Immune function in SLE is paradoxically characterized by active T cell help for autoantibody production, along with impaired T cell proliferative and cytokine responses in vitro. To reconcile these observations, we investigated the possibility that the accelerated spontaneous cell death of SLE lymphocytes in vitro is caused by an activation-induced cell death process initiated in vivo. 27 SLE patients, three patients with systemic vasculitis, seven patients with arthritis, and 14 healthy subjects were studied. Patients with clinically active SLE or systemic vasculitis had accelerated spontaneous death of PBMC with features of apoptosis at day 5 of culture. A prominent role for IL-10 in the induction of apoptosis was observed, as neutralizing anti-IL-10 mAb markedly reduced cell death in the active SLE patients by 50%, from 22.3 Ϯ 5.2% to 11.2 Ϯ 2.8%, and the addition of IL-10 decreased viability in the active SLE group, but not in the control group, by 38%. In addition, apoptosis was shown to be actively induced through the

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Despite the fact that nonmotor symptoms (NMS) like gastrointestinal (GI) complaints are frequently reported in Parkinson’s disease (PD), no therapeutic guidelines are available. This study aimed to manage some lower GI-NMS in a group of patients with PD. A total of 40 patients (17 males, 23 females; mean age 76.05±2.09 years) were randomly selected for this study. Patients were confirmed to have PD (modified Hoehn–Yars scale: 2.075±0.4) who had undergone levodopa or dopamine agonist treatment. In the non-motor symptoms questionnaire (NMS-Quest), regarding GI complaints, the following were recorded: abdominal pain, bloating, and constipation of mild-to-moderate severity. Laboratory studies, abdominal ultrasound, and upper and lower digestive endoscopies were performed to rule out organic issues. All patients increased their water intake to 2 L/d and alimentary fiber to 20–25 g/d. Twenty patients received trimebutine 200 mg three times daily half an hour before meals. The other 20 patients received probiotics (60 mg per-tablet of two lactic bacteria: Lactobacillus acidophilus and Bifidobacterium infantis), 2×/d, 1 hour after meals for 3 months along with the reassessment of GI complaints. Our results demonstrated that there were significant statistical differences in all assessed symptoms in the first group: 1.55±0.51 vs 0.6±0.5 (P<0.0001) for abdominal pain; 1.6±0.5 vs 0.45±0.51 (P<0.0001) for bloating; and 1.5±0.51 vs 0.85±0.67 (P=0.0014) for constipation with incomplete defecation. The second group displayed statistical differences only for abdominal pain 1.45±0.51 vs 1.05±0.69 (P=0.00432) and bloating 1.4±0.5 vs 0.3±0.47 (P<0.0001). For constipation with incomplete defecation, there was a slight improvement. Thus, there was no significant statistical difference: 1.35±0.49 vs 1.15±0.49 (P=0.2040). In conclusion, lower GI-NMS are frequently present, isolated or associated with other autonomic issues, even before the diagnosis of PD. Treatment with probiotics could improve abdominal pain and bloating as much as with trimebutine, but less for constipation with incomplete evacuation, where trimebutine showed better results.

Objective. To determine the frequencies and clinical associations of antiribosomal P antibodies (anti-P) in a large multiethnic cohort of patients with systemic lupus erythematosus (SLE), and to assess whether anti-P was associated with any major histocompatibility complex (MHC) class I1 alleles or shared amino acid sequences.Methods. Sera from 394 SLE patients were studied for anti-P using an enzyme-linked immunosorbent assay, and MHC class I1 alleles (HLA-DRB1, DQA1, and DQBl) were determined by DNA oligotyping.Results. Anti-P antibodies were found in 13-2W of patients in the majority of ethnic groups, but were perhaps more frequent in Chinese patients (36%) and less common in Bulgarian patients (6%). Neuropsychiatric lupus (psychosis and/or depression) was significantly associated with anti-P. The HLA-DR2, DQ6 haplotypes DRB1*1501 or *1503, DQA1*0102, and DQB1*0602 were increased in anti-P-positive whites, blacks, and Mexican Americans. The HLA-DQB1*0602 allele showed the strongest association with anti-P when these 3 ethnic groups were combined and compared with both race-matched anti-P-negative SLE patients and normal controls. The HLA-DQS specificity (DQB1*0302) was increased both in whites and in Mexican-Americans with anti-P who were negative for HLA-DQB1*0602, and perhaps also increased in Greeks, but not in blacks, in whom HLA-DQB1*0301 was increased. A shared amino acid sequence in HLADQBl (at position 26 of leucine and position 30 of tyrosine) was strongly associated with anti-P positivity (70%) versus anti-P negativity (42%) across ethnic lines.Conclusion. The anti-P response in SLE patients, occurring in -15% of patients, was strongly influenced by certain MHC class I1 alleles and was correlated with diffuse neuropsychiatric dysfunction.