Monitored Supplementation of Vitamin D in Preterm Infants: A Randomized Controlled Trial

Appropriate supplementation of vitamin D can affect infections, allergy, and mental and behavioral development. This study aimed to assess the effectiveness of monitored vitamin D supplementation in a population of preterm infants. 109 preterm infants (24 0/7–32 6/7 weeks of gestation) were randomized to receive 500 IU vitamin D standard therapy (n=55; approximately 800-1000 IU from combined sources) or monitored therapy (n=54; with an option of dose modification). 25(OH)D concentrations were measured at birth, 4 weeks of age, and 35, 40, and 52±2 weeks of post-conceptional age (PCA). Vitamin D supplementation was discontinued in 23% of infants subjected to standard treatment due to increased potentially toxic 25(OH)D concentrations (>90 ng/mL) at 40 weeks of PCA. A significantly higher infants’ percentage in the monitored group had safe vitamin D levels (20–80 ng/mL) at 52 weeks of PCA (p=0.017). We observed increased vitamin D levels and abnormal ultrasound findings in five infants. Biochemical markers of vitamin D toxicity were observed in two patients at 52 weeks of PCA in the control group. Inadequate and excessive amounts of vitamin D can lead to serious health problems. Supplementation with 800–1000 IU of vitamin D prevents deficiency and should be monitored to avoid overdose.

Vitamin D Toxicity Managed with Peritoneal Dialysis

Vitamin D deficiency is a global health issue that afflicts more than one billion children and adults worldwide. Vitamin D supplementation has increased over the years, whether through medical prescriptions, over-the-counter, or online purchasing. This is driven by a more recognized association between vitamin D sufficiency status and lower risk of cancer. In addition, more recently, it is used as a potential prophylactic and treatment for COVID-19 infection. This can lead to toxicity from overingestion. While rare, it has been reported in the literature. In this case report, we present a 75-year-old man with severe hypercalcemia secondary to vitamin D toxicity managed with peritoneal dialysis. He presented with biochemical evidence of hypercalcemia, acute kidney injury, and pancreatitis. Workup for his hypercalcemia led to the diagnosis of vitamin D toxicity as shown by a level greater than 200 ng/dL (Ref: 20–50 ng/mL) was confirmed by liquid chromatography-mass spectroscopy. Cornerstone medical management of hypercalcemia was provided which included aggressive intravenous fluid hydration, intravenous diuretics, calcitonin, bisphosphonate, and corticosteroid therapy. At every interruption of therapy, calcium levels trended upward. A thorough literature review yielded the finding of a sole case report from 1966 presented at the Third International Congress of Nephrology, in which peritoneal dialysis was used in the management of vitamin D toxicity and hypercalcemia. This modality is established to cause vitamin D deficiency. In collaboration with the nephrology team, 10 sessions of peritoneal dialysis were undertaken with resolution of hypercalcemia and downtrend in 25-hydroxyvitamin D levels as measured by dilution.

A Case Report on Hypervitaminosis D Mediated Juvenile Idiopathic Arthritis

Juvenile Idiopathic Arthritis (JIA) may be defined as prevailing persistent rheumatic malady of unknown etiology in childhood and predominantly presents with peripheral arthritis. Oligoarticular Juvenile Idiopathic Arthritis (OJIA) was prevailing betwixt young female patients which consistently accompanied by anti-nuclear antibodies incontrovertibility and anterior uveitis. Disease complications differ from maturation retardation, osteoporosis and bone deformities. Due to severe Macrophage Activation System (MAS) leads to multi-organ insufficiency and loss of function. The primary goals of treatment are to distribute normal joint function, to perpetuate normal growth and to thwart long-term joint damage and retain normal body homeostasis. Key words: Juvenile Idiopathic Arthritis, Vitamin D Toxicity, Hypercalciuria, Hypervitaminosis.

A Challenging Case of Vitamin D Toxicity Responding to Cinacalcet

Background: Interest in the role of vitamin D in various physiological processes, the prevalence of its deficiency and importance of replacement has increased significantly over the past few decades. However, many formulations of vitamin D are not regulated and are available to the public without clear guidance on safe administration, which has contributed to the uptrend in the incidence and severity of vitamin D toxicity cases. Clinical Case A 57- year-old man with a medical history significant for amyotrophic lateral sclerosis, cervical myelopathy, and oropharyngeal dysphagia presented with weakness, constipation, polydipsia, polyuria and was found to have hypercalcemia with a total Calcium level of 15.5 mg/dL (n 8.6- 10.4), and albumin 4.2 g/dL (n 3.5–5.1). He soon developed acute hypoxic respiratory failure requiring prolonged intubation followed by tracheostomy. Evaluation of the hypercalcemia revealed an elevated 25-hydroxyvitamin D [25(OH)D] > 392 ng/mL (n 30–80), 1,25- dihydroxyvitamin D [1,25(OH)D] >600 pg/mL (n 19.9 - 79.3), PTH 8 pg/mL (n 12–88), and PTHrP 0.7 pmol/L (n< 4.2). The patient had initially stated that he was taking 5000 IU of vitamin D daily but further discussion with his wife revealed that he had been taking 2 teaspoons of a powder cholecalciferol preparation with 125 mcg (5000 IU of vitamin D) per 50 mg, which would be about 800,000 IU/day. He was treated with aggressive IV hydration, calcitonin and received 2 doses of pamidronate with an initial improvement in his Calcium level down to 10 mg/dL followed by recurrence of hypercalcemia. Work up for granulomatous disease and multiple myeloma revealed latent TB. At significantly elevated [25(OH)D] levels, toxicity is partially caused by the direct action of [25(OH)D] on the vitamin D receptor (VDR), and [25(OH)D] can also cross-react with the [1,25(OH)D] assay causing false elevation. Steroids were avoided because of his recent diagnosis of latent TB; hence he was started on Cinacalcet which was gradually increased to 60 mg twice a day with sustained Calcium normalization. Repeat labs showed improvement in [25(OH)D] to 292, and normalization of [1,25(OH)D] at 69.4. He was discharged on Cinacalcet 30 mg twice a day. Conclusion PTH-independent hypercalcemia is usually treated with hydration, anti-resorptive agents including bisphosphonates, denosumab and calcitonin, in addition to steroids in cases of increased 1 αλπηα-hydroxylase activity. Cinacalcet acts on the Calcium sensing receptor (CaSR) in parathyroid tissue, kidneys, bones and the intestine and was recently shown to improve hypercalcemia of malignancy in a report of 2 cases by Sheehan et al. Cinacalcet has helped our patient and might have a potential role for the prompt treatment of vitamin D toxicity, but more data is needed.