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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 1  |  Issue : 1  |  Page : 33-35

Hypoparathyroidism precipitated by mumps: An unusual temporal association


1 Department of Pediatrics, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India
2 Department of Diagnostic and Interventional Radiology, All India Institute of Medical Sciences, Jodhpur, Rajasthan, India

Date of Submission15-Oct-2020
Date of Decision04-Nov-2020
Date of Acceptance27-Nov-2020
Date of Web Publication27-Feb-2021

Correspondence Address:
Dr. Varuna Vyas
Department of Pediatrics, Academic Block, All India Institute of Medical Sciences, Jodhpur - 342 005, Rajasthan
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ipcares.ipcares_22_21

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  Abstract 

Background: Hypoparathyroidism is a condition characterized by hypocalcemia and hyperphosphatemia due to insufficient secretion of parathyroid hormone (PTH). The common causes of hypoparathyroidism are postsurgical and autoimmune. We describe a case of hypoparathyroidism precipitated by mumps. Clinical Description: A 17-year-old boy was brought to us with altered sensorium following 2 episodes of generalized tonic-clonic seizures within the last 4 h. He required mechanical ventilation, but severe laryngospasm made intubation difficult. He had been suffering from a febrile illness that appeared to be mumps for the preceding 4 days. The only salient biochemical abnormality was hypocalcemia and hyperphosphatemia. Neuroimaging and cerebrospinal fluid examination were normal. Hypoparathyroidism was suspected and confirmed by low PTH levels. He also developed secondary hypothyroidism. Management and Outcome: The child had no symptoms of hypocalcemia in the past. He was started on intravenous calcium and calcitriol. He showed dramatic improvement in sensorium with normalization of serum calcium levels. He was extubated after a week. At discharge, there were no neurological sequelae and the sick euthyroid syndrome had resolved. Viral serology for mumps was reactive by the 3rd week of illness. Conclusion: Although viral infections have been described as triggers for other endocrinopathies, we could not find any association with hypoparathyroidism. An exhaustive literature search we could not find any similar case reports of hypoparathyroidism during or following mumps. Whether mumps infection had any role in the pathogenesis of the hypoparathyroidism or only unmasked an underlying endocrinopathy remains uncertain.

Keywords: Hypoparathyroidism, mumps, sick euthyroid syndrome


How to cite this article:
Vyas V, Khera D, Didel S, Yadav T, Singh K. Hypoparathyroidism precipitated by mumps: An unusual temporal association. Indian Pediatr Case Rep 2021;1:33-5

How to cite this URL:
Vyas V, Khera D, Didel S, Yadav T, Singh K. Hypoparathyroidism precipitated by mumps: An unusual temporal association. Indian Pediatr Case Rep [serial online] 2021 [cited 2023 Feb 3];1:33-5. Available from: http://www.ipcares.org/text.asp?2021/1/1/33/310220

Parathyroid hormone (PTH) is an important hormone involved in maintaining calcium and phosphorus balance in the body. Hypoparathyroidism is a relatively uncommon condition with an estimated prevalence of 22–37 per 100,000 person-years in different countries.[1] It is characterized by low PTH levels which results in low serum calcium and high serum phosphorus levels. Congenital hypoparathyroidism is due to developmental anomalies of the parathyroid gland or genetic mutations, whereas acquired hypoparathyroidism develops due to the destruction of the parathyroid gland by surgery, radiation, or an autoimmune disorder. The most common cause, however, is postsurgical, found in nearly 75% of patients.[2] The clinical features of hypoparathyroidism depend on the severity of hypocalcemia. They can vary from fatigue and irritability to tetanic spasms and seizures. It can rarely also lead to renal stones and intracerebral calcifications.

We describe an adolescent who presented to us with hypocalcemic seizures due to acquired hypoparathyroidism that was preceded by mumps. Despite an extensive review of literature, we could not find the report of any other case with this temporal association.


  Clinical Description Top


A 17-year-old boy presented to the hospital with an altered sensorium immediately following two brief episodes of generalized tonic-clonic seizures within 4 h. In view of the emergency setting, the process of history taking, examination, investigations, and management were started simultaneously. At admission, the patient was in altered sensorium with a Glasgow Coma Scale score of 10/15 (E3, V3, M4). He had an audible stridor with clenching of teeth and low blood oxygen saturation levels. He was not in shock and peripheral perfusion was maintained. Emergency intubation was initiated, during which it was noted that the patient had severe laryngospasm and it was difficult to visualize the glottic opening. He was placed on mechanical ventilation on synchronized intermittent mandatory ventilation mode. On the spot, blood glucose was normal. He was loaded with anticonvulsants. After stabilization, emergency blood samples for baseline hematological, and biochemical samples were drawn as per standard protocol for seizures and altered sensorium.

