We examined the effectiveness of 2 models of arthritis self-care intervention, the home study model and the small group model. The effects of disease diagnosis and duration, self-care behavior, perceived helplessness, social support, treatment choice, and formal education level on outcomes among persons with arthritis who participated in these programs were evaluated. A pretest-posttest control group design was utilized in the initial experimental study; comparison group designs were used in the longitudinal studies. Three hundred seventy-four subjects completed the interventions and 12 months of research followup. We found that the intervention models had a statistically significant positive impact on arthritis knowledge, selfcare behavior, perceived helplessness, and pain. These findings did not vary when the effects of education level, disease diagnosis and duration, informal social support, and treatment choice were controlled.

The clinical and serologic characteristics of 17 patients with onset of systemic lupus erythematosus (SLE) after age 50 were compared with those of 49 younger patients. All patients were followed prospectively for a mean duration of 47 months. A clinical and serologic data base was established for each patient, and information collected at each visit to a lupus clinic was analyzed by computer. The clinical features distinguishing old-age SLE were a low incidence of significant renal disease and prominent pleuropericarditis and arthritis throughout the period of followup. Serologic abnormalities were milder in older patients. Thus, hypocomple-

Serologic studies were performed on 25 patients with systemic lupus erythematosus (SLE) during 29 acute episodes of central nervous system (CNS) disease. Increased anti-DNA antibody and decreased total serum hemolytic complement activity were observed only in those patients with associated extra-CNS disease manifestations. Patients with isolated CNS disease were otherwise in apparent clinical and serological remission regarding these two indices. No special association of cold-reactive IgM antilymphocyte antibodies was demonstrable in patients with ongoing CNS injury. Of special interest was an increased incidence of anti-Sm antibodies in the patients with CNS dysfunction relative to that in a large group BRUNNER, and DAVID KOFFLER of patients without neuropsychiatric disease. The incidence of anti-RNP was not increased.The data do not support direct involvement in SLE brain injury of either DNA/anti-DNA complexes or of lymphocytotoxic antibodies cross-reactive with brain cells, but do suggest an association of anti-Sm with CNS disease in this disorder.The pathogenesis of neuropsychiatric manifestations of systemic lupus erythematosus (SLE) has not been clearly defined. The enigma of central nervous system (CNS) injury contrasts with the considerable evidence implicating immune complexes as mediators of tissue injury in glomerulonephritis in SLE (1). Previous investigation of the mechanisms involved in brain injury has assumed an analogy with glomerulonephritis. Efforts directed toward complement (2-4), immunoglobulin (4,5), and anti-DNA or DNA/anti-DNA immune complex (4,6,7) determinations in cerebrospinal fluid have yielded conflicting data and have failed to establish clearly defined pathogenetic factors. The frequent absence of gross changes in cerebrospinal fluid protein and of pleocytosis (4,8,9) suggests that any abnormalities, if present, may be subtle.Distinctive serologic indices have not been identified, although little information is available in this area. Of interest is a recent demonstration of free DNA in the plasma of patients with CNS disease (lo), an observation suggesting participation of unusual antigen excess DNA/anti-DNA complexes in brain injury. Direct at-

The complement mediated binding of prepared antib~dy/~H-dsDNA immune complexes to the red blood cells obtained from a number of patient populations has been investigated. Patients with solid tumors have binding activity similar to that seen in a normal group of individuals. However, a significant fraction of patients with systemic lupus erythematosus, rheumatoid arthritis, and hematologic malignancies have lowered binding activity compared with normal subjects. Quantitative studies indicate the lowered activity probably arises due to a decrease in complement receptors on the respective red blood cells. The potential importance and implications of these findings are briefly discussed. It is well established that complement-fixing antibody/dsDNA immune complexes play a key role in the pathogenesis of SLE (17,18). We have previously performed quantitative experiments (5-8) which demonstrate that large, soluble antibody/dsDNA immune complexes bind to the CR, receptors of normal human