Tumor necrosis factor alpha (TNF alpha) and interleukin-6 (IL-6) play a main role in inducing acute phase protein production by hepatocytes. This study describes the serum levels of TNF alpha and IL-6 in relation to serum levels of C-reactive protein (CRP) and alpha 1-acid glycoprotein (alpha 1AG) in three systemic lupus erythematosus (SLE) patients. Disease courses of these patients were divided in a total of 19 clinical periods, according to the clinical symptoms and interleukin profiles. Significantly elevated TNF alpha levels were found in all but three of the defined periods, without being associated with disease activity. In only four of the defined periods elevated TNF alpha were observed combined with elevated IL-6 and CRP levels. Two of these periods coincided with minor symptoms of SLE, one with an exacerbation and the other one with a systemic infection while SLE activity was low. All other periods showed varying combinations of elevated TNF alpha and/or IL-6 levels being followed or not by elevated CRP levels. Significantly raised alpha 1AG levels were measured in all clinical periods. In most of the observed periods a dissociation was found between TNF alpha and IL-6 and also between the different cytokine (TNF alpha and IL-6) levels and acute phase protein (CRP and alpha 1AG) levels. These data could not be explained by differences in disease course or influences of medication. We conclude that more factors other than TNF alpha and IL-6 must play a role in the regulatory pathway of the acute phase response in SLE.(ABSTRACT TRUNCATED AT 250 WORDS)

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Recently, an enzyme-linked immunosorbent assay (ELISA), using purified recombinant non-fusion proteins, has been introduced to detect and quantify Ro/SS-A and La/SS-B autoantibodies. We compared this method with anti-Ro/SS-A and anti-La/SS-B detection by means of counterimmunoelectrophoresis and immunoblotting in patients with primary Sjögren's syndrome (SS), patients suspected of the syndrome and controls. The sensitivity and specificity of the newly developed ELISA for anti-Ro/SS-A were 53% and 100%, respectively, and for anti-La/SS-B, 40% and 98%, respectively. No significant difference was found between these results and those obtained from both other assays. Titres of Ro/SS-A and La/SS-B autoantibodies correlated with the presence of an abnormal parotid gland sialogram and hypergammaglobulinaemia. We concluded that the new ELISA did not enhance the diagnostic yield in cases of suspicion of primary Sjögren's syndrome. Longitudinal studies of large groups of patients with primary Sjögren's syndrome are necessary to demonstrate whether following the course of the titres of these autoantibodies would be of value for prediction of disease exacerbations.