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BACKGROUND AND OBJECTIVE: Indoleamine 2,3-dioxygenase (IDO) is one of the major pathways for metabolism of tryptophan in a variety of cells, including immune cells. Increasing evidence indicates that IDO is a critical player in establishing the balance between immunity and tolerance and ultimately in the maintenance of homeostasis. By inducing inflammation in gingival tissue, we tested the hypothesis that IDO is a pivotal player in regulating the immune and inflammatory responses of gingiva. MATERIAL AND METHODS: We utilized the IDO knockout mouse model in conjunction with lipopolysaccharide (LPS)-induced inflammation. Accordingly, wild-type and IDO knockout mice were injected with LPS or vehicle in the anterior mandibular gingiva, twice over a 2-wk period, which was followed by procurement of gingival tissue for histopathology and preparation of tissue for flow cytometry-based studies. RESULTS: Clinical and histological examinations revealed a marked adverse impact of IDO deficiency on gingival inflammation. These observations were consistent with a more marked increase in the number of cells positive for the proinflammatory cytokine interleukin (IL)-17, but no significant change in the number of cells positive for the anti-inflammatory cytokine IL-10, in LPS-treated IDO knockout mice. Consistent with the more marked proinflammatory impact of IDO deficiency, the percentage of regulatory T cells was much reduced in gingival tissue of LPS-treated IDO knockout mice than in gingival tissue of wild-type mice. These proinflammatory changes were accompanied with a prominent increase in apoptotic and necrotic cell death in gingival tissue of IDO knockout mice compared with wild-type mice. CONCLUSION: Collectively, our findings support a major role for IDO in the development of gingival inflammation, as an example of an inflammatory condition, and lay the foundation for subsequent studies to explore it as a novel immunotherapy target.

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OBJECTIVE: To determine the incidence and pattern of thyroid dysfunction (TD) in patients on chronic amiodarone therapy. METHODS: A retrospective study which evaluated 59 patients who had received amiodarone therapy regularly for at least 12 months from a period of 3 years from October 2007 to October 2010. The patients were followed-up at the cardiac clinic at Sultan Qaboos University Hospital, Muscat, Oman. RESULTS: The mean age of the cohort was 63 ± 13 years ranging from 27 to 98 years. Fifty-one percent (n = 30) of the patients were female. There were 11 (19%) cases of thyroid dysfunction (TD). Seven (12%) patients were hypothyroid, 3 (5%) had hyperthyroidism and 1 (2%) patient had sub-clinical hypothyroidism; no cases of sub-clinical hyperthyroidism were noted. Female gender and presence of anti-thyroid peroxidase antibodies were significantly associated with amiodarone-induced hypothyroidism (p = 0.001) while age, amiodarone dose and duration of therapy were not correlated with the development of TD (all p-values > 0.05). CONCLUSION: Amiodarone-induced thyroid dysfunction is prevalent. Hypothyroidism was more frequent and seen more in female patients and those who had positive anti-thyroid peroxidase antibodies. Initial screening and periodic monitoring of thyroid function is mandatory for all patients on amiodarone therapy.

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