Neuropsychiatric syndromes in patients with systemic lupus erythematosus and rheumatoid arthritis.
ABSTRACT The cause of neurologic (N) and psychiatric (P) syndromes in patients with systemic lupus erythematosus (SLE) is mutifactorial and includes primary immunopathogenic mechanisms, nonspecific sequelae of chronic disease, and concurrent illnesses. We compared the prevalence, diversity, and clinical significance of NP syndromes in patients with SLE and rheumatoid arthritis (RA).
Fifty-three patients with SLE were matched by age and sex to 53 patients with RA attending ambulatory clinics in a single academic medical center. All fulfilled the American College of Rheumatology (ACR) classification criteria for either SLE or RA. Cumulative NP manifestations were determined using the ACR nomenclature and case definitions for 19 NP syndromes. Depression and anxiety were measured by the Hospital Anxiety and Depression Scales (HADS) and symptoms of cognitive dysfunction were assessed by the Cognitive Symptoms Inventory (CSI). Health related quality of life (HRQOL) was evaluated by the SF-36 and fatigue by a 10 point Likert scale.
The patients were well matched with regard to age, sex, disease duration, and years of education. There were no significant differences in self-reported HRQOL, fatigue, anxiety, depression, and cognitive symptoms between the 2 groups. The proportion of patients with cumulative NP events was higher in RA than in SLE patients (47% vs 28%; p = 0.045), and of these the occurrence of multiple NP events in individual patients was comparable in both groups (SLE 53%; RA 48%; p = 0.75). Fifty-five percent and 66% of NP events occurred prior to the diagnosis of SLE and RA, respectively. NP events common to both SLE and RA patients were headaches, mood disorders, acute confusional states, anxiety, cerebrovascular disease, and cognitive dysfunction. Seizures and demyelinating syndrome occurred only in SLE patients, but were rare. Depression scores (HADS) were significantly higher in SLE patients with a history of cumulative NP events compared to RA patients with NP events (p = 0.02). Similarly, symptoms of cognitive dysfunction (CSI) were more common in SLE patients with a history of NP manifestations (p = 0.02). However, there were no significant differences in SF-36 subscale or fatigue scores between SLE and RA patients with cumulative NP events.
NP syndromes, regardless of etiology, are common in both SLE and RA patients. SLE patients with NP syndromes report more symptoms of depression and cognitive dysfunction compared to RA patients with NP syndromes, but do not report significantly poorer HRQOL. These results emphasize the presence of non-disease-specific causes of NP manifestations in SLE patients, which should be acknowledged in future studies of pathogenesis and treatment.
[Show abstract] [Hide abstract]
ABSTRACT: Objective. Findings from previous studies of predictors of depression among patients with systemic lupus erythematosus (SLE) have been inconsistent. The aim of our study was to identify risk factors that preceded incident depression based on a large, closely followed longitudinal cohort. Methods. Data regarding 1609 patients with SLE in the Hopkins Lupus Cohort who had no history of depression prior to cohort entry were analyzed. Demographic variables, SLE manifestations, laboratory tests, physician's global assessment, Safety of Estrogens in Lupus Erythematosus National Assessment-SLE Disease Activity Index (SELENA-SLEDAI), cumulative organ damage (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index), and onset of depression were recorded at enrollment and each quarterly visit. Rates of incident depression were calculated overall, and in subgroups defined by demographic and clinical variables. Adjusted estimates of association were derived using pooled logistic regression. Results. The incidence of depression was 29.7 episodes per 1000 person-years. In the multivariable analysis, these variables remained as independent predictors of incident depression: recent SLE diagnosis, non-Asian ethnicity, disability, cutaneous activity, longitudinal myelitis, and current prednisone use of 20 mg/day or higher. Global disease activity (SELENA-SLEDAI) was not a significant predictor after controlling for prednisone use. Conclusion. Depression in SLE is multifactorial. Higher-dose prednisone (>= 20 mg daily) is 1 important independent risk factor. Global disease activity is not a risk factor, but cutaneous activity and certain types of neurologic activity (myelitis) are predictive of depression. The independent effect of prednisone provides clinicians with an additional incentive to avoid and reduce high-dose prednisone exposure in SLE.The Journal of Rheumatology 08/2014; 41(9). DOI:10.3899/jrheum.140111 · 3.17 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Objective Inflammatory processes, which provoke alternations of neurotransmitter metabolism, neuroendocrine function, and neuroplasticity in the brain, might promote depression. In depression patients who do not exhibit risk factors, including hypertension, diabetes, coronary heart disease, stroke, Parkinson’s disease and dementia, particularly in young people, inflammation is a likely risk factor for depression. We explored whether chronic osteomyelitis (COM), a chronic inflammatory disease, increases depression risk. Methods A Taiwanese national insurance claims dataset of more than 22 million enrollees was used to select 15,529 COM patients without depression history and 62,116 randomly selected age- and gender-matched controls without depression and COM history to trace depression development for an 8-year follow-up period from January 1, 1999 to December 31, 2006. The depression risk was analyzed using the Cox proportional hazards regression model. Results Above-mentioned risk factors for depression were more frequent in the COM cohort, who exhibited significantly higher depression risk than the control group did. Comparing only those without comorbidities, the COM group exhibited higher depression risk than the control group did (hazard ratio [HR] = 3.04, 95% confidence interval [CI]: 2.55-3.62). The younger population carried even greater risk (age < 45: HR = 6.08, 95% CI: 1.71-7.85; age > 65: HR = 1.75, 95% CI: 1.39-2.19). Conclusions This is the first study connecting COM to increased risk of developing depression. The outcomes suggest that COM is a substantial depression predictor and call for a closer focus on these patients for more rigorous depression prevention, particularly in young people.Journal of psychosomatic research 09/2014; DOI:10.1016/j.jpsychores.2014.09.008 · 2.84 Impact Factor
Neuro-immune interaction in the adult central nervous system, 01/2013: chapter 1: pages 1-22;