A newly developing case of adrenal insufficiency developing after Coronavirus disease

Abstract

Abstract Introduction Although some short and long-term effects of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) infection on the endocrine system are shown, there are still much more remaining to be clarified. A few case reports have shown that adrenal insufficiency can develop after COVID-19 infection due to adrenal hemorrhage or infarction. However, the exact effects of infection on cortisol dynamics are still poorly understood. This case report highlights an unusual case of acute adrenal insufficiency in a Covid-19. Clinical Case A 30-year-old female patient with no history of chronic disease applied with complaints of nausea, abdominal pain, and weakness for nearly 2 weeks. She was hospitalized. Her vitals were stable at the admission. Her initial laboratory evaluation showed serum sodium: 119 mEq/L, potassium: 5.38 mEq/L, creatinine: 1.35 mg/dL, aldosterone 2.33 ng/dL (1.46–17.4), plasma renin activity 40.56 ng/ml/h (0.06–4.69). Hemogram and liver function tests were normal. The basal ACTH value was measured 1142 pg/mL (7.2–63.3), and cortisol was 0.29 (6.24–18).The diagnosis of tuberculosis was ruled out with the quantiferon and the PPD test performed. In the detailed questioning of the patient, it was learned that she had Covid-19 infection about 3 months before the onset of symptoms. In this process, the patient's skin color was significantly darkened, and it was confirmed in comparison with the old photographs and from the patient's declaration. She was diagnosed with adrenal crisis, and corticosteroid therapy (80 mg/day intravenous methylprednisolone) and intravenous hydration were started. On the other hand, imaging and endoscopic evaluations were performed to exclude other intra-abdominal pathologies. No pathology was detected. Adrenal glands were normal in abdominal tomography. Stress dose steroid therapy was adjusted by reducing the daily dose. In the follow-up, the patient's complaints decreased and disappeared. Fludrocortisone was added to her treatment because electrolyte disturbances continued as hyponatremia and hyperkalemia. In the first week of treatment the patient's electrolyte disturbances improved and she was discharged with oral hydrocortisone and fludrocortisone treatment. The patient's skin color was observed lighter than before in the control examination, one week after discharge. Conclusion Although cases of adrenal insufficiency due to Covid-19 infection are found in the literature, their number is limited. The underlying causes are usually shown as hemorrhage and thrombosis. The absence of these findings in our case supports that the underlying cause is autoimmune and brought a different perspective to the issue. Our case also drives attention to the evaluation of patients in terms of adrenal insufficiency not only in the acute period but also in the later periods, since the diagnosis was made 3 months after the disease.