Differentiating persistent from self-limiting symmetrical synovitis in an early arthritis clinic.

Early rheumatoid arthritis (RA) must be differentiated from benign self-limiting polyarthritis because of the risks associated with treatment of RA. Conventional, widely available clinical and laboratory variables, measured at first clinic visit, were studied for their ability to predict persistence in 112 patients with up to 6 months of joint symptoms. Those 65 patients with symmetrical peripheral polyarthritis were followed for 1 year: 36 who underwent spontaneous remission were classified self-limiting synovitis (SLS); the remaining 29 were termed persistent synovitis (PS). Univariate analysis suggested more severe disease in PS at presentation but showing considerable overlap with SLS, making clinical discrimination difficult. Multivariate analysis confirmed this overlap but identified a subset of most helpful variables. The RA latex was the most powerful variable, yet accounted for only 45% of the variability in outcome. Combining a positive RA latex with an ESR > 30 mm/h carried a relative risk for PS of 4.33, with specificity 94% but sensitivity only 69%. Self-limiting synovitis initially could not be distinguished from early RA: hence RA may exist in two forms, the traditional persistent form and a less well recognized abortive form.

Immunodeficiencies associated with sulphasalazine therapy in inflammatory arthritis.

Abnormalities in serum immunoglobulin levels (Igs) are documented in a series of 350 patients with rheumatoid arthritis (RA) and other inflammatory joint diseases treated with sulphasalazine (SASP) for up to 10 years. Low Ig levels occurred in just over 10% of patients after therapy. Three per cent developed selective IgA deficiency between 8 and 20 weeks after starting SASP. Low IgG levels occurred in 2% at 4-52 weeks and low IgM levels in 5% after 3-7 months. One per cent developed panhypogammaglobulinaemia (hypo gamma) 3-7 months after commencing therapy. Most immunodeficiencies were not accompanied by other toxic reactions and SASP was continued in all but one patient with a rash and thrombocytopenia. A good clinical response was observed in most patients particularly those with selective IgA deficiency and hypo gamma. Two patients with hypo gamma developed chest infections which responded to antibiotics. A low level of individual Igs is not usually an indication to stop SASP unless accompanied by other reactions. Panhypo gamma is potentially serious and should be monitored carefully and replacement therapy should be considered in these patients if infections occur.

Sulphasalazine in rheumatoid arthritis: haematological problems and changes in haematological indices associated with therapy.

This prospective study documents the haematological responses in 300 rheumatoid patients (RA) treated with sulphasalazine (SASP) for between 1 and 9 years. It also examines the effect of SASP on the total white cell and platelet counts over 2 years in relation to disease activity in 80 RA patients. Neutropenia occurred in six (2%) (three severe--neutrophil count less than 0.8 X 10(9)/l) after 3 and 12 weeks. The drug was withdrawn in six immediately and in one patient after 21 months when the neutrophil count fell to 0.7 X 10(9)/l. An additional 11 (3.7%) developed mild or transient leucopenia between 2 weeks and 24 months, and eight continued therapy. Thrombocytopenia occurred in one patient at 18 weeks associated with other reactions. Four with Felty's syndrome developed a further fall in the total WBC associated with thrombocytopenia in two. A rise in mean cell volume was common (72%), and macrocytosis (MCV greater than 98 fl) occurred in 27 (9%). Macrocytic anaemia was rare (less than 1%). All haematological problems were reversible. In 80 patients treated with SASP for 2 years there was a significant fall in the median white cell and platelet counts at 3 months associated with improvement in disease activity.