The aim of our study was to analyse the serum interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interferon-gamma (IFN-gamma) levels in patients with AS and their relationship with disease activity. An ELISA test was used to analyse serum cytokine (IL-6, TNF-alpha, IL-1 beta and IFN-gamma) levels in 69 patients with AS. Results were compared with those from 43 patients with RA and 36 patients with non-inflammatory back pain. The relationship between serum concentrations of the different cytokines and parameters of disease activity and severity in AS patients was also evaluated. IL-6 and TNF-alpha serum levels, but not IL-1 beta and IFN-gamma, were significantly higher in AS than in NIBP. However, patients with RA showed higher serum levels of IL-6, TNF-alpha and IFN-gamma than both AS and NIBP patients. In AS, IL-6 correlated with clinical parameters of disease activity with significant correlation being observed with laboratory parameters of inflammation such as ESR, CRP, platelet count and clinical parameters of severity such as vertebral mobility. TNF-alpha did not correlate with laboratory or clinical parameters of activity. Macrophagic cytokines (TNF-alpha and IL-6), are increased in AS patients and IL-6 closely correlated with the activity of the disease.

Between April 1982 and March 1984 7 pathologically confirmed cases of progressive multifocal leukoencephalopathy (PML) were diagnosed at our institution. Only 1 case had been seen in the preceding twenty years. Four patients had acquired immunodeficiency syndrome (AIDS). The others had chronic lymphocytic leukemia, Hodgkin's lymphoma, and systemic lupus erythematosus. All patients presented with progressive neurological deficits. In most, the initial computed tomographic (CT) scan was disproportionately less abnormal than the clinical findings. In 5 patients the first CT scan revealed hypodensities of the cerebral white matter which lacked mass effect and did not enhance with contrast agent. The lesions were observed to enlarge progressively on CT scans but often lagged behind the rate of clinical evolution. Although 3 patients were treated with cytosine arabinoside, none improved. PML had similar clinical, radiographic, and pathological features in the AIDS and non-AIDs patients. Of 79 AIDS patients cared for at our institution between December 1979 and December 1983, 3.8% had PML. PML should be suspected in AIDS patients in the presence of the characteristic CT features, especially when CT-clinical dissociation occurs.

In a 36‐month period, 240 patients at our institution received kidney transplants from cadaver donors. Cyclosporin A (CsA) was used as the initial immunosuppressive therapy. Seven patients (5 men and 2 women) developed severe pain, periarticular soft tissue swelling with no effusion, and vasomotor changes in affected areas. Although articular mobility was conserved, most of the patients had great difficulty in walking. A patchy osteoporotic pattern was seen radiographically and increased uptake of 99mtechnetium with a periarticular distribution in the clinically affected areas were found. All of these symptoms and radiographic and scintigraphic signs are compatible with definite reflex sympathetic dystrophy syndrome (RSDS). Articular symptoms began within 3 months after kidney transplantation in all patients; all but 1 patient had plasma CsA levels >200 ng/ml at that time. When the dosage of CsA was reduced, there was concomitant improvement in the RSDS, which appeared when the plasma CsA levels declined to <200 ng/ml. The mean duration of the clinical symptoms of RSDS was 8 months. We believe RSDS should be added to the list of complications that may appear in kidney transplant patients who receive CsA treatment.

Interleukin 1-beta (IL-1 beta), IL-2, IL-4, IL-5, IL-6, IL-8, tumour necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta) and granulocyte-macrophage colony-stimulating factor (GM-CSF) gene expression was determined in knee synovium of 16 patients with rheumatoid arthritis (RA) and 16 patients with seronegative spondyloarthropathies (SSP), by using polymerase chain reaction (PCR) amplification. The pattern of cytokines observed in RA synovium is of the macrophage-fibroblast type, with the highest expression of IL-1 beta and TGF-beta. GM-CSF and IL-2 bands were visualized in a minority of patients. Neither IL-4 nor IL-5 could be detected. No significant differences were observed in the cytokine profile between patients with early (< 12 months) and more advanced disease. No differences were observed according to gender, age, rheumatoid factor status and the duration of knee synovitis. The pattern of cytokines in the synovium of SSP patients is similar to that observed in RA patients and does not change in relation to disease duration. IL-2 was the only T-cell cytokine observed. These data provide evidence that the macrophage-fibroblast cells have an important role in early and more advanced rheumatoid synovitis, and show that this is also true for SSP peripheral synovitis.

In a case-controlled study, serum creatinine kinase (CK) activity was significantly lower in 40 patients with RA than in 40 age- and sex-matched patients with non-inflammatory arthropathies [mean 37.6 (S.D. 29.2) vs 77.7 (S.D. 45.3) IU/l respectively P < 0.0001]. In contrast, serum levels of aldolase and myosin were not significantly lower in RA patients. A significant inverse correlation between CK activity and ESR, CRP and platelet count was observed in RA. There was also a positive correlation between haemoglobin levels and CK values. No correlation was found between CK activity and a meager mass index, disease duration and radiological erosion. No inhibitor of CK activity in the sera of RA patients was found. CK serum activity was markedly reduced in RA, and is related to the inflammatory activity of the disease. This finding may stimulate further exploration on the effect of inflammatory response in muscle metabolism.