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Background Alexithymia is considered as a reduced capacity to be aware of, to clearly recognize, and to define one’s feelings with a limited fantasy and a concrete, externally oriented cognitive style. Some studies have stated that alexithymia is more common in systemic lupus erythematosus patients (SLE) than in general population but there is a paucity of studies in such context. Aim To study the prevalence of alexithymia in a sample of SLE patients looking for associated epidemiological and clinical findings and its relationship to quality of life. Methods Cross-sectional study in 93 SLE patients collecting clinical, epidemiological, and serological data, data on quality of life by 12 item short health survey (SF-12), and alexithymia by Toronto scale (TAS-26). Disease’s cumulative damage was measured by Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage index. Results In this sample (90.3% females and median age of 46 years), 55.9% had alexithymia; 22/92 (23.9%) did not and 19/93 (20.4%) had inconclusive results. Alexithymia presence had a positive association with age ( p = 0.01) and a negative association with presence of glomerulonephritis (25% vs 59%; p = 0.005) and glucocorticoid use (19.2% vs 59.0%; p = 0.0007). A negative correlation of TAS-26 was observed with mental domain of ( r = −0.46; p < 0.0001) and physical domain ( r = −0.32; p = 0.004) of SF-12, but not with cumulative damage index. Conclusion We found a high prevalence of alexithymia in this sample of SLE patients that negatively associated with quality of life, but not with cumulative damage index.

Background Cognitive dysfunction (CD) is frequently found in patients with systemic lupus erythematosus (SLE) and contributes to impairment in the patient’s quality of life. Aim To study CD in a sample of patients and the possible associations with cumulative damage, disease activity, clinical/serological profile, and cumulative glucocorticoid dose. Methods Included in this study are 103 patients with SLE and 95 controls for cognitive performance through MoCA (Montreal Cognitive Assessment) and MMSE (Mini-Mental State Examination). Disease activity was measured by SLEDAI (Systemic Lupus Erythematosus Disease Activity Index) and cumulative organ damage by SLICC/ACR/DI (Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index). CES-D (Center for Epidemiological Studies-Depression) scale was used to evaluate depression. Data on clinical and serological profile, treatment, and cumulative glucocorticoid dose were also collected. Results Patients with SLE had worse performance in the MoCA ( p = 0.009) and MMSE ( p = 0.01) than controls. The MoCA results showed that visuospatial and abstraction domains ( p = 0.03 and p = 0.002, respectively) were impaired, and the MMSE results showed that language and spatial orientation were reduced ( p = 0.002 and p = 0.01, respectively) when compared to controls. Both questionnaires (MoCA with r = −0.29 and MMSE r = −0.21) correlated negatively with SLICC/ACR/DI and the MoCA with SLEDAI (r = −0.22). No associations were found with cumulative glucocorticoid dose, degree of depression, and clinical or serological profile. Conclusions According to the MoCA, visuospatial cognition and abstraction were impaired, and according to the MMSE, spatial orientation and language were impaired in patients with SLE. The CD was correlated with cumulative damage and disease activity. These findings demonstrate that both disease-activity and disease-injury associated CD is found broadly in SLE patients in a Brazilian population, supporting the prior reports of CD in other regional SLE populations.

Background Systemic lupus erythematosus (SLE) may have a different serological and clinical profile according to age of disease onset. Aim To compare clinical presentation and serological data from patients with SLE onset in childhood (cSLE) with disease onset in adulthood (aSLE) in a sample of Brazilian patients. Methods Retrospective study of 614 SLE patients from a single Rheumatology Unit from Brazil: 77 (12.5%) cSLE and 537 (87.4%) aSLE. Clinical and serological data were obtained from the charts. Comparisons of cSLE with aSLE in general and according to patient’s gender were made. Results The comparison of whole sample showed that children had more malar rash (p = 0.04), seizures (p Conclusion Children had a higher frequency of severe manifestations (glomerulonephritis and central nervous system) than adults. The difference in glomerulonephritis occurrence disappeared when only males were compared.

