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Aim: The aim of this study was to identify factors predictive of serious infections over time in patients with systemic lupus erythematosus (SLE). Methods: A multi-ethnic, multi-national Latin American SLE cohort was studied. Serious infection was defined as one that required hospitalization, occurred during a hospitalization or led to death. Potential predictors included were sociodemographic factors, clinical manifestations (per organ involved, lymphopenia and leukopenia, independently) and previous infections at baseline. Disease activity (SLEDAI), damage (SLICC/ACR Damage Index), non-serious infections, glucocorticoids, antimalarials (users and non-users), and immunosuppressive drugs use; the last six variables were examined as time-dependent covariates. Cox regression models were used to evaluate the predictors of serious infections using a backward elimination procedure. Univariable and multivariable analyses were performed. Results: Of the 1243 patients included, 1116 (89.8%) were female. The median (interquartile range) age at diagnosis and follow-up time were 27 (20–37) years and 47.8 (17.9–68.6) months, respectively. The incidence rate of serious infections was 3.8 cases per 100 person-years. Antimalarial use (hazard ratio: 0.69; 95% confidence interval (CI): 0.48–0.99; p = 0.0440) was protective, while doses of prednisone >15 and ≤60 mg/day (hazard ratio: 4.18; 95 %CI: 1.69–10.31; p = 0.0019) and >60 mg/day (hazard ratio: 4.71; 95% CI: 1.35–16.49; p = 0.0153), use of methylprednisolone pulses (hazard ratio: 1.53; 95% CI: 1.10–2.13; p = 0.0124), increase in disease activity (hazard ratio: 1.03; 95% CI: 1.01–1.04; p = 0.0016) and damage accrual (hazard ratio: 1.22; 95% CI: 1.11–1.34; p < 0.0001) were predictive factors of serious infections. Conclusions: Over time, prednisone doses higher than 15 mg/day, use of methylprednisolone pulses, increase in disease activity and damage accrual were predictive of infections, whereas antimalarial use was protective against them in SLE patients. [ABSTRACT FROM AUTHOR]

Antiphospholipid syndrome (APS) is characterized by arterial and/or venous thrombosis, pregnancy morbidity and persistent antiphospholipid antibodies (aPL).[8] Patients with APS still develop significant morbidity and mortality despite treatment, as shown in a 10-year multicentre prospective European study of 1000 patients. Development and initial validation of a damage index (DIAPS) in patients with thrombotic antiphospholipid syndrome (APS). [Extracted from the article]

The objective of this work was to determine markers of endothelial cell activation in valves from patients with antiphospholipid syndrome (APS) and heart valve involvement, in order to establish a role for endothelial cells in the pathogenesis of the valvular disease. Sixteen valves from ten patients with APS, obtained from autopsies or removed during valve replacement, were studied. Two groups of valves were used as controls. One group included seven normal valves from patients who died from non-cardiac diseases. The other group of valves were obtained from patients with bacterial endocarditis during autopsies or valve replacement operations. Immunoperoxidase and immunofluorescence stainings with antibodies to human immunoglobulins, endothelial cells, α[sub 3] β[sub 1] integrin, collagen IV, laminin and fibronectin were employed.Three histopathological patterns were apparent: normal valves, valves with verrucous endocarditis and valves with fibrocalcific changes. In all the valves with verrucous endocarditis the following findings were observed: (1) increased expression of the α[sub 3] β[sub 1] integrin on the endothelial cells, (2) increased amount of collagen IV, laminin and fibronectin, (3) proliferation of blood vessels and (4) linear subendothelial deposition of immunoglobulins and complement. The valves with fibrocalcific changes were deformed and showed a thick layer of collagen IV, laminin and fibronectin, yet in two valves the indothelial cells showed an expression of the α[sub 3] β[sub 1] integrin. The control valves did not express the integrin and had only a thin subendothelial band of collagen IV.In valves from patients with APS,[sup 1] markers of endothelial cell activation are upregulated while the inflammatory exudate is scant. There is also a prominent deposition of immunoglobulins in the valves from patients with APS, suggesting a possible association between the deposition of the antibodies and the activ... [ABSTRACT FROM AUTHOR]

Two complete years of operation of two grid-tied PV facilities is presented. Energetic and economic performance of both installations has been compared. Located in the same place, the installation of these facilities followed the same construction criteria - PV panels, panel support system and wiring - and the facilities are exposed to the same atmospheric temperature and solar radiation. They differ with regard to their inverter topology used: one facility uses a central inverter and the other a string inverter configuration. The performance of the facilities has been determined using a procedure based on a small number of easily obtained parameters and the knowledge of the analyzed system and its operation mode. Electrical losses have been calculated for both systems and a complete comparison between them has been carried out. The results have shown better performance for distributed system in economic and energetic terms. [ABSTRACT FROM AUTHOR]

Introduction: There is a strong link between female sex hormones and sleep. This implies the existence of sex differences both in the structure of sleep as in the incidence of various sleep disorders., Aim: To review the changes in the pattern of sleep experienced by women along different stages of their life cycle (fertile period, menstruation, pregnancy, menopause and postmenopause), as well as the most frequent sleeping pathologies in which there exist more gender differences (insomnia, obstructive sleep apnea syndrome, restless legs syndrome and narcolepsy)., Development: About normal sleeping has been reported a higher quality of it, in women compared with men (increased sleeping time, reduced sleep onset latency, and a greater efficiency of sleeping), but they frequently complain of sleep problems. Moreover, different stages in the life of women are associated with significant physiological and hormonal changes that favour the disruption of normal sleep pattern and by this way, possibly, increase risk to suffer sleep disorders., Conclusions: The reasons that underlie in gender differences in sleeping disorders are attributed to differences in normal sleep pattern, in the clinical manifestations and risk factors for sleep disorders, and in the results and optimal dose of treatments.

