Case Presentation: 44 yr old black male presented to ED with weakness, generalized bone pain, and swollen jaw bilaterally. Subsequently found to have a calcium level of > 19 and shortly admitted thereafter. 2 weeks prior he had battled acute COVID-19 with relatively minimal symptoms. Once in the hospital started on therapy with aggressive fluid hydrations, bisphosphates and calcitonin. Workup for underlying etiology did not fit under any known algorithm. Follow up in the clinic setting eventually showed normalization of his PTH and calcium levels. Our theory is, COVID-19, with its known inflammatory state, caused a parathyroiditis leading to a dramatic acute elevation of his blood calcium through the release of large amounts of PTH.
Discussion: In this setting, where the hypercalcemia cannot be explained by an academically-recognized disorder, the development of an autoinflammatory parathyroiditis triggered by severe COVID-19 pneumonia is postulated. While case reports on the autoimmune sequelae of COVID-19 is limited, hematological, gastrointestinal, neurological, and cardiovascular cases have been documented (1). Currently, case reports regarding related endocrinopathies have not been previous documented; however, explorations into the links between COVID-19 lung damage and dysregulation of the parathyroid gland as well as electrolyte abnormalities, including calcium, have recently been recognized (5,6,7). While the mechanism behind the development of COVID-triggered autoimmunity is not elucidated, parallels between the developments of ground-glass opacities from COVID-19 pneumonia and those of autoimmune as well as autoinflammatory diseases have been established – these include polyangiitis with granulomatosis, rheumatic arthritis, systemic sclerosis, and systemic juvenile idiopathic arthritis (9,10,11,12). At this time, there is limited literature available discussing the likelihood of developing autoimmunity in genetically predisposed patients (13). Regarding the development of COVID-19-related autoimmunity, one prevalent theory thus far identifies the commonalities between the peptide sequences of the viral pathogen and human proteins as the pathologic mechanism (14,15). Another popular theory identifies the associated cytokine storm release as one of the major instigators of autoimmunity (16). This theorized mechanism underlies the ongoing discussion regarding the management of severe COVID-19 pneumonia and the development of regimens with immunosuppressant drugs, such as tocilizumab (17). However, further trials are needed before immunosuppressant protocols in the treatment of COVID-19 pneumonia become commonplace.
Conclusions: COVID-19 is a disease of inflammation as much if not more as of infection. Unexplained etiologies of inflammatory conditions should have COVID-19 in the differential. We have mountains of data showing links with autoimmune etiologies, hypercoagulable states and overall inflammatory conditions. What we can do to prevent and or treat the subsequent sequelae of COVID-19 remains to be seen, but the first step is to gather data.