Vitamin D intoxication: case report

Marins, Tatiana Aporta; Galvão, Tatiana; Korkes, Fernando; Malerbi, Domingos Augusto Cherino; Ganc, Arnaldo José; Korn, D; Wagner, Jairo; Guerra, João Carlos de Campos; Filho, Wladimir Mendes Borges; Ferracini, Fábio Teixeira; Korkes, Hélio

doi:10.1590/s1679-45082014rc2860

Cited by 23 publications

(24 citation statements)

References 9 publications

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“…Seven paediatric cases of hypercalcaemia due to vitamin D intoxication were reported in association with a fish oil supplement, where the stated dose was roughly 4000 times less than the actual dose [31]; in one of these cases, an infant in whom the stated daily dose was 2000 IU day -1 was actually taking 6000 IU day -1 [30]. Toxicity associated with inaccurately manufactured and labelled vitamin D supplements is a globally reported problem [32,[34][35][36][37][38][39][40][41][42][43]. To our knowledge, such errant labelling has not been reported in conjunction with licensed formulations.…”

Section: Causes Of Vitamin D Toxicitymentioning

confidence: 99%

A review of the growing risk of vitamin D toxicity from inappropriate practice

Taylor

Davies

2018

Brit J Clinical Pharma

134

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Vitamin D is a particularly important sterol hormone, with evidence emerging of its beneficial effects well beyond bone. In consequence of this and increased global recognition of vitamin D deficiency in the general population, there has been a resurgence in treatment with vitamin D preparations. However, the increasing use of vitamin D treatments has also seen a substantial increase in the number of reports of vitamin D intoxication, with the majority (75%) of reports published since 2010. Many of these cases are a consequence of inappropriate prescribing, and the use of high-dose over-the-counter preparations or unlicensed preparations. This review highlights that the majority of cases were preventable and discusses the inappropriate use of poorly formulated, and unlicensed vitamin D preparations.

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Section: Causes Of Vitamin D Toxicitymentioning

confidence: 99%

A review of the growing risk of vitamin D toxicity from inappropriate practice

Taylor

Davies

2018

Brit J Clinical Pharma

134

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“…The daily intake of 100,000 IU or more could cause VD toxicity ( 68 ), while an increased intake of up to 2000 fold against the prescribed dosage could lead to renal failure ( 82 ). It has also been reported that an annual treatment of 500,000 IU VD 3 increases fracture risk ( 83 , 84 ).…”

Section: Limitations Of the Use Of Vitamin D As Therapeuticsmentioning

confidence: 99%

Vitamin D: Possible Therapeutic Roles in Hepatocellular Carcinoma

Adelani

Rotimi

Maduagwu³

et al. 2021

Front. Oncol.

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Hepatocellular carcinoma (HCC) is a unique type of liver cancer instigated by underlying liver diseases. Pre-clinical evidence suggests that HCC progression, like other cancers, could be aided by vitamin D deficiency. Vitamin D is a lipid-soluble hormone usually obtained through sunlight. Vitamin D elucidates its biological responses by binding the vitamin D receptor; thus, promoting skeletal mineralization, and maintain calcium homeostasis. Other reported Vitamin D functions include specific roles in proliferation, angiogenesis, apoptosis, inflammation, and cell differentiation. This review highlighted studies on vitamin D’s functional roles in HCC and discussed the specific therapeutic targets from various in vivo, in vitro and clinical studies over the years. Furthermore, it described recent advancements in vitamin D’s anticancer effects and its metabolizing enzymes’ roles in HCC development. In summary, the review elucidated specific vitamin D-associated target genes that play critical functions in the inhibition of tumorigenesis through inflammation, oxidative stress, invasion, and apoptosis in HCC progression.

