” on pathological examination. Following excision of the tumor, the patient’s Ca and P values returned to normal range. The development of TIO in the presence of a GIST and thyroid CA is an unusual occurrence. As a matter of fact, the cause of hypophosphatemia was TIO which induced by a third primary tumor in this patient. To the best of our knowledge, TIO due to a third primary tumor is the first and only case in the literature. Another primary tumor focus should be suspected and carefully investigated if the patient already has a primary tumor and that tumor is not among those frequently inducing TIO.

Reduction in Hypercalcemia Following Readjustment of Target Serum 25-Hydroxy Vitamin D Concentration during Cholecalciferol Therapy in Vitamin D-Deficient Critically Ill Patients.

The intent of this study was an evaluation of our effort to reduce the incidence of hypercalcemia in critically ill vitamin D-deficient patients with multiple traumatic injuries given cholecalciferol. Vitamin D deficiency was defined as a serum 25-hydroxy vitamin D concentration (25-OH vit D) of <20 ng/mL. Adult patients (>17 years of age) were given 10,000 IU of cholecalciferol daily with an intended target 25-OH vit D of >19.9 ng/mL. These patients were compared to a historical control group that underwent therapy with a higher target of >29.9 ng/mL. Patients received cholecalciferol via the feeding tube along with enteral nutrition (EN) until the target 25-OH vit D was achieved, EN discontinued, the nutrition support service signed off the patient, or the patient was discharged from the TICU. Patients were included if two consecutive weekly 25-OH vit D were measured. One hundred and three critically ill trauma patients were retrospectively studied. Fifty were given cholecalciferol therapy with the new lower target 25-OH vit D, and 53 were from a historical cohort aiming for the higher target. Hypercalcemia (serum ionized calcium concentration > 1.32 mmol/L) was reduced from 40% (21 out of 53 patients) to 4% (2 out of 50 patients; p < 0.001). None of the hypercalcemic patients were symptomatic. Readjustment of target 25-OH vit D concentration resulted in a ten-fold decrease in the rate of hypercalcemia and improved the safety of cholecalciferol therapy for critically ill patients with traumatic injuries.

The role of serum 25 (OH) vitamin D level in the correlation between lipid profile, body mass index (BMI), and blood pressure

Since the prevalence of vitamin D deficiency is high in some countries, such as Iran, and the trend of hypertension and obesity is increasing, this study aimed to investigate the serum level of vitamin D and explore its correlation and association with obesity, blood pressure, fasting blood sugar (FBS), and lipid profile. Our hypothesis is that serum vitamin D levels are associated with risk factors for cardiometabolic disease such as hypertension. The results of this article were extracted from a cross-sectional study with a sample size of 720 people in the winter of 2020. The serum level of 25 OH vit D was measured using the ELISA method. In addition, lipid profiles were measured using the Auto Analyzer photometry method. Serum levels of vitamin D (25 (OH) vitamin D) were significantly higher in the control group compared to the case group (29.5±16.3 vs. 26.7±14.5; P-value=0.016). The significant association between body mass index (BMI) and FBS (Beta unadjusted:0.024, 95%CI 0.009:0.038; Beta adjusted:0.020,95%CI 0.005:0.034), and triglyceride (Beta unadjusted:0.009, 95%CI 0.006:0.012; Beta adjusted:0.008,95%CI 0.005:0.011), and an inverse association HDL-C (Beta unadjusted:-0.079,95%CI -0.123:-0.036; Beta adjusted:-0.065,95%CI -0.111:-0.019) were seen in both unadjusted and adjusted models. In conclusion, we report that obese people had significantly lower serum vitamin D levels than normal-weight people. There is also a significant correlation between BMI and blood pressure.

