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Abstract Hypervitaminosis D leads to toxic effects, including hypercalcemia, which can cause severe damage to various organs. Fetuin-A, a glycoprotein with anti-inflammatory properties, may protect tissues from such damage. This study explores the role of Fetuin-A in mitigating hypervitaminosis D-induced damage in renal, hepatic, and cardiac tissues. The objectives of this study were to: (1) Assess the extent of tissue damage from high-dose vitamin D in a murine model by examining the histopathological changes in liver, kidney and heart. (2) Investigate Fetuin-A's protective effect against this damage. Thirty-six albino rats were divided into four groups: (1) control, (2) vitamin D toxicity, (3) Fetuin-A + vitamin D, and (4) Fetuin-A only. Vitamin D was administered subcutaneously at 250 μg/20 g/day for 3 days. Fetuin-A was given at 100 μl/20 g, starting 7 days before vitamin D treatment. Histopathological analysis of liver, kidney, and heart tissues was performed using H&E and Alizarin Red staining and findings were analysed statistically. Vitamin D toxicity caused significant tissue damage, including apoptosis, inflammation, and calcification in the liver, kidneys, and heart. Pre-treatment with Fetuin-A reduced calcification and inflammation, preserving tissue architecture. Fetuin-A-only rats showed no damage or calcification. Fetuin-A provided statistically significant protection against vitamin D-induced damage, reducing oxidative stress and calcification in affected organs. These findings suggest Fetuin-A could be a potential therapeutic agent for hypervitaminosis D.

High dose bolus cholecalciferol supplementation has been associated with falls and fracture, and this does not appear to be due to hypercalcaemia. The primary aim of this study was to determine the change in free vitamin D and metabolites after high dose bolus supplementation. This was a single centre, double-blinded, randomised, controlled trial of three different oral bolus doses of vitamin D3 (50,000 IU, 150,000 IU, and 500,000 IU) in otherwise healthy, vitamin D deficient (total 25-hydroxylated vitamin 25(OH)D < 30 nmol/L) postmenopausal women. Thirty-three women were randomized to one of the three treatment groups. Twenty-seven vitamin D sufficient (25(OH)D > 50 nmol/L) postmenopausal women were recruited as a concurrent control group. Participants attended five study visits over three months. We measured total 25(OH)D3 and free 25(OH)D, total and free 1,25(OH)2D, parathyroid hormone, fibroblast-growth factor-23, serum calcium, ionised calcium, urinary calcium excretion, and bone turnover markers (procollagen I N-propeptide (PINP), serum C-telopeptides of type I collagen (CTX-I) and Osteocalcin (OC)). We assessed muscle strength and function with grip strength and a short physical performance battery. Postural blood pressure and aldosterone:renin ratio (ARR) was also measured. Total 25(OH)D3 and free 25(OH)D increased in response to dose, and there were proportionate increases in total and free metabolites. Treatment did not affect serum calcium, postural blood pressure, ARR, or physical function. Bone turnover markers increased transiently one week after administration of 500,000 IU. High dose bolus cholecalciferol supplementation does not cause disproportionate increases in free vitamin D or metabolites. We did not identify any effect on blood pressure regulation or physical function that would explain increased falls after high dose treatment. A transient increase in bone turnover markers one week after a 500,000 IU bolus suggests that very high doses can have acute effects on bone metabolism, but the clinical significance of this transient increase is uncertain. [ABSTRACT FROM AUTHOR]

During the COVID-19 pandemic, vitamin D was used along with vitamin C and zinc as a preventive and curative therapy against SARS-CoV-2 infection. Vitamin D toxicity, even if it is rare, occurs when serum concentrations exceed 150 ng/mL and is usually manifested by hypercalcemia phenomena.

Introduction: Hypervitaminosis D is a relatively uncommon etiology of hypercalcemia. Toxicity is usually caused by very high doses, mostly secondary to erroneous prescription or administration of vitamin D, and less commonly, contaminated foods or manufacturing errors of vitamin D-containing supplements. Case Presentation: A 16-year-old male, previously healthy, presented with 2-week history of nonspecific symptoms (fatigue, gastrointestinal complaints). Investigations showed acute kidney injury and hypercalcemia (total calcium 3.81 mmol/L). Further diagnostic workup revealed markedly elevated 25-hydroxyvitamin D levels (1,910 nmol/L). He denied taking any vitamin D supplements; however, he reported consumption of creatine and protein supplements. Mass spectrometry analysis of the creatine supplement estimated a vitamin D content of 425,000 IU per serving (100 times the upper tolerable daily dose). A few months later, another previously healthy adolescent presented with severe hypercalcemia and acute kidney injury secondary to hypervitaminosis D. He was also using a creatine supplement, from the same manufacturer brand and lot. Both patients were treated with intravenous hydration, calcitonin, and pamidronate. They maintained normocalcemia after their initial presentation but required low-calcium diets and laboratory testing for months after this exposure. Discussion/Conclusion: We present 2 cases of hypervitaminosis D caused by a manufacturing error of a natural health product which did not claim to contain vitamin D. The use of dietary supplements is highly prevalent; this should be incorporated while taking medical history, and considered a potential source of toxicity when an alternative source cannot be found, regardless of the product label. [ABSTRACT FROM AUTHOR]

