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| CASE IN POINT: VITAMIN D SUPPLEMENTATION |
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| Year : 2015 | Volume
: 2
| Issue : 2 | Page : 103-104 |
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Too much of anything is good for nothing
Ramita Sardana
Department of Physical Medicine and Rehabilitation, All India Institute of Medical Sciences, New Delhi, India
| Date of Web Publication | 28-Dec-2015 |
Correspondence Address:
Ramita Sardana
Department of Physical Medicine and Rehabilitation, All India Institute of Medical Sciences, New Delhi
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2349-0977.172680
How to cite this article:
Sardana R. Too much of anything is good for nothing. Astrocyte 2015;2:103-4 |
A 60-year-old female presented with low back pain with generalized musculoskeletal pain, fatigue, anorexia, gait imbalance, and nausea. There was no history of fever, weight loss, cough, headache, trauma, focal weakness, tremors, decreased sensation, or urinary symptoms. She was taking treatment from orthopedics for some generalized bone pain for past 3 months and had been prescribed cholecalceferol sachet 60,000 IU/week and calcium supplements (elemental calcium 500 mg/day). On conducting a general physical examination, she was bit depressed but oriented. The rest of the general physical examination was within normal limits. Her neurological examination was performed and no abnormality was detected in her mental status, tone, power, sensation, deep tendon reflexes, and cerebellar signs. On examination, her cardiovascular, respiratory, and abdominal systems were within normal limits. Blood investigations (hematological and biochemistry) were advised which showed serum calcium - 13.8 mg/dl (8.1–10.5 mg/dl); Vitamin D (25 [OH])−152 ng/dl (41–80 ng/dl); plasma PTH - 12.2 pg/ml (10–65 pg/ml); serum creatinine - 1.6 mg/dl (0.6–1.2 mg/dl); urea - 42 mg% (20–40 mg/dl); and alkaline phosphatase - 60 mg/dl (30–140 IU/L). X-ray lumbosacral spine showed few degenerative changes. Other radiological investigations like chest X-ray, computed tomography chest, neck, and abdomen and magnetic resonance imaging brain were found to be normal. To find etiology of hypercalcemia, all previous investigations and prescriptions of the patient were checked thoroughly. A look at medications she was already taking revealed that she was prescribed cholecalceferol 60,000 IU/week sachet by some local practitioner. On asking she told that she was taking that sachet daily for past 3 months. Therefore a diagnosis of hypervitaminosis D leading to hypercalcemia was made, which was confirmed by high serum calcium, high serum Vitamin D and normal PTH levels. Her calcium and Vitamin D supplements were immediately stopped. Calcium restricted diet was prescribed. In addition, she was prescribed adequate hydration with plenty of fluids. Medicines prescribed included tablet aceclofenac 50 mg bid for 5 days and then as and when required; bisphosphonates (pamidronate) 90 mg in 100 ml 0.9% NaCl intravenous (IV) over 2–4 h (single dose); prednisolone 20 mg daily for 10 days then 10 mg daily for 4 days. She was called for follow-up after 2 weeks and 8 weeks. After 2 weeks, clinically her condition had improved, and serum calcium levels were found to be 11.2 mg/dl. After 8 weeks, her serum calcium level decreased to 10.2 mg/dl and Vitamin D level was found to be 76.87 ng/ml. She was symptomatically much better. The patient is on regular follow-up in PMR OPD and is doing well.
As we know Vitamin D supplements are prescribed and taken by more and more patients these days (Vitamin D deficiency being so common). Though rare but hypervitaminosis D is a possibility. Healthcare providers and patients should be educated on advantages and risks associated with Vitamin D supplementation. As physicians, it is our duty to not only diagnose a disease and prescribe medications but also to correctly explain the patient about the dosage and risks of medications, see previous prescriptions and monitor the therapy regularly.
