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Background Both C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) can be elevated in systemic lupus erythematosus (SLE) flare and infection, and are therefore of limited utility for distinguishing between the two conditions in febrile SLE patients. Methods A medical records review of hospitalizations (1997-2006) of SLE patients in the Michigan Lupus Cohort was performed. Eligible hospitalizations were those in which patients presented with a temperature of >100.3°F or with subjective fevers as a presenting complaint at admission. Detailed demographic, clinical, and laboratory data were collected. Multivariable logistic regression was used to examine the associations between ESR and CRP and the outcome of flare vs infection, adjusted for confounders. Results Among 557 SLE patients screened, there were 53 eligible hospitalizations (28 flares and 25 infections). Each unit increase in the ratio of ESR:CRP was associated with a 17% increase in the odds of fever being attributable to SLE flare compared to infection (OR 1.17, 95% CI 1.04, 1.31; p = 0.009), when adjusted for white blood cell count, SLE duration, sex, race, and age. ESR and CRP were not individually associated with flare vs infection when modeled with their ratio. Conclusions The ratio of ESR:CRP may provide diagnostic value beyond individual ESR and CRP levels in distinguishing flare vs infection in SLE patients presenting with fever.

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BACKGROUND: Long-term follow-up was completed in 84 mother-infant pairs of 118 women who completed a randomized controlled trial of prenatal supplementation with EPA- or DHA-rich fish oil or soy oil placebo. The goal of this study was to determine whether prenatal omega-3 fatty acid supplementation protects offspring against development of early childhood allergies. METHODS AND FINDINGS: Assessment of childhood allergic/atopic disease among offspring at age 36 months was performed by maternal interview using the National Health Interview Survey (NHIS) questions for childhood digestive allergies, wheezing, eczema or skin allergy, and respiratory allergy. Multiple logistic regressions examined the association between prenatal supplementation and childhood outcomes, adjusted for covariates. Eczema was reported in 26/84 (31%) of offspring at age 36 months, and was significantly more prevalent in the omega-3 supplementation groups vs. placebo: EPA 13/31 (41.9%); DHA 10/26 (38.5%); placebo 3/27 (11.1%), p=0.019. Compared to placebo, EPA and DHA were associated with ≥5 times risk of offspring eczema [odds ratios (ORs): EPA 5.8 (95% CI 1.4-23.3); DHA 5.0 (95% CI 1.2-21.0)]. After adjusting for other potential risk factors (race, birth weight, vaginal/Cesarean delivery, and maternal eczema) the magnitudes of association for omega-3 supplementation increased: EPA OR 8.1 (95% CI 1.4-45.6); DHA OR 9.6 (95% CI 1.6-58.5). Maternal eczema was also significantly associated with offspring eczema in the adjusted model: OR 10.8 (95% CI 2.1-54.3). CONCLUSION: Contrary to our hypothesis, acids supplementation compared to soy oil was associated with a substantial increase in risk of childhood eczema. This association was not observed on childhood respiratory or digestive outcomes. It is unclear if these findings were driven by unfavorable effects of omega-3s, or whether there may have been unanticipated protective effects of the soy-based placebo with regards to eczema.

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A dose-dependent combination of environmental exposures, estrogenic hormones and genetic predisposition is thought to be required for lupus to develop and flare, but how the environment modifies the immune system in genetically predisposed people is unclear. Current evidence indicates that environmental agents that inhibit DNA methylation can convert normal antigen-specific CD4+ T lymphocytes into autoreactive, cytotoxic, pro-inflammatory cells that are sufficient to cause lupus-like autoimmunity in animal models, and that the same changes in DNA methylation characterize CD4+ T cells from patients with active lupus. Environmental agents implicated in inhibiting T-cell DNA methylation include the lupus-inducing drugs procainamide and hydralazine, as well as diet, and agents causing oxidative stress, such as smoking, UV light exposure, and infections, which have been associated with lupus onset or disease activity. Other studies demonstrate that demethylated T cells cause only anti-DNA antibodies in mice lacking a genetic predisposition to lupus, but are sufficient to cause lupus-like autoimmunity in genetically predisposed mice and likely people, and that estrogens augment the disease. Collectively, these studies suggest that environmental agents that inhibit DNA methylation, together with lupus genes and estrogens or endocrine disruptors, combine in a dose-dependent fashion to cause lupus flares.

