Mifepristone-Induced Hypothyroidism.

Medications are known to affect the thyroid physiology and are a known cause of hypothyroidism. There is an ever-growing list of medications that affect the thyroid by 1 or more mechanisms. Mifepristone is presently used for the treatment of mild autonomous cortisol secretion (MACS). Hypothyroidism is not a known side effect of this medication. We present a 71-year-old woman with newly diagnosed impaired fasting glucose, dyslipidemia, and osteopenia presenting with a 3-year history of unintentional 15-pound weight gain (despite exercise and a good diet) and increased anxiety. Her physical examination was pertinent for mild lower extremity edema, easy bruising, and skin thinning. Workup revealed adrenocorticotropic hormone (ACTH)-independent MACS from bilateral micronodular hyperplasia of the adrenals. Since she was not a surgical candidate, medical management with mifepristone was chosen. While on mifepristone, she complained of excessive fatigue, a workup done revealed new-onset hypothyroidism. Given her symptoms and bloodwork, she was started on levothyroxine. After stopping mifepristone, she was biochemically and clinically euthyroid and was eventually off levothyroxine. The mechanism by which mifepristone induces hypothyroidism is unknown. Except for a multicenter case series suggesting that mifepristone increases thyroid hormone requirements in patients with central hypothyroidism, to the best of our knowledge, the literature on euthyroid patients developing hypothyroidism secondary to mifepristone is scarce. In conclusion, while the hypothyroidism seems reversible our case highlights the importance of getting baseline thyroid function tests (TFTs) and repeating them while on the medication. Treatment of hypothyroidism is based on symptoms and bloodwork.

Takayasu Arteritis: A Difficult Diagnosis in a Patient With an Extensive Cardiovascular History.

Large vessel vasculitides, such as Takayasu arteritis (TAK), are rare inflammatory conditions primarily affecting the aorta and its major branches. Its nonspecific symptoms and potential resemblance to atherosclerotic disease often pose diagnostic challenges. We present a case of a 57-year-old male with a history of extensive cardiovascular disease, initially attributed to atherosclerosis, resulting in several interventions, such as catheterization and major cardiac surgery, which didn't help improve his symptoms. Further evaluation revealed diffuse wall thickening of the aorta and its roots, as well as labs that suggested elevated inflammatory markers, comprehensive review of his chart and previous admissions, revealed that he had a well-documented aortitis for which he underwent a biopsy, which at the time was unrevealing. Furthermore, as he had significant aortic aneurysmal dilation, a thoracic cardiovascular surgeon remitted him to the rheumatology clinic, where he was placed on a prednisone taper and methotrexate regimen. Unfortunately, he redeveloped symptoms, and plans were made to transition to a tumor necrosis alpha (TNF-alpha) inhibitor. Our case highlights the importance of an accurate diagnosis and the prompt initiation of appropriate treatment in challenging cases of large vessel vasculitides. This case also underscores the need for heightened clinical awareness and interdisciplinary collaboration to ensure optimal patient care.

A Case of Antisynthetase Syndrome in the Setting of SARS-Cov-2 Infection.

Antisynthetase syndrome is a complex autoimmune disorder, and one of the key criteria for diagnosis is the presence of myositis. Additionally, evidence of interstitial lung disease (ILD) is another important indicator for diagnosis; other clinical features associated with antisynthetase syndrome include arthritis, unexplained and persistent fever, Raynaud's phenomenon, and the presence of mechanic's hands. We report a case of a 36-year-old male who presented to the emergency department with shortness of breath and proximal muscle weakness in the setting of severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2) infection, as his inflammatory markers were elevated and he exhibited features suspicious for antisynthetase syndrome, he was started on methylprednisolone 40 mg intravenously every eight hours, and a myositis panel was checked. In addition, a chest computed tomography (CT) exhibited ground-glass opacities which were compatible with coronavirus disease 2019 (COVID-19). A magnetic resonance image (MRI) of both thighs was done, revealing significant swelling and confirming the suspicion of myositis as his muscle strength in his lower extremities took significant time to improve. As days passed, his muscle strength improved significantly and his creatine phosphatase kinase (CPK) values trended down, indicating that his myositis was improving as well. He was transitioned to oral prednisone 60 mg daily and was discharged home with a rheumatology follow-up to define long-term treatment. A myositis panel revealed anti-glycyl-transferRNA synthetase (EJ) autoantibody positivity and a diagnosis was established. Our case revealed how sometimes laboratory values do not necessarily correlate with disease severity and how we have to do a thorough history of present illness and physical exam to think about unusual diagnoses before putting laboratory data into context.