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Rheumatoid arthritis and major depre...

Johnston, Sandra K.

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Rheumatoid arthritis and major depression: Effects of antidepressant therapy on markers of inflammation.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Rheumatoid arthritis and major depression: Effects of antidepressant therapy on markers of inflammation./
Author:	Johnston, Sandra K.
Description:	160 p.
Notes:	Chair: Patricia Prinz.
Contained By:	Dissertation Abstracts International65-04B.
Subject:	Health Sciences, Immunology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3131170
ISBN:	9780496784141

Rheumatoid arthritis and major depression: Effects of antidepressant therapy on markers of inflammation.
Johnston, Sandra K.

Rheumatoid arthritis and major depression: Effects of antidepressant therapy on markers of inflammation. - 160 p.

Chair: Patricia Prinz.

Thesis (Ph.D.)--University of Washington, 2004.

Purpose. Evidence exists of systemic inflammation in both rheumatoid arthritis (RA) and major depression (MD). However, little is known about the effects of antidepressants on systemic inflammation. The purpose of this study was to examine the effects of effective antidepressant treatment on inflammatory immune markers (Tumor Necrosis Factor alpha---TNF-alpha, Interleukin-1 Receptor Antagonist---IL-1Ra, and C-reactive protein---CRP) in persons with combined RA and MD. Methods. This was a secondary analysis of a study in which subjects (n = 54) with RA received cognitive-behavioral and pharmacologic treatment for MD (Parker et al., 2003) and on-going rheumatology care. The current study focused on a subset of subjects (n = 38) treated for 15 months with sertraline. Serum TNF-alpha, IL-1Ra, and CRP levels; depression (Hamilton Depression Rating Scale), RA health status, and joint disease activity were obtained at baseline and following 15 months of antidepressant treatment with sertraline. Serum TNF-alpha and IL-1Ra levels were obtained by enzyme-linked immunosorbent assay; Serum CRP levels were obtained by high sensitivity CRP chemiluminescent immunoassay. Results. Following 15 months of antidepressant treatment, significant reductions were noted for depression severity (p = .001); 87% of subjects had at least a 50% reduction in depression severity scores. There was a near significant (p = .06) decrease in serum TNF-alpha levels; while serum IL-1Ra and CRP levels remained unchanged (p = .62, p = .97, respectively). Baseline serum TNF-alpha and IL-1Ra levels predicted the amount of reduction in depression severity (R2 =35, p =.002). Subjects with lower baseline serum levels of the inflammatory cytokine TNF-alpha had greater reductions in depression severity scores; subjects with higher baseline serum levels of the anti-inflammatory cytokine IL-1Ra had greater reductions in depression severity scores. Conclusions . This study provides preliminary evidence that baseline serum TNF-alpha and IL-1Ra levels in persons with RA and MD predict the amount of improvement in depression severity with antidepressant treatment. Serum TNF-alpha levels decreased following antidepressant treatment. These findings support the importance of vigilance in monitoring for and successfully managing MD in persons with RA.

ISBN: 9780496784141Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

Rheumatoid arthritis and major depression: Effects of antidepressant therapy on markers of inflammation.
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020 $a 9780496784141
035 $a (UnM)AAI3131170
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100 1 $a Johnston, Sandra K. $3 1288327
245 1 0 $a Rheumatoid arthritis and major depression: Effects of antidepressant therapy on markers of inflammation.
300 $a 160 p.
500 $a Chair: Patricia Prinz.
500 $a Source: Dissertation Abstracts International, Volume: 65-04, Section: B, page: 1765.
502 $a Thesis (Ph.D.)--University of Washington, 2004.
520 $a Purpose. Evidence exists of systemic inflammation in both rheumatoid arthritis (RA) and major depression (MD). However, little is known about the effects of antidepressants on systemic inflammation. The purpose of this study was to examine the effects of effective antidepressant treatment on inflammatory immune markers (Tumor Necrosis Factor alpha---TNF-alpha, Interleukin-1 Receptor Antagonist---IL-1Ra, and C-reactive protein---CRP) in persons with combined RA and MD. Methods. This was a secondary analysis of a study in which subjects (n = 54) with RA received cognitive-behavioral and pharmacologic treatment for MD (Parker et al., 2003) and on-going rheumatology care. The current study focused on a subset of subjects (n = 38) treated for 15 months with sertraline. Serum TNF-alpha, IL-1Ra, and CRP levels; depression (Hamilton Depression Rating Scale), RA health status, and joint disease activity were obtained at baseline and following 15 months of antidepressant treatment with sertraline. Serum TNF-alpha and IL-1Ra levels were obtained by enzyme-linked immunosorbent assay; Serum CRP levels were obtained by high sensitivity CRP chemiluminescent immunoassay. Results. Following 15 months of antidepressant treatment, significant reductions were noted for depression severity (p = .001); 87% of subjects had at least a 50% reduction in depression severity scores. There was a near significant (p = .06) decrease in serum TNF-alpha levels; while serum IL-1Ra and CRP levels remained unchanged (p = .62, p = .97, respectively). Baseline serum TNF-alpha and IL-1Ra levels predicted the amount of reduction in depression severity (R2 =35, p =.002). Subjects with lower baseline serum levels of the inflammatory cytokine TNF-alpha had greater reductions in depression severity scores; subjects with higher baseline serum levels of the anti-inflammatory cytokine IL-1Ra had greater reductions in depression severity scores. Conclusions . This study provides preliminary evidence that baseline serum TNF-alpha and IL-1Ra levels in persons with RA and MD predict the amount of improvement in depression severity with antidepressant treatment. Serum TNF-alpha levels decreased following antidepressant treatment. These findings support the importance of vigilance in monitoring for and successfully managing MD in persons with RA.
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