Clinical associations of incidentally detected parotid gland calcification on CT.

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.

The thyroid hormone degrading type 3 deiodinase is the primary deiodinase active in murine epidermis.

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 (T(4)) to the active hormone triiodothyronine because athyreotic humans can be treated with T(4) 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.

Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D.

CONTEXT: Two reports suggested that vitamin D2 is less effective than vitamin D3 in maintaining vitamin D status. OBJECTIVE: Our objective was to determine whether vitamin D2 was less effective than vitamin D3 in maintaining serum 25-hydroxyvitamin D levels or increased the catabolism of 25-hydroxyvitamin D3. SUBJECTS AND DESIGN: This was a randomized, placebo-controlled, double-blinded study of healthy adults ages 18-84 yr who received placebo, 1000 IU vitamin D3, 1000 IU vitamin D2, or 500 IU vitamin D2 plus 500 IU vitamin D3 daily for 11 wk at the end of the winter. RESULTS: Sixty percent of the healthy adults were vitamin D deficient at the start of the study. The circulating levels of 25-hydroxyvitamin D (mean+/-sd) increased to the same extent in the groups that received 1000 IU daily as vitamin D2 (baseline 16.9+/-10.5 ng/ml; 11 wk 26.8+/-9.6 ng/ml), vitamin D3 (baseline 19.6+/-11.1 ng/ml; 11 wk 28.9+/-11.0 ng/ml), or a combination of 500 IU vitamin D2 and 500 IU vitamin D3 (baseline 20.2+/-10.4 ng/ml; 11 wk 28.4+/-7.7 ng/ml). The 25-hydroxyvitamin D3 levels did not change in the group that received 1000 IU vitamin D2 daily. The 1000 IU dose of vitamin D2 or vitamin D3 did not raise 25-hydroxyvitamin D levels in vitamin D-deficient subjects above 30 ng/ml. CONCLUSION: A 1000 IU dose of vitamin D2 daily was as effective as 1000 IU vitamin D3 in maintaining serum 25-hydroxyvitamin D levels and did not negatively influence serum 25-hydroxyvitamin D3 levels. Therefore, vitamin D2 is equally as effective as vitamin D3 in maintaining 25-hydroxyvitamin D status.