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JOURNAL ARTICLE
RESEARCH SUPPORT, N.I.H., EXTRAMURAL
Association of Trauma and Posttraumatic Stress Disorder With Incident Systemic Lupus Erythematosus in a Longitudinal Cohort of Women.
Arthritis & Rheumatology 2017 November
OBJECTIVE: To conduct the first longitudinal study examining whether trauma exposure and posttraumatic stress disorder (PTSD) are associated with increased risk of incident systemic lupus erythematosus (SLE) in a civilian cohort.
METHODS: We examined the association of trauma exposure and PTSD symptoms with SLE incidence over 24 years of follow-up in a US longitudinal cohort of women (n = 54,763). Incident SLE in women meeting ≥4 American College of Rheumatology criteria was ascertained by self-report and confirmed by medical record review. PTSD and trauma exposure were assessed with the Short Screening Scale for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition PTSD and the Brief Trauma Questionnaire, respectively. Women were categorized as having no trauma, trauma and no PTSD symptoms, subclinical PTSD (1-3 symptoms), or probable PTSD (4-7 symptoms). We examined whether longitudinally assessed health risk factors (e.g., smoking, body mass index [BMI], oral contraceptive use) accounted for increased SLE risk among women with trauma exposure and PTSD versus those without.
RESULTS: During follow-up, 73 cases of SLE occurred. Compared to women with no trauma, probable PTSD was associated with increased SLE risk (for 4-7 symptoms, hazard ratio [HR] 2.94 [95% confidence interval {95% CI} 1.19-7.26], P < 0.05). Subclinical PTSD was associated with increased SLE risk, although this did not reach statistical significance (for 1-3 symptoms, HR 1.83 [95% CI 0.74-4.56], P = 0.19). Smoking, BMI, and oral contraceptive use slightly attenuated the associations (e.g., for 4-7 symptoms, adjusted HR 2.62 [95% CI 1.09-6.48], P < 0.05). Trauma exposure, regardless of PTSD symptoms, was strongly associated with incident SLE (HR 2.83 [95% CI 1.29-6.21], P < 0.01).
CONCLUSION: This study contributes to growing evidence that psychosocial trauma and associated stress responses may lead to autoimmune disease.
METHODS: We examined the association of trauma exposure and PTSD symptoms with SLE incidence over 24 years of follow-up in a US longitudinal cohort of women (n = 54,763). Incident SLE in women meeting ≥4 American College of Rheumatology criteria was ascertained by self-report and confirmed by medical record review. PTSD and trauma exposure were assessed with the Short Screening Scale for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition PTSD and the Brief Trauma Questionnaire, respectively. Women were categorized as having no trauma, trauma and no PTSD symptoms, subclinical PTSD (1-3 symptoms), or probable PTSD (4-7 symptoms). We examined whether longitudinally assessed health risk factors (e.g., smoking, body mass index [BMI], oral contraceptive use) accounted for increased SLE risk among women with trauma exposure and PTSD versus those without.
RESULTS: During follow-up, 73 cases of SLE occurred. Compared to women with no trauma, probable PTSD was associated with increased SLE risk (for 4-7 symptoms, hazard ratio [HR] 2.94 [95% confidence interval {95% CI} 1.19-7.26], P < 0.05). Subclinical PTSD was associated with increased SLE risk, although this did not reach statistical significance (for 1-3 symptoms, HR 1.83 [95% CI 0.74-4.56], P = 0.19). Smoking, BMI, and oral contraceptive use slightly attenuated the associations (e.g., for 4-7 symptoms, adjusted HR 2.62 [95% CI 1.09-6.48], P < 0.05). Trauma exposure, regardless of PTSD symptoms, was strongly associated with incident SLE (HR 2.83 [95% CI 1.29-6.21], P < 0.01).
CONCLUSION: This study contributes to growing evidence that psychosocial trauma and associated stress responses may lead to autoimmune disease.
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