| Discussion | |  |
Calcium is required in the human body for nerve conduction, muscle contraction, coagulation, electrolyte, and enzyme regulation.[1] Vitamin D metabolic disorders are among important causes of calcium imbalance in the body. Recommended daily allowance of Vitamin D for an adult is 600–800 IU/day while it's no adverse effect level is 10,000 IU per day.[2] The half-life of Vitamin D (25-hydroxyvitamin D3) is 20–29 days and half-life of 1,25(OH)2D3 is 15 h.[3] Vitamin D metabolic disorders include intoxication, sarcoidosis, granulomatous disorders, hyperthyroidism, prolonged immobilization, thiazide use, Vitamin A intoxication, Paget's disease of bone, renal failure, lithium use, etc.[4] Vitamin D in excess may lead to increased calcium absorption from the gastrointestinal tract, which may further lead to increased bone resorption and loss of renal concentrating ability causing hypercalcemia.[5] There is increased risk of hypervitaminosis D with supplements if the patient is already having kidney disease, liver disease, tuberculosis, hyperparathyroidism, sarcoidosis or histoplasmosis. Food sources rich in Vitamin D are Fatty fish, beef liver, cheese, egg yolk, and some mushroom. Main signs and symptoms of hypervitaminosis D include nausea, vomiting, weakness, altered level of consciousness, polyuria, excessive thirst, painful articular calcinosis, nephrocalcinosis, hypertension, band keratopathy, dehydration, constipation, fatigue, muscle weakness, decreased appetite, and hearing loss.[6] For management of hypervitaminosis D one should discontinue Vitamin D and calcium supplements, the patient should be prescribed a calcium-restricted diet, hydration in the form of IV or oral fluids. Loop diuretics like frusemide may also be prescribed to permit continue large volume intake, minimize the risk of blood volume overload and to depress renal calcium absorption.[7] Bisphosphonates are prescribed to bind to bone hydroxyapatite and inhibit calcium release by interfering with osteoclast-mediated bone resorption.[8] Prescription of calcitonin helps in blocking bone resorption and in increasing urinary calcium excretion. Glucocorticoids may help by decreasing endogenous overproduction of calcitriol. On having a look at review of literature it was seen that Parvaiz et al. concluded in their study titled “Vitamin D toxicity in adults” that Hypervitaminosis D must be considered in the differential diagnosis of patients with hypercalcemia in endemically Vitamin D deficient areas.[9] Bischoff-Ferrari et al. published a review article titled “benefit-risk assessment for Vitamin D” and selected 10,000 IU of daily Vitamin D as the upper limit of Vitamin D.[10] Hence, it can be concluded that as Vitamin D supplements are prescribed and taken by more and more patients these days (Vitamin D deficiency being so common). Though rare but Hypervitaminosis D is a possibility. Healthcare providers and patients should be educated on advantages and risks associated with Vitamin D supplementation. Being physicians it is our duty to not only diagnose a disease and prescribe medications but also to correctly explain the patient about the dosage and risks of medications, see previous prescriptions and monitor the therapy regularly.
Acknowledgment
I express my gratefulness to the head of my department Prof. U. Singh, who understood and solved any problem in this case. I am also thankful to my teachers Prof. Sanjay Wadhwa, Prof. S. L. Yadav and Prof. Gita Handa for their kind support and guidance.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 4. | Chan FK, Koberle LM, Thys-Jacobs S, Bilezikian JP. Differential diagnosis, causes, and management of hypercalcemia. Curr Probl Surg 1997;34:445-523. |
| 5. | Reichel H, Koeffler HP, Norman AW. The role of the vitamin D endocrine system in health and disease. N Engl J Med 1989;320:980-91. |
| 6. | Attie MF. Treatment of hypercalcemia. Endocrinol Metab Clin North Am 1989;18:807-28. |
| 7. | Bilezikian JP. Management of acute hypercalcemia. N Engl J Med 1992;326:1196-203. |
| 8. | Dominguez LJ, Di Bella G, Belvedere M, Barbagallo M. Physiology of the aging bone and mechanisms of action of bisphosphonates. Biogerontology 2011;12:397-408. |
| 9. | Koul PA, Ashraf M, Jan RA, Shah S, Khan UH, Ahmad F, et al. An elderly male with tubercular osteomyelitis of the chest wall. BMJ Case Rep 2011;2011. pii: Bcr1220103638. |
| 10. | Bischoff-Ferrari HA, Shao A, Dawson-Hughes B, Hathcock J, Giovannucci E, Willett WC. Benefit-risk assessment of vitamin D supplementation. Osteoporos Int 2010;21:1121-32. |
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