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Horm Res Paediatr ; 95(4): 397-401, 2022.
Article in English | MEDLINE | ID: covidwho-1861727

ABSTRACT

INTRODUCTION: There is emerging speculation that the inflammatory state associated with SARS-CoV-2 infection may trigger autoimmune conditions, but no causal link is established. There are reports of autoimmune thyroiditis and adrenal insufficiency in adults post-COVID-19. We describe the first pediatric report of adrenal insufficiency and autoimmune hypothyroidism after COVID-19. CASE PRESENTATION: A 14-year-old previously healthy girl, with vitiligo, presented in shock following 1 week of fever, lethargy, diarrhea, and vomiting. Three weeks prior, she had congestion and fatigue and known familial exposure for COVID-19. Labs were remarkable for sodium 129 mmol/L, K 4.3 mmol/L, creatinine 2.9 mg/dL, hemoglobin 8.3 g/dL, and positive COVID-19 PCR and SARS-CoV-2 IgG. She was resuscitated with normal saline and required pressor support. EKG showed abnormal repolarization presumed secondary to myocarditis. She met the criteria for multisystem inflammatory syndrome in children (MIS-C), received intravenous immune globulin and IL-1R antagonist and was admitted for intensive care. Persistent hypotension despite improved inflammatory markers and undetectable cortisol led to initiation of hydrocortisone. She was then able to rapidly wean off pressors and hydrocortisone within 48 h. Thereafter, tests undertaken for persistent bradycardia confirmed autoimmune hypothyroidism with TSH 131 µU/mL, free T4 0.85 ng/dL, and positive thyroid autoantibodies. Basal and stimulated cortisol were <1 µg/dL on a standard 250 µg cosyntropin stimulation test, with baseline ACTH >1,250 pg/mL confirming primary adrenal insufficiency. Treatment was initiated with hydrocortisone, levothyroxine, and fludrocortisone. Adrenal sonogram did not reveal any hemorrhage and anti-adrenal antibody titers were positive. The family retrospectively reported oligomenorrhea, increased salt craving in the months prior, and a family history of autoimmune thyroiditis. The cytokine panel was notably different from other cases of MIS-C. CONCLUSION: This is the first pediatric report, to our knowledge, of primary adrenal insufficiency and hypothyroidism following COVID-19, leading to a unique presentation of autoimmune polyglandular syndrome type 2. The initial presentation was attributed to MIS-C, but the subsequent clinical course suggests the possibility of adrenal crisis. It remains unknown if COVID-19 had a causal relationship in triggering the autoimmune adrenal insufficiency and hypothyroidism.


Subject(s)
Addison Disease , Adrenal Insufficiency , COVID-19 , Hypothyroidism , Thyroiditis, Autoimmune , Addison Disease/complications , Addison Disease/drug therapy , Adolescent , Adrenal Insufficiency/diagnosis , Adrenal Insufficiency/drug therapy , Adrenal Insufficiency/etiology , Adult , Autoantibodies , COVID-19/complications , Child , Cosyntropin , Creatinine/therapeutic use , Cytokines , Female , Fludrocortisone , Hashimoto Disease , Humans , Hydrocortisone/therapeutic use , Hypothyroidism/complications , Hypothyroidism/drug therapy , Immunoglobulins, Intravenous/therapeutic use , Retrospective Studies , SARS-CoV-2 , Saline Solution/therapeutic use , Sodium/therapeutic use , Systemic Inflammatory Response Syndrome , Thyroiditis, Autoimmune/complications , Thyroiditis, Autoimmune/diagnosis , Thyroiditis, Autoimmune/drug therapy , Thyrotropin , Thyroxine/therapeutic use
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