Calcium and bone metabolism

This chapter covers calcium and bone metabolism. It starts with the physiology of bone, investigation of the bones, imaging, mass measurements, and biopsy, then goes on to investigation of calcium, phosphate, and magnesium. Urine excretion and calcium-regulating hormones are explained. It goes on to hypercalcaemia, primary hyperparathyroidism and its treatment, vitamin D intoxication, sarcoidosis, and hypocalcaemia. Vitamin D deficiency, Paget’s disease, and inherited disorders of bone are all included. The pathology, epidemiology, presentation, investigation, and treatment of osteoporosis are covered in detail.

Calcinosis in Alpaca Crias (Vicugna pacos) Due to Vitamin D Intoxication—Clinical, Laboratory and Pathological Findings with a Focus on Kidney Function

Alpacas kept in Central Europe are often deficient in vitamin D3, which is supplemented orally or by injection by the owners or veterinarians. Vitamin D3 can be specified in two different units (IU and µg), which differ by a factor of 40. By mixing up these units, an overdosage can be induced. In this study, three alpaca crias were examined after vitamin D3 intoxication, with particular reference to kidney function. All three animals developed non-specific clinical alterations 1–2 weeks after a vitamin D3 overdose of approximately 40 times. Plasma of the animals revealed several alterations. The main findings were severe azotemia, hypercalcemia and hyperphosphatemia, 15 days after treatment. Kidney function analysis (endogenous creatinine clearance) in two of the crias revealed severe glomerular damage. All crias died despite intensive treatment within 23 days after vitamin D3 treatment. Necropsy revealed calcification in different organs, mainly the kidneys, lungs and liver. Since nine other crias in the same group were treated with comparable doses of vitamin D3 and no clinical signs were observed in these animals, it is concluded that individual animals show different levels of sensitivity to vitamin D3.

Vitamin D Intoxication and Nephrocalcinosis in a Young Breastfed Infant

Numerous studies were performed assessing the benefits and side effects of vitamin D. Vitamin D helps in regulating the calcium and phosphate metabolism leading to a healthy mineral and bone development. Vitamin D intoxication is an uncommon event that leads to hypercalcemia which can be associated with both immediate and late morbidities that can cause severe renal complications. Here, we present a case of a 4-month-old girl with a history of decreased feed and activity due hypercalcemia and high vitamin D level, which led to nephrocalcinosis. The patient received IV fluids, IV diuretics, methylprednisolone, and bisphosphonate in order to normalize the calcium level in blood. With clear verbal and written instructions for the dosage and administration of vitamin D supplements, as well as clear warnings of the potential risks of overdose, vitamin D intoxication could be an easily avoidable condition.

CLINICAL CASE OF VITAMIN D OVERDOSE IN A YOUNG CHILD

The article describes a case of vitamin D intoxication (cholecalociferol) in a premature baby (born at the 33rd week of pregnancy) at the age of 8 weeks. An excess of the vitamin D dose by 15 times (15 000 IU/day instead of 1000 IU/day prescribed by the doctor) led to a concentration of 25(OH)D of 210 ng/ml and to a clinical picture of intoxication. During detoxification therapy, the 25(OH)D concentration decreased to the normal range in 4 weeks after vitamin D discontinuation. It is necessary to focus parental attention to the accuracy of adherence to the vitamin D regimen prescribed by the pediatrician.

Vitamin D Intoxication Presenting as Subacute Encephalopathy—A Case Report

Vitamin D intoxication is uncommon in children and is more commonly suspected in the setting of ingestion of high doses of vitamin D. Its manifestations can be non specific and varied ranging from mild like constipation and vomiting to life threatening like arrhythmias and encephalopathy. Here we present a 14 month female who presented with loss of milestones, floppiness, and poor interaction with mother. She was detected to have hypercalcemia and was subsequently diagnosed with vitamin D intoxication. She was successfully treated with hydration, furosemide, prednisolone and frequent monitoring of electrolytes, electrocardiography and volume status. Subsequently as her serum calcium levels normalized with therapy, she became alert, conscious and started achieving developmental milestones.

How Much Vitamin D is Too Much? A Case Report and Review of the Literature

Background: The beneficial effects of vitamin D, together with the high prevalence of vitamin D deficiency, have led to an expanding use of vitamin D analogues. While inappropriate consumption is a recognized cause of harm, definition of doses at which vitamin D becomes toxic remain elusive. Case presentation: A 56-year woman was admitted to our Hospital following a 3-week history of nausea, vomiting and muscle weakness. The patient had been assuming very high dose of cholecalciferol since 20 months (cumulative 78,000,000UI, mean daily 130,000UI), as indicated by a non-conventional protocol for multiple sclerosis. Before starting vitamin D integration, serum calcium and phosphorus levels were normal, while 25OH-vitamin D levels were very low (12.25 nmol/L). On admission, hypercalcemia (3.23 mmol/L) and acute kidney injury (eGFR 20 mL/min) were detected, associated with high concentrations of 25OH-vitamin D (920 nmol/L), confirming the suspicion of vitamin D intoxication. Vitamin D integration was stopped and, in a week, hypercalcemia normalized. It took about 6 months for renal function and 18 months for vitamin D values to go back to normal. Conclusions: This case confirms that vitamin D intoxication is possible albeit with a really high dose. The doses used in clinical practice are far lower than these and, therefore, intoxication rarely occurs even in those individuals whose baseline vitamin D serum levels have never been assessed. Repeated measurements of vitamin D are not necessary in patients under standard integrative therapy. However, patients and clinicians should be aware of the potential dangers of vitamin D overdose.

Long-term hypervitaminosis D-induced hypercalcaemia treated with glucocorticoids and bisphosphonates

Hypercalcaemia is a common diagnosis with the majority of cases resulting from hyperparathyroidism or malignancy. We report a rare case of persistent symptomatic hypervitaminosis D-induced hypercalcaemia in an individual taking 50 000 IU of vitamin D supplement daily for several months following a diagnosis of vitamin D deficiency. His hypercalcaemia was initially treated with calcitonin and intravenous fluids, but due to recurrent symptomatic hypercalcaemia after discharge, additional treatment with glucocorticoids and bisphosphonates was warranted during his second admission. The pathophysiology of hypercalcaemia from vitamin D intoxication results from the long-term effects of vitamin D storage in adipose tissue. In the present case, we discuss this pathophysiology and treatment approaches in the context of increasing awareness of and testing for vitamin D deficiency, and growing access to over-the-counter supplements.