Thyroid hormone resistance (THR) is a rare syndrome of reduced end organ sensitivity. Patients with THR have elevated serum free thyroxine (FT4), free triiodothyronine (FT3), but normal or slightly elevated serum thyrotropin values. The characteristic clinical feature is goitre without symptoms and metabolic consequences of thyroid hormone excess. THR can be classified on the basis of tissue resistance into pituitary, peripheral or generalised (both pituitary and peripheral) types. Mutations in the TRbeta gene, cell membrane transporter and genes controlling intracellular metabolism of thyroid hormone have been implicated. THR is differentiated from thyroid stimulating hormone (TSH) secreting pituitary adenoma by history of THR in the family. No specific treatment is often required for THR; patients with features of hypo- or hyperthyroidism are appropriately treated with levo-triiodothyronine (L-T3), levo-thyroxine (L-T4), dextro-thyroxine(D-T4) or 3,3,5 triiodo-thyroacetic acid (TRIAC). The diagnosis helps in appropriate genetic counselling of the family.

The ongoing coronavirus disease-2019 (COVID-19) pandemic has been the focus of health care workers as it has affected millions of people and cost hundreds of thousands of lives around the world. As hospitals struggle to identify and care for those afflicted with COVID-19, it is easy to overlook endemic diseases that potentially worsen or mimic the pulmonary manifestations or may coinfect those with COVID-19. In this case report, we present the case of a 48-year-old Hispanic female who was admitted with respiratory distress from an acute COVID-19 infection but was also found to have acute pulmonary coccidioidomycosis infection and was treated successfully.

No abstract

No abstract