Serum sclerostin in acute kidney injury patients

BackgroundMany of the mineral metabolite abnormalities encountered in chronic kidney disease (CKD) patients were found also associated with acute kidney injury (AKI). In the last decade, sclerostin was found to intimately affect bone mineral metabolism in CKD patients. Nothing is known about sclerostin in AKI. ObjectiveWe looked for serum level of sclerostin in AKI patients in comparison to normal control subjects and if there is an impact on metabolic derangement, endothelial function or clinical outcome. Cases and methodsThis is a cross sectional case control observational study of 219 AKI cases (group I) beside 219 age matched normal control subjects (group II). All cases of group I were in the intensive care because of sepsis; 86 had acute on CKD (group Ib), while 133 had de novo AKI (group Ia). All studied subjects underwent estimation of serum sclerostin, parathyroid hormone (PTH), 25 hydroxy vitamin D (25 OH vit D), fibroblast growth factor 23 (FGF23), C-reactive protein (CRP), interleukin 6 (IL6), Homeostatic Model Assessment for Insulin Resistance (Homa IR), beside the routine CBC, kidney and liver function tests, serum calcium, and phosphorus, and flow mediated vasodilation of brachial artery (FMD). Follow-up of group I cases was done till they recovered or passed away. ResultsSerum sclerostin, PTH, FGF23, phosphorus, CRP, IL6, HOMA IR, creatinine, urea, uric acid, ALT, AST and white blood cell count (WBC) were significantly higher while serum calcium, 25 OH vit D, hemoglobin, platelet count and FMD were significantly lower in group I compared to group II (P<0.001 in all). On the other hand, there was no significant difference in serum sclerostin, PTH, FGfF23, 25 OH vit D, CRP, IL6, Homa IR and FMD between group Ia and Ib. Survivors were younger in age (median 55.5 vs. 60 years, P<0.04), had lower AST (30.5 vs. 58 units, P<0.001), had higher platelet count (206 vs 162×109/L, P<0.001), otherwise, there was no significant difference in any of the other parameters between survivors and patients that were lost. Serum sclerostin had strong correlation with FGF23 in group I (r=0.99, P<0.001) and group II (r=1, P<0.001). Homa IR had positive correlation with serum sclerostin (r=0.148, P=0.014) and serum FGF23 (r=0.142, P=0.018) in group I. ConclusionSclerostin is intimately related to FGF23. Sclerostin level increases in AKI patients. Both sclerostin and FGF23 might increase insulin resistance but have no impact on FMD. Neither sclerostin nor FGF23 interfere with AKI outcome.

A clinical registry of multisystemic presentation of hypovitaminosis D in hospital attendees in Kolkata

Background: Vitamin D (Vit D) is a steroid hormone essential for maintaining functional homeostasis in the body. Hypovitaminosis D has been a recognized worldwide problem affecting all age groups and sex. Its prevalence is very high in South Asia. Aims and Objectives: Therefore, this study was aimed to determine the spectrum of presentation of biochemical levels of hypovitaminosis D in Indian population in terms of age, sex, and multisystemic disorders. Materials and Methods: A cross-sectional study carried out on selective study population attending a tertiary care hospital from July 2019 to December 2020 with clinical presentations suspected to arise due to Vit D deficiency. Serum 25OH Vit D level was estimated by chemiluminescence method. Data were analyzed using GraphPad Prism 8. Results: Of the study population (n = 685), average serum 25(OH)D level in females and males was 24.13 ng/ml and 28.59 ng/ml, respectively. Significant difference in mean value of Vit D existed in males and females in the 21–40 years age group (p = 0.0048). Females in the Vit D deficient group (Vit D level&lt;20) mostly presented with mastalgia (20.45%), low back pain (17.61%), and joint pain (11.36%). Common clinical presentation in males with Vit D levels less than 20 ng/ml was diabetes mellitus without CKD (18.34%), non-diabetic CKD (19.27%), and low back pain (16.51%). Conclusion: Low Vit D levels manifest itself as signs and symptoms involving various multisystemic disorders involving different age groups in both sexes. Early recognition and replacement can prevent the progress of complications which Vit D deficiency makes us prone to develop.

Assessment of 25 Hydroxy Cholecalceferol Level in Autistic Children; is there a role for it in Treatment of Autism Spectrum Disorder?

Abstract Background Autism is a group of neurodevelopmental disabilities with various genetic and environmental risk factors. Vitamin D is an important neurosteroid hormone which can affect brain development and function, but research on its use in treating autism has been limited. Objectives The current study aimed at assessing the level of 25 OH vit D3level in a group of autistic infants and children compared to controls and correlating it with the severity of autistic manifestations and evaluation of the role of therapeutic doses of vitamin D on the severity of autistic manifestations. Methodology Thirty autistic Egyptian children (group I) and 30 clinically healthy age and sex matched controls were enrolled (group II). Therapeutic doses of vitamin D were given for autistic children who showed insufficient levels of 25 OH cholecalceferol for a period of 4-6 weeks followed by maintenance doses for another 6 weeks. Psychometric and laboratory evaluation for this group was done thrice: at the onset of study, at 6 week after enrollment in the study, and at 12 weeks after that enrollment. Results Serum vitamin D level was substantially reduced in patients with ASD in comparison to control group, and on the other hand, 25 (OH) vitamin D level was significantly negatively correlated with ATEC score and Total CARS score. Autistic children who received vitamin D3 treatment had significant improvement of CARS and ATEC scores. Conclusion vitamin D supplementation significantly improved the outcome of enrolled autistic children. It is recommended to follow up our studied sample to check the consolidation of improvement for how long it will be needed.

