摘要
Thyroid abnormalities have been reported in persons with HIV infection, although data have been inconsistent with respect to its frequency and association with specific medications. The purpose of this study was to explore thyroid system response to thyroid releasing hormone stimulation in persons with and without HIV infection and determine the extent to which their response was associated with depression. As part of a larger study of neuroendocrine response persons with HIV-1 infection, control and HIV-1 infected individuals were evaluated. Participants' response to TRH stimulation was evaluated via TSH, total T3, and T4 levels at baseline and 15, 30, 45, and 60 minutes after TRH stimulation. Participants with HIV infection had a more robust response to TRH stimulation as measured by higher levels of TSH, lower levels of T4 and modestly higher levels of T3. Depressed persons had a reduced TSH response to stimulation and lower levels of both T4 and T3, although the effect of depression on T4 was not statistically significant. These results suggest that TSH response to TRH-stimulation may be exaggerated in individuals with HIV infection but reduced in those with depression. They also suggest that the effects of depression and HIV infection may interact, and may provide a partial explanation for observed thyroid abnormalities in HIV-infected individuals. Results thus provide a partial explanation for findings on thyroid and depression in those affected by HIV infection.
Thyroid abnormalities have been reported in persons with HIV infection, although data have been inconsistent with respect to its frequency and association with specific medications. The purpose of this study was to explore thyroid system response to thyroid releasing hormone stimulation in persons with and without HIV infection and determine the extent to which their response was associated with depression. As part of a larger study of neuroendocrine response persons with HIV-1 infection, control and HIV-1 infected individuals were evaluated. Participants' response to TRH stimulation was evaluated via TSH, total T3, and T4 levels at baseline and 15, 30, 45, and 60 minutes after TRH stimulation. Participants with HIV infection had a more robust response to TRH stimulation as measured by higher levels of TSH, lower levels of T4 and modestly higher levels of T3. Depressed persons had a reduced TSH response to stimulation and lower levels of both T4 and T3, although the effect of depression on T4 was not statistically significant. These results suggest that TSH response to TRH-stimulation may be exaggerated in individuals with HIV infection but reduced in those with depression. They also suggest that the effects of depression and HIV infection may interact, and may provide a partial explanation for observed thyroid abnormalities in HIV-infected individuals. Results thus provide a partial explanation for findings on thyroid and depression in those affected by HIV infection.
