SUN-010 A Unique Case of Central Hypothyroidism Due to Infective Endocarditis Presenting as Myxedema Coma

Abstract B. Godasi: None. N.R. Jannareddy: None. C. Lovato: None. Introduction: Central hypothyroidism is characterized by a deficiency of thyroid hormone either by insufficient production of thyrotropin releasing hormone and/or insufficient production of thyroid stimulating hormone from the pituitary. Acquired central hypothyroidism can result from invasive or compressive lesions of the sella, iatrogenic causes, trauma, vascular accidents, autoimmune diseases, infiltrative diseases, and infections. Clinical Case: A 31-year-old Hispanic female patient with a past medical history of end-stage kidney disease on hemodialysis, hypertension, non-ischemic cardiomyopathy, and cirrhosis was transferred from an outside hospital to our facility for MSSA endocarditis with multiple cerebral and pulmonary embolic abscesses from an infected dialysis catheter, new-onset seizures, and right frontal lobe intra-parenchymal hemorrhage secondary to mycotic aneurysm. At the time of presentation, the patient’s TSH was mildly elevated at 6.710 uIU/ml (n 0.270-4.20 uIU/ml), and free T4 was normal at 1.3 ng/dl (n 0.9-1.7 ng/dl). Eight days later, repeat TSH was inappropriately normal at 3.300 uIU/ml with undetectable free T4 < 0.2 ng/dl. She was discharged from the hospital without any levothyroxine supplementation. She was hospitalized 3 weeks later due to hypotension and somnolence. She developed bradycardia and hypoxia. Repeat labs showed undetectable free T4 < 0.2 ng/dl and mildly high TSH 5.710 uIU/ml. The patient was started on treatment for myxedema coma with IV hydrocortisone, IV levothyroxine, and IV liothyronine. The patient began to improve clinically and was transitioned to oral levothyroxine and was titrated off hydrocortisone. However, her free T4 levels did not improve into the normal range, likely secondary to poor absorption from gut edema and anasarca. She was transitioned back to IV levothyroxine with normalization of free T4 levels. Morning serum cortisol was 34.8 µg/dL (n 6.0-18.4 µg/dL) and prolactin was 18.7 ng/ml (n 4.8-23.3 ng/ml). MRI of the brain without contrast did not show a pituitary mass. However, the pituitary was T1 hyperintense and thought to potentially reflect sequelae of prior apoplexy/hemorrhage, prior hypophysitis or protein deposition. We suspect that the patient had a septic embolism to the pituitary that resulted in central hypothyroidism. The patient ultimately died from other medical complications during her hospitalization. Discussion: This is a rare case of central hypothyroidism resulting from infective endocarditis. To our knowledge, there is only one other case of endocarditis that resulted in hypopituitarism. Our case is unique as it resulted in an isolated central hypothyroidism. Physicians should be aware of potential pituitary complications of endocarditis, as these hormonal deficiencies can cause significant morbidity and mortality. Sunday, June 2, 2024