These data reinforce the role of oxidative stress and especially lipid peroxidation products in the progression of SLE disease.

The purpose of this study was to evaluate the effects of partial sleep deprivation (PSD) on circulating concentrations of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in relation to the secretory profiles of growth hormone (GH), cortisol, and testosterone during a repeated brief sprint interval exercise. Thirty healthy football players (mean age: 21.1 [range: 18-24] years; body mass index [BMI]: 22.6 [range: 18.47-24.46] Kg/m(2)) completed two test sessions at 08:00 h, one scheduled after a baseline night (bedtime: from 22:30 to 07:00 h) and the other after a PSD night caused by an early awakening (bedtime: from 22:30 to 03:00 h). During each session, participants performed 4 × 250-m run on a treadmill at a constant intensity of 80% of the personal maximal speed with a 3-min recovery in between. Tests session were performed at 08:00 h. Blood samples were collected before, immediately after the first and the fourth 250-m run, and 60 min after the exercise. The results showed that cortisol concentrations were not affected by the PSD. However, GH and testosterone concentrations were higher (p < .05) 60 min after the exercise during PSD in comparison with baseline. Likewise, plasma concentrations of IL-6 and TNF-α were higher (p < .05) after PSD during the exercise (i.e., the first and the fourth run) and remained elevated during the recovery period (i.e., 60 min after the exercise). In conclusion, these results showed that sleep restriction increases the proinflammatory cytokine, GH, and testosterone concentrations after physical exercise but did not affect the cortisol responses.

This study does not seem to confirm the described association of anti-P antibodies with neuropsychiatric manifestations of SLE. However, it supports the anti-P antibody association with arthritis and disease activity as well as the presence of aCL. Based on our study and other related studies, we propose that, akin to anti-Sm and anti-dsDNA, anti-P antibodies detected by one agreed method may be considered for inclusion as a criterion for the classification of SLE.

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Autoantibodies other than anti-desmoglein antibodies are not rare in pemphigus patients. Clinical and serological follow-up of pemphigus patients with positive autoantibodies are needed to clarify their impact in disease evolution.

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The aim of this study was to investigate the clinical significance of antinucleosome antibodies in Tunisian systemic lupus erythematosus (SLE) patients. IgG antinucleosome antibodies were detected by a qualitative enzyme immunoassay (immunodot) in the sera of SLE patients at onset of disease. The patients were divided into two groups according to the result of the antinucleosome antibodies test: positive (group A) and negative (group B). The two groups were also evaluated for clinical and biological parameters. Of 84 patients with SLE, 66 (78.6%) had antinucleosome antibodies. Among 21 patients negative for anti-double-stranded DNA (anti-dsDNA), 5 (23.8%) were antinucleosome positive. The most common initial features were haematological disorders (80.1%) and arthritis or arthralgias (79.8%). Renal disorders, observed in 59.5% of SLE patients, were more common in group A compared to group B (65 vs 38%) (p=0.04). The European Consensus Lupus Activity Measurement (ECLAM) mean score was higher in group A (6.42) than in group B (4.44) (p=0.002). Antinucleosome antibodies were positive in nearly one-fourth of SLE patients negative for anti-dsDNA. We found a correlation between antinucleosome antibodies, nephritis and SLE disease activity. Therefore, the determination of circulating antinucleosome antibodies could be a useful parameter for early diagnosis and follow-up of SLE patients.

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