Calcium Homeostasis in the human body is regulated by hormones, including parathyroid hormone and vitamin D3. Dysfunction in the form of hypoparathyroidism causes hypocalcaemia. In patients treated for primary hypoparathyroidism with activated vitamin D replacement, iatrogenic hypercalcaemia can occur. This must be investigated to exclude other aetiologies, such as malignancy and granulomatous disease. In this case report, we describe a 73-year-old man with a distant history of chronic hypoparathyroidism treated with vitamin D3 who presented with lethargy, confusion, polyuria, and polydipsia. On admission, he was found to be hypercalcaemic at 3.22 mmol/L. He presented on two previous occasions with symptomatic hypocalcaemia that resulted in a reduction and subsequent cessation of his vitamin D supplementation. This hypercalcaemia persisted, prompting investigations of non-iatrogenic causes. Computer tomography (CT) and positron emission tomography (PET) scans showed bilateral hilar lymphadenopathy and ruled out malignancy. Serum angiotensin-converting enzyme was three times the normal range while calcitriol levels were inappropriately raised, suggesting sarcoidosis as the likely aetiology of the hypercalcaemia. The patient was very responsive to steroid therapy, with serum calcium dropping to normal levels over a four-week admission. The patient developed hypocalcaemia within weeks of discharge, eventually requiring the recommencement of his vitamin D replacement, which has been titrated to maintain normal serum calcium levels. This case highlights a rare occurrence of two infiltrative disorders with simultaneous differential adverse effects on calcium metabolism, leading to a series of acute hospitalisations often alternating between severe hypocalcaemia or severe hypercalcaemia., Competing Interests: Human subjects: Consent for treatment and open access publication was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Sola-Oladokun et al.)

Background: Vitamin D is a steroid based hormone that has crucial role in calcium metabolism and bone homeostasis and potential role in fibrosis including liver. Patients with chronic liver disease has tendency for vitamin D deficiency with possible sequalae including hepatic osteodystrophy. Safe and effective regime of vitamin D that can be used in children with chronic liver disease is still not well established. Moreover, the potentiality of reversing fibrosis process or halting it by correction of vitamin D is still not well studied. Aim of work: The primary aim of the study is to assess the efficacy and safety of vitamin D regime using two different mode of administration. The secondary aim is to assess the possible antifibrotic effect of vitamin D therapy by assessment of fibroscan. Methodology: Twenty four children with different etiologies of chronic liver disease but age and sex matched as well as anthropometric measures are enrolled in the study. They were distributed randomly among the two arms of the study and followed up for 6 months using different laboratory and imaging variables. The two regimes were group A who received intramuscular stoss dose once (200.000 IU) vitamin D therapy while group B received oral vitamin D therapy with dose 50.000 IU for four weeks. All children received maintenance vitamin D (600 IU) and Ca doses thereafter for the whole follow up period. All patients were subjected to complete history taking, complete clinical examination including abdominal examination, signs of liver decompensation and signs of vitamin D deficiency. As regard laboratory investigations done were CBC, liver function tests, serum calcium and phosphorous. Serum vitamin D level and fibroscan were also done at the beginning and the end. Results: There were significant improvement of vitamin D level in both arms with no development of toxic s/o of vitamin D toxicity with p-value of < 0.001 and 0.000 respectively in group A and B. The difference of improvements between both arms were not significant display the equal efficacy of both regimes (P = 0.885). There were no significant improvement of fibroscan parameters following vitamin D treatment in either group A or B with p-value 0.637 and 0.931 respectively. Conclusion: Stoss and oral vitamin D regimes suggested in the study are both equally effective and safe in the treatment of vitamin D deficiency among children with chronic liver disease. Despite no proof of antifibrotic effect upon vitamin D correction, further study is required to evaluate this issue. [ABSTRACT FROM AUTHOR]

Apart from maintaining healthy bones, vitamin D is also required for cell differentiation, cell growth inhibition, and immune modulation. Vitamin D deficiency is common in the Indian subcontinent. Vitamin D presenting toxicity, leading to hypercalcemia, acute kidney injury, and altered sensorium is very rare. Here we present a case of a 65-year-old man who presented to emergency with persistent vomiting, altered sensorium, and acute kidney injury. The cause of which was an unchecked intake of vitamin D for non-specific musculoskeletal pain. When treated with intravenous fluid, diuretics, calcitonin, and steroids, the patient improved clinically. Therefore, for any patient presenting with persistent vomiting, altered sensorium, and hypercalcemia, with normal to low parathyroid hormone levels, a diagnosis of an overdose of vitamin D should be considered. Early treatment of this condition not only improves the symptoms but also prevents further kidney damage.

