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 Table of Contents  
CASE REPORT
Year : 2012  |  Volume : 1  |  Issue : 2  |  Page : 112-114

A rare case of hypocalcemia in hyperthyroidism


Department of General Medicine, Dr. B.R. Ambedkar Medical College, Kadugondanahalli, Bangalore - 560 045, Karnataka, India

Date of Web Publication27-Sep-2012

Correspondence Address:
Jayashankar C Anjanappa
Department of General Medicine, Dr. B. R. Ambedkar Medical College, Kadugondanahalli, Bangalore - 560 045, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-344X.101713

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  Abstract 

A 35-year-old woman presented with multinodular goitre with features of hyperthyroidism of two years' duration. While on treatment for hyperthyroidism she developed clinical features of tetany. Evaluation revealed low serum calcium, low serum parathyroid hormone (PTH), no hyperventilation, normal serum albumin level, normal serum cortisol, normal serum magnesium, no previous surgical or radio iodine therapy for thyroid dysfunction. She responded to treatment with antithyroid drug and calcium supplements and symptoms improved after two weeks. This rare association of hypoparathyroidism (idiopathic) in multinodular goitre with hyperthyroidism is presented.

Keywords: Hyperthyroidism, hypocalcemia, idiopathic hypoparathyroidism


How to cite this article:
Raja SB, Anjanappa JC. A rare case of hypocalcemia in hyperthyroidism. Int J Health Allied Sci 2012;1:112-4

How to cite this URL:
Raja SB, Anjanappa JC. A rare case of hypocalcemia in hyperthyroidism. Int J Health Allied Sci [serial online] 2012 [cited 2024 Mar 28];1:112-4. Available from: https://www.ijhas.in/text.asp?2012/1/2/112/101713


  Introduction Top


Hypercalcemia is well known in hyperthyroidism, but hypocalcemia is rarely seen. Hypocalcemia in hyperthyroidisms occur as a complication following surgery on thyroid gland or following radio iodine therapy. Hypoalbuminemia and hypomagnesemia as a cause of hypocalcemia was excluded in this case. Parathyroid surgery is known to cause hypocalcemia. A few cases of hypocalcemia are being reported following medical treatment for hyperthyroidism simulating Hungry bone syndrome.


  Case Report Top


A 35-year-old female was admitted to our hospital on 10 May 2010 with history of a progressively increasing swelling in the anterior aspect of the neck, palpitations, tremors in hands, nervousness, excessive sweating and loss of weight of 8 kg since two years. There was no history of diarrhoea, jaundice, diabetes mellitus, oligomennorhoea, family history of thyroid disease or any treatment received. Her previous medical and obstetric history was normal. She is a mother of two children, the age of the younger child being six years. There was no history suggestive of thyroid dysfunction during her pregnancies.

On examination, anthropometry: height was 150 cm, weight 50 kg and body mass index was 20. Pulse was 130/min (tachycardia), regular in rhythm. Blood pressure (BP) was 120/80 mm Hg. Both hands were warm and fine tremors were noticed. There was no lymphadenopathy, pretibial edema and clubbing or eye signs. Examination of neck revealed non-tender multinodular goitre with right lobe measuring 5 cm × 3 cm and left lobe measuring 5 cm × 3 cm but no bruit heard over it. Cardiac examination revealed loud first and second heart sounds. Other systemic examinations were clinically normal.

Laboratory studies on admission revealed Hb% of 11.3 gm%, total white cells count was 6,900/mm 3 , platelets were 2,15,000/mm 3 , random blood glucose 174 mg/dl, blood urea was 34.9 mg/dl and serum creatinine 0.6 mg/dl. Her total serum triiodothyronine (T3) was > 6.51 (normal: 0.5-2.0 ng/dl), total serum thyroxine (T4) was > 24.86 μg/dl (normal: 4.8-14 μg/dl) and serum TSH was < 0.005 μIU/ml (normal: 0.3-6.0 μIU/ml).

Electrocardiogram demonstrated sinus tachycardia. Ultrasound thyroid scan revealed multiple nodular goitre with no retrosternal extension.

Anti-thyroid peroxidase was 26 (Negative < 35 U/mL, Positive > 50 U/mL ELISA).

