Case Report Shows COVID-19 May Worsen Well-controlled Hypoparathyroidism
The study, “Decompensated primary hypoparathyroidism in a patient with COVID-19,” was published in the journal Annales d’Endocrinologie.
Hypoparathyroidism is characterized by low levels of parathyroid hormone (PTH) in the blood. PTH causes the kidneys to produce active vitamin D, which helps the absorption of calcium from food.
PTH also is a key regulator of the balance between calcium and phosphorus. When PTH levels drop, vitamin D and calcium levels in the blood are reduced, and phosphorus levels increase.
Low calcium levels — a condition called hypocalcemia — have been suggested as an important indicator of COVID-19 severity, and appears to be specific to COVID-19 relative to other acute respiratory disorders.
Research has indicated that hypocalcemia in COVID-19 patients may be related to vitamin D deficiency, with a previous study reporting a link between vitamin D supplements and a reduced risk for COVID-19-related infection and death.
However, the effect of such supplementation on the prevalence of COVID-19 has not yet been shown.
Now, a team from the Centre Hospitalier Universitaire de Montpellier, in France, described the case of an 82-year-old man with both a COVID-19 infection and hypocalcemia.
The patient was hospitalized in November 2020 in a COVID-19 unit and started a 12-day treatment with the anti-inflammatory dexamethasone, at a dose of 6 mg.
At admission, his blood levels of calcium were 1.74 millimoles per liter (mmol/L), decreasing to 1.68 mmol/L on the next day and confirming hypocalcemia — normal values are typically indicated as 2.2 mmol/l. A prior measurement in December 2019 showed a calcium level of 2.05 mmol/L, indicating that hypocalcemia preceded COVID-19.
PTH levels in the blood also were low at 0.954 picomol/L — normal values range from 1.590-6.893 picomol/mL — suggesting the presence of hypoparathyroidism. In contrast, blood levels of vitamin D were within normal values.
The patient showed a long QT interval, which measures how long the heart’s electrical system takes to recharge between beats, at 470 millisecond. Notably, hypocalcemia is known to both impair heart contractility and prolong the QT interval.
To stabilize the QT interval and calcium levels in the blood, the man was given intravenous (IV, or into-the-vein) supplements with 2 g of calcium hydrochloride, once daily, for four days.
Assessment of blood pH and gases indicated the presence of respiratory alkalosis, which is characterized by low carbon dioxide levels in the blood due to breathing excessively.
C-reactive protein, a marker of inflammation, was higher than normal at 123.60 mg/L. Normal levels are below 10 mg/L.
A complete stabilization of calcium levels was achieved when the IV supplements were replaced by oral supplementation of calcium — at a daily dose of 4 g — and alfacalcidol, a form of vitamin D, at 1 microgram once daily.
At 28 days of inpatient care, the patient’s calcium level improved to 2.90 mmol/L and supplementation was stopped. Two months after hospital admission, PTH also improved to 2.12 picomol/L.
Altogether, these findings suggest that this may be a case of deterioration of primary hypoparathyroidism during COVID-19 infection.
Despite prior reports of decompensation of primary hypoparathyroidism in people infected with SARS-CoV-2 (the virus that causes COVID-19), the scientists said no research supports viral infiltration of SARS-Cov-2 in the parathyroid gland.
“This observation should remind us that, although SARS-Cov-2 does not present a known [infection risk] for the parathyroid gland, the severity of the infection can lead to decompensation of pathologies [disorders] that were well tolerated before, even in the absence of vitamin D deficiency,” the scientists wrote.