Background and aims: The profile of hypercalcaemia in hospitalized patients in India seems to be changing. However, studies evaluating the profile of hypercalcaemia in hospitalized settings in India are extremely limited. This prospective study aims to evaluate the clinical and biochemical profile of hospitalized patients with hypercalcaemia from a tertiary care centre in north India. Materials and methods: Clinical and biochemical profiles of subjects with hypercalcaemia detected during hospitalization/hospitalized with hypercalcaemia were assessed. A total of 91 subjects with sustained hypercalcaemia, who were eligible, underwent further investigation as per the institutional protocol and the data collected were analyzed. Results: The mean age of participants was 57.88 ± 14.23 years, with 62.64% of participants being females. The most common symptoms were nausea and anorexia, which were observed in all patients. The most common clinical sign was dehydration, which was observed in 32.97% of subjects. Primary hyperparathyroidism was the most common cause (41.76%), followed by suspected or confirmed malignancy/solid tumours in 15.38% of subjects. Other causes were advanced chronic liver disease (10.99%), multiple myeloma (9.89%), vitamin D toxicity (8.79%), granulomatous disorders (2.20%) and drug-i nduced disorders (1.10%). Forty-one subjects (45.05%) developed acute kidney injury and 14 subjects (15.38%) developed acute pancreatitis as a complication. Six subjects (6.59%) died during the course of hospitalization because of either primary disease or other secondary complications. Conclusions: Clinicians should be aware of changing patterns of hypercalcaemia in a hospital setting. Hypercalcaemia in hospitalized patients is associated with significant complications and mortality. Further large-scale prospective studies are needed to understand the changing pattern of hypercalcaemia in hospitalized patients from India., Competing Interests: Disclosures: Aman Kumar, Deepak Khandelwal, Lovely Gupta, Upasana Agrawal, Suresh Mittal, Vivek Aggarwal, Nishikant Avinash Damle, Monika Garg, Deep Dutta and Sanjay Kalra have no financial or non-financial relationships or activities to declare in relation to this article., (© Touch Medical Media 2024.)

Vitamin D toxicity is a rare but potentially serious condition that can lead to severe hypercalcaemia and subsequent complications, such as acute renal failure, nephrocalcinosis, congestive heart failure and coronary calcium deposition, resulting in myocardial injury. We present a case of a 76-year-old male patient who developed severe hypercalcaemia and acute kidney injury due to excessive long-term over-the-counter vitamin D supplementation. The patient was initially treated with aggressive intravenous fluids and furosemide. However, a failed effective response prompted the addition of pamidronate, resulting in the gradual improvement of hypercalcaemia and renal function. We have presented, in this case, a rare adverse effect of vitamin D toxicity and its multiorgan effect., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Khan et al.)

Summary: Vitamin D intake over the recommended dose is usually associated with high serum 25(OH)D levels and generally not associated with symptoms of hypercalcemia. High doses of cholecalciferol need to be avoided to protect against vitamin D toxicity and related complications. Strict adherence to the clinical guidelines for treating vitamin D deficiency can ensure safe and effective treatment. Purpose: We observed a tendency to use high doses of cholecalciferol for vitamin D deficiency treatment or vitamin D supplementation. We aimed to determine the biochemical characteristics of patients with high normal and elevated serum 25(OH)D levels. Methods: An online invitation was sent to all tertiary endocrinology clinics in Turkey to complete an online retrospective survey (DeVIT-TOX Survey) for patients diagnosed with high serum 25(OH)D levels (> 88 ng/mL) between January 2019 and December 2019. The patients were evaluated according to the presence of signs and symptoms of hypercalcemia and doses of vitamin D intake, evaluated into the following three groups according to their 25(OH)D levels: group 1, > 150 ng/mL; group 2, 149–100 ng/mL; and group 3, 99–88 ng/mL. Results: A total of 253 patients were included in the final analysis (female/male: 215/38; mean age, 51.5 ± 15.6 years). The average serum 25(OH)D level was 119.9 ± 33 (range, 88–455) ng/mL, and the average serum calcium level was 9.8 ± 0.7 (range, 8.1–13.1) mg/dL. Most (n = 201; 75.4%) patients were asymptomatic despite having high serum 25(OH)D and calcium levels. The serum 25(OH)D level was significantly higher in the symptomatic groups than in the asymptomatic groups (138.6 ± 64 ng/mL vs. 117.7 ± 31 ng/mL, p < 0.05). The most common cause (73.5%) associated with high serum 25(OH)D levels was the inappropriate prescription of a high dose of oral vitamin D (600.000–1.500.000 IU) for treating vitamin D deficiency/insufficiency in a short time (1–3 months). The cut-off value of 25 (OH) D level in patients with hypercalcemia was found to be 89 ng/mL [median 116.5 (89–216)]. Conclusions: High dose of vitamin D intake is associated with a high serum 25 OH D level, without symptoms of hypercalcemia. Inappropriate prescription of vitamin D is the primary cause for elevated 25(OH) D levels and related hypercalcemia. Hypercalcemia may not be observed in every patient at very high 25(OH) D levels. Adherence to the recommendation of guidelines is essential to ensure safe and effective treatment of vitamin D deficiency. [ABSTRACT FROM AUTHOR]

