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Objectives/Hypothesis Parotid gland calcifications can be incidental findings on computed tomography (CT) and have been reported to be associated with chronic inflammatory conditions. Associations between parotid gland calcification and other common medical conditions have not been reported. Methods Following institutional review board approval, 1,571 patients who underwent noncontrast head CT with 1.25-mm slice thickness on a 64-detector row CT between January 2011 and July 2011 were retrospectively reviewed for parotid gland calcifications. Medical records were reviewed for chronic kidney disease, alcoholism, autoimmune conditions, endocrine disorders, elevated alkaline phosphatase, and HIV (human immunodeficiency virus) status. Statistical analyses were performed using Fisher's exact test and multiple logistic regression. Results Sixty-three of 1,571 (4%) patients had parotid gland calcifications. Significant associations were observed between parotid gland calcifications and HIV infection ( P = 0.002), chronic kidney disease ( P < 0.0001), alcoholism ( P < 0.0001), elevated alkaline phosphatase ( P = 0.003), and autoimmune disease ( P = 0.02). Conclusion Parotid gland calcifications were associated with HIV, alcoholism, chronic kidney disease, autoimmune disease, and elevated alkaline phosphatase. Level of Evidence 4. Laryngoscope, 125:1360-1365, 2015 [ABSTRACT FROM AUTHOR]

Introduction: Many tissues express thyroid hormone metabolizing deiodinases that both activate and inactivate thyroid hormones through conversion processes. Many believe that the primary role of thyroid hormone deiodinases is the activation of the prohormone thyroxine (T4) to the active hormone triiodothyronine because athyreotic humans can be treated with T4 alone. In our hands a nonspecific deiodinase inhibitor (iopanoic acid [IOP]) decreased cutaneous cell proliferation in vitro, so we hypothesized that topical IOP would inhibit epidermal proliferation in vivo. Methods: IOP was applied topically to mice. Treatments were applied daily for 1 week. Skin biopsies were either stained for 5-bromo-2-deoxyuridine or flash-frozen to assay for deiodinase activity. Results: Topical IOP resulted in a dose-dependent increase in epidermal proliferation. Assay revealed significant inactivating type 3 deiodinase (Dio3) activity in the epidermis but little or no activating (Dio1 or Dio2) activity. Dio3 activity was decreased 44%±21% in epidermis from mice treated with low-dose IOP and 80%±4% in epidermis from mice treated with high-dose IOP ( p<0.001). Conclusion: We hypothesize that keratinocytes express Dio3 in vivo to maintain cutaneous health and prevent the skin from becoming hyperproliferative. Our data support the developing recognition that the primary role of thyroid hormone deiodinases in some tissues may be the degradation of thyroid hormone to protect the tissue against thyrotoxicosis. [ABSTRACT FROM AUTHOR]