Neurologic involvement as first sign of Behcet's syndrome.
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Biomedical subjects
Publications and source records attributed to C Salvarani.
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OBJECTIVE: 38 untreated patients suffering from rheumatoid arthritis (RA) were studied to evaluate the relationship between serum sIL-2R levels and laboratory and clinical indexes of disease activity and circulating lymphocyte subpopulations. Furthermore, we serially analyzed the correlation between the clinical response to oral gold (Auranofin) treatment and serum sIL-2R levels in 28 RA patients. METHODS: Patients received a complete rheumatological examination at entry and every 3 months during the study. A complete biochemical analysis was executed every month. Serum sIL-2R levels were evaluated before entering and at the 3rd and 6th month by ELISA: Phenotype analysis of peripheral blood mononuclear cells was performed by a two-color technique using the association of specific monoclonal antibodies. Samples were analyzed by a FACS-scan 440 cytofluorimeter with a single Argonion laser. RESULTS: Serum sIL-2R were significantly higher in RA patients than in controls and had a significant negative correlation with disease duration and a positive correlation with serum IgG and C3 levels. A significant positive correlation was found between serum sIL-2R levels and circulating CD3 + HLADR+, CD3-HLADR+ and CD20 + CD5-cells. After 6 months of auranofin therapy no differences in serum sIL-2R in comparison with basal levels were found in either responders or in non-responders. CONCLUSION: Serum sIL-2R level is not a good index of activity in RA patients and is not a useful marker of response to AU therapy.
Low molecular weight IgM (LMW IgM), the monomeric subunit of pentameric IgM, was measured in the serum of 27 patients with primary Sjögren's syndrome. LMW IgM was also measured in a control group consisting of 24 patients with psoriatic arthritis (PA) and 8 patients with active rheumatoid arthritis (RA). LMW IgM was found in the majority of patients with primary SS (63%) and those patients had a longer disease duration than those without SS (80.7 +/- 43.9 months vs 37 +/- 18.3, p = 0.01). Although the differences were not significant, SS patients with LMW IgM showed higher rates of: seropositive disease (71% vs 50%), anti-Ro (59% vs 30%) and anti-La antibodies (12% vs 0%), extraglandular involvement (76% vs 60%) and raised gammaglobulins levels (47% vs 30%) compared to those without LMW IgM. Our only two patients with active RA and vasculitis had LMW IgM. None of the patients with PA showed LMW IgM, regardless of their Kammer subgroup classification, disease activity or radiological evidence of erosions. The presence of LMW IgM in a high percentage of patients with primary SS appears to be the expression of a dysregulation of B cell state that may predispose these patients to developing malignant lymphoproliferation.
We present an additional case of focal myositis which, after surgical excision of the muscular mass, did not evolve to generalized polymyositis. To our knowledge immunological evaluations of this disease have never before been carried out. Immunohistochemical analysis of the muscular mass showed the presence of activated endothelial cells, CD4 and macrophage cells in the perivascular and endomysial areas, suggesting an immune-mediated mechanism of muscular damage. At the same time the normal distribution of the peripheral blood lymphocyte subpopulations and the normal levels of serum IL-1 beta, IL-6, TNF-alpha, soluble IL-2R and soluble CD8 underline the non-systemic nature of the disease.
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OBJECTIVE: Evaluation of serum concentrations of chemotactic cytokines (chemokines) in patients with polymyalgia rheumatica at disease diagnosis and during a six-month period of corticosteroid treatment. METHODS: Sera were obtained from patients at the time of PMR diagnosis and subsequently after one week, two weeks, one month, three months and six months. At each time point a clinical and laboratory evaluation was performed. Serum concentrations of IL-8, GRO alpha, RANTES, MCP-1, and MIP1 alpha were evaluated by commercial ELISA kits. RESULTS: Only RANTES serum levels were significantly higher in PMR patients than in controls. No correlation was found between RANTES concentrations and laboratory and clinical features. Chemokine levels reached their lowest level after one month of steroid treatment and remained in the normal range thereafter. CONCLUSIONS: The production of RANTES is enhanced in untreated PMR patients; corticosteroid treatment results in a normalization of chemokine levels.
Patients are said to have inflammatory spinal pain if they fulfill at presentation 4 of the following 5 criteria: duration of spinal discomfort for at least 3 months, spinal morning stiffness, age less than 40, insidious onset of symptoms, and no relief from pain with rest, but improvement with exercise. Inflammatory spinal pain is typical of the spondylarthropathies. Only in a minority of the cases it is found in other rheumatic disorders such as rheumatoid arthritis, fibromyalgia or infectious spondyilitis. Tuberculous spondylitis is rarely mentioned as a possible cause of inflammatory spinal pain. We describe 4 patients with tuberculous spondylitis seen over a 3-year period who met the clinical criteria for inflammatory spinal pain at presentation. We conclude that inflammatory spinal pain may be a presenting feature, albeit rare, of tuberculous spondylitis. Awareness of this finding should help facilitate the proper diagnosis and the institution of appropriate therapy.