Dr Saedis Saevarsdottir and Prof

Dr Saedis Saevarsdottir and Prof. (95% CI 3.80, 6.54). Four SNPs were associated with PF in RA: rs35705950 [(mucin 5B) gene [10C13], but several other genes involving host defence, cellCcell adhesion, signalling and telomere maintenance have been associated with IPF [10C12, 14, 15]. The association between the promoter variant and ILD in RA patients has been confirmed with similar point estimates for risk as for IPF in the general population [16]. In addition, a study using exome sequencing has identified 13 heterozygous mutations in the coding regions of and as associated with ILD in RA [17]. Predictive factors for the development of PF in RA have been reported to be similar to those for IPF and ILD in general, e.g. male sex, age and tobacco smoking [18], in addition to RA-related factors such as positive RF and/or ACPAs and disease activity [19C21]. In this study we aimed to evaluate the development BMS-509744 of PF in relation to the previously identified gene loci for IPF in our inception cohort of patients with early RA followed prospectively within the catchment area of northern Sweden. The impact of disease-related factors was also evaluated in relation to PF. Materials and methods Subjects and collection of clinical data An inception cohort of patients diagnosed with early RA according to the American College of Rheumatology Classification Criteria [22] were analysed in this study. The patients with early RA (symptomatic 12?months before diagnosis) were consecutively included in the study at the time BMS-509744 of RA diagnosis (index date) between 1 January 1996 and 31 December 2016 at any of the five rheumatology clinics in northern Sweden. They were simultaneously included in the Swedish Rheumatology Quality Register (SRQ) [23]. Clinical data, e.g. the 28-joint DAS (DAS28) [24] and starting and ongoing pharmacological treatment, were registered. These data were systematically recorded at baseline and at 6, 12, 18 and 24?months after diagnosis and thereafter at all clinical visits. Data on smoking habits were collected at inclusion (the index date) and previous and current smoking was registered as smoking ever non-smoking. BMI (in m/kg2) was also recorded. ACPAs were analysed in plasma samples collected at baseline (the index date) and preserved at ?80 C until analysed using the anti-CCP2 test (Euro Diagnostica, Malm?, BMS-509744 Sweden), as previously described [25]. RF was assessed at baseline using routine laboratory methods. Radiographs of the lungs were obtained at baseline as part of the clinical routine in 95% of the cases. Thereafter, radiological examinations were performed in patients presenting any symptoms of cough, dyspnoea or chest pain and before initiating biologic DMARDs (bDMARDs). If there was any sign of pathology around the routine plain X-rays, clinically suspected pulmonary involvement or other clinical indication of ILD, high-resolution CT (HRCT) was performed. At the index date, 83 (7%) of the RA patients had a pulmonary diagnosis: asthma in 55 (4.7%), chronic obstructive pulmonary disease (COPD) in 22 (1.9%), both diagnoses in 3 and a diagnosis of bronchiectasis, chronic bronchitis or pleura plaque in 3. In 2016 the patients completed a questionnaire regarding disease progression and the incidence of lung involvement, e.g. self-reported symptoms of cough, dyspnoea or chest pain. The answers to the questionnaires were validated by reviewing the patients medical records and analysing the radiological examinations of the lungs. In this study of the originally recruited RA patients with DNA collected at baseline, 1184 were eligible, although 66 patients (5.6%) declined to participate by not answering the questionnaires. Consequently they were excluded and their hospital records were not examined, resulting in 1118 patients remaining for the analysis of PF. Since their inclusion in the study, 157 patients have died and BMS-509744 therefore did not answer the questionnaire. For these individuals, medical records were reviewed and the radiological examinations Rabbit Polyclonal to ZNF682 were analysed. The results of the X-rays and HRCT examinations were reassessed at the end of the follow-up by an experienced pulmonologist. The diagnosis of PF was based on the results of HRCT, with the exception of five patients for whom the PF diagnosis was based on the routine plain X-ray examinations. The HRCT findings defined as PF were reticular pattern, honeycombing or traction bronchiectasis of variable degree and with BMS-509744 ground-glass in a few cases [26]..