Introduction: Antiphospholipid syndrome (APS) is a systemic autoimmune disease, associated not only with a hypercoagulable state and recurrent fetal loss but with many diverse clinical manifestations including heart involvement, neurological manifestations, as well as skin, kidney and hematologic abnormalities. Cardiac manifestations include coronary by-pass graft and angioplasty occlusions, cardiomyopathy, cyanotic congenital heart disease, intracardiac thrombus and complications of cardiovascular surgery. The valvular heart disease was defined as Libman-Sacks nonbacterial endocarditis. Previously, we have shown a linear subendothelial deposition of anti-cardiolipin/beta2 glycoprotein I (beta2GPI) antibodies in the valve specimens derived from APS patients. The involvement of complement C3c in the pathogenesis was documented. We assessed the beta2GPI-related target epitope recognized by the anti-beta2GPI Abs on the valves., Materials and Methods: In order to find the beta2GPI-related target epitopes recognized by the anti-beta2GPI antibodies on the valves, we used beta2GPI-related synthetic peptides. The presence of anti-beta2GPI Abs on the studied valves was detected by anti-idiotypic antibody, followed by immunoperoxidase analysis. Biotin attached to the N-terminal of beta2GPI-related synthetic peptides and control peptide were used to identify the epitope addressed by the anti-beta2GPI Abs deposited on the patient's valve. The binding was probed by streptavidin-peroxidase and appropriate substrate. The specificity was confirmed by competition assays with control peptide and anti-idiotypic antibody., Results: Among the beta2GPI-related synthetic peptides, two peptides were found in previous studies to mimic common pathogens either bacteriae or viruses, which raised a possible infectious origin for APS. One of these peptides, TLRVYK, is a specific target for anti-beta2GPI Abs deposited on the APS valves. This synthetic peptide was able to displace the anti-anti-beta2GPI anti-idiotypic Abs for binding the anti-beta2GPI Abs on the valve by a competition assay., Conclusion: We point to the possibility that Libman-Sacks nonbacterial endocarditis may have an infectious origin.

The results of prospective large cohort studies of patients with different clinical subsets of APS have been reported recently. A significant impact of the disease on long-term survival has been documented in these studies. Cumulative irreversible damage secondary to thrombosis results in organ dysfunction and morbidity. To assess prognosis and treatment in APS, it is imperative to quantify damage. We have recently created and validated an Antiphospholipid Damage Index, which is currently undergoing improvements. Having APS, whether primary or secondary, definitely confers a poor prognosis.

A growing body of evidence suggests that aPL are not only serological markers of the antiphospholipid syndrome (APS), but may also directly contribute to the development of thrombosis and other manifestations, including the APS vasculopathy. The latter has been documented in leptmeninges, lung, skin, myocardium, peripheral arteries, and kidney. Renal lesions, a common feature of primary antiphospholipid syndrome (PAPS), include occlusion of principal renal arteries or their main branches, TMA, cortical ischemia, and renal vein thrombosis. Within the cardiac manifestations associated with aPL, valvular involvement is the most common. Histologic findings in valve specimens are consistent with a noninflammatory lesion characterized by intravalvular capillary thrombosis, laminar or verrucous superficial thrombosis, vascular proliferation, fibrosis, and calcification. Even though there is general consensus that endothelial damage triggers the chain of events that results in valve thickening, fusion, rigidity, and ultimately functional abnormalities, we believe that more experimental work remains to be done on the initial valve insult in APS.

APS is found in 20% to 35% of patients with SLE. PAPS and secondary APS have similar features and aPL specificities. The clinical course of the secondary syndrome is independent of the activity and severity of lupus, but the presence of APS worsens the prognosis of patients with lupus. Some features of SLE may result from thrombosis in patients with APS; thus, these patients require anticoagulation rather than corticosteroids. Novel preliminary classification criteria for APS were formulated during a postconference workshop held in Sapporo, Japan, following the Eight International Symposium on Antiphospholipid Antibodies. Treatment of APS remains empirical because of limited controlled prospective data. There is strong evidence that patients with aPL-associated thrombosis are subject to recurrences and require prophylactic therapy. APS is a treatable cause of recurrent fetal loss in women with SLE. The treatment of choice is anticoagulation with heparin, either standard unfractionated heparin or LMWH. One of the main reasons for the improving outcomes in APS pregnancies is closer obstetric surveillance.