Background: Serum 25-hydroxyvitamin D (25(OH)D) assays have become readily available in India over the past decade. A large number of cross-sectional studies have been performed on the vitamin D status and the prevalence of vitamin D deficiency (VDD) in India. However, seasonal and long-term trends in serum 25(OH)D levels have been reported less frequently. Aim: To determine the seasonal and year-wise variation in vitamin D status at a tertiary care hospital in north India. Materials and Methods: Using hospital records, the data on serum 25(OH)D assays performed in its endocrinology laboratory between 2008 and 2016 were obtained. For analysis of seasonal trends, the months of a year were divided into following seasons: March to June (summer season), July to October (rainy season), and November to February (winter season). VDD was defined as serum 25(OH)D concentration 100 ng/mL) and vitamin D toxicity (serum 25(OH)D >150 ng/mL) were seen in 319 (1.2%) and 27 (0.1%) assays, respectively. Conclusions: This study provides data on seasonal and year-wise trends in vitamin D status over a long period of time at a tertiary care hospital in north India. A long-term trend toward improving vitamin D status, especially in females, was noted in the study. The prevalence of VDD was found to decrease in the analyzed samples during the study period.

The risk of vitamin D insufficiency in humans is a global problem that requires improving ways to increase vitamin D intake. Supplements are a primary means for increasing vitamin D intake, but without a clear consensus on what constitutes vitamin D sufficiency, there is toxicity risk with taking supplements. Chickens have been used in many vitamin-D-related research studies, especially studies involving vitamin D supplementation. Our state-of-the-art review evaluates vitamin D metabolism and how the different hydroxylated forms are synthesized. We provide an overview of how vitamin D is absorbed, transported, excreted, and what tissues in the body store vitamin D metabolites. We also discuss a number of studies involving vitamin D supplementation with broilers and laying hens. Vitamin D deficiency and toxicity are also described and how they can be caused. The vitamin D receptor (VDR) is important for vitamin D metabolism; however, there is much more to understand about VDR in chickens. Potential research aims involving vitamin D and chickens should explore VDR mechanisms that could lead to newer insights into VDR. Utilizing chickens in future research to help elucidate vitamin D mechanisms has great potential to advance human nutrition. Finding ways to increase vitamin D intake will be necessary because the coronavirus disease 2019 (COVID-19) pandemic is leading to increased risk of vitamin D deficiency in many populations. Chickens can provide a dual purpose with addressing pandemic-caused vitamin D deficiency: 1) vitamin D supplementation gives chickens added-value with the possibility of leading to vitamin-D-enriched meat and egg products; and 2) using chickens in research provides data for translational research. We believe expanding vitamin-D-related research in chickens to include more nutritional aims in vitamin D status has great implications for developing better strategies to improve human health. [ABSTRACT FROM AUTHOR]

Calcium compounds and vitamin D supplements are readily available as over-the-counter preparations. Whilst integral in maintaining calcium homeostasis in certain patients, excess exogenous intake of these preparations can have deleterious effects, particularly in terms of renal function. We look at the cases of two patients, aged 52 and 34, who were referred into hospital with hypercalcaemia and acute kidney injury (AKI). Both individuals reported regular and prolonged self-medication with unregulated over-the-counter supplements containing calcium carbonate and vitamin D, respectively. Prompt investigation and treatment enabled an element of reversibility of the AKI in both the cases, with further improvement in renal function over time. We emphasise the importance of recognising the overuse of exogenous vitamin D supplements and calcium compounds as rare yet treatable causes of AKI associated with hypercalcaemia and discuss how raising public awareness into the risks posed by self-medication of over-the-counter medicines is paramount. [ABSTRACT FROM AUTHOR]