Poster Abstracts

Purpose: The protective role of Vitamin D as an immunomodulator has been demonstrated in different pathologies included the viral etiology. This effect has been described by different mechanisms among these acting as an immunoprotein inducer, participates in growth and cell differentiation and acts as a mediator of apoptosis. Some evidence suggests that it could influence the SARS-COV 2 infection and its prognosis. Kidney transplant (KT) patients are more susceptible to 25 (OH) VitD (Calcidiol) deficiencies. The purpose of this study is to evaluate the Vitamin D status in transplant patients who have been diagnosed with COVID-19 and its possible correlation with prognosis. Methods: It is an observational, retrospective, cross-sectional and descriptive study that includes kidney transplant patients diagnosed with COVID-19 and with serum 25 (OH) Vit D Results: 79 patients were evaluated. The mean age was 58 years, 60.8% were men. 86% were KT, 11% were simultaneous pancreas and kidney transplant (SPK). 39 (48%) presented neumonia, 22 (28%)flu-like syndrom. 14 (17%) asyntomatic and 2(2,5%) fever. From this patients 39,2% had not changes in the antiinflamatorie therapy, 20.3%, required increased dose of corticosteroids, and 30.4% required methylprednisolone bolus or initiation of anti-interleukin therapy. The mean of Vit D was 21.41+/- 11% we found that 52% has Vit D 30 ng / dl In 32 patientes who required intensification of treatment we found that 73% had Vit D levels <20 ng. 11 patients need an citical care unit, of these 62.5% had levels below <20 ng / dl. There were 12 deaths. 66% of deaths had vitamin D values <20 ng / dl. Conclusions: We were able to observe that vitamin D levels could influence in the prognosis of SARS-COV 2 infection. Vitamin D deficiency was found in a high percentage of transplant patients with COVID 19. Low levels of 25 OH Vit D were evidenced in patients who required greater intensification of antiinflamatory treatment and in deaths.

Low vitamin D levels and increased neutrophil in patients admitted at ICU with COVID-19.

Background & aimsSystemic inflammation has been reported as a new predictor for COVID-19 outcomes. Thus, we hypothesized that ICU patients infected by COVID-19 had lower blood vitamin D levels and increased systemic inflammation. Therefore, this is the first Brazilian study to evaluate the vitamin D concentrations and NLR as a systemic inflammation in patients infected by COVID-19 admitted in ICU.MethodsThis cross-sectional study selected twenty-six patients from COVID-19 Data Sharing/FAPESP, Brazil. Twenty-five patients were enrolled from a single hospital and those with blood vitamin D and neutrophil and lymphocyte data were included and had all available data analyzed. Patients were divided in two groups: low vitamin D concentration when ≤20 ng/mL (low Vit D group, n = 8, 5M/3F, 62.7 ± 8.4 years old), and normal vitamin D when > 20 ng/mL (normal Vit D group, n = 17, 9M/8F, 74 ± 8.2 years old). Serum 25-hydroxy-vitamin D, C reactive protein (CRP), and count of neutrophils and lymphocytes concentrations were collected from COVID-19 Data Sharing/FAPESP. Statistical analyses were performed using the Prism version 5.0 and Student T test was applied to verify any difference between the groups.ResultsLow vitamin D group had 15.5 ± 3.3 ng/mL of 25OH Vit D concentrations and normal vitamin D group had 35.9 ± 8.8 ng/mL. Although no difference between groups for CRP concentrations (low Vit D: 4.5 ± 3.3 vs. normal Vit D: 4.2 ± 4.0 mg/dL, p = 0.45), we found higher neutrophil count and NLR values in the low Vit D group when compared to normal Vit D group (low Vit D: 6049.8 ± 3719.7 vs. normal Vit D: 3741.8 ± 1704.1 ng/mL, p = 0.02) and (low Vit D: 9.0 ± 8.6 vs. normal Vit D: 4.2 ± 4.0 ng/mL, p = 0.03), respectively.ConclusionThis data sharing-derived cases of COVID-19 in patients admitted at ICU showed that patients infected by COVID-19 had lower serum 25-hydroxy vitamin D and enhanced systemic inflammation when assessed by NLR values.

