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 Table of Contents  
Year : 2021  |  Volume : 8  |  Issue : 1  |  Page : 36-38

Hypoparathyroidism in pregnancy

1 Department of Obstetrics and Gynecology, Mahatma Gandhi Medical College and Research Institute, Puducherry, India
2 Department of General Medicine, Mahatma Gandhi Medical College and Research Institute, Puducherry, India

Date of Submission18-Sep-2020
Date of Decision25-Feb-2021
Date of Acceptance18-May-2021
Date of Web Publication30-Jun-2021

Correspondence Address:
Sendhil A Coumary
Department of Obstetrics and Gynecology, Mahatma Gandhi Medical College and Research Institute, Puducherry
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijamr.ijamr_223_20

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Hypoparathyroidism is a disorder rarely observed during pregnancy. It poses a major challenge in managing a patient appropriately to prevent maternal and fetal complications. We report a case of a 21-year-old gravid woman, a diagnosed case of hypoparathyroidism. She was successfully treated with calcium and calcitriol before pregnancy. Dosage was adjusted according to serum calcium values, and she delivered a healthy baby with normal serum calcium level.

Keywords: Calcitriol, hypoparathyroidism, pregnancy, serum calcium, tetany

How to cite this article:
Coumary SA, Janarthanam S, Dutta TK, Habeebullah S. Hypoparathyroidism in pregnancy. Int J Adv Med Health Res 2021;8:36-8

How to cite this URL:
Coumary SA, Janarthanam S, Dutta TK, Habeebullah S. Hypoparathyroidism in pregnancy. Int J Adv Med Health Res [serial online] 2021 [cited 2023 Mar 25];8:36-8. Available from: https://www.ijamhrjournal.org/text.asp?2021/8/1/36/319774

  Introduction Top

Idiopathic hypoparathyroidism is an extremely rare endocrine disorder, with a prevalence of 37/100,000 in general population. There is no estimated incidence in pregnancy.[1] The most common acquired cause of hypoparathyroidism is head and neck surgery.[2] Hypocalcemia due to hypoparathyroidism may be undetected or misdiagnosed. Hypocalcemia has a variety of presenting symptoms.[3] A high level of suspicion should be maintained for timely diagnosis and treatment. If left untreated during pregnancy, mid-trimester abortions, stillbirths, and preterm labor can occur.[1] Prolonged maternal hypocalcemia will cause fetal parathyroid hyperplasia, leading to fetal subperiosteal bone resorption, genetic skeletal deformities, and osteitis fibrosa. Maternal hypercalcemia can cause suppression of fetal parathyroid glands.[4] In pregnancy, maintaining normocalcemia in response to treatment is the biggest challenge.

  Case Report Top

A 21-year-old primigravida presented to the outpatient department for regular antenatal checkup at 17 + 5 weeks of pregnancy. She was a known case of idiopathic hypoparathyroidism. She was on calcium replacements along with calcitriol. It was a spontaneous conception 2 years following the diagnosis of idiopathic hypoparathyroidism. During the first trimester of pregnancy, parathyroid hormone (PTH) and serum calcium were estimated. PTH was found to be <1 pg/ml and serum calcium was 8 mg/dl. Hence, she was continued on her regular calcitriol 0.25 μg twice a day and calcium carbonate 500 mg twice a day. Serial monitoring of serum calcium was done throughout pregnancy. In the third trimester, serum calcium was found to be 12.5 mg/dl, and hence, oral calcium was stopped. After 1 week, she developed complaints of weakness and numbness of all four limbs and was restarted on calcium 2 g/day and calcitriol 0.5 μg/day. She went into spontaneous labor at term and delivered a healthy female child of 2.6 kg. Postnatal serum calcium was 8.5 mg/dl, and the patient was continued on elemental calcium 1.2 g/day and calcitriol 0.5 μg/day. Serum calcium was estimated for the baby and found to be 9.1 mg/dl. The patient was advised to continue breastfeeding and review monthly for 3 months.

