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Untitled-36Hypercalcaemic Crisis — A Case Study of Three
Unusual Cases of Iatrogenic Vitamin D and Calcium
I n t o x i c a t i o n
Bhakti Desai*, Anand Gokani**, Alpana Shukla***, PS Tampi****
A b s t r a c t
Severe hypercalcaemia is potentially life-threatening complication of several diseases. Most
commonly it is caused by cancers that enhance bone resorption. Though rare, Vitamin D intoxi-
cation is an important cause of hypercalcaemia. Massive doses of ergocalciferol continue to be
prescribed inappropriately or without adequate supervision and the dangers to this therapy
are still not appreciated. We studied such three unusual cases of Vitamin D and calcium intoxi-
cation due to overcorrection of osteoporosis treatment.
C a s e R e p o r t
I n t r o d u c t i o n
A n 8 0 y r o l d m a l e , k n o w n h y p e r t e n s i v e w a s admitted with chief complaints of nausea, loss of adequate intake is 5 micrograms (200 IU) daily appetite, constipation and progressive weakness. On for all individuals (males, females, pregnant/ e x a m i n a t i o n p a t i e n t ' s g e n e r a l a n d s y s t e m i c lactating women) under the age of 50 years, e x a m i n a t i o n w a s n o r m a l . I n v e s t i g a t i o n s r e v e a l e d Calcium – 18.5 mg/dl, Creatinine – 2.70 mg/dl, Albumin – 3.2 gm%, Vitamin D – 150 ng/dl, Plasma micrograms daily (600 IU) for those who are over the age of 70 years. The recommended Urea – 50 mg %, Alkaline Phosphatase – 66 mu /dl.
Treatment was started immediately with infusion of dose 1200 mg /day of elemental calcium and I.V Isotonic saline (500 ml /6 hrs) over 24 hrs followed by loop diuretics. A single dose of Bisphosphonates i.e. I.V Zolendronate 4 mg diluted in100 ml of 0.9 % treatment of Vitamin D deficiency especially NaCl was given followed by Inj Calcitonin 100 mg i.m 8 hrly. During the hospital stay patient developed v o m i t i n g , o l i g u r i a w i t h f l u i d r e t e n t i o n a n dbronchospasm. Appropriate I.C.U management with hypercalcaemia which is potentially life- diuretics, bronchodilators improved the condition.
threatening. There is little relationship Repeat Calcium levels were reduced. On discharge between symptoms of hypercalcaemia and the p a t i e n t w a s a s k e d t o s t o p c a l c i u m s u p p l e m e n t s .
actual level of blood calcium. Hence early and Repeated calcium, PTH and urine analysis report were found to be normal. Detailed history revealed, patienthad taken 18 injections of Vitamin D for bone pain.
hypercalcaemia though difficult, is important.
A 6 7 y r p o s t m e n o p a u s a l f e m a l e a d m i t t e d w i t h * R e s i d e n t M e d i c a l O f f i c e r ; * * C o n s u l t a n t complaints of nausea, vomiting, loss of appetite and D i a b e t o l o g i s t ; * * * C o n s u l t a n t E n d o c r i n o l o g i s t ; low back pain. General and systemic examination was ****Consultant Chest Physician, Bombay Hospital.
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normal. Biochemistry showed Calcium – 16.7 mg%, Creatinine – 1.8 mg/dl, Albumin – 3.10 mg%, Alkaline phosphatase-64 mu/dl Plasma P.T.H – 8.67 pg/dl.
Immediate treatment with isotonic saline infusion, Calcitonin along with single dose of Bisphosphonates (Pamidronate) 90 mg in 100 ml of 0.9% NaCl started.
level in the blood (Normal range: 9-10.5 mg/ P a t i e n t r e s p o n d e d w e l l t o t h i s t r e a t m e n t v o m i t i n g stopped and appetite was improved. Repeat calcium excessive skeletal calcium release, increased levels were normal serially. On discharge, patient was intestinal calcium absorption, or decreased advised to stop calcium supplements and low calcium diet was prescribed. On follow up patient’s calcium r e p o r t s w h i c h w e r e f o u n d t o b e n o r m a l . D e t a i l e d parathyroidism and malignancy account for history that patient had taken 3 Vitamin D injections ~90% of cases. Other causes include Vitamin- from orthopaedic doctor for backache.