History revealed that he had been running fever for 4 days that was associated with painful swellings of both sides of the jaw, causing difficulty in chewing. There was no past history of similar illness, but a significant history of a classmate being diagnosed with mumps was elicited. The child had not received the Measles-Mumps-Rubella vaccination. On the fourth day of his illness he developed generalized tonic clonic seizures and altered sensorium following which he was brought to us. A clinical diagnosis of mumps was kept, and the altered sensorium and seizures were attributed to acute mumps meningoencephalitis. Nevertheless, pending investigations, he was started on broad-spectrum intravenous antibiotics and acyclovir to cover for complicated acute bacterial meningitis and viral meningoencephalitis, respectively.

Hypocalcemia was detected with ionized (i) Ca2 + 0.46 mmoles/L (normal 1.15–1.3 mmoles/L), for which intravenous calcium supplementation was started, whereas Na + was 133 mEq/L and K + 3.54 mEq/L. The hemogram reports revealed hemoglobin 14.8 g/dL, total leukocyte count 8390/mm3 with 90% neutrophils, and platelet count 1.83 lakh/mm3. The C-reactive protein was elevated (31.19 mg/L), but procalcitonin was normal (0.1 ng/mL). The cerebrospinal fluid had no cells with normal biochemistry (sugar 89 mg/dl and protein 26 mg/dl) and sterile culture. The blood culture was also sterile. Computerized tomography of the brain did not detect cerebral edema, meningeal enhancement, or other features of meningoencephalitis, but identified calcification in the basal ganglia and right frontal hemisphere at the gray white matter junction [Figure 1]. In the meantime, it was noted that the serum iCa2 + and total serum Ca2 + were persistently low despite infusion of calcium gluconate, with P of 7.19 mg/dl and serum alkaline phosphatase 71 IU/L. Since this suggested hypoparathyroidism, intact PTH was ordered, which was 1.7 pg/ml (normal 10–65 pg/ml). Since PTH is unstable and prone to preanalytical errors,[3] PTH was repeated and confirmed to be low on one more occasion. Since the sensorium remained depressed that was out of proportion to the anticonvulsants, sedation, muscle relaxants, and absence of meningoencephalitis, a thyroid function test (TFT) was done. This revealed undetectable free T3, low free T4, and low thyroid-stimulating hormone (TSH); FT4 0.40 ng/dL and TSH 0.52 mIU/L. This was attributed to sick euthyroid state.
Figure 1: (a) Axial and (b) sagittal reformats of noncontrast CT scan show bilateral basal ganglia calcifications (straight arrow). Subcortical calcifications (curved arrow in b) are also seen in the frontal region. (c) Contrast-enhanced CT axial image reveals enlarged right parotid gland with increased enhancement (black arrow) as compared to the left side (white arrow) suggestive of right parotitis. CT: Computed tomography

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Management and Outcome

Once the diagnosis of hypoparathyroidism was established, oral calcitriol (0.250 μg twice a day) was added to the intravenous calcium. Although he could be extubated as he had spontaneous respiratory efforts and his laryngospasm resolved with the initiation of treatment, his sensorium remained depressed till calcium levels stabilized at >7 mg/dL.

As the calcium level increased, the sensorium of the patient improved. However, he developed ventilator-associated pneumonia which was successfully managed with intravenous antibiotics. At discharge, 19 days after admission, he was conscious with no neurological sequelae. The TFT had normalized. Serological confirmation of the clinical diagnosis was obtained 18 days after the onset of illness, with reactive mumps specific IgM and IgG levels; 56.11 NTU and 24.3 NTU, respectively.


