Necrotising myopathy and concurrent thyroiditis in a patient
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A 76-year-old man presented to the hospital with 1?week of shortness of breath, cough, fatigue and myalgias. His medical history was significant for hyperlipidemia, hypogonadism on testosterone replacement and bronchiolitis associated with hypogammaglobulinemia for which he received monthly intravenous immunoglobulin (IVIG) infusions, with last infusion 12 weeks prior to admission. He was a former athlete who participated in 45 min of cardiovascular workouts daily before this admission.

His oxygen saturation on hospital presentation was 89% on room air and he required 4 L/min of supplemental oxygen via a nasal cannula which increased saturations to 93%. His heart rate was 54 beats/min. He was afebrile and otherwise stable. The only significant physical examination abnormality was scattered coarse inspiratory breath sounds. Neurological examination including strength testing was normal.

His symptoms were highly suspicious for a COVID-19 infection and PCR testing for SARS-CoV-2 testing was found to be positive. Initial chest X-ray demonstrated patchy bilateral mid-to-lower lung infiltrates suspicious for pneumonia. Given hypoxia and chest infiltrates with positive PCR, he was diagnosed with severe COVID-19 pneumonia. C reactive protein was elevated on admission at 5.93 mg/dL and peaked at 9.57 mg/dL on hospital day 6, then declined thereafter. Ferritin was high on admission and peaked at day 3 at 2767 µg/mL and declined thereafter. D-dimer was elevated on admission and peaked on day 9 at 3.83 µg/mL. Interleukin-6 levels were not checked.

He initially received empiric treatment for bacterial pneumonia with one-time doses of ceftriaxone and doxycycline, which were discontinued after normal procalcitonin and negative blood cultures. In addition, he was treated for COVID-19 pneumonia with a 5-day course of remdesivir and 6?mg intravenous dexamethasone daily for the first 5 days. His home atorvastatin 80 mg was continued; however, his home testosterone replacement was held.

On hospital day 5, his hypoxia and oxygen requirements acutely worsened, necessitating transfer to the intensive care unit (ICU). In the ICU, given his severe COVID-19 infection, he was administered convalescent plasma and high-flow oxygen, and his steroids were increased to methylprednisolone 60 mg every 6 hours. His condition improved in the ICU without the need for intubation, antibiotics or paralytics, and he was discharged to a medical ward on hospital day 14.

Initial creatine kinase (CK) was 236 IU/L, which trended down to 39 IU/L in the following week. On hospital day 16, the patient reported new-onset muscle weakness amid an attempt to taper his steroid treatment. Physical examination was significant for symmetrical 4/5 proximal upper extremity strength and 3/5 proximal lower extremity strength.

Upper and lower distal extremity strengths were 5/5 bilaterally. Repeat CK was found to be elevated to 3665 IU/L. Transaminases were elevated with an aspartate aminotransferase (AST) of 123 IU/L and an alanine aminotransferase (ALT) of 137 IU/L. Owing to concern that his hypolipidemic agents were contributing to his clinical decline, his atorvastatin and fenofibrate were discontinued. The patient’s IVIG treatment was continued, and he received an infusion on hospital day 18.

Despite discontinuing his hypolipidemic agents and tapering steroids, his serum CK continued to rise. A thyroid function panel was ordered to investigate potential thyroid myopathy. The panel revealed thyroid stimulating hormone (TSH) of 0.026 µIU/mL, free thyroxine (T4) of 2.66 ng/dL and free triiodothyronine (T3) of 2.30 pg/mL. He had no tremor, tachycardia, eye symptoms or prior thyroid disease. Thyroid examination revealed symmetrical, normal-sized and non-tender thyroid without nodules. A thyroid uptake and scan following capsule of I-123 revealed diffusely decreased thyroid uptake, consistent with thyroiditis. Anti-thyroid peroxidase was 1.7 IU/mL. TSH and free T4 levels were followed 10 days later still demonstrating a hyperthyroid pattern. Two weeks after, the TSH and free T4 levels normalised without antithyroid treatment.