Serum sclerostin in acute kidney injury patients

BackgroundMany of the mineral metabolite abnormalities encountered in chronic kidney disease (CKD) patients were found also associated with acute kidney injury (AKI). In the last decade, sclerostin was found to intimately affect bone mineral metabolism in CKD patients. Nothing is known about sclerostin in AKI. ObjectiveWe looked for serum level of sclerostin in AKI patients in comparison to normal control subjects and if there is an impact on metabolic derangement, endothelial function or clinical outcome. Cases and methodsThis is a cross sectional case control observational study of 219 AKI cases (group I) beside 219 age matched normal control subjects (group II). All cases of group I were in the intensive care because of sepsis; 86 had acute on CKD (group Ib), while 133 had de novo AKI (group Ia). All studied subjects underwent estimation of serum sclerostin, parathyroid hormone (PTH), 25 hydroxy vitamin D (25 OH vit D), fibroblast growth factor 23 (FGF23), C-reactive protein (CRP), interleukin 6 (IL6), Homeostatic Model Assessment for Insulin Resistance (Homa IR), beside the routine CBC, kidney and liver function tests, serum calcium, and phosphorus, and flow mediated vasodilation of brachial artery (FMD). Follow-up of group I cases was done till they recovered or passed away. ResultsSerum sclerostin, PTH, FGF23, phosphorus, CRP, IL6, HOMA IR, creatinine, urea, uric acid, ALT, AST and white blood cell count (WBC) were significantly higher while serum calcium, 25 OH vit D, hemoglobin, platelet count and FMD were significantly lower in group I compared to group II (P<0.001 in all). On the other hand, there was no significant difference in serum sclerostin, PTH, FGfF23, 25 OH vit D, CRP, IL6, Homa IR and FMD between group Ia and Ib. Survivors were younger in age (median 55.5 vs. 60 years, P<0.04), had lower AST (30.5 vs. 58 units, P<0.001), had higher platelet count (206 vs 162×109/L, P<0.001), otherwise, there was no significant difference in any of the other parameters between survivors and patients that were lost. Serum sclerostin had strong correlation with FGF23 in group I (r=0.99, P<0.001) and group II (r=1, P<0.001). Homa IR had positive correlation with serum sclerostin (r=0.148, P=0.014) and serum FGF23 (r=0.142, P=0.018) in group I. ConclusionSclerostin is intimately related to FGF23. Sclerostin level increases in AKI patients. Both sclerostin and FGF23 might increase insulin resistance but have no impact on FMD. Neither sclerostin nor FGF23 interfere with AKI outcome.

Hypervitaminosis A: A Rare Cause of Hypercalcemia

Abstract Introduction: Hypercalcemia is a rather common clinical problem and a majority of cases are found to be secondary to primary hyperparathyroidism and malignancy. A rare cause of hypercalcemia is associated with high levels of vitamin A and thought to be secondary to the effect of vitamin A on bone to stimulate osteoclastic resorption or inhibit osteoblastic formation. Clinical Case: A 54 year-old male with a past medical history of CKD stage 3 secondary to medullary sponge kidney presented for hypercalcemia. He complained of chronic constipation, joint pain, mood changes and recurrent kidney stones. Reported multivitamin use (including 1000mcg of vitamin A) for years but was discontinued one year prior to visit. Lab work showed calcium of 11.5 mg/dL (8.7–10.2mg/dL), albumin 4.9 g/dL (3.8–4.9g/dL), elevated 24h urine calcium, eGFR 40 mL/min/1.73, parathyroid hormone 5 pg/mL (15-65pg/mL,) normal 1,25-OH vit D and 25-OH vit D, PTHrP &amp;lt;2.0 pmol/L, serum protein electrophoresis unremarkable. His vitamin A level was elevated to 103 ug/dL (20.1–62.0ug/dL). CT chest showed no findings concerning for sarcoidosis. Bone density scan showed normal bone mineral density. Patient diagnosed with hypercalcemia secondary to elevated vitamin A levels. Current limited literature shows stopping the vitamin A supplement will normalize vitamin A levels and correct the hypercalcemia. This patient had discontinued his multivitamin 1 year prior and vitamin A remained elevated, thought to be due to his poor kidney function. Treatment was targeted at improving his hypercalcemia and reducing his symptoms. He was prescribed a one-week course of prednisone 40 mg daily. His calcium level improved to 10.5 mg/dL. Prednisone was reduced to 20 mg daily with normalization of calcium to 10.3 mg/dL (8.7–10.2mg/dL). Conclusion: Hypercalcemia is a rare but known complication of vitamin D toxicity. The liver, kidney and adrenal glands store vitamin A and it is excreted in the urine. Liver and kidney disease pose higher risk of vitamin A toxicity. We present a unique case of Hypercalcemia secondary to elevated vitamin A levels in a patient with moderate chronic kidney disease who was not taking excessive amounts of vitamin A and whose calcium and vitamin A did not normalize once vitamin A supplements were discontinued. The CKD 3 may have reduced vitamin A clearance and increased its toxicity. Hypercalcemia is not the only concern regarding vitamin A toxicity, the increasing use of dietary supplements and over the counter medications may pose significant risks for osteoporosis and bone fractures. A high clinical suspicion and thorough workup to exclude other causes of hypercalcemia is warranted to diagnose hypervitaminosis A as the etiology. Steroids can reduce gastrointestinal absorption of calcium, however, its role in vitamin A toxicity remains unclear. Further research is needed to investigate the appropriate treatment for these patients.

