The aim of this study was to evaluate health-related quality of life (HR-QOL) in patients with primary Sjögren's syndrome (pSS) using both Short-Form 36 (SF-36) and World Health Organization Quality of Life Assessment-BREF (WHOQOL-BREF) questionnaires and to determine the effects of anxiety and depression on HR-QOL using the Hospital Anxiety-Depression Scale (HADS). In this cross-sectional study, 107 female patients with pSS (mean age 54.10 ± 10.2 years), fulfilling US-European Consensus Criteria and 109 female controls (mean age 53.4 ± 10.9 years) were included. Student's t test, Mann-Whitney U test, and analysis of variance (ANOVA) were used for statistical analysis. P values > 0.05 were accepted as significant. All domains of the SF-36, with the exception of "Vitality", and all domains of the WHOQOL-BREF with the exception of "Environment", were significantly lower in pSS patients compared with healthy controls. In pSS patients having anxiety according to HADS, the scores of all domains of WHOQOL-BREF were significantly lower, and in patients having depression according to HADS, three of four domains of WHOQOL-BREF were significantly lower compared with the rest of the group. However, the scores of two domains of the SF-36, namely "Role-Physical" and "Role-Emotional" domains, were significantly higher in pSS patients having depression according to HADS. We confirmed the presence of impaired HR-QOL in pSS. Whereas the presence of anxiety and/or depression generally showed a negative affect on HR-QOL, interestingly, depression seemed to improve the scores of "Role-Physical" and "Role-Emotional" domains of the SF-36. This surprising finding might be related to adaptation to changing health. Social support based upon cultural traditions might also have contributed.

Smoking is well known to contribute to the pathogenesis and severity of some systemic autoimmune rheumatic diseases and especially to the production of certain autoantibodies. Primary Sjögren's syndrome (pSS) is an autoimmune disease, affecting primarily the exocrine glands. It may also cause extraglandular involvement in some cases. In this study, we aimed to determine the frequency of smoking habits in our cohort of pSS patients and to investigate whether the frequencies of autoantibody positivity and extraglandular involvement were significantly different between patients with and without smoking. In this cross-sectional study, 207 patients with pSS (F/M 203/4), fulfilling the United States-European Consensus Criteria, and 602 healthy controls (F/M 534/68) were included. Patients and controls were classified into five groups: never smokers, current smokers, former smokers; ever smokers, and passive smokers. The χ(2) and Kruskal-Wallis tests were used for statistical analysis; a p value of less than 0.05 was accepted as statistically significant. While the frequency of current smokers was significantly lower in the pSS group compared with the healthy controls (11.6 vs 22.3%), the frequencies of former smokers (30.4 vs 11.8%), ever smokers (42.0 vs 34.1%), and passive smokers (47.3 vs 37.5%) were significantly higher in the pSS group compared with the healthy controls. In pSS patients, only antinuclear antibody (ANA) positivity was significantly associated with smoking habits, while there was no significant association with other autoantibodies or with the presence of extraglandular involvement. We found that in pSS patients smoking was significantly associated only with ANA positivity. Unlike the deleterious effects of smoking upon disease severity and anti-cyclic citrullinated protein (CCP) antibody production in rheumatoid arthritis, we could not find any association of smoking with extraglandular involvement and/or anti-Ro/anti-La antibody positivity in pSS. These results are indeed in line with the limited number of previous studies reported in the literature. Further studies with higher numbers of pSS patients are required to confirm the seemingly negative association of smoking with pSS.

A possible relationship between Takayasu arteritis (TA) and tuberculosis (TB) has been suggested. An increased frequency of tuberculin skin test (TST) was observed in TA patients. Quantiferon-TB Gold test (QFT) is a new in vitro assay measuring interferon-gamma response to M. tuberculosis antigens and helpful in diagnosing latent TB infection. The aim of this study was to investigate latent TB infection among TA patients by the use of both TST and QFT Gold test. Ninety-four (male/female: 7/87) TA patients fulfilling ACR 1990 TA criteria from three different university hospitals in Turkey and 107 control subjects without inflammatory diseases were included in the study. Data about medical history (TA and TB) were collected for both groups. TST and QFT were performed. TST values > or =5 mm for TA patients and > or =15 mm for controls was accepted as TST positivity. Even though TA group was older (40 +/- 12 vs. 32 +/- 8, P < 0.001), there was no significant difference between TA patients and controls regarding demographic characteristics. Six TA patients and one control had a history of previous TB infection (P = 0.054). Although TST positivity was higher in TA group [55 patients (62.5%) vs. 24 controls (41.4%), P = 0.008], QFT positivity was similar between two groups [21 patients (22.3%) vs. 24 controls (22.4%), P > 0.05]. QFT was negative in two of six TA patients with previous TB history. Rate of latent TB infection in TA patients measured with QFT is no more than controls. QFT seems to be a good and favorable test compared with TST in detecting LTBI in TA.