Background: Vitamin D toxicity (VDT), a “not uncommon” cause of hypercalcemia, can be life-threatening and cause substantial morbidity, if not treated promptly. Aims: To describe presentation, management, and outcome in 32 patients with VDT diagnosed over 3 years. Materials and Methods: Patients presenting with VDT at a tertiary care centre in Srinagar Kashmir India were included. Evaluation included detailed history and biochemical tests including serum calcium, phosphate, creatinine, intact parathyroid hormone (iPTH), 25-hydroxy Vitamin D (25-OHD), and 24-hour urinary calcium. Results: The clinical manifestations of the 32 patients (median age 65; range 3–77 years) included gastrointestinal symptoms (constipation and vomiting), polyuria/polydipsia, altered sensorium, pancreatitis, acute kidney injury, and nephrocalcinosis. The median total serum calcium level was 13.95 (range 11.10-17.20) mg/dl and median 25-OHD level was 306 (range 105–2800) ng/ml. All patients had suppressed or low normal iPTH and hypercalciuria and 78% had azotemia. All patients had received multiple intramuscular injections of vitamin D3. The median cumulative dose was 4,200,000 (range, 1,800,000-30,000,000) IU. The median time to resolution of hypercalcemia was 7 months (range 4–18 months). Conclusion: We conclude that VDT is an increasingly common cause of symptomatic hypercalcemia. VDT needs prolonged follow up as it takes months to abate its toxicity. Enhancing awareness among general practitioners regarding the toxicity resulting from high doses of vitamin D is the key to prevent VDT. We suggest that VDT be considered in patients, especially the elderly, presenting with polyuria, polydispsia, vomiting, azotemia, or encephalopathy.

Apart from maintaining healthy bones, vitamin D is also required for cell differentiation, cell growth inhibition, and immune modulation. Vitamin D deficiency is common in the Indian subcontinent. Vitamin D presenting toxicity, leading to hypercalcemia, acute kidney injury, and altered sensorium is very rare. Here we present a case of a 65-year-old man who presented to emergency with persistent vomiting, altered sensorium, and acute kidney injury. The cause of which was an unchecked intake of vitamin D for non-specific musculoskeletal pain. When treated with intravenous fluid, diuretics, calcitonin, and steroids, the patient improved clinically. Therefore, for any patient presenting with persistent vomiting, altered sensorium, and hypercalcemia, with normal to low parathyroid hormone levels, a diagnosis of an overdose of vitamin D should be considered. Early treatment of this condition not only improves the symptoms but also prevents further kidney damage. [ABSTRACT FROM AUTHOR]

About 50 million of the U.S. adult population suffer from chronic pain. It is a complex disease in its own right for which currently available analgesics have been deemed woefully inadequate since ~20% of the sufferers derive no benefit. Vitamin D, known for its role in calcium homeostasis and bone metabolism, is thought to be of clinical benefit in treating chronic pain without the side-effects of currently available analgesics. A strong correlation between hypovitaminosis D and incidence of bone pain is known. However, the potential underlying mechanisms by which vitamin D might exert its analgesic effects are poorly understood. In this review, we discuss pathways involved in pain sensing and processing primarily at the level of dorsal root ganglion (DRG) neurons and the potential interplay between vitamin D, its receptor (VDR) and known specific pain signaling pathways including nerve growth factor (NGF), glial-derived neurotrophic factor (GDNF), epidermal growth factor receptor (EGFR), and opioid receptors. We also discuss how vitamin D/VDR might influence immune cells and pain sensitization as well as review the increasingly important topic of vitamin D toxicity. Further in vitro and in vivo experimental studies will be required to study these potential interactions specifically in pain models. Such studies could highlight the potential usefulness of vitamin D either alone or in combination with existing analgesics to better treat chronic pain. [ABSTRACT FROM AUTHOR]

Background: Serum 25-hydroxyvitamin D (25(OH)D) assays have become readily available in India over the past decade. A large number of cross-sectional studies have been performed on the vitamin D status and the prevalence of vitamin D deficiency (VDD) in India. However, seasonal and long-term trends in serum 25(OH)D levels have been reported less frequently. Aim: To determine the seasonal and year-wise variation in vitamin D status at a tertiary care hospital in north India. Materials and Methods: Using hospital records, the data on serum 25(OH)D assays performed in its endocrinology laboratory between 2008 and 2016 were obtained. For analysis of seasonal trends, the months of a year were divided into following seasons: March to June (summer season), July to October (rainy season), and November to February (winter season). VDD was defined as serum 25(OH)D concentration ង ng/mL. Results: A total of 26,339 assays of serum 25(OH)D were analyzed in the study. The year-wise assay numbers increased steadily from 2008 to peak in the year 2012, followed by a decline and a second smaller peak in the year 2016. The mean serum 25(OH)D concentration increased from 19.1 ± 16.4 ng/mL in 2008 to 21.7 ± 17.1 ng/mL in 2016 (P = 0.02). Between 2008 and 2016, the prevalence of VDD decreased from 71.9% to 54.3% in females, and from 56.7% to 52.1% in males. The levels in rainy season were significantly higher as compared to winters and summers (P < 0.05 for both). Hypervitaminosis D (serum 25(OH)D >100 ng/mL) and vitamin D toxicity (serum 25(OH)D >150 ng/mL) were seen in 319 (1.2%) and 27 (0.1%) assays, respectively. Conclusions: This study provides data on seasonal and year-wise trends in vitamin D status over a long period of time at a tertiary care hospital in north India. A long-term trend toward improving vitamin D status, especially in females, was noted in the study. The prevalence of VDD was found to decrease in the analyzed samples during the study period. [ABSTRACT FROM AUTHOR]