A 74 yr old, postmenopausal female was admitted with complaints of generalized weakness, anorexia 1,25(OH) D), disorders related to high bone- a n d m e n t a l c o n f u s i o n . S h e w a s a k n o w n c a s e o f h y p e r t e n s i o n , d i a b e t e s , i s c h a e m i c h e a r t d i s e a s e , c h r o n i c k i d n e y d i s e a s e a n d h y p e r t h y r o i d i s m o nt r e a t m e n t . S h e a l s o h a d a h i s t o r y o f m u l t i p l e vitamin A intoxication, Paget’s disease of the compression fractures between D2 – D12 levels. On bone) renal failure (e.g. severe secondary e x a m i n a t i o n s h e w a s d r o w s y b u t o r i e n t e d w i t h hyperparathyroidism), lithium use.1
bradycardia. Systemic examination essentially normal. On investigating, the Serum calcium – 15.10 Creatinine – 2.9 mg/dl , Urea – 158 mg %, Albumin – 1.7 mg, Vitamin D3 – 145 ng/dl ( normal < 75 ng/dl) increased urination; Severe hypercalcaemia with normal PTH levels and thyroid function test. CT Scan of Brain was also normal. Patient was shifted to threatening.2 At these levels, coma and
I.C.U. and immediate treatment for hypercalcaemia was started with isotonic saline infusion, followed byd i u r e t i c s . C a l c i t o n i n a n d B i s p h o s p h o n a t e s (Zolendronate) was administered under close cardiac however mislead like in our cases where the monitoring. With this management the serum calcium patient's clinical symptoms didn’t correlate gradually reverted to normal over next 24 to 48 hours a n d t h e p a t i e n t ' s g e n e r a l c o n d i t i o n s t a b i l i z e d .
Hypervitaminosis D is a well known cause of S u b s e q u e n t l y t h e p a t i e n t d e v e l o p e d f e v e r a n dsepticaemia (ESBL producing Klebsiella was cultured from blood). As her O saturation and B.P dropped, suspected when some of the above symptoms she had to be intubated and placed on ventilatory develop in a patient receiving vitamin D.3
support with inotropic infusion. The azotaemia was managed with dialysis. Despite energetic and c o n t i n u e d m a n a g e m e n t , t h e p a t i e n t c o n t i n u e d t o d e t e r i o r a t e w i t h m u l t i o r g a n f a i l u r e a n d f i n a l l y resorption, as well as there is consequent lossof renal concentrating ability causing D i s c u s s i o n
hypercalcaemia. Also an increase in albumin Calcium plays an important role in cellular of 1 g/dL over normal increases measure total calcium by 0.8 mg/dL. 4 T h e s e r u m
Bombay Hospital Journal, Vol. 50, No. 2, 2008
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phosphorus and alkaline phosphatase levels C o n c l u s i o n
This case report is to sensitize about the overcorrection of osteoporosis with Vitamin D and Calcium leading to hypercalcaemia.
Treatment of vitamin intoxication consists Massive doses of ergocalciferol continued to of discontinuing treatment with vitamin D, a be prescribed without adequate supervision low-calcium diet.5 Hydration is needed
and the dangers of this therapy are still not generally appreciated. A vigorous emphasis to vomiting or renal defects in concentrating on the use of Vitamin D and calcium as of urine. After rehydration, a loop diuretic such other vitamins , implies several risk and must b e p r e s c r i b e d o n l y w h e n n e e d e d a n d u n d e r continued large volume intravenous salt and water replacement while minimizing the risk R e f e r e n c e s
of blood volume overload. In addition, loop Chan FK, Koberle LM, Thys-Jacobs S, Bilezikian reabsorption thereby helping to lower blood management of hypercalcemia. Curr Prob Surg calcium levels by 1-3 mg/dL within 24 hours.
Attie MF. Treatment of hypercalcemia, Endocrinol B i s p h o s p h o n a t e s a r e p y r o p h o s p h a t e Metab. Clin North Am 1989; 18 (3) : 807–28.
D a v i e s M , A d a m P H . T h e c o n t i n u i n g r i s k o f especially areas of high bone-turnover. They Vitamin D intoxication. Lancet 1980; 1 : 1308.
are relatively contraindicated in renal failure.
Buchinsky DA, Monk RD. Calcium. Lancet 1998; Calcitonin blocks bone resorption and also B i l e z i k i a n J P . M a n a g e m e n t o f a c u t eh y p e r c a l c e m i a . N E n g l J M e d 1 9 9 2 ; 3 2 6 : inhibiting renal calcium reabsorption.
TREATING ACUTE MYOCARDIAL INFARCTION : SOMETHING IN THE WIND?
The preservation of healthy myocardium during a heart attack is the holy grail of contemporary c a r d i o l o g y . P r i m a r y a n g i o p l a s t y t o r e s t o r e p e r f u s i o n i s a n i m p o r t a n t a d v a n c e b u t r o o m f o r improvement remains. Over the past 40 years, hundreds of experimental interventions have beenreported to protect the myocardium in animal models, but except for early reperfusion, none have J-WIND-ANP studied atrial natriuretic peptide (ANP) and I-WIND-KATP studied nicorandil. By
contrast, intravenous nicorandil showed no acute benefits.
Richard Bogle, Martin Wilkins, The Lancet, 2007; 370 : 1461-62.
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