The association between vitamin D levels and the clinical severity and inflammation markers in pediatric COVID-19 patients: single-center experience from a pandemic hospital.

Vitamin D has an immunomodulating property that regulates the inflammatory response. In this study, the aim was to evaluate the relationship between vitamin D levels and clinical severity and inflammation markers in children and adolescents with COVID-19. The clinical and laboratory records of 103 pediatric cases with COVID-19, whose vitamin D levels had been measured, were retrospectively reviewed. The cases were divided into groups according to their clinical severity (asymptomatic, mild, and moderate-to-severe) and vitamin D levels. The moderate-to-severe clinical group had significantly higher inflammation markers (CRP, procalcitonin, fibrinogen, d-dimer) and a lower lymphocyte count compared to both the mild and asymptomatic groups. The 25 OH vitamin D levels were also significantly lower (p < 0.001), and the ratio of vitamin D deficiency was 70.6% in the moderate-to-severe group. The vitamin D–deficient group had a significantly higher age and fibrinogen levels while also having a lower lymphocyte count compared to the insufficient and normal groups. The 25 OH vitamin D level was correlated positively with the lymphocyte count (r = 0.375, p = <0.001), and negatively with age (r = −0.496, p = <0.001), CRP (r = −0.309, p = 0.002) and fibrinogen levels (r = −0.381, p = <0.001). In a logistic regression analysis, vitamin D deficiency, d-dimer, and fibrinogen levels on admission were independent predictors of severe clinical course.Conclusion: This study revealed an association between vitamin D deficiency and clinical severity, in addition to inflammation markers in pediatric COVID-19 cases. Prophylactic vitamin D supplementation may be considered, especially in the adolescent age group. What is Known:• • The pathology of COVID-19 involves a complex interaction between the SARS-CoV-2 and the immune system. Hyperinflammation/cytokine storm is held responsible for the severity of the disease.• Vitamin D has multiple roles in the immune system that can modulate the body reaction to an infection.What is New:• • Clinically more severe group had significantly lower vit D levels and significantly higher inflammation markers.• Lower 25 OH vit D levels were associated with higher inflammation markers, suggesting an important role of vitamin D in the clinical course of COVID-19 in children and adolescents probably by regulating the systemic inflammatory response.Supplementary InformationThe online version contains supplementary material available at 10.1007/s00431-021-04030-1.

Evaluation of Vitamin D3 metabolite (25-OH Vit D3), Neurotransmitter (ACh), and the Expression of Proinflammatory Cytokines (IL-6 and TNF-α) in Tissue Homogenate after Administration of Biofield Energy Healing-based Novel Proprietary Test Formulation and Biofield Treatment per se to the Animals in Vitamin D3 Deficiency Diet (VDD)-induced Sprague Dawley Rats

A novel proprietary test formulation was designed which included minerals, vitamins, β-carotene, cannabidiol isolate,and Panax ginseng extract. This present study was evaluated the impact of the Trivedi Effect® on novel proprietary test formulation in male Sprague Dawley rats, fed with vitamin D3 deficiency diet (VDD). The novel test formulation was divided into two parts; one part was defined as untreated test formulation, while the other part was defined as the Biofield Energy Treated sample, which received the Biofield Energy Healing Treatment by renowned Biofield Energy Healer, Mr. Mahendra Kumar Trivedi. The level of 25-OH Vit. D3 was measured in brain homogenate, which was found to be increased by 20.13%, 24.12%, 45.86%, 14.79%, and 29.96% in the G5 group treated with Biofield Treated test formulation, Biofield Energy Treatment per se to the animals (G6), 15 days pre-treatment of Biofield Energy Treated test formulation (G7), Biofield Energy Treatment per se plus Biofield Energy Treated test formulation from day -15 (G8), and untreated test formulation to the Biofield Energy Treated animals (G9) groups respectively, as compared with the disease control (G2) group. Brain acetylcholine (ACh) level was increased by 61.33% in the G7 group as compared with the untreated test formulation (G4) group. The expression of interleukin-6 (IL-6) was significantly reduced by 43.44% (p≤0.01), 30.93%, 21.42%, 45.99% (p≤0.01), and 60.85% (p≤0.01), respectively as compared with the G4. Lung pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α) level was significantly reduced in the G5, G6, G7, and G8 by 24.86%, 32.55% (p≤0.01), 30.12% (p≤0.01), and 42.69% (p≤0.01), respectively, as compared with the G4 group. Altogether, the Biofield Treated test formulation and/or per se treatment to the animals significantly improved the levels of active form of vitamin D3 metabolite (25-OH Vit D3) and neurotransmitter (ACh); consequently significantly lowered the expression of proinflammatory cytokines (IL-6 and TNF-α). Therefore, the energized test formulation or per se treatment could be effectively useful against neuronal damage and inflammation for the management of brain disorders such as Alzheimer’s disease, dementias, brain cancer, epilepsy and other seizure disorders, mental disorders, and Parkinson’s. Thus, the results showed a significant slowdown of disease progression and all other disease-related complications/symptoms in the preventive Biofield Energy Treatment group per se and the Biofield Energy Treated Test formulation groups (viz. G6, G7, G8, and G9) as compared to the disease control group.

