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Interstitial keratitis and vestibuloauditory symptoms (vertigo and hearing loss) are the typical signs of Cogan's syndrome, a rare inflammatory vascular disease. Signs of vasculitis in many organ systems may appear, among which neurologic problems are sometime predominant. The efficacy of glucocorticoids on the ocular and systemic symptoms is established, but their effect on hearing loss is unknown. We describe a case of Cogan's syndrome with neurological involvement in which early treatment with combination therapy (prednisolone and cyclosporin) failed to bring ear inflammation under control.

Objective: To identify the time point of the greatest degree of improvement in daily living activities, pain and depression in patients with osteoarthritis (OA) of the knee during 6 months of treatment with NSAIDs, in order to define compliance and drop-out rate., Methods: 107 patients were recruited into a multicentre, prospective, randomized, controlled trial comparing two treatments, piroxicam-beta-cyclodextrin (PBCD) and slow release diclofenac (DCL)., Results: The greatest improvement in quality of life occurred in both groups after 3 months, with a slight further gain observed by the end of treatment. The Stanford Health Assessment Questionnaire score improved (p < 0.05 vs baseline) at 3 and 6 months with PBCD and at 6 months with DCL. The Arthritis Impact Measurement Scale score improved (p < 0.05 vs baseline) after 6 months in both groups. Significant (p < 0.05 vs baseline) improvement in other psychological and pain scores were recorded in both groups after 3 and 6 months. Compliance with treatment at 3 months was 73% for PBCD and 72% for DCL, and was 60% in both groups at 6 months., Conclusions: The results of this study indicate that the optimal length of time for an NSAID trial in OA patients is 3 months, when assessment of daily living activities is considered as the main outcome criterion.

Objective: To verify the distribution of different types of beta 1 integrin on the plasma membrane of chondrocytes and to correlate the pattern of integrin expression to the severity of osteoarthritis (OA)., Methods: The articular cartilage of ten OA patients who had undergone surgical knee replacement for "genu varum" were studied. The cartilage was separated into three zones that macroscopically and microscopically showed a decreasing degree of anatomic lesions. After enzymatic digestion, the isolated chondrocytes were immediately challenged with monoclonal antibodies against the beta 1, alpha 1-6 and alpha v chains. The phenotypic study was paralleled by a cell cycle analysis performed by flow cytometry on chondrocytes stained with propidium iodide., Results: Chondrocytes isolated from the articular cartilage of osteoarthritic patients expressed, in different percentages, all the alpha chains (alpha 1-6 and alpha v) of the beta 1 integrins. The alpha chain most frequently expressed was alpha 1, followed by alpha 3, alpha 5, alpha 2 and alpha v, with lesser amounts of alpha 4 and alpha 6. The beta 1 chain was expressed (on average) on the 40% of the chondrocytes regardless of the zone they were isolated from. Differential phenotypic analysis of the three zones showed that beta 1 integrins correlate inversely with the severity of the anatomic lesions and the cycle phase of the chondrocytes (the G0/G1 phase prevailed in the anatomically normal cartilage of the least damaged zone, and the S-phase in the most damaged zone)., Conclusions: This study provides evidence of the existence of beta 1 integrins on the surface of chondrocytes from human OA cartilage, all of the alpha chains being represented, although in different percentages. Moreover, an inverse correlation was demonstrated between the severity of the anatomical changes found in the zones and the phenotypic/metabolic changes of the cells. These results, together with the well known inside-out signaling function of the adhesion molecules, highlight the key role of matrix interactions in the pathogenesis of the anatomic changes in OA.

We studied interleukin-10 (IL-10) levels in the blood and synovial fluid (SF) of 15 patients with RA and in the blood of 15 healthy donors (HD). RA IL-10 levels were significantly higher in SF than in blood (p = 0.001) and did not correlate with the disease activity nor with the therapy. RA patients showed significantly reduced blood IL-10 levels compared to the HD (p = 0.002), suggesting that IL-10 synthesis is depressed in RA. Since IL-10 has anti-inflammatory properties, reducing pro-inflammatory cytokine release by monocytes and down-modulating T cell function, its defect in RA may play a role in perpetuating RA synovitis.

