Endocrine Abstracts

Background: Subacute thyroiditis, autoimmune thyroiditis and an atypical form of thyroiditis due to primary injury of the thyroid gland by SARS Cov2 itself are complications of COVID-19. Angiotensin-converting enzyme 2 is also expressed in the thyroid gland. On the other hand, both untreated thyrotoxicosis and COVID-19 affects heart, generating cardiac complications.

Case report: A 36-year-old woman resident in an iodine sufficient area, heavy smoker, presented for palpitations, resting dyspnea, pedal edema, 40 kg weight loss in the past 2 months, tremor and asthenia. She denies cough, sore throat, rhinorrhea, smell or taste loss, myalgias or diarrhea. Physical examination reveals resting dyspnea, SaO2-95-96%, atrial fibrillation with arrhythmic HR=200/min, severe heart failure with right pleural effusion and pedal edema, small goiter, tremor, low fever, agitation. Biochemical assessment revealed autoimmune thyrotoxicosis (TSH=0.0007 mIU/l; FT4=40.06 pmol/l, total T3=309.88 ng/dl, increased TRAb (160 UI/l) and TPO Abs (209.7 IU/ml), anemia, leukopenia (3680/mm3) with lymphopenia. ESR, fibrinogen, C-reactive protein, procalcitonin were normal. Liver enzymes are elevated, hyperbilirubinemia was present (total bilirubin=2.6 mg/dl, direct bilirubin=1.9 mg/dl), alkaline phosphatase (180 U/l) and GGT were also increased. From cardiac point of view, D-Dimers were increased (403.925 ng/ml), CK MB was slightly increased (32 UI/l), troponin was normal, but NTproBNP was significantly increased (6112 pg/ml). RT PCR for SARS Cov2 was positive, IgM Abs against SARSCov 2 were slightly elevated, Ig G Abs were negative. A native CT scan confirmed right massive pleural effusion, without significant pulmonary involvement. Thyroid diffuse enlargement and markedly increased color flow Doppler signal with diffuse homogeneous distribution were present on thyroid ultrasound.

Treatment: During the hospitalization, antithyroid drugs were initiated, well tolerated, with significant decrease of FT4 within 3 days from 40.6 pmol/l to 23.64 pmol/l. High dose beta blockers, digoxin, double diuretic medication and anticoagulation with NOAC were administered for controlling heart rate and severe heart failure.

Follow-up: Despite having initially an increased score for thyroid storm (85), this patient with concomitant Graves disease and COVID-19 infection had a significant improvement within 4 weeks: weight gain, atrial fibrillation converted to sinus rhythm, FT4 was low-normal (8.43 pmol/l), NTproBNP significantly decrease (1007 pg/ml). No pleural effusion was described on her chest X-Ray; Her RT-PCR test was still positive for SARS-CoV-2 and Ig G Abs were increased (43IU/ml).

Conclusion: concomitant Graves disease and COVID-19 infection may be a cause of atrial fibrillation and severe heart failure during SARS Cov2 pandemic.