The complement system contributes to the pathogenesis of systemic lupus erythematosus (SLE). Mannose-binding lectin (MBL) is a key molecule of the lectin pathway of complement and seems to be related to the clinical manifestations of this disease. We evaluated the serum levels of MBL and its relationship with disease onset and clinical findings in SLE patients. Serum samples were analysed in 195 patients and 145 healthy controls from southern Brazil. Patients with high MBL levels (above 2000 ng/ml) showed a significant increase in the frequency of thrombocytopaenia ( p = 0.007; OR = 2.71; 95% CI = 1.32–5.55); and seizures ( p = 0.034; OR = 2.61; 95% CI = 1.07–6.37). A positive correlation between disease activity and MBL levels (>2000 ng/ml; p = 0.031, rho = 0.279) as well as of MBL concentration with accumulated organ damage ( p = 0.021; rho = 0.232) was observed. Our results suggest a role for MBL in the development of clinical manifestations such as thrombocytopaenia and seizures in SLE patients. These findings corroborate the participation of the lectin pathway of complement in the pathophysiologic mechanisms underlying clinical manifestations of SLE.

Background Patients with systemic lupus erythematosus (SLE) may form clusters with clinical manifestations and autoantibodies. Objective The objective of this report is to study whether SLE patients with positive rheumatoid factor (RF) have a special clinical and/or serological profile. Methods A retrospective study of 467 SLE patients seen at a single rheumatology unit was conducted. Epidemiological data (age, gender, age at disease onset, ethnic background and tobacco use), clinical data (malar rash, photosensitivity, oral ulcers, discoid lesions, serositis, glomerulonephritis, convulsions, psychosis, hemolytic anemia, leukopenia, lymphocytopenia, arthritis and hypothyroidism) and serological profile (anti-dsDNA, anti-Ro/SS-A, anti-La/SS-B, anti-RNP, anti-Sm, IgG aCL, IgM aCL, lupus anticoagulant, direct Coombs and RF) were collected. Patients with positive and negative RF were compared. Results RF was found in 24.9% of the sample. In univariate analysis, RF was positively associated with butterfly rash ( p = 0.04), anti-Ro ( p = 0.03), anti-Sm antibodies ( p = 0.01) and hypothyroidism ( p = 0.01) and negatively associated with glomerulonephritis ( p = 0.003). Logistic regression showed that only glomerulonephritis ( p = 0.03; OR = 0.45; 95% CI = 0.21–0.93) and anti-Ro ( p = 0.009; OR = 2.3; 95% CI = 1.24–4.57) were independent associations. Conclusion In our sample RF was associated with protection from glomerulonephritis and with higher prevalence of anti-Ro antibodies.

Background B factor (BF) from the alternative complement pathway seems to participate in the pathophysiology of systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Objective To study the allotypic variability of BF in SLE and their associations with clinical and autoantibodies profile. Methods BF allotypes were determined by high-voltage agarose gel electrophoresis, under constant cooling, followed by immunofixation with anti-human BF antibody, in 188 SLE patients and 103 controls. Clinical and serological data were obtained from medical examination and records. Results No significant differences of BF variants between patients and controls were found, neither in relation to epidemiologic or clinical manifestations. Associations of phenotype BF SS07 and allotype BF*S07 were found with anticardiolipin IgM (aCl-IgM) antibodies ( p = 0.014 and p = 0.009 respectively), but not with aCl-IgG, lupus anticoagulant (LA), anti β2GPI or clinical APS. A significant decrease in BF*F allotype ( p = 0.043) and BF SF phenotype ( p = 0.018) was detected in patients with anti-phospholipid antibodies as a whole (aCl-IgG, aCl-IgM, LA and anti β2GPI). Conclusions There is a link between phenotype BF SS07 and allotype BF*S07 with aCl-IgM in SLE patients; BF*F allotype could be considered a marker of protection against the development of antiphospholipid antibodies in these patients.