Association between the concentration of CYP24A1, 25-OH vit D3 and calcium-phosphate metabolism with an increased risk of multiple sclerosis in Iraqi patients

Growing research has shown that multiple sclerosis (MS) patients have lower levels of 25-OHvitD3 than healthy controls. The purpose of this study was to evaluate the serum concentration of 25-OHvitD3, CYP24Alenzyme in MS patients and calcium-phosphate metabolism indices depending on the different disease lines and gender. Furthermore, we elevated the relationship between study parameters and gender with degree of motor disability according to the Expanded Disability Status Scale (EDSS). Serum of 110 Iraqi MS patients (50 male and 60 female) and 63 healthy individuals (30 male and 33 female) as control groups were used in our study. Serum level of 25-OHvitD3, CYP24A1and PTH were measured by ELISA. Serum level for calcium, phosphorus and magnesium were performed with a BioSystems A25 and A15 analyzers. Significantly lower level of CYP24A1 and 25-OHvitD3 was found in MS patients when compared to control groups. The Levels of CYP24A1 and 25-OHvitD3 were positively correlated in female and significantly decreased with EDSS in female groups. Also, in MS patients a highly significant decrease in calcium, a considerable increase in level of PTH, phosphorous and magnesium. In this study the negative correlation between 25-OHvitD3 and the degree of motor disability, according to EDSS in MS patients was confirmed. We identified a non-significant difference in the level of 25-OHvitD3 regarding on gender. Still, we confirmed the association between gender and MS disease development regarding the levels of 25-OHvitD3, PTH and phosphorus.

Low 25-OH vitamin D level are associated with increased postoperative acute kidney injury, broch pleural fistula after lung transplantation

Background: Vitamin D (Vit D) deficiency is found in over two-thirds of lung transplantation (LT) candidates, which is greater than in general population. In addition to bone metabolism, low serum level of 25-hydroxyvitamin D[25(OH)D] is known to be associat ed with higher incidence of infections, cancer, and cardiovascular disease. So, it is important to investigate association between Vit D level and post LT complications. Methods: In this single-center study, we reviewed 237 LT patients from January 2013 to July 2019 at Severance Hospital, Seoul, Korea. Thirty-nine patients were excluded due to missed level of preoperative Vit D. Enrolled patients were divided into Vit D defi ciency group (range, 0-10 ng/mL), Vit D insufficiency (range, 10-30 ng/mL), and Vit D sufficiency group (>30 ng/mL). Analysis of variance and chi-square tests were used for comparing variables. Results: Forty-nine patients (24.7%) were Vit D deficiency, 128 patients (64.6%) were Vit D insufficiency, and 21 patients (10.6%) were Vit D sufficiency. There were no significant differences between three groups with respect to age, sex, comorbidities, and primary lung disease. Low Vit D level was associated higher occurrence of postoperative acute kidney injury (AKI; deficiency vs. insufficiency vs. sufficiency, 10 [22.2] vs. 11 [9.5] vs. 1 [5.0]; P<0.05). Prevalence of broncho pleura fistula was higher in Vit D sufficiency group: deficiency vs. insufficiency vs. sufficiency, 0 (0.0) vs. 14 (10.9) vs. 0 (0.0); P=0.016. We further evaluate postop erative broch pleural fistula (BPF) in Vit D increase and Vit D decrease group within 6-month follow-up, and Vit D decrease group show high prevalence of BPF: decrease vs. increase, 9 (12.3) vs. 1 (1.1); P=0.002. Low Vit D level was also associated with post operative anxiety, but it was not statically meaning. Conclusions: Low 25-OH Vit D level is associated with increased incidence of post LT complications such as AKI, BPF, and anxi ety. Also, Vit D decrease during postoperative period showed higher incidence of BPF.

Cytokines, 25-OH vit D and disease activity in patients with juvenile-onset systemic lupus erythematosus.