The patient was initially diagnosed to have seizure disorder following an episode of involuntary movements of all four limbs 6 years ago. She was then put on regular antiepileptic drugs. Three years ago, she presented to the casualty as a known case of seizure disorder following an epileptic attack. During examination, on checking her blood pressure, the patient developed carpopedal spasm (Trousseau's sign positive). Chvostek sign was also found to be positive suggesting hypocalcemia. However, she had no history of perioral or acral paresthesias, facial twitching, irritability, depression, psychosis, or laryngeal spasms. She had no history of thyroid surgeries or family history of endocrine or autoimmune disorders. All baseline blood investigations, including complete electrolyte profile, were done, and she was found to have hypocalcemia (4.6 mg/dl) with mild hyperphosphatemia (5.3 mg/dl) and normal renal function. Electrocardiogram (ECG) was done and showed prolonged Q-T interval. Hypoparathyroidism was suspected and PTH assay was done. PTH was <1 pg/ml with normal Vitamin D3 level (25.8 ng/ml). Ophthalmological evaluation showed bilateral posterior subcapsular cataract. Computed tomography (CT) brain showed multiple soft calcifications involving the bilateral capsuloganglionic region; bilateral caudate, lentiform, and dentate nucleus; and thalamus and in subcortical regions. All findings were consistent with idiopathic hypoparathyroidism, and she was started on elemental calcium 2.4 g/day and calcitriol 0.5 μg/day. Antiepileptics were stopped and she had no further seizure episodes. The patient's serum calcium, phosphorous, and magnesium levels were reviewed monthly and calcium and calcitriol doses changed accordingly.

  Discussion Top

Hypoparathyroidism is characterized by deficiency of PTH. This results in decreased serum calcium levels and increased serum phosphorus levels. Normal body calcium homeostasis is delicate. It is maintained by serum calcium, PTH level, and 1,25 dihydroxycholecalciferol levels.[5] A decrease in serum calcium increases PTH-mediated bone resorption and 1,25 dihydroxycholecalciferol-mediated intestinal absorption and reduces urinary excretion. Hypocalcemia leads to a hyperexcitable neuromuscular system followed by full-blown tetany.[5] This leads to perioral and distal numbness and paresthesias, carpopedal spasm, and diffuse muscle cramps. Other unusual symptoms include depression, psychosis, laryngeal spams, respiratory arrest, and convulsions.[4] Increased intracranial pressure, papilledema, and convulsions can also be presenting symptoms, leading to confusion in the primary diagnosis.[4]

During the first and second trimester, patients with a normal calcium store have normal or slightly suppressed PTH levels. Serum calcium is normally decreased due to hemodilution. However, due to increased fetal calcium requirement of around 25–30 g/day during the third trimester, serum calcium level gradually increases to mid-normal range.[6],[7],[8],[9] Thus, the combined effects of increased intestinal absorption of calcium, 1,25-dihydroxycholecalciferol, urinary calcium excretion, and bone resorption increase serum calcium level to meet the increased need during pregnancy.[8]

The most common acquired condition of hypoparathyroidism is thyroid surgery, with an incidence of 0.2%–3.5%. Idiopathic hypoparathyroidism may be isolated or due genetic conditions, such as thymus agenesis (Di-George syndrome), or due to familial causes.[4] Pseudohypoparathyroidism is an entity which presents with hypocalcemia and hyperphosphatemia but with increased levels of intact PTH.[2]

Investigations to be done include serum calcium, phosphate, and magnesium; renal function tests; 24-h urine calcium creatinine ratio; serum PTH level and 1,25 dihydroxycholecalciferol and cholecalciferol level. ECG and CT brain can give additional information.[4]

Treatment of hypoparathyroidism involves correction of Vitamin D3 level. Calcitriol is preferred as it has a predictable bioavailability and short half-life. A dose of 0.25–3 μg/day can be given, usually starting with a low split dose to avoid nocturnal hypocalcemia. Calcium supplementation can be given; 1200 mg of elemental calcium should be given daily.[4]

Hypoparathyroidism can be less cumbersome during pregnancy, due to the normal physiology of calcium homeostasis in pregnancy. Increased fetal demands causes increase in 1,25 dihydroxycholecalciferol and intestinal calcium absorption, which may compensate the low level of serum calcium.[10] Thus, the preconceptional dosage of calcium and calcitriol may be reduced. However, in some cases, hypoparathyroidism may worsen and fetal calcium requirement cannot be met.[11]

In pregnant patients with hypoparathyroidism, the absence of PTH along with increased calcium demands during pregnancy can result in hypocalcaemia, if not adequately supplemented. This is of great concern, especially in the third trimester. Risk of hypocalcemic complications manifesting with symptoms such as seizures, cramps, tetany, and heart failure increase.[9] Ionized calcium should be maintained in the low to mid-normal range. Maternal hypocalcemia must be avoided as it increases the risk of premature labor and fetal hyperparathyroidism. However, overtreatment with calcitriol causes maternal hypercalcemia, leading to suppression of the fetal and neonatal parathyroids and fetal hypocalcemia.[12] Thus, calcium homeostasis is vital during the entire period of pregnancy.

