Iloprost is effective for the short-term palliation of severe Raynaud phenomenon in patients with systemic sclerosis.

No abstract

A patient with seropositive rheumatoid arthritis developed ascites while taking weekly doses of methotrexate (MTX). Her serum transaminase and albumin levels were normal. A liver biopsy revealed chronic hepatitis with bridging fibrosis and piecemeal necrosis. Upon discontinuation of MTX, her ascites resolved, and her arthritis became more active. This is the third report of reversible hepatic decompensation associated with prolonged MTX therapy in patients with rheumatoid arthritis.

LETTERSthe IgG galactose deficiency seen in rheumatoid arthritis and in a relatively small number of patients with systemic lupus erythematosus (SLE) and Crohn's disease as evidence that changes in carbohydrate are merely a consequence of chronic inflammation.We have set out at some length (2) the arguments for the view that structural changes involving galactose in the Fcy oligosaccharides are restricted to certain diseases. In particular, we have determined the percentage of IgG oligosaccharide chains lacking galactose in over 300 patient sera representing 25 different disease states, and concluded that the galactose glycosylation defect is confined to juvenile and adult rheumatoid arthritis, SLE associated with Sjogren's syndrome, active Crohn's disease, and untreated pulmonary tuberculosis (3). Normal galactose values were obtained not only in SLE uncomplicated by symptoms of Sjogren's disease, but also in primary Sjogren's syndrome, ankylosing spondylitis, psoriatic arthropathy, myositis, scleroderma, leprosy, Klebsiella infection, and other disorders. These findings have recently been confirmed using a novel lectinbinding assay (4). Thus, the data from our laboratories show that this intriguing defect is not a characteristic feature of the chronic inflammatory state in general, but has important associations with certain diseases.The authors' earlier comments concerning decreased lymphocytic galactosyltransferase were prophetic (5).

In 28 serum and plasma samples from patients with systemic lupus erythematosus, we examined the importance of antibody class with respect to complement-mediated binding to human red blood cells (RBC) of antibody/DNA immune complexes (IC) prepared with anti-DNA antibodies. We used both 3H-double-stranded DNA and 3H-single-stranded DNA (ssDNA). Generally, double-stranded DNA IC showed considerably higher binding than did ssDNA IC in the RBC binding assay. Further analysis indicated that although ssDNA IC fix complement, it is necessary that these IC contain IgM anti-DNA antibodies in order for them to bind to RBC. The results suggest that the mechanisms of clearance and pathogenic potential of these IC may depend upon both the DNA conformation and antibody class. In particular, complement-fixing IC which contain IgG anti-DNA antibodies and ssDNA may not be cleared via the erythrocyte clearance mechanism, and therefore, Address reprint requests to Ronald P. Taylor, PhD, Department of Biochemistry, University of Virginia School of Medicine, Charlottesville, VA 22908.Submitted for publication March 19, 1986; accepted in revised form September 10, 1986. could be more likely to deposit in certain tissues and initiate inflammatory reactions.The results of extensive studies from a number of different laboratories indicate that complementfixing (CF) IgG antibody/double-stranded DNA (dsDNA) immune complexes (IC) play a significant role in the pathogenesis of systemic lupus erythematosus (SLE) (1-5). Although it is also believed that IC containing single-stranded DNA (ssDNA) may contribute to the pathogenesis of SLE (6,7), studies of these IC have been less frequent. This is because antibodies to dsDNA are more specific for SLE (3,8,9). In fact, care has often been taken to ensure that the DNA antigen used in SLE studies is not contaminated with ss regions (9-11). However, it has been demonstrated that IC prepared with ssDNA, and SLE sera containing anti-DNA antibodies, do fix complement, as defined by immune hemolysis techniques (12).Recently, Cornacoff and colleagues' findings in baboons (13) have raised considerable interest in the role of red blood cells (RBC) in the clearance of CF IC from the circulation. Their studies indicate that injected CF bovine serum albumin (BSA)/anti-BSA IC rapidly bind to the complement receptors of the baboon RBCs and are then taken to the liver, where the IC (but not the RBC) are removed from the circulation. In vitro studies (14) have shown that C F antibody/dsDNA IC also bind to the C3b receptors of human RBC, so it is likely that a similar clearance mechanism is operative in humans. The recent finding of a reduction in either the number of RBC C3b receptors or in their IC binding capacity, in ICmediated diseases such as SLE and rheumatoid arthri-