Objective: The aim of this study is to assess the efficacy and safety of nintedanib (NTD) therapy in a real world population of patients with connective tissue diseases related interstitial lung disease (CTDs-ILD). Methods: Our multicenter retrospective study included patients with a CTD-ILD diagnosis who started NTD treatment due to the development of PPF during follow-up. The results of the percentage predicted forced vital capacity (%pFVC) and percentage predicted diffusion capacity (%pDLCO) of patients before NTD treatment and 6, 12 and 18 months after the start of NTD treatment were evaluated. In addition, the patients were divided into two groups, SSc-ILD and other CTDs-ILD, and compared in terms of the efficacy and safety of the NTD. Results: In all patients (n = 66), %pFVC and %pDLCO values stabilised after 6, 12 and 18 months compared to baseline values. All patients received at least one immunosuppressive therapy in combination with NTD treatment. The most common side effect after NTD treatment was diarrhoea (n = 20, 30.3%). When we divided the patients into two groups, SSc-ILD (n = 35) and other CTDs-ILDs (n = 31), no significant difference was found between the groups in the change in %pFVC (p values = 0.498, 0.595 and 0.376, respectively) and in the change in %pDLCO (p values = 0.817, 0.185 and 0.399, respectively) at 6, 12 and 18 months follow-up. Again, there was no statistically significant difference between the two groups in terms of adverse events and safety data after NTD treatment (p > 0.05). Conclusion: In summary, the use of NTD in combination with immunosuppressive therapies was effective and safe in SSc-ILD patients as well as in other CTDs-ILD patients. Key Points• This multicenter study provides real-world data on the use of nintedanib in patients with connective tissue disease-interstitial lung disease.• Nintedanib treatment is as effective and safe in patients with other connective tissue disease as in patients with systemic sclerosis.

In August 2015, FDA published a black box declaring that DPP-4 inhibitors may cause severe joint pains. The impact on autoimmunity marker positivity of these drugs has not been comprehensively evaluated. We compared the incidence of arthritis/arthralgia in patients with T2DM who were using DPP-4 inhibitors and patients who were not using. A number of 93 DPP-4 inhibitor users and 107 non-users were included into the study. Arthritis/arthralgia were found in 41 of 93 (44.1%) DPP-4 inhibitor users and in 19 of 107 (17.8%) non-users (p0.05). After adjusting for gender the incidence for arthritis/arthralgia was significantly increased in the DPP-4 inhibitor user group (p value for any DPP-inhibitor <0.05). There was 3.77 times increased risk for arthritis/arthralgia in the DPP-4 inhibitor using group (p value= 0.001) and this risk increases 2.43 times for each year of DPP-4 inhibitor usage. Arthritis/arthralgia were more common among T2DM patients who were using DPP-4 inhibitors compared to non-users, but the seropositivity did not differ between DPP-4 inhibitor users and non-users.

Objectives: To investigate the ability of quantitative parameters to assess the severity of rheumatoid arthritis (RA)–associated interstitial lung disease (ILD). Methods: Thorax CT images and pulmonary function tests of RA patients followed up in a tertiary reference center were retrospectively examined. Radiologically, patients were divided into two groups as limited and extensive ILD, using two semiquantitative scoring systems. Two different methods (Method 1, Method 2) were used for quantitative image analysis, in which different Hounsfield unit values were selected as thresholds. Spearman’s