Background: Vitamin D toxicity (VDT), a "not uncommon" cause of hypercalcemia, can be life-threatening and cause substantial morbidity, if not treated promptly. Aims: To describe presentation, management, and outcome in 32 patients with VDT diagnosed over 3 years. Materials and Methods: Patients presenting with VDT at a tertiary care centre in Srinagar Kashmir India were included. Evaluation included detailed history and biochemical tests including serum calcium, phosphate, creatinine, intact parathyroid hormone (iPTH), 25-hydroxy Vitamin D (25-OHD), and 24-hour urinary calcium. Results: The clinical manifestations of the 32 patients (median age 65; range 3–77 years) included gastrointestinal symptoms (constipation and vomiting), polyuria/polydipsia, altered sensorium, pancreatitis, acute kidney injury, and nephrocalcinosis. The median total serum calcium level was 13.95 (range 11.10-17.20) mg/dl and median 25-OHD level was 306 (range 105–2800) ng/ml. All patients had suppressed or low normal iPTH and hypercalciuria and 78% had azotemia. All patients had received multiple intramuscular injections of vitamin D3. The median cumulative dose was 4,200,000 (range, 1,800,000-30,000,000) IU. The median time to resolution of hypercalcemia was 7 months (range 4–18 months). Conclusion: We conclude that VDT is an increasingly common cause of symptomatic hypercalcemia. VDT needs prolonged follow up as it takes months to abate its toxicity. Enhancing awareness among general practitioners regarding the toxicity resulting from high doses of vitamin D is the key to prevent VDT. We suggest that VDT be considered in patients, especially the elderly, presenting with polyuria, polydispsia, vomiting, azotemia, or encephalopathy. [ABSTRACT FROM AUTHOR]

Vitamin D deficiency is an increasing problem affecting all ages. Patients should be assessed for risk factors as part of preventive health maintenance. Vitamin D toxicity is a rare occurrence caused by oversupplementation and errors in food fortification. The connection between vitamin D deficiency and osteoporosis, is well established. However, a cause and effect relationship has yet to be established between vitamin D deficiency and many chronic illnesses. An evidence-based approach is treating patients for an underlying vitamin D deficiency in hopes of improving many chronic illnesses. [ABSTRACT FROM AUTHOR]

Background: Interest in vitamin D has increased during the past 2 decades, with a corresponding increase in laboratory testing of 25-hydroxyvitamin D [25(OH)D]. The vast majority of specimens tested display normal or deficient levels of 25(OH)D; concentrations rarely fall in the potentially toxic range. Methods: We performed a retrospective investigation of elevated 25(OH) D levels during a 16-year period at the University of Iowa Hospitals and Clinics (UIHC), a 734-bed tertiary-/quaternary-care academic medical center in the midwestern United States. Detailed medical-record review was performed for patients with serum/plasma 25(OH)D concentrations higher than 120 ng per mL. Results: A total of 127,932 serum/plasma 25(OH)D measurements were performed on 73,779 unique patients. Of these patients, 780 (1.05%) had results that exceeded 80 ng per mL and 89 patients (0.12%) had results that exceeded 120 ng per mL. Only 4 patients showed symptoms of vitamin D toxicity. Three of these cases involved inadvertent misdosing of liquid formulations. Conclusions: Symptomatic vitamin D toxicity is uncommon, and elevated levels of 25(OH)D do not strongly correlate with clinical symptoms or total serum/plasma calcium levels. Our study highlights the potential risks of the liquid formulation of vitamin D. [ABSTRACT FROM AUTHOR]

Vitamin D deficiency and insufficiency is a global health issue that afflicts more than one billion children and adults worldwide. The consequences of vitamin D deficiency cannot be under estimated. There has been an association of vitamin D deficiency with a myriad of acute and chronic illnesses including preeclampsia, childhood dental caries, periodontitis, autoimmune disorders, infectious diseases, cardiovascular disease, deadly cancers, type 2 diabetes and neurological disorders. This review is to put into perspective the controversy surrounding the definition for vitamin D deficiency and insufficiency as well as providing guidance for how to treat and prevent vitamin D deficiency. [ABSTRACT FROM AUTHOR]

We describe a patient with hypercalcemia associated with the injection of high doses vitamin D as supplement for a period of six months. A 76-year-old woman had been taking an intramuscular injection of vitamin D 300,000 IU every ten days for six months. She was hospitalized with symptoms of hypercalcemia: chronic constipation, unstable gait, a chronic generalized musculoskeletal pain and increased fatigue. On admission her 25 (OH) vitamin D and Calcium levels were 559 nmol/L and 13.85 mg/dL respectively, and Parathyroid Hormone (PTH) level was 7.1 pg/mL. Immediately she received diuresis therapy with saline and furosemide in conjunction with calcitonin and pamidronate. At discharge her serum calcium level was 11.5 mg/dL. To lower endogenous overproduction of calcitriol, prednisolone 20 mg/day for 10 days was administered at discharge time.