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“…Hypercalcaemia has many causes; more than 90% of cases result from primary hyperthyroidism or malignancy 1. Other causes of hypercalcaemia include chronic lithium therapy, thiazide diuretics, pheochromocytoma, adrenal insufficiency, theophylline toxicity and vitamin D poisoning,2 and there was a fatal case of hypercalcaemia due to calcium channel blocker ingestion. In general, treatment of hypercalcaemia is aimed at lowering serum calcium levels.…”

Section: Descriptionmentioning

confidence: 99%

Fatal case of commercial moisture absorber ingestion

et al. 2018

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DesCripTionOne of the most commercially available moisture absorbers is a dehydrating agent containing calcium chloride. In humid environments such as basements, kitchens, cabinets and closets, calcium chloride provides effective moisture absorption by becoming highly concentrated calcium chloride brine. Ingestion of calcium chloride can lead to severe hypercalcaemia and can be fatal. In our case, hypercalcaemia developed from intentional ingestion of moisture absorber and the patient eventually died. To our knowledge, fatality from commercial moisture of absorber ingestion has not been reported. A 31-year-old man presented to the emergency department (ED) 20 min after intentionally ingesting 300 mL of commercial moisture absorber solution. It contained 300 g of calcium chloride (figure 1). The patient had a history of a pervasive developmental disorder. When the patient first presented to ED, he was alert. The patient's initial symptoms were nausea and vomiting. Gastric lavage was done, and activated charcoal was used. Although initial vital signs were relatively stable, initial ECGs revealed sinus bradycardia (36 bpm), with corrected QT interval of 421 ms (<430 ms) which, in subsequent study, increased to 512 ms. The results of the laboratory studies were as follows: serum total calcium 20.7 mg/ dL (8.2-10.8 mg/dL), ionised calcium 3.82 mmol/L (1.13-1.32 mmol/L), blood urea nitrogen 18.9 mg/ dL (7.8-22.0 mg/dL), creatinine 0.78 mg/dL (0.7-1.2 mg/dL), albumin 4.2 g/dL (3.1-5.2 g/dL), phosphorus 5.3 mg/dL (2.5-5.5 mg/dL), creatine kinase 94 IU/L (38-174 IU/L), sodium 139 mmol/L, potassium 4.0 mmol/L and chloride 107 mmol/L. Blood analysis results were pH 7.37, paCO 2 45 mm Hg, paO 2 81 mmHg and bicarbonate 26 mmol/L on room air. Urinary calcium excretion was not measured. Patient was given adequate normal saline, pamidronate and then furosemide intravenously. The second arterial blood gas analysis was done 1 hour and 40 min after the patient's arrival. pH of 7.25, PaCO 2 43 mm Hg, PaO 2 123 mm Hg and bicarbonate 18.9 mmol/L were measured. For the treatment of advanced metabolic acidosis, we had to manage it with haemodialysis. At that time, however, there was no continuous renal replacement therapy (CRRT) equipment available at our hospital, so the patient had to be transferred to nearby hospital. CRRT device w as applied immediately after the patient's transfer, but unfortunately symptoms. did not improve. On the fifth day of hospitalisation, the patient eventually died of multiple organ failure. Hypercalcaemia has many causes; more than 90% of cases result from primary hyperthyroidism or malignancy. Other causes of hypercalcaemia include chronic lithium therapy, thiazide diuretics, pheochromocytoma, adrenal insufficiency, theophylline toxicity and vitamin D poisoning, 2 and there was a fatal case of hypercalcaemia due to calcium channel blocker ingestion. In general, treatment of hypercalcaemia is aimed at lowering serum calcium levels. Despite best efforts, the patient remained in shock with signs of renal fa...

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Vitamin D intoxication: case report

Cited by 23 publications

References 9 publications

A review of the growing risk of vitamin D toxicity from inappropriate practice

A review of the growing risk of vitamin D toxicity from inappropriate practice

Vitamin D: Possible Therapeutic Roles in Hepatocellular Carcinoma

Fatal case of commercial moisture absorber ingestion

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