Juvenile onset systemic lupus erythematosus JO-SLE patients usually exhibit a more aggressive disease course compared to adult patients. Vitamin D deficiency is proposed to be associated with increased disease activity and flares of numerous autoimmune diseases like SLE, rheumatoid arthritis, and scleroderma. To evaluate the level of IL-17, IFN-γ, and 25-OH Vit D in JO-SLE patients versus healthy controls, and determine the correlation of those inflammatory mediators with SLE disease activity and damage scores. Furthermore, to analyze the relationship between 25-OH Vit D levels with the inflammatory cytokines (IFN-γ and IL-17) in JO-SLE patients. Fifty JO-SLE patients and 25 controls were included in this study. Clinical and laboratory data of patients at the time of the study were recorded. SLE disease activity and damage were assessed using the SLEDAI-2K disease score and SLICC damage index, respectively. Plasma 25-OH Vit D, IFN-γ, and IL-17 concentrations were determined using the human ELISA kit. Plasma 25-OH Vit D levels (20 ng/mL) were significantly lower in JO-SLE patients compared to (31 ng/mL) controls (P = 0.014). Plasma levels of IFN-γ and IL-17 were significantly higher (163.5 and 25.5 pg./mL) in JO-SLE patients than (68.3 and 3 pg./mL) that of controls (P = 0.016 and P = 0.013). There was a significant negative correlation between 25-OH Vit D levels and SLEDAI-2K (R= -0.431) as well as IFN-γ (R= -0.471) plasma level (P = 0.022 and P = 0.027). IFN-γ and IL-17 were significantly higher in JO-SLE patients, while 25-OH Vit D was significantly lower compared to controls. There was a negative correlation between 25-OH Vit D and each of SLEDAI-2K and IFN-γ.

Vit D Status and Osteoporosis in Tobacco Consuming Men in Rural Region Surrounding Wardha City, Maharashtra, Central Part of India

Background: Awareness towards tobacco consumption has increased and it is well accepted too but will ithelp to cease the consumption. With widespread menace of tobacco consumption in developing country likeIndia, not much data of study is available currently about tobacco consumption and osteoporosis around therural region of Wardha a central part of India.Aim: Vit D status and osteoporosis in tobacco consumers and non consumers.Objective: To asses influence of tobacco consumption on Sr. Vit D, Sr. ionized Ca, Sr. Phosphate, Sr.parathyroid hormones the biochemical markers of bone turnover and Bone mineral density in a cohort of214 healthy men in rural area surrounding Wardha region of Maharashtra.Design: A cross sectional studySubjects: 214 healthy men aged around 30-50 years with no disease history were included in the study.Results: Tobacco consumers had significantly reduced levels of Sr 25 OH Vit D (P&lt;0.02), PTH (P&lt;0.001).There was no significant difference in Sr ionized Calcium between tobacco consumers and Non tobaccoconsumers. We got negative effect of tobacco consumption on Sr Osteocalcin (P&lt;0.01).Conclusion: Calcium and Vit D metabolism is significantly deranged by habit of tobacco consumption andcannot be explained by life style factors. Vitamin D- PTH system depression among tobacco consumersrepresent a other mechanism for the deleterious effects of tobacco consumption on the bones and contributeto reported risk of osteoporosis among tobacco consumers.Sponsorship: Intra mural Grant from DMIMS(DU)

P0866EVALUATION OF ERYPTOSIS IN PATIENTS WITH CHRONIC KIDNEY DISEASE

Abstract Background and Aims One of the many factors in the pathogenesis of renal anaemia, is eryptosis. The aim of this study is to evaluate eryptosis in patients with chronic renal disease stage 3-5 and 5 dialysis (5D). Method Patients with CKD who were monitored in our nephrology department were included in the study. The age range of the patient groups was 18-80 years and haemoglobin levels were &amp;lt;13 g / dl in men and &amp;lt;12 g / dl in women. As parameters of eryptosis, flow cytometric annexin V binding and intracellular calcium, and superoxide dismutase (SOD) activity with ELISA method were measured in 59 predialysis patient (eGFR&amp;lt;60 mL / min 1.73 m2), 26 haemodialysis patient, 21 peritoneal dialysis patient and 29 healthy volunteers with similar age (control). Haematological and biochemical tests including complete blood count(CBC), erythrocyte sedimentation rate (ESR), Parathormone (PTH), 25-OH vit D3, Blood urea nitrogen (BUN), Creatinine (Cr), C-reactive protein (CRP), Na, K, phosphor (P), ionized and total Calcium, Ferritin, B12 and Folate, were performed. IBM SPSS Statistics Version 20.0 was used for statistical analysis of the data Results The amount of intracellular calcium were 3.05 ± 1.66 in predialysis group, 2.24 ± 0.99 in haemodialysis group, 2.38 ± 0.87 in peritoneal dialysis group and 1.71 ± 0.46 in control group. For intracellular calcium there was statistically significant difference only between predialysis group and control group (p &amp;lt;0. 000). Annexin V binding were calculated as 1.05 ± 0.99 in predialysis group, 1.15 ± 0.56 in haemodialysis group, 1.06 ± 0.87 in peritoneal dialysis group and 0.88 ± 0.86 in control group. Comparing to control group annexin V binding in predialysis, haemodialysis and peritoneal dialysis groups, were statistically significantly increased (for all p &amp;lt;0.000). SOD activity was 0.07 ± 0.07 in predialysis group, 0.13 ± 0.08 in haemodialysis group, 0.14 ± 0.07 in peritoneal dialysis group and 0.03 ± 0.01 in control group. The difference between the control group and dialysis group was statistically significant (p &amp;lt;0. 00). Comparing to nonusers; patients using calcium channel blockers (CCB) had low annexin V binding level (p = 0.013). Patients using erythropoietin (EPO) had elevated annexin V binding level (p &amp;lt;0.000) and lower intracellular calcium (p = 0.014) according to non- users. Conclusion We determined increased eryptosis in patients with CKD stage 3-5 and 5D in our study. Inflammation and elevated parathormone were also associated with increased eryptosis. Therefore, eryptosis may be an important factor in the pathogenesis of renal anaemia. Inflammation associated CKD may increase eryptosis. In addition, this effect can be taken into consideration in the planning of treatment because of the lower incidence of eryptosis in patients using calcium channel blocker and EPO.