In patients with tuberculosis, abnormal extrarenal production of 1,25-dihydroxyvitamin D3 by activated macrophages in granulomatous tissues may result in hypercalcaemia. More commonly reported in adults with active pulmonary tuberculosis, this complication may rarely occur in extrapulmonary tuberculosis, and children. The hypercalcaemia may be precipitated by usually recommended vitamin D and calcium supplementation in patients with tuberculosis. We report here an infant with tubercular meningitis who developed hypercalcaemia 12 days after starting routine vitamin D and calcium supplementation. This communication highlights the importance of close monitoring of calcium levels in patients with tuberculosis, especially if started on vitamin D and calcium replacement before antitubercular therapy.

Summary Background & aims Recent interest in vitamin D has led to a substantial increase in the use of vitamin D supplements. Vitamin D intoxication may be a concern as hypervitaminosis D can result in irreversible calcification of soft tissues so that it is important to detect early markers of vitamin D intoxication. Our aim was to assess the simultaneous presence of biochemical markers of vitamin D toxicity (i.e. hypervitaminosis D, hypercalcemia) and determine the concentrations of 25-OH-vitamin D at which the risk of hypercalcemia, and thus toxicity, might begin. Methods We evaluated retrospectively a 6-year period during which 25.567 samples were assessed for 25-OH-vitamin D status by UHPLC. Hypervitaminosis D was defined at serum 25-OH-vitamin D >160 nmol/L. Serum and urine calcium, phosphorus and iPTH were also recorded, if available. Medical history revision was performed in subjects displaying simultaneously hypervitaminosis D and hypercalcemia. Results Overall, hypervitaminosis D was found in 475 samples (1.86%) of which 51 displayed hypercalcemia (11.1%). A total of 382 samples were identified as the first record of hypervitaminosis D and 39 presented hypercalcemia (10.2%), most of them at 25-OH-vitamin D levels between 161 and 375 nmol/L. Only in 15 subjects, hypercalcemia could be directly attributed to vitamin D and serum 25-OH-vitamin D ranged between 164 and 1139 nmol/l. In no case, serum calcium achieved concentrations considered as critical values (>13 mg/dl). Conclusion Hypercalcemia due to vitamin D represented <4% of the total hypervitaminosis D detected and <0.1% of the tests performed. However, a highly variable response was observed and most subjects presented hypercalcemia at serum concentrations of 25-OH-vitamin D < 375 nmol/L. [ABSTRACT FROM AUTHOR]

Vitamin D is a fat-soluble vitamin essential for calcium homeostasis and bone health. Vitamin D toxicity or hypervitaminosis D is extremely rare. We describe the case of a 73-year-old man who presented with life-threatening hypervitaminosis D and hypercalcaemia resulting from self-medicated doses of vitamin D supplements. This case, alongside other global case reports, highlights the potential dangers of unlicensed vitamin D replacement. We discuss the evidence for vitamin D replacement and remind readers of the current guidance on daily intake and supplementation. [ABSTRACT FROM AUTHOR]

Vitamin D deficiency is widely prevalent across the globe. This has lead to widespread use of vitamin D supplements in populations. We present our experience of vitamin D toxicity in a subject resulting in hypercalcemia and CHB (Complete Heart Block). A 70-year-old female, known hypertensive for thirty five years and diabetic for seven years underwent total knee replacement (TKR) for osteoarthritis left knee in December 2010. For perioperative glycemic control, multiple subcutaneous injections of insulin were advised. Patient later presented with poor glycemic control, decreased appetite and constipation for last 1 month with history of episodes of transient loss of consciousness for 15 days and recurrent vomiting. Biochemical work-up showed hypercalcemia (Serum calcium 12.4 mg/dL). Sr. albumin, ALP, Sr. phosphorus and PTH levels were normal, thus suggesting PTH independent hypercalcemia. Strong suspicion led us to check vitamin D levels in dilution which were 2016 ng/mL, thus confirming vitamin D toxicity. Retrospective analysis of treatment history revealed patient receiving 4 injections of Architol (6 Lac units im) prior to presentation. Work-up for malignancy was negative, brain imaging and EEG were normal. Holter was suggestive of intermittent CHB. Patient was given hydration, injection calcitonin 100 I.U. subcutaneously, injection pamidronate 60 mg infusion, with serum calcium levels normalizing, with relief in constipation, vomiting and behavioral improvement. However, persistence of rhythm disturbances led to permanent pacemaker placement. The present case highlights the dangers of indiscriminate vitamin D usage, exposing patients to potentially life threatening complications.

