Risks of the ‘Sunshine pill’ – a case of hypervitaminosis D

Abstract

Case presentationA 73-year-old man presented with a 4-week history of diarrhoea and 2-week history of confusion. He was a retired nuclear scientist who was previously fully independent with no history of cognitive impairment. There was no history of smoking, alcohol or substance abuse.His wife reported cognitive disturbances including being unable to use a cassette player or turn on his electric razor and he had started urinating in the sink. He was visited by his GP who found him confused, drowsy and dehydrated. Observations were unremarkable but a rectal examination showed hard stool in the rectum. Presuming a urinary tract infection, laxatives and trimethoprim were prescribed and he was transferred to hospital for further investigations.On admission there were no infective signs or symptoms. His cardiovascular, respiratory and abdominal examinations were unremarkable. He was extremely delirious requiring sedation and occasional reasonable physical restraint. He scored 3/10 on the Abbreviated Mental Test Score (AMTS) but had no other neurological signs. His electrocardiogram (ECG), chest X-ray (CXR) and computed tomography (CT) brain were all normal. Admission blood test results are shown in Table 1 . DiagnosisInvestigations for his hypercalcaemia revealed low parathyroid hormone 0.6 pmol/L and a toxic 25-hydroxyvitamin D (25[OH]D) ABSTRACT concentration 881 nmol/L (normal range 25-100 nmol/L), suggesting a diagnosis of hypervitaminosis D. Other causes of hypercalcaemia such as malignancy, thyroid disease and sarcoidosis were excluded. On further questioning his daughter reported he had been taking 60,000 IU vitamin D capsules per day for the last 2 years having read a book advocating its health benefits.

Vitamin D intoxication and severe hypercalcaemia complicating nutritional supplements misuse

“…Given its slow turnover (half-life of approximately 2 months), during which vitamin D toxicity develops, symptoms can last for several weeks. 2 …”

Risco de hipervitaminose na população idosa e o papel do farmacêutico

“…Um estudo realizado por Ellis et al, (2018), relatou um caso de paciente, homem de 73 anos, com Hipervitaminose D, ocasionada pela automedicação de suplementos, apresentando risco de vida e hipercalcemia. Neste relato, os autores evidenciaram o histórico de comprometimento cognitivo do paciente relacionado à elevada ingestão de doses diárias de vitamina D, onde o senhor chegou a apresentar desidratação, sonolência, confusão e até incapacidade para realização de atividades básicas, como ligar seu barbeador elétrico.…”

“…Embora, no geral, tenham evidenciado a importância da familiarização de médicos e farmacêuticos quanto a composição de oligoelementos, suplementos vitamínicos e suas respectivas toxicidades potenciais associadas à superdosagem (Ruiz, Souza & Paiva, 2021). Para que possam possuir, assim, conhecimento suficiente para evitar a automedicação e orientar pacientes sobre perigo potenciais da ingestão vitamínica excessiva (Ellis et al, 2018;Malet et al, 2019;Melliez et al, 2020).…”

“…Todos os artigos estavam no idioma inglês, sendo predominantemente publicados nos Estados Unidos (Blank et al, 1995;Jacobsen et al, 2011;Kim et al, 2017;Rooney et al, 2017). Outros países presentes na amostra foram: França (Malet et al, 2019;Melliez et al, 2020), Reino Unido (Ellis et al, 2018), Espanha (Granado-Lorencio et al, 2012), Bélgica (Nollevaux et al, 2006) e Itália (Cirillo et al, 2016).…”

Calcium Alkali Syndrome Treated With Hemodialysis

“…Miacalcin's acute effect on decreasing high plasma levels of calcium ceases after 24-48 h due to the development of drug tolerance over time by the kidneys [5]. Unfortunately, our choices for long-acting agents were not good as patient presented with acute kidney injury (AKI) and bisphosphonates (Aredia and Zometa) can exacerbate the severity of AKI in the setting of hypercalcemia [5][6][7]. There is evidence that both drugs renally accumulate and are retained in the renal cortex and medulla, likely via endocytosis [5,7].…”