No abstract

The objective was to determine whether the frequency of flare in systemic lupus erythematosus (SLE), patients is increased during pregnancy and the puerperium. Seventy-eight pregnancies in 68 SLE patients attending the lupus pregnancy clinic, at St. Thomas' Hospital, during the last 5 yr were included. The pregnancy period and 8 weeks post-delivery were considered. This group was compared with a control group of 50 consecutive, non-pregnant, age-matched SLE patients attending our weekly lupus clinic. Additionally, 43 of the pregnant patients carried on attending the lupus clinic for the year after puerperium, and their course was compared with themselves during pregnancy. SLE activity was assessed using the Lupus Activity Index (LAI) score. An increase > or = 0.26 in the score was considered as a flare of the disease. Pregnancy and control groups were homogeneous for age, race, disease duration and distribution of autoantibodies. Sixty-five per cent of the patients flared during pregnancy and/or the puerperium and 42% flared in the control group (P = 0.015). The rates of flare per patients/month were 0.082 +/- 0.004 for the pregnancy group and 0.039 +/- 0.003 for the control group (P < 0.001). The 43 patients whose course was controlled after the puerperium flared more frequently during pregnancy that thereafter (McNemar test, P = 0.003). The rates of flare per patient/month were 0.093 +/- 0.006 during pregnancy and the puerperium, and 0.049 +/- 0.004 after the puerperium (P = 0.0015). Kidney and central nervous system involvement was not different between the pregnancy and control groups. In terms of frequency of flares, there was no difference in any of the groups between patients taking and not taking steroids. We conclude that SLE tends to flare during pregnancy. Flares are maximal during the second and third trimester and the puerperium. Flares are not more severe than in non-pregnant patients, and most of the flares can be managed conservatively. Prednisolone does not prevent flares.

Objective. To determine the prevalence of antihigh-density lipoprotein (anti-HDL) antibodies and to establish a possible relationship between anti-HDL, anticardiolipin antibodies (aCL), anti-␤ 2 -glycoprotein I (anti-␤ 2 GPI), and paraoxonase (PON) activity in patients with systemic lupus erythematosus (SLE) and primary antiphospholipid syndrome (APS).Methods. Thirty-two patients with SLE and 36 with primary APS were enrolled in a cross-sectional study. Twenty age-and sex-matched healthy subjects were used as controls. Serum levels of IgG and IgM aCL, anti-␤ 2 GPI, and antiprothrombin antibodies and IgG anti-HDL were measured by enzyme-linked immunosorbent assay. Total cholesterol, HDL cholesterol, HDL 2 , and HDL 3 were determined by standard enzymatic techniques. PON activity was assessed by quantification of nitrophenol formation, and total antioxidant capacity (TAC) by chemiluminescence.Results. Levels of total HDL, HDL 2 , and HDL 3 were reduced in patients with SLE compared with controls (mean ؎ SD 0.51 ؎ 0.3, 0.37 ؎ 0.3, and 0.14 ؎ 0.1 mmoles/liter, respectively, versus 1.42 ؎ 0.9, 1.01 ؎ 0.7, and 0.40 ؎ 0.2). Patients with SLE and primary APS had higher titers of anti-HDL antibodies and lower PON activity than controls. In the SLE population, PON activity was inversely correlated with IgG anti-HDL titers (r ‫؍‬ ؊0.48, P ‫؍‬ 0.005) whereas in the primary APS population, IgG anti-␤ 2 GPI was the only independent predictor of PON activity (r ‫؍‬ ؊0.483, P ‫؍‬ 0.003). In the SLE group, anti-HDL was inversely correlated with TAC (r ‫؍‬ ؊0.40, P < 0.02), and PON activity was positively correlated with TAC (r ‫؍‬ 0.43, P < 0.02).Conclusion. IgG anti-HDL and IgG anti-␤ 2 GPI antibodies are associated with reduced PON activity in patients with SLE and primary APS. Since the physiologic role of PON is to prevent low-density lipoprotein oxidation with its attendant atherogenic effects, the reported interactions may be relevant to the development of atherosclerosis in SLE and primary APS.

Context Accelerated atherosclerosis has been described in antiphospholipid syndrome, but the vascular abnormalities and the underlying mechanisms remain unclear.Objectives To compare vascular structure and function in patients with positive antiphospholipid antibodies (aPL) with controls and to assess their relationship with paraoxonase activity. Design, Setting, and ParticipantsA cross-sectional study of 77 women with positive antiphospholipid antibodies from a lupus outpatient clinic in London, England (90% of the eligible population) and 77 controls matched on frequency basis for age and cardiovascular risk factors between June 2006 and April 2009. Carotid intima media thickness (CIMT), flow-mediated dilatation, pulse wave velocity, and paraoxonase activity were measured in all patients. Anti-inflammatory and antioxidant properties of high-density lipoprotein (HDL) were examined.Main Outcome Measures CIMT, pulse wave velocity, flow-mediated dilatation, and paraoxonase. ResultsWomen with aPL had greater CIMT and pulse wave velocity compared with controls (mean [SD], 0.75 [0.16] vs 0.64 [0.

Objective. To determine whether antibodies against high-density lipoprotein (aHDL) and apolipoprotein A-I (aApo A-I) interfere with the anti-atherogenic functions of high-density lipoprotein (HDL) and relate to disease activity and damage in SLE. Methods. Seventy-seven SLE patients were compared with an age-and sex-frequency matched control group. Immunoglobulin G (IgG) aHDL, IgG aApoA-I, soluble vascular cell and intracellular cell adhesion molecules (VCAM-1 and ICAM-1, respectively) were measured by ELISA, paraoxonase (PON) activity by spectrophotometry, nitric oxide (NOx) metabolites by the Griess reaction, and total anti-oxidant capacity (TAC) by chemiluminescence. Results. Compared with controls, SLE patients showed higher titres of IgG aHDL (P < 0.0001) and IgG aApo A-I (P < 0.0001), lower PON activity (P < 0.0001), increased NOx (P < 0.