Fine Needle Aspiration Cytology of thyroid gland showed follicular epithelial cells (in clusters) with fragile cytoplasm, histiocyte and little colloid. Due to paucity of resources, radionuclide scan of thyroid gland could not be carried out.

She was treated for hyperthyroidism with oral carbimazole 10 mg TID and propranolol 10 mg TID.

Three days later she had circumoral paraesthesia and spasm in both hands and feet typical of carpopedal spasm but no Chvostek's sign.

Investigation for cause of tetany showed total serum calcium of 8.3 mgs/dl, and other lab investigation details are given in [Table 1].
Table 1: Lab investigations

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Hepatitis B surface antigen was negative. Arterial blood gas analysis showed no features of respiratory alkalosis. Electrocardiography showed normal QT interval. 2 D-Echocardiography revealed sclerotic aortic valve, Grade I aortic regurgitation. Chest X-ray was normal. Slit-lamp examination of eyes did not reveal any Kayser Fleischer ring which is seen in Wilson disease. Wilson disease can cause hypocalcemia due to hypoparathyroidism.

A diagnosis of hypoparathyroidism was considered in view of tetany, hypocalcemia, and low intact parathyroid hormone (PTH). This hypoparathyroidism was considered idiopathic as serum phosphorous was normal, no radiological findings of osteomalacia, and no evidence of renal insufficiency. In addition there was no history of neck surgery or radioiodine therapy. Signs for pseudohypoparathyroidism like brachydactyly and dwarfing, and low serum cortisol was also not present. A complete diagnosis of 'Hypocalcemia due to Idiopathic Hypoparathyroidism following Carbimazole therapy for Hyperthyroidism in a Multinodular goitre' was made.

Patient was started on 10 ml of 10% calcium gluconate IV infusion (90 mgs of elemental calcium/10 ml) TID, oral calcium carbonate and 1,25 hydroxy D3. Calcium gluconate infusion had to be continued for 10 days in view of persistent low serum calcium on daily follow-up and later oral calcium supplements and 1,25 hydroxy D 3 was continued. Serum calcium was restored to normal (10 mgs/ dl) by the 15 th day of treatment. In addition there was a decrease in hyperthyroidism signs like palpitation and nervousness. In view of correction of hypocalcaemia and improvement of hyperthyroidism features she was discharged and followed up. Her total serum triiodothyronine (T3) was 1.9 ng/dl (normal: 0.5-2.0 ng/dl), total serum thyroxin (T4) was 13 μg/dl (normal: 4.8-14 μg/dl) and serum TSH was 5 μIU/ml (normal: 0.3-6.0 μIU/ml) on follow-up.


  Discussion Top


This case who presented with hyperthyroid symptoms was detected to have dominant multinodular goitre. Absence of Anti-TPO excluded the possibility of autoimmune status. FNAC confirmed multinodularity. In view of the above, subacute thyroiditis and Graves' disease was considered unlikely and hyperthyroidism due to hyperfunctioning of nodule was entertained. Radioactive uptake study of thyroid gland could have confirmed presence of overfunctioning nodule. However, this could not be carried out due to paucity of resources. Thus available evidence strongly supported overfunctioning nodule in a multinodular goitre.

This case of toxic multinodular goitre while on treatment with Carbimazole developed tetany. Investigation revealed persistent hypocalcemia, low intact PTH, normal serum alkaline phosphatase and upper limit of serum phosphate level.

Most cases of hyperthyroidism usually cause hypercalcemia. [1] Only a few cases of hypocalcemia have been reported [2] but none from India. In the absence of parathyroid surgery or radioactive iodine therapy for thyroid gland, the most possible cause of low serum intact PTH is considered to be idiopathic hypoparathyroidism. This is also supported by the presence of a normal serum magnesium level, absence of roentgenologic findings of osteomalacia, absence of renal insufficiency, absence of diarrhoea, absence of signs of pseudohypoparathyroidism like brachydactyly and dwarfing. [3]

Surgery on parathyroid gland for hyperparathyroidism has been reported to cause hypocalcemia due to Hungry bone syndrome. [ 4] A few cases of Hungry bone syndrome have been reported to cause hypocalcemia after medical treatment of thyrotoxicosis. [5],[6] In the absence of diagnostic criteria, Hungry bone syndrome was not considered. [7] In our case, absence of parathyroid surgery and available investigations point in favour of idiopathic hypoparathyroidism as a cause of hypocalcemia. Hungry bone syndrome is unlikely as it does not fulfill the existing diagnostic criteria and no parathyroid interference was done.