No abstract

Spinal new bone formation is a major but incompletely understood manifestation of ankylosing spondylitis (AS). We explored the relationship between spinal new bone formation and ultrasound (US)-determined Achilles enthesophytes to test the hypothesis that spinal new bone formation is part of a generalized enthesis bone-forming phenotype. A multicenter, case control study of 225 consecutive AS patients and 95 age/body mass index (BMI) matched healthy controls (HC) was performed. US scans of Achilles tendons and cervical and lumbar spine radiographs were obtained. All images were centrally scored by one investigator for US and one for radiographs, blinded to medical data. The relation between syndesmophytes (by modified Stoke Ankylosing Spondylitis Spine Score (mSASSS) and the number of syndesmophytes) and enthesophytes (with a semi-quantitative scoring of the US findings) was investigated. AS patients had significantly higher US enthesophyte scores than HCs (2.1(1.6) vs. 1.6(1.6); p = 0.004). The difference was significant in males (p = 0.001) but not in females (p = 0.5). The enthesophyte scores significantly correlated with mSASSS scores (ρ = 0.274, p < 0.0001) with the association even stronger in males (enthesophyte scores vs. mSASSS ρ = 0.337, p < 0.0001). In multiple regression analysis, age, BMI, enthesophyte scores and disease duration were significantly associated with syndesmophytes in males, and keeping all other variables constant, increasing US enthesophyte scores increased the odds of having syndesmophytes by 67%. Male AS patients that have more severe US-determined Achilles enthesophyte also associated spinal syndesmophytes suggesting a bone-forming gender-specific phenotype that could be a useful marker predicting of new bone formation.

Smoking is well known to contribute to the pathogenesis and severity of some systemic autoimmune rheumatic diseases and especially to the production of certain autoantibodies. Primary Sjögren's syndrome (pSS) is an autoimmune disease, affecting primarily the exocrine glands. It may also cause extraglandular involvement in some cases. In this study, we aimed to determine the frequency of smoking habits in our cohort of pSS patients and to investigate whether the frequencies of autoantibody positivity and extraglandular involvement were significantly different between patients with and without smoking. In this cross-sectional study, 207 patients with pSS (F/M 203/4), fulfilling the United States-European Consensus Criteria, and 602 healthy controls (F/M 534/68) were included. Patients and controls were classified into five groups: never smokers, current smokers, former smokers; ever smokers, and passive smokers. The χ(2) and Kruskal-Wallis tests were used for statistical analysis; a p value of less than 0.05 was accepted as statistically significant. While the frequency of current smokers was significantly lower in the pSS group compared with the healthy controls (11.6 vs 22.3%), the frequencies of former smokers (30.4 vs 11.8%), ever smokers (42.0 vs 34.1%), and passive smokers (47.3 vs 37.5%) were significantly higher in the pSS group compared with the healthy controls. In pSS patients, only antinuclear antibody (ANA) positivity was significantly associated with smoking habits, while there was no significant association with other autoantibodies or with the presence of extraglandular involvement. We found that in pSS patients smoking was significantly associated only with ANA positivity. Unlike the deleterious effects of smoking upon disease severity and anti-cyclic citrullinated protein (CCP) antibody production in rheumatoid arthritis, we could not find any association of smoking with extraglandular involvement and/or anti-Ro/anti-La antibody positivity in pSS. These results are indeed in line with the limited number of previous studies reported in the literature. Further studies with higher numbers of pSS patients are required to confirm the seemingly negative association of smoking with pSS.

It has been well known that anti-TNF drugs might increase lymphoma risk in rheumatoid arthritis (RA), where the rate of lymphoma has already been increased. However, unlike RA, an increased rate of lymphoma has not been reported in ankylosing spondylitis (AS). Hereby, we present a case with AS developing Hodgkin's lymphoma (HL) following 6 months of etanercept treatment. Pathological analysis revealed mixed cellular type of HL. Although we report a single case, it should be kept in mind that anti-TNF drugs might cause lymphoma development not only in RA, but also in AS.

Using Doppler echocardiography (DE), we measured pulmonary arterial systolic pressure (PASP) in rheumatoid arthritis (RA) patients without coexisting cardiopulmonary diseases. Accepting the normal upper limit of PASP as 30 mmHg, we found elevated PASP in 11 out of 40 (27.5%) RA patients, values being mostly 30-40 mmHg, indicating mild pulmonary hypertension (PHT). Although estimation of PASP by DE is not as reliable as cardiac catheterisation, it is possible that mild elevations in PASP may contribute to the high incidence of cardiovascular events not explained by traditional cardiac risk factors in patients with RA. Long-term follow-up will be obviously necessary to ascertain the impact of mild PHT on the prognosis and mortality rate of RA patients.