Monitoring of serum calcium should be done on a frequent basis, for example, every 2–3 weeks throughout pregnancy.[13] Special care should be taken during lactation period as there is hypersensitivity to Vitamin D3 due to increased parathormone related peptide (PTHrP) which stimulates endogenous calcitriol. In the first 1–2 weeks of lactation, hypercalcemia should be carefully avoided.[4]

In this case report, the patient was initially thought to have seizure disorder. This atypical presentation misled the physicians to a delayed diagnosis of hypoparathyroidism. However, on a second admission, a routine blood pressure measurement accidently revealed Trousseau's sign and a suspicion of hypocalcemia rose. This was confirmed by low serum calcium levels in the same visit. The diagnosis of hypoparathyroidism was confirmed by subnormal PTH levels and hypocalcemia. During pregnancy and intrapartum, serum calcium was monitored regularly and calcium and calcitriol supplementation was changed accordingly. She had a relatively normal pregnancy period with good fetal outcome. The diagnosis of idiopathic hypoparathyroidism in our patient was based on clinical evidence of tetany, associated with low serum calcium and undetectable PTH levels. Posterior subcapsular cataracts and calcifications on CT brain added to the diagnosis.

A high degree of suspicion is needed to diagnose hypoparathyroidism in women of reproductive age group. Monitoring of serum calcium and supplementation of calcium prenatally and every 2–3 weeks antenatally can avoid catastrophic maternal and fetal complications. The patient should be followed up during lactation period to avoid hypercalcemia. Serum calcium monitoring in the newborn is also required to prevent early neonatal complications.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Parkes I, Schenker JG, Shufaro Y. Parathyroid and calcium metabolism disorders during pregnancy. Gynecol Endocrinol 2013;29:515-9.  Back to cited text no. 1
Bilezikian JP, Khan A, Potts JT Jr., Brandi ML, Clarke BL, Shoback D, et al. Hypoparathyroidism in the adult: Epidemiology, diagnosis, pathophysiology, target-organ involvement, treatment, and challenges for future research. J Bone Miner Res 2011;26:2317-37.  Back to cited text no. 2
Eastell R, Edmonds CJ, de Chayal RC, McFadyen IR. Prolonged hypoparathyroidism presenting eventually as second trimester abortion. Br Med J (Clin Res Ed) 1985;291:955-6.  Back to cited text no. 3
Powrie RO, editor. De Swiet's Medical Disorders in Obstetric Practice. 5th ed. Oxford: Wiley-Blackwell; 2010. p. 793.  Back to cited text no. 4
Barrett KE, Ganong WF, editors. Ganong's Review of Medical Physiology. 24th ed. New York: McGraw-Hill Med; 2012. p. 752.  Back to cited text no. 5
Kaspar DL, editor. Harrison's principles of internal medicine. 19th ed. New York: McGraw Hill Education; 2015. p. 2466.  Back to cited text no. 6
Shah KH, Bhat S, Shetty S, Umakanth S. Hypoparathyroidism in Shah KH, Bhat S, Shetty S, Umakanth S. Hypoparathyroidism in pregnancy. BMJ Case Reports 2018;2018:bcr-2015-210228corr2.  Back to cited text no. 7
Richa CG, Issa AI, Echtay AS, El Rawas MS. Idiopathic hypoparathyroidism and severe hypocalcemia in pregnancy. Case Rep Endocrinol 2018;2018:8316017.  Back to cited text no. 8
Hatswell BL, Allan CA, Teng J, Wong P, Ebeling PR, Wallace EM, et al. Management of hypoparathyroidism in pregnancy and lactation – A report of 10 cases. Bone Rep 2015;30;3:15-9.  Back to cited text no. 9
Krysiak R, Kobielusz-Gembala I, Okopien B. Hypoparathyroidism in pregnancy. Gynecol Endocrinol 2011;27:529-32.  Back to cited text no. 10
Khan AA, Clarke B, Rejnmark L, Brandi ML. Management of endocrine disease: Hypoparathyroidism in pregnancy: Review and evidence-based recommendations for management. Eur J Endocrinol 2019;180:R37-44.  Back to cited text no. 11
Kovacs CS. Calcium and bone metabolism disorders during pregnancy and lactation. Endocrinol Metab Clin North Am 2011;40:795-826.  Back to cited text no. 12
Cooper MS. Disorders of calcium metabolism and parathyroid disease. Best Pract Res Clin Endocrinol Metab 2011;25:975-83.  Back to cited text no. 13


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