Vedat Inal

Cigarette smoking in primary Sjögren’s syndrome: positive association only with ANA positivity

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 χ2 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.

Primary Systemic Al Amyloidosis Presenting as Temporal Arteritis

Temporal arteritis is most common vasculitis in elderly and imitated by miscellaneous disorders. Temporal artery biopsy is the gold standard test in the diagnosis of giant cell arteritis (GCA). Hereby, we describe a case of a 67-year-old man who presented initially with temporal arteritis; however, a lip biopsy then revealed AL amyloidosis. In this respect, temporal artery biopsy should be performed for definitive diagnosis of GCA particularly patients with systemic symptoms and treatment resistant.

Frequency of pulmonary hypertension in transthoracic echocardiography screening is not increased in Takayasu arteritis: Experience from a single center in Turkey

Objective Pulmonary hypertension (PH) may occur in Takayasu arteritis (TA), mostly due to pulmonary arteritis, but also due to left heart disease and/or chronic thromboembolism (CTE). Using transthoracic echocardiography (TTE), we investigated the frequency of PH caused by pulmonary arteritis. Methods This cross-sectional study included 70 patients with TA fulfilling the 1990 ACR criteria, 68 healthy controls, and 67 patients with systemic sclerosis (SSc) fulfilling the 1980 ACR criteria representing the disease control group. Patients with severe left heart disease or CTE were excluded. The ESC-ERS guideline definition was considered for diagnosis of PH. Results The mean systolic pulmonary artery pressure (SPAP) values in TA, SSc, and healthy control groups were 20.93±6.06, 31.57±12.75, and 18.88±5.39 mmHg, respectively. While the SPAP values were similar between TA and healthy groups, the SPAP values in the SSc group were significantly higher than in other groups. Based on conventional and/or magnetic resonance angiography findings, pulmonary arteritis was present in 4 out of 70 TA patients; however, PH was not detected in any patients with TA, including those with pulmonary arteritis. Conclusion The TTE findings suggested that the frequency of PH was not increased in TA. However, a low frequency of pulmonary arteritis in our series might have affected our results.

Serum and bronchoalveolar lavage fluid nitric oxide levels in diffuse systemic sclerosis.

Dear Sir, DiVuse systemic sclerosis (SSc) is a multisystem disorder characterized by excessive Wbrosis in skin and various organs such as lungs, heart, gastrointestinal tract, and kidney. It is often complicated by interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH) which are major causes of mortality. Pathogenesis of SSc and lung involvement are still unclear but most accused mechanisms are autoimmunity and vascular endothelial cell damage [1]. Nitric oxide (NO) is an essential molecule in host defense and also an inXammatory mediator associated with various pathologies such as endothelial dysfunction [1, 2]. Although NO is indeed a vasodilatory agent, depending upon physiopathological situations, higher NO concentrations may also cause endothelial dysfunction/cell damage due to its role in oxidation. NO can be synthesized by diVerent kinds of cells, such as macrophages. We also know that lung macrophages obtained from SSc patients express a higher level of inducible nitric oxide synthase than those of healthy subjects [3]. There have been controversial Wndings as to whether serum NO levels are increased or decreased in SSc [4–8]. Standing from this point, we aimed to measure NO levels in serum and bronchoalveolar lavage (BAL) Xuid of SSc patients. Sixteen patients with diVuse SSc having pulmonary Wbrosis (F/M:14/2), who met the American College of Rheumatology criteria for SSc [9] were included the study. All patients undervent a high-resolution CT (HRCT) scan and carbon monoxide diVusion capacity (DLCO) of the lungs. As the disease control group, 4 (F/M:3/1) patients with idiopathic interstitial lung disease (ILD) were included in the study. Fifteen healthy controls were also included, only for serum NO measurements. Patients with lung diseases other than interstitial Wbrosis and/or treated with prednisolone >10 mg/day were excluded. Demographic and laboratory features were summarized in Table 1. Serum and BAL Xuid nitrate levels were determined spectrophotometrically, based on the reduction of nitrate to nitrite by reductase (EC.1.6.6.2), in the presence of NADPH. The oxidation of NADPH was recorded as the decrease in absorbance at 340 nm. Nitrite levels were measured by the Griess reaction [10] which was the simplest and most commonly used assay method. Measured NO level represented the sum of the nitrate and the nitrite levels. Statistical comparisons were performed using Mann– Whitney U-test. P values <0.05 were accepted as signiWcant (conWdence interval = 95%, = 0.05). Although serum and BAL NO levels in diVuse SSc were higher than idiopathic ILD, there was no signiWcant diVerence between these two groups (P > 0.05). However, serum NO levels in diVuse SSc and in idiopathic ILD were signiWcantly higher than healthy controls (P = 0.016). There was no statistically signiWcant correlation between DLCO and serum/BAL NO (for serum NO P:0.906, for BAL NO P:0.985). V. Inal · K. Aksu · G. Keser · E. Doganavsargil Department of Internal Medicine, Division of Rheumatology, Ege University School of Medicine, Izmir, Turkey