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BACKGROUND: We measured antimullerian hormone (AMH), a marker of ovarian reserve, in women with lupus treated with cyclophosphamide (CYC) (group I), CYC plus gonadotropin-releasing hormone agonist (GnRH-a) (group II) or neither (group III). We hypothesized that AMH would be diminished in women exposed to CYC versus women receiving adjunctive GnRH-a treatment or no CYC exposure. METHODS: Forty-eight premenopausal lupus patients were retrospectively divided into three treatment groups: CYC alone (group I, n = 11), CYC + GnRH-a (group II, n = 10) and neither (group III, n = 27). Serum AMH levels between groups were compared using a nonparametric test (Wilcoxon rank-sum). Multiple linear regression adjusting for age was performed. RESULTS: AMH (ng/mL) levels at the last collection were significantly lower in group I versus group III (mean ± SD: 0.18 ± 0.20 group I vs 1.33 ± 1.59 group III; p = 0.015), and versus group II (mean ± SD: 0.86 ± 1.06; p = 0.018). When centered on age 30 years, average AMH levels for group I, group II and group III were 0.20, 0.44 and 1.00, respectively. When adjusted for age, AMH between all groups was significantly different (p<0.0001). CONCLUSION: Posttreatment AMH levels were significantly higher among patients receiving CYC + GnRH-a compared to CYC alone, suggesting that GnRH-a coadministration mitigates CYC-induced ovarian injury.

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DHEA (dehydroepiandrosterone) is a weak androgen with proposed efficacy in the treatment of mild to moderate lupus, and possible beneficial effects on cardiovascular risk and bone mineral density. We hypothesized that treatment with 200 mg a day of Prasterone (DHEA) would improve pre-clinical measures of atherosclerosis: flow-mediated dilatation (FMD), nitroglycerin-mediated dilatation (NMD), and circulating apoptotic endothelial cells (CD 146(AnnV +)), as well markers of bone metabolism. Thirteen premenopausal female patients with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI)

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OBJECTIVE: To describe and analyse the clinical and immunological characteristics of a large series of patients with delayed lupus nephritis (LN). METHODS: A cross-sectional study was carried out. Patients with systemic lupus erythematosus (SLE) who developed renal involvement >or=5 years after the first manifestation(s) of the disease (delayed LN, n = 48) were compared with patients with SLE in whom LN developed within 5 years or less after SLE appeared (early-onset LN, n = 187). A control group, the no LN (NLN) group, comprised patients with longstanding SLE (duration of disease >10 years) who had never shown signs of renal involvement (n = 164). RESULTS: The group with delayed LN was positively associated with Sjögren's syndrome, lung involvement and antiphospholipid syndrome as compared with early LN. However, its renal clinical expression and histopathological patterns were similar to those of early-onset LN. The frequency of anti-dsDNA, anti-Sm and anti-RNP antibodies was higher in patients with LN than in the NLN group, as was the frequency of low complement levels. Jaccoud's arthropathy was a protective factor for nephritis. CONCLUSIONS: Delayed LN is not uncommon in patients with SLE. The identified risk factors might aid in its diagnosis and enhance the ability to identify patients at risk for this complication of SLE.

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OBJECTIVE: To compare disease progression and mortality between idiopathic interstitial pneumonia (IIP) and interstitial lung disease (ILD) due to connective tissue diseases (CTD) including scleroderma, rheumatoid arthritis, systemic lupus, polymyositis, dermatomyositis, Sjögren's syndrome, and mixed CTD. METHODS: A case-control study of patients with CTD-ILD (n = 46) and IIP controls (n = 51), seen at the University of Michigan between July 1,1998 and June 30,1999 and followed until March 30, 2002, was conducted. Survival analysis and Cox regression were performed to estimate survival, accounting for demographic and clinical parameters, including pulmonary function tests and high resolution computed tomography (HRCT) diagnosis and scoring. RESULTS: Median followup time was 4.4 person-years. Five-year survival in the IIP group was 51.9% (95% confidence interval [95% CI] 30.8-69.4) versus 43.4% (95% CI 21.1-63.9) in the CTD-ILD group. There were no significant differences among HRCT diagnostic categories between IIP and CTD-ILD. A fibrotic score > or = 2 was associated with decreased survival among the entire group. Age at diagnosis and most recent forced vital capacity were significant predictors of mortality when adjusted for IIP versus CTD-ILD diagnosis, sex, and interstitial score. CONCLUSION: Contrary to expectation, CTD-ILD compared with IIP appears to be associated with a worse prognosis when adjusted for age. A higher fibrotic score is suggestive of decreased survival.

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