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Cytotoxic therapy, especially with cyclophosphamide in the dose 8–20 mg/kg used as intermittent pulses, has been shown to improve both patient and renal survival in systematic lupus erythematosus (SLE), but to date there is no cure for the disease. Owing to the paucity of recognisable clones, the rationale and goal of cytotoxic immunosuppressive therapy in the treatment of immune-mediated diseases as against malignancies is to suppress the aberrant inflammation and immune-mediated reactions responsible for tissue damage, without dangerously suppressing the normal host defence mechanism(s). We report the case of a patient suffering from SLE with nephritis who has remained in sustained remission over the past 8 years without any maintenance therapy following an accidental administration of a single dose of 5000 mg of intravenous cyclophosphamide (44.2 mg/kg body weight). The patient recovered fully from pancytopenia following the injection. Presently, she is asymptomatic and working gainfully. Her laboratory parameters including blood counts, urine analysis, FANA and anti-dsDNA have reverted to normal. Cyclophosphamide in the dose of 30–160 mg/kg has been safely and effectively used in various neoplastic conditions with the aim of destroying every possible tumour cell. The experience of the present case suggests that such an approach may be applicable to SLE. [ABSTRACT FROM AUTHOR]

Two dimensional echocardiography with doppler examination was performed in 54 patients with systemic lupus erythematosus (SLE). Nine (17%) had significant cardiac involvement (four left ventricular hypertrophy, one moderate pericardial effusion, one severe aortic regurgitation, and three ventricular systolic dysfunction). We further studied diastolic function in 45 patients who did not have a major abnormality in echo. SLE was graded as active in 16 patients (SLEDAI>5) and inactive in 29 patients. Twenty age- and sex-matched subjects acted as controls. The data were compared using one way ANOVA test. Patients with active disease had significant diastolic dysfunction compared to inactive patients and controls as indicated by increased peak A (P<0.01) and decreased E/A ratio (P<0.01). There was no linear correlation between disease activity and diastolic dysfunction if SLEDAI was considered as a continuous variable (r=0.29 for E/A). Anticardiolipin antibodies (both IgG and IgM) were elevated in five patients (13 studied). One of them had severe mitral regurgitation, one had trace mitral and aortic regurgitation and one had diastolic dysfunction. We conclude that asymptomatic diastolic dysfunction is present in SLE patients. [ABSTRACT FROM AUTHOR]