Amyloid arthritis associated with IgM kappa lymphoplasmacytoid lymphoma.

Amyloid arthritis is an uncommon cause of locomotor disease and may closely resemble RA. Macroglobulinaemia is rarely associated with amyloidosis and there has been only one report of amyloid arthritis in this setting, the patient having had Waldenstrom's macroglobulinaemia. We report the occurrence of amyloid joint disease in the course of an IgM kappa B-cell dyscrasia which evolved over 16 years to an overt lymphoplasmacytoid lymphoma.

Arthritis artefacta: factitious disease in rheumatology.

Self-induced disease can be difficult to diagnose and costly of time and money to investigate. The key is to think of the possibility. Five patients in whom the evidence for factitious rheumatological illness was strong are discussed and their histories, physical signs and family backgrounds are explored in relationship to factitious disease presenting in other fields. Young immature individuals seem most at risk and the discrepancy between physical signs and understandable pathological mechanisms may suggest the diagnosis. The outlook seems frequently poor.

C reactive protein and immunoglobulin G in synovial fluid and serum in joint disease.

C reactive protein (CRP) and immunoglobulin G (IgG) were measured in synovial fluid and serum of 72 patients (29 with rheumatoid arthritis (RA), 17 with osteoarthritis, 11 with crystal synovitis, seven with undifferentiated arthritis, and eight with seronegative arthritis). The synovial fluid:serum (SF:S) ratios were compared with those calculated from the SF:S ratios of transferrin, caeruloplasmin, and alpha 2 macroglobulin, using the binomial test within groups and the Mann-Whitney test between groups. In RA synovial fluid CRP concentrations were lower than expected and IgG concentrations higher than expected. In osteoarthritis CRP concentrations were higher than expected. In seronegative arthritis IgG concentrations were raised. The ratio of CRP:IgG was depressed in RA. These findings are consistent with a role for CRP in the inflammatory process of RA, while the CRP:IgG ratio may be of value in the differential diagnosis of joint disease.

Arthritis and coeliac disease.

We report six patients with coeliac disease in whom arthritis was prominent at diagnosis and who improved with dietary therapy. Joint pain preceded diagnosis by up to three years in five patients and 15 years in one patient. Joints most commonly involved were lumbar spine, hips, and knees (four cases). In three cases there were no bowel symptoms. All were seronegative. X-rays were abnormal in two cases. HLA-type A1, B8, DR3 was present in five and B27 in two patients. Circulating immune complexes showed no consistent pattern before or after treatment. Coeliac disease was diagnosed in all patients by jejunal biopsy, and joint symptoms in all responded to a gluten-free diet. Gluten challenge (for up to three weeks) failed to provoke arthritis in three patients tested. In a separate study of 160 treated coeliac patients attending regular follow up no arthritis attributable to coeliac disease and no ankylosing spondylitis was identified, though in a control group of 100 patients with Crohn's disease the expected incidence of seronegative polyarthritis (23%) and ankylosing spondylitis (5%) was found (p less than 0.01). Arthritis appears to be a rare manifestation of coeliac disease. This relationship may provide important clues to the role of gastrointestinal antigens in rheumatic diseases.

Twice-daily cimetidine does not increase gastric bacterial flora.

Thirty patients with peptic ulcer (20 duodenal, 10 gastric) underwent glucose-hydrogen (H2) breath tests before and after 6 weeks treatment with cimetidine, 400 mg twice daily. For the group as a whole, basal breath H2 and integrated H2 output over a 2.5 hr test period was unchanged by cimetidine treatment. We conclude that there was no evidence of significant gastric bacterial colonization following twice daily cimetidine treatment.

Mononuclear phagocytes in rheumatoid arthritis: Fc-receptor expression by peripheral blood monocytes.

Fc receptor expression by enriched monocytes from rheumatoid arthritis (RA) patients and age and sex matched controls (healthy subjects) was compared by measuring the uptake of IgG on monocytes in a competitive radioassay. The association constant (Ka) between IgG and the monocytes and the number of Fc binding sites per cell was calculated from Scatchard plots of 4 degrees C binding data. RA monocytes had increased expression of Fc receptors as compared with those of controls. This increase was particularly pronounced in those RA patients affected by extra-articular disease. There were significant correlations between the numbers of Fc receptors on monocytes and both C1q binding and anticomplementary activity but none between monocyte Fc receptor numbers and serum rheumatoid factors (IgG and IgM). It is considered that monocyte handling of circulating immune complexes is unimpaired in RA and that monocytes make an adaptive response to increased levels of immune complexes.

Indolent Wegener's granulomatosis.

Classical Wegener's granulomatosis is a relentlessly progressive and rapidly fatal disease. A pulmonary 'limited form' is associated with a much better prognosis. We report 3 cases of Wegener's granulomatosis which ran a prolonged indolent course despite major manifestations outside the lower respiratory tract and review the literature on survival.

Studies of mononuclear phagocyte function in the rat. I. Saturation and recovery following intravenous administration of soluble human serum albumin (HSA)--anti-HSA complexes.

We have attempted to demonstrate saturation of the mononuclear phagocyte system (MPS) in the Long Evans rat following intravenous administration of increasing doses of soluble HSA--125I-anti-HSA complexes. The fate of large (greater than 11S) complexes was followed by sucrose density gradient ultracentrifugation of serial serum samples in rats receiving 0.005-0.16 mg anti-HSA/g body weight. Administration of complexes provoked a rapid and profound increase in vascular permeability. Under these conditions no steady state clearance velocity for greater than 11S complexes could be established. The quantity of greater than 11S complexes removed from the circulation in the 1st hr never became independent of the initial dose. Specific immune complex uptake by the liver reached a maximum in rats receiving 0.09 mg anti-HSA/g body weight. Above this dose specific uptake decreased. Clearance of a tracer dose of complexes in rats pre-loaded with complexes containing 0.06 mg anti-HSA/g body weight was delayed for more than 3 hr. This was cautiously interpreted to indicate the period required for MPS recovery. The pattern of immune complex clearance in the context of marked changes in vascular permeability raised the possibility that maximum uptake was determined not by saturation of the mononuclear phagocyte system but by impaired hepatic perfusion.