SAT-340 Familial Hypocalciuric Hypercalcemia Due to a C.571G&amp;gt;A (p.Glu191Lys) Variant in the GNA11 Gene

Background: Familial hypocalciuric hypercalcemia (FHH) type 1 is caused by inactivating pathogenic variants in the calcium sensing receptor (CASR) gene and clinically presents with serum hypercalcemia, low urine calcium excretion, and inappropriately normal PTH response. In a minority of patients with CASR-negative FHH (up to 26%), variants in AP2S1 are linked to FHH type 3. Similarly, inactivating pathogenic variants in the GNA11 gene have been shown to cause FHH type 2 in up to 10% of CASR and AP2S1 negative cases.1 Clinical case: A four-month old male presented to the ED for symptoms of polyphagia and polyuria. Biochemical evaluation found a serum calcium of 11.9 mg/dL (8.7-11.0 mg/dL), magnesium 2.4 mg/dL (1.6-2.3 mg/dL), 25-OH Vit D 38 ng/mL (30 -100 mg/dL) and intact PTH 27.8 pg/mL (15-65 pg/mL). His further labwork fit clinically with FHH with a urine calcium-creatinine ratio < 0.09 (<= 0.20), accompanied by a serum calcium level of 11.9 mg/dL and iCal of 1.48 mmol/L (1.13 – 1.37 mmol/L). Subsequent monitoring of serum calcium levels showed improvement with time, along with improvement in polyphagia and polyuria.Of note, mother also has a history of hypercalcemia that was diagnosed at age fifteen as part of a rheumatology evaluation. At diagnosis, her calcium was 12.1 mg/dL (9.3-10.6 mg/dL), Mg 2.3 mg/dL, phosphorous 3.3 mg/dL (2.3-4.8 mg/dL), intact PTH 39 pg/mL, and urine calcium-creatinine ratio of 0.04 (<= 0.20). She was treated with calcitonin, during which she developed hypercalciuria with elevated PTH of 88 pg/mL. A parathyroid uptake scan was concerning for adenomatous changes in the right upper parathyroid gland, but she was subsequently lost to follow-up without additional evaluation.Sequencing of the AP2S1, CASR, CDC73, CYP24A1, GCM2, GNA11, MEN1, PTH1R, or SLC34A1 genes by Next-generation sequencing methodology was completed in the patient and only revealed a maternally inherited missense variant of unknown significance of c.571G>A (p.Glu191Lys) in GNA11. This G to A transition in exon 4 substitutes a glutamic acid for a lysine at codon 191 of a highly conserved amino acid. This variant has not been previously reported in affected individuals nor has it been observed in the healthy population per the gnomAD population database. It is predicted to be deleterious/probably damaging by in silico tools (SIFT, PolyPhen2). Conclusion: To our knowledge, this is the first case demonstrating the presence of a c.571G>A (p.Glu191Lys) variant in the GNA11 gene, in a child with familial hypocalciuric hypercalcemia as well as in his affected mother. In cases with strong suspicion of FHH despite negative CASR and AP2S1 analyses, genetic analysis of GNA11 should also be considered.Reference:(1) Hovden, S., Rejnmark, L., Ladefoged, S., & Nissen, P. (2017). AP2S1 and GNA11 mutations – not a common cause of familial hypocalciuric hypercalcemia, European Journal of Endocrinology, 176(2), 177-185.