Dysmagnesemia Is the Most Common Disturbance of the Calcium–Magnesium–Phosphorous Balance among Older Hospitalized People in Warsaw

The elderly are at great risk of developing life-threatening disturbances in calcium–magnesium–phosphate homeostasis because of comorbidities, long-term medication use, and dietary deficiencies, but it is still not known how often they occur in this group of patients. This study aimed to assess the prevalence of these disturbances in a group of hospitalized patients over 65 years of age according to age and sex. The study was conducted between January 2018 and September 2020 at the Central Clinical Hospital in Warsaw. A total of 66,450 calcium, magnesium, phosphate, and vitamin D concentration results were included in the analysis. Dysmagnesemia was present in 33% of the calcium results, dyscalcemia, dysphosphatemia, and dysvitaminosis D—in 23.5%, 26%, and 70% of the results, respectively. The magnesium concentration was found to be age-dependent, and older people were found to be at higher risk of developing abnormal magnesium concentrations (p < 0.001). Sex influenced the occurrence of abnormal magnesium (p < 0.001), vitamin D (p < 0.001), and calcium (p < 0.00001) concentrations, with hypercalcemia and hypervitaminosis D disorders being significantly more common in women (p < 0.0001). In conclusion, disorders of the calcium–magnesium–phosphate metabolism are common in hospitalized patients over 65 years of age, and the concentrations of these substances should be routinely monitored in this group.

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.

Coexistent CYP24A1 and PHEX Gene Mutations With Hypervitaminosis D Plus Hypercalcemia Treated With Fluconazole

Background: CYP24A1 and PHEX gene mutations are rare and can cause hypercalcemia, hypervitaminosis D and elevated FGF23 levels. Fluconazole, an antifungal medication, has shown therapeutic benefit in achieving normocalcemia plus normalisation of vitamin D levels in this case report. Clinical Case: A 42 year old man was referred to the endocrine clinic with a history of severe nephrocalcinosis and recurrent nephrolithiasis requiring surgical intervention and gradual decline in kidney function over 20 years. Biochemical investigations revealed hypercalcaemia with adjusted calcium levels of 2.83 mmol/L (R 2.2–2.6 nmol/L) and suppressed PTH 1.1 pmol/L(R 1.6–6.9 pmol/L). Twenty-four hour urine calcium/creatinine clearance ratio was above 0.0578 mmol/mmol indicating hypercalciuria. Vitamin D metabolites 25 OH Vitamin D was elevated at 201 nmol/L, (R 50–120 nmol/L) along with intermittently elevated 1,25 OH Vitamin D 147 pmol/L(R 55–139 pml/L). 24,25 Vitamin D was low at 2.0 nmol/L producing a 25:24,25 dihydroxyvitamin D ratio of 80 (n&lt;25). This biochemical data was highly suggestive of a loss of function mutation in the CYP24A1 gene that codes for the enzyme 24-hydroxylase, which is responsible for conversion of 1,25 vitamin D to 24,25 vitamin D. A pathogenic variant (heterozygous c.756G&gt;A) was confirmed on genetic testing. Plasma FGF23 (immutopics) was raised (with a peak of 596 RU/mL, n&lt;100 RU/mL) but a full body octreotide scan did not reveal malignancy or other paraneoplastic syndromes such as oncogenic osteomalacia. A pathogenic variant in his PHEX gene (homozygous c.1874A&gt;T) was also identified that has been associated with increased levels of FGF23 plus hypophosphataemia. Fluconazole at 50 mg once daily was initiated. Azoles inhibit cytochrome P450 enzymes and have been used in sarcoidosis to block vitamin D-synthesizing enzymes such as 25-hydroxylases and 1-α-hydroxylase that are P450 dependent. Few cases of CYP24A1 gene defects have been treated with fluconazole, which has a favourable side effect profile and yields good results. Adjusted calcium reduced to 2.62 nmol/L, 25 OH Vitamin D normalised to 111 nmol/L and 24:24,25 dihydroxyvitamin D ratio is now 17. Patient’s liver functions and full blood count has been monitored regularly during the course of treatment and the drug was well tolerated. Conclusion: Genetic causes of hypercalcemia can be left undiagnosed for long periods and there is a lack of proven or definitive therapeutic agents for correction of elevated calcium. Here fluconazole has been shown to reduce the hypercalcaemic burden and effectively lowered the Vitamin D levels in this case of a CYP24A1 mutation. This study augments fluconazole use in these cases but further studies are needed to elucidate the long term safe usage.

Hypervitaminosis D in Infants

Objective of the Paper: To describe a case history of the diagnosis and management of hypervitaminosis D in a 3-month baby. Key Points. Hypervitaminosis D can be caused either by intake of high doses of this product, or hypersensitivity to its toxic effects. This paper describes a clinical history of diagnosis and management of hypervitaminosis D in a 3-month baby boy. Medical history (daily intake of vitamin D in doses manifold exceeding the age-specific preventive dose for 2 months), laboratory tests (increased blood concentrations of 25-hydroxycholecalciferol and calcium, reduced parathormone levels) made it possible to diagnose hypervitaminosis D. The condition of the baby improved after withdrawal of vitamin D and therapy aiming at normalisation of the hydro-electrolytic balance and body functions. It was recommended not to take vitamin D until the 25-hydroxycholecalciferol level normalises. Conclusion. In order to prevent hypervitaminosis D, it is essential to strictly adhere to the preventive and therapeutic doses of vitamin D, preferably with blood calcidiol monitoring. Keywords: hypervitaminosis D, 25-hydroxycholecalciferol, intoxication, preventive dose, therapeutic dose.