Objective: To evaluate the cell surface expression of cell membrane-bound peptidases CD10 and CD26 on osteoarthritic (OA) chondrocytes, correlating it with the cell cycle phase and with the severity of OA lesions found in different load zones of the cartilage from human knees., Methods: Chondrocytes freshly isolated from three different load zones of cartilage, obtained from 10 OA patients undergoing surgical knee replacement, were analyzed for the expression of CD10 and CD26 and for their cell cycle phase by flow cytometry. Statistical analysis was carried out using the multifactorial analysis of the variance with the LSD (least square difference) range test. The Chi square test was used to compare the cell cycle phases., Results: Analysis of the chondrocyte cell cycle showed a significantly high proportion of cells in the S-phase in the maximum load zone in comparison with the minimum load zone (p < 0.001); the percentage of resting cells (G0/G1 phase) was significantly higher in the minimum load zone than in the maximum load zone (p < 0.001). The expression of CD10 and CD26 on chondrocytes was significantly reduced in the maximum load zone of the cartilage and was directly related to the progressive worsening of osteoarthritic lesions., Conclusions: These data demonstrate, for the first time, that articular chondrocytes express on their surface CD10 and CD26 peptidases. Neprilysin 3.4.24.11 (CD10) and dipeptidyl peptidase IV 3.4.14.15 (CD26) have been shown to play a specific role in the control of growth and differentiation of many cell types by cleaving growth factors able to promote cellular proliferation. Our results indicate that CD10 and CD26 are down-regulated in the maximum load zone of the knee OA cartilage: this condition may allow the increase of local levels of growth factors causing chondrocyte activation. Furthermore, as CD26 mediates cell binding to fibronectin and collagen, its reduction in osteoarthritic cartilage may reflect a perturbation of chondrocyte interactions with the extracellular matrix.

Objective: Rheumatic diseases are a group of systemic disorders that may be concurrent with Raynaud's phenomenon and involvement of the internal organs, in particular the esophagus. Esophageal motor abnormalities have been widely described in systemic sclerosis, but have not frequently been reported in other diseases. In the present study we have examined the prevalence and pattern of esophageal motility disorders in different rheumatic diseases., Methods: Esophageal manometry was performed on 150 patients, 21 males and 129 females, suffering from different rheumatic diseases (SSc, RA, SLE, MCTD, undifferentiated CTD, or DM/PM) and on 30 healthy controls., Results: Functional involvement of the esophagus was demonstrated in all the rheumatic diseases considered, although at varying percentages. The frequencies of the functional abnormalities differed when each disease was considered separately. In SSc patients abnormalities were found more frequently in the lower esophageal sphincter (81.8%) and in the esophageal body (84.8%); data for the DM/PM and MCTD patients broadly overlapped. On the contrary, in SLE the lower sphincter appeared to be less (or even not at all) impaired, while the most specific disorder was an isolated abnormal peristalsis. RP did not always correlate with manometric changes in all of the groups studied., Conclusions: Three conclusions derive from our study: i) motor disorders affecting the esophagus were not only found in SSc, but also in all forms of non-lupus CTD; ii) the simultaneous involvement of the esophageal body and the lower esophageal sphincter is discriminant between non-lupus CTD and SLE; and iii) RP may be regarded as a condition pathogenetically unrelated to manometrically detected esophageal motor abnormalities.

The occurrence of certain antibacterial antibodies was studied in the sera of 22 healthy donors (HD) and 66 patients with different diseases. The cases investigated included 22 rheumatoid arthritis (RA), 22 non-arthritic-psoriasis (NAP), and 22 psoriatic arthritis (PA) patients. A complement fixation test was used with Yersinia enterocolitica 0:3 type (YEC), Yersinia pseudotuberculosis (YPT), Campylobacter jejuni (CJ), and Campylobacter fetus (CF) antigens; the detection of anti-Chlamydia trachomatis (CT) antibodies was carried out using an immunoperoxidase colorimetric slide test that allowed the detection of isotypes of specific antibodies. It was found that the synthesis of anti-CF, CJ, YEC, and YPT antibodies in NAP patients does not differ significantly from that of the HD group; on the contrary, the antibody levels were statistically higher in PA than in the other disease groups or in the healthy controls, although only anti-CF antibodies seemed to significantly differentiate (p = 0.000003) the PA group from the others. Anti-CT IgA antibody titers were found to be significantly higher in the PA as well as in the RA groups when compared with the controls, while the antibody levels in NAP patients showed no clear-cut difference with respect to those of either the arthritic patients or the healthy controls. By showing that anti-enterobacterial antibodies are increased in PA but not in NAP patients, our data furnish additional support to the thesis of a pathogenic role of bacterial infections in psoriatic arthritis.