Malignant neoplasms in autoimmune rheumatic diseases: examination of the risk of developing a malignancy among five different rheumatic diseases in one institution.

Relationships between autoimmune rheumatic diseases and malignant neoplasms have been discussed, but there is no study of the different rheumatic diseases examining the risk of developing cancer. Our study has examined probabilities for developing malignancy among patients with connective tissue diseases seen in a single institution. Patients with autoimmune rheumatic disease and malignancy were compared with patients with the same autoimmune rheumatic diseases without malignancy. All cases identified through record-linkage from 1964 to 1996 were selected. Four controls per case were randomly selected from a pool of 3228 patients. The rheumatic diseases considered were rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), primary Sjögren's syndrome (pSS), dermatomyositis-polymyositis (DM-PM), and systemic sclerosis (Scl). The statistical analysis was conducted by conditional logistic regression, testing rheumatic disease as main effect. We identified 72 cases and 288 controls. Fifty-three of the cases had solid tumors, and 19 had lymphoproliferative neoplasms. The risk of developing a malignancy was considerably higher in DM-PM than in SLE (odds ratio [OR] = 17.5, 95% confidence interval [CI] 4.1-75.7), in pSS than in SLE (OR = 5.7, 95% CI 2.2-15.1), and in Scl than in SLE (OR = 5.4, 95% CI 1.6-18.0). These risks persisted after controlling for rheumatic disease duration, the time the disease was active, and anti-rheumatic treatment. RA had an OR of 1.8 (95% CI 0.9-3.4) with respect to SLE. This is the first study which describes the magnitude of risks among rheumatic diseases associated with the probability of developing a malignant neoplasm whether lymphoproliferative or solid. The risks in this series depend on the primary rheumatic disease, with DM-PM, pSS, and Scl all having greater risk than SLE.

Objective and subjective sleep disturbances in patients with systemic lupus erythematosus.

OBJECTIVE: To assess objective and subjective evidence of sleep disorders in patients with systemic lupus erythematosus (SLE) and to examine correlations between parameters of lupus activity, depression, and sleep disturbances. METHODS: Fourteen SLE patients and 11 normal control subjects of similar age underwent all-night polysomnography on 3 consecutive nights. The patients and controls were also evaluated for daytime sleepiness by the Multiple Sleep Latency Test and completed a sleep disorders questionnaire and the Beck Depression Inventory. RESULTS: The polysomnographic data showed that sleep in SLE patients was characterized by respiratory and movement disorders. These intrinsic primary sleep disorders are related to the symptom of restless, poor sleep at night. Lupus patients were more sleepy during the day, and their sleepiness was related to sleep fragmentation, with more arousals and stage transitions than the control group. Disease activity was associated with decreases in sleep efficiency and delta sleep and with increases in sleep fragmentation. Depression was not correlated with the activity of the disease. CONCLUSION: There is an enhanced presence of sleep disorders in patients with SLE. The most frequent primary sleep disorders are respiratory and movement disorders.

Genetic analysis of the contribution of IL10 to systemic lupus erythematosus.

OBJECTIVE: To study the contribution of the IL10 gene to the susceptibility to systemic lupus erythematosus (SLE). METHODS: Analysis by fluorescent-semiautomated genotyping of a dinucleotide repeat located in the promoter region of the IL10 locus (microsatellite G). RESULTS: No significant difference was found in the frequencies of the microsatellite alleles of 330 Mexican patients with SLE compared to 368 controls from the same population. Two-point linkage analyses were carried out using 13 Mexican, 13 Swedish, and 8 Icelandic families with 2 or more cases with SLE. No linkage was revealed between IL10 and SLE, using a variety of parameter settings. CONCLUSION: Our results do not support that the IL10 gene contributes to the susceptibility to SLE in the populations we studied.

A comparison of genome-scans performed in multicase families with systemic lupus erythematosus from different population groups.

Systemic lupus erythematosus is a disease of unknown etiology. Multiple genetic factors are believed to be involved in its pathogenesis. In addition, and due to genetic heterogeneity, these factors and/or their combinations may be different in different ethnic groups, while some might be shared between populations. We have performed genome scans in multicase families from three different population groups, two from Northern Europe, with a high degree of homogeneity, and the third from a recently admixed population of Mexican Mestizos. Although our family material is relatively small, the results presented here show that using family sets from well defined populations are sufficient to detect susceptibility loci for SLE. Our results also reveal the chromosomal regions most likely to contain susceptibility genes for SLE.