The exact mechanism of the development of hypoparathyroidism in a patient with hyperthyroidism is not known. However, it is postulated that an enlarged thyroid gland in hyperthyroidism will compress the blood vessels supplying the parathyroid glands leading to ischemic necrosis of the parathyroid gland and thereby development of hypoparathyroidism.

Also, such destruction of one parathyroid gland might induce the formation of antiparathyroid substances, which in turn cause inflammation of the remaining parathyroids. [8]

Idiopathic hypoparathyroidism is a rare condition that may be isolated or associated with familial polyglandular endocrinopathy Type 2 (mucocutaneous candidiasis, Addison's disease, or hypoparathyroidism). It usually presents in childhood. Other rare causes of hypoparathyroidism include DiGeorge syndrome [congenital condition characterized by cardiac defects (conotruncal), abnormal facies, thymic hypoplasia, cleft palate, hypocalcaemia 22 q11 deletions] and Wilson's disease due to copper deposition in parathyroid gland. [9]


  Conclusion Top


This 35-year-old lady with hyperfunctioning multinodular goitre, while on treatment with carbimazole for three days developed tetany due to hypocalcemia. Other causes of hypocalcemia like hyperventilation, surgery on thyroid gland or radioiodine therapy of thyroid gland, hypoalbuminemia, hypomagnesemia, and chronic renal failure were excluded. Treatment for hyperthyroidism and hypocalcemia improved her clinical state in two weeks. This rare case of idiopathic hypoparathyroidism presenting with hypocalcemic tetany while on treatment with Carbimazole for hyperthyroidism in a multinodular goitre is reported for rarity. This case report is to increase the awareness of clinician to be aware of this entity while treating such cases.

 
  References Top

1.Baxter JD, Bondy PK. Hypercalcemia of thyrotoxicosis. Ann Intern Med 1966; 65:429-42.  Back to cited text no. 1
[PUBMED]    
2.Meek CL, Kaplan F, Pereira RS, Viljoen A. Hypocalcemia following treatment for hyperthyroidism. Clin Chem 2011; 57:811-4.  Back to cited text no. 2
[PUBMED]    
3.Bronsky D, Kushner DS, Dubin A, Snapper I. Idiopathic hypoparathyroidism and pseudohypoparathyroidism: Case reports and review of the literature. Medicine 1958;37:317-52.  Back to cited text no. 3
[PUBMED]    
4.Simsek E, Arikan Y, Dallar Y, Akkus MA. Prolonged hungry bone syndrome in a 10-year-old child with parathyroid adenoma. Indian Pediatr 2009;46:178-80.  Back to cited text no. 4
[PUBMED]    
5.Grieff M. The hungry bone syndrome after medical treatment of thyrotoxicosis. Ann Intern Med 2003;139:706-7.  Back to cited text no. 5
[PUBMED]    
6.Sanguin F, Camozzi V, Mantero F, Luisetto G. A case of hungry bone syndrome during therapy with methimazole for hyperthyroidism. Endocrine Abstracts 2008;16:P148.  Back to cited text no. 6
    
7.Bhattacharyya A. Hungry bone syndrome - revisited. J R Coll Physicians Edinb 2002;32:83-6.  Back to cited text no. 7
    
8.Dahl JR, McFadden SD, Eisenberg E. Idiopathic hypoparathyroidism associated with hyperthyroidism. Ann Intern Med 1962;57:635-8.  Back to cited text no. 8
[PUBMED]    
9.McMahon GT. Hypocalcemia. In: Mushlin SB, Greene HL, editors. Decision Making in Medicine. An Algorithmic Approach, third ed. Philadelphia, United States of America: MOSBY, Elsevier; 2010. p.132.  Back to cited text no. 9
    



 
 
    Tables

  [Table 1]


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