Despite the rare occurrence of vitamin D toxicity in infants, increased use of vitamin D formulations as well as incorrect supplement concentration by manufacturing pharmaceutical companies, has contributed to an increased incidence of vitamin D toxicity. Over-the-counter vitamin D preparation constitutes variable concentrations that can render life-threatening consequences in children., Case Presentation: Here, we present a case of a 2.5-month-old infant presenting with failure to thrive. The clinical presentations were nasal blockage, noisy breathing, poor feeding, lethargy, dehydration, and fever for 3 days with decreased appetite. Her urine culture report showed a urinary tract infection. The biochemical evaluation demonstrated raised total serum calcium (6.0 mmol/l) and serum 25-hydroxy vitamin D (>160 ng/ml) with suppressed parathyroid hormone concentration (3.7 pg/ml), which was the major concern to the clinicians. On ultrasonographical examination, nephrocalcinosis was observed. Further evaluation unveiled that the vitamin D supplement administered to the infant constituted a deucedly high dose of 42 000 IU instead of the recommended dose of 0.5 ml of 800 IU., Clinical Discussion: The patient developed vitamin D toxicity after consuming a mega dose of vitamin D supplements due to a manufacturer error., Conclusions: Hypervitaminosis D has severe life-threatening consequences like failure to thrive in otherwise healthy-born infants. Regular monitoring of vitamin D supplements administered in infants by medicinal practitioners and strict supervision of all stages of the production process by pharmaceutical companies is crucial to prevent complications from supplement overdose., Competing Interests: There are no conflicts of interest., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Vitamin D toxicity also known as hypervitaminosis D was previously believed to be rare. But with an increase in vitamin D supplementation several cases have been reported in literature. Fat soluble vitamins like Vitamin D, due to their ability to accumulate in the body, have a higher potential for toxicity than water soluble vitamins. The main clinical consequence of vitamin D toxicity is hypercalcemia. In this report we describe an adult female patient who developed very high serum Vitamin D levels (746 ng/mL, RI: 20 to 50) as a result of medication error. Inspite of such high serum concentrations the patient was without any clinical symptoms and had normal serum calcium. We critically discuss the mechanism of toxicity and hypothesize the possible molecular/metabolic factors which might have been responsible for this nontoxic presentation. This case study highlights the fact that physicians need to consider the risk of medication errors while prescribing Vitamin D therapy. Clinical trials to study Vitamin D toxicity in humans is not possible ethically. Thus the evidence base regarding the safety profile of Vitamin D supplementation in humans has been build through case reports. This review of the paradoxical clinico-laboratory manifestation of hypervitaminosis D could possibly contribute to existing literature. [ABSTRACT FROM AUTHOR]

The article presents a case study of a 30-year-old female patient who was diagnosed with hypercalcemia caused by vitamin D toxicity. Topics include the role of vitamin D in Ca2+ homeostasis, the symptoms and other causes of vitamin D toxicity, and zeolite supplements and their contribution to electrolyte abnormalities.

Background and objective  Around 25-30% of elderly patients present to emergency departments (ED) with altered mental status (AMS), with hypercalcemia being one of the metabolic causes. Elderly patients, due to their multiple vulnerability factors and relative homeostenosis, are susceptible to alterations in mental state at even milder grades of hypercalcemia. There is a trend of overzealous prescription of higher doses of vitamin D in elderly patients for various ailments, which often exceeds the requirements of the patients. In this study, we aimed to establish vitamin D toxicity (VDT) as an underlying cause of AMS in elderly patients presenting to the hospital. Methods This was a descriptive case study conducted at a tertiary care university hospital in North India, from January 2015 to March 2020 for a total duration of five years. Elderly patients (aged ≥60 years) who were admitted with VDT as a cause for underlying hypercalcemia were included. The evaluation included patient history regarding the dosage of vitamin D received, route of administration, and biochemical parameters, such as serum calcium, intact parathyroid hormone (iPTH), 25-hydroxy vitamin D [25(OH)D], and albumin. All other potential causes for hypercalcemia and AMS were ruled out concurrently. Results A total of 19 patients were enrolled in the study, with a mean age of 72.3 years (range: 62-86 years). All patients had received injectable vitamin D formulation. The mean serum calcium among the patients was 12.52 ± 1.12 mg/dL (range: 11.2-15.7 mg/dL), whereas the mean 25(OH)D was 196.34 ± 70.44 ng/mL (range: 107-356 ng/mL). The mean cumulative vitamin D supplement intake was 2.594 ± 0.841 million IU (range: 1.2 million-4.2 million IU). While six patients had mild hypercalcemia, 12 had moderate, and one person had severe hypercalcemia, with altered sensorium (85%) being the most common complaint for presenting to ED, followed by generalized weakness (15%). Conclusion VDT can manifest with AMS as an initial presenting complaint. The geriatric population, due to various underlying vulnerability factors, is more susceptible than their younger counterparts. We strongly recommend that in elderly patients, higher doses of vitamin D should be prescribed only after checking their serum levels, and frequent monitoring of vitamin D should be performed., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2022, Khan et al.)