  Discussion Top


This case was very interesting from an endocrine perspective. Our patient presented with acute symptomatic hypocalcemia (seizures, altered sensorium, and laryngospasm) and hypoparathyroidism that appeared to have been precipitated by mumps. There were no symptoms of hypocalcemia in the past. His sensorium started improving with normalisation of calcium levels. The fact that the phosphorus levels were relatively lower than what is usually seen with hypoparathyroidism may suggest that it was of short duration. However, intracranial calcification was present. Goswami et al. found basal ganglia calcification in 73.8% of patients with idiopathic hypoparathyroidism and gray white matter junction calcification in 39.8%.[4] Basal ganglia calcification was associated with a lower calcium to phosphorus ratio and more likely to cause seizures, rather than tetany. The minimum duration of hypoparathyroidism that leads to calcification is unknown.

The presumption that the hypoparathyroidism was due to mumps is by the exclusion of other causes. Autoimmune polyendocrine syndrome type 1[5] was unlikely due to the absence of ectodermal dysplasia, candidal infection, adrenal insufficiency, or any other endocrinopathy. The assumption that the hypothyroidism was sick euthyroid syndrome was confirmed by the transient nature and normalization of TFT with recovery. The severity of change in thyroid hormone is proportional to the severity of illness, length of admission, and mortality rate.[6] TSH is the first parameter to recover, with normalization of T4 levels lagging behind.[7]

There was no history of thyroid surgery or traumatic injury to the neck. That left us with the possibility of the disease being autoimmune. Viruses, including mumps, have been cited as environmental factors responsible for triggering autoimmune thyroid diseases.[8],[9] There is evidence of the presence of mumps virus in Hashimoto's thyroiditis, but whether it is causative or a silent bystander is not clear. An earlier case report has described mumps infection as a trigger for fulminant type 1 diabetes.[10] We were unable to find any previous reports of a temporal association between mumps and hypoparathyroidism. Due to financial constraints, antiparathyroid antibodies could not be tested. In these circumstances, it is difficult to say whether the autoimmunity was triggered by mumps, or whether it was an incidental illness that simply unmasked an idiopathic hypoparathyroidism.

Hypoparathyroidism is a rare condition and hence requires a high index of suspicion to be diagnosed. The symptoms of hypoparathyroidism are primarily secondary to hypocalcemia. The purpose of reporting this case is to sensitize clinicians to screen for hypocalcemia in children with mumps and consider hypoparathyroidism if investigations are suggestive. If more cases are identified, it could generate some worthwhile research questions to explore the relationship between mumps and hypoparathyroidism.



Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Clarke BL, Brown EM, Collins MT, et al. Epidemiology and Diagnosis of Hypoparathyroidism. J Clin Endocrinol Metab 2016;101:2284-99.  Back to cited text no. 1
    
2.
Lopes MP, Kliemann BS, Bini IB, et al. Hypoparathyroidism and pseudohypoparathyroidism: Etiology, laboratory features and complications. Arch Endocrinol Metab 2016;60:532-6.  Back to cited text no. 2
    
3.
Hanon EA, Sturgeon CM, Lamb EJ. Sampling and storage conditions influencing the measurement of parathyroid hormone in blood samples: A systematic review. Clin Chem Lab Med 2013;51:1925-41.  Back to cited text no. 3
    
4.
Goswami R, Sharma R, Sreenivas V, et al. Prevalence and progression of basal ganglia calcification and its pathogenic mechanism in patients with idiopathic hypoparathyroidism. Clin Endocrinol (Oxf) 2012;77:200-6.  Back to cited text no. 4
    
5.
Husebye ES, Anderson MS, Kämpe O. Autoimmune Polyendocrine Syndromes. N Engl J Med 2018;378:1132-41.  Back to cited text no. 5
    
6.
Maiden MJ, Torpy DJ. Thyroid Hormones in Critical Illness. Crit Care Clin 2019;35:375-88.  Back to cited text no. 6
    
7.
Economidou F, Douka E, Tzanela M, et al. Thyroid function during critical illness. Hormones (Athens) 2011;10:117-24.  Back to cited text no. 7
    
8.
Desailloud R, Hober D. Viruses and thyroiditis: An update. Virol J 2009;6:5.  Back to cited text no. 8
    
9.
Parmar RC, Bavdekar SB, Sahu DR, et al. Thyroiditis as a presenting feature of mumps. Pediatr Infect Dis J 2001;20:637-8.  Back to cited text no. 9
    
10.
Goto A, Takahashi Y, Kishimoto M, et al. A case of fulminant type 1 diabetes associated with significant elevation of mumps titers. Endocr J 2008;55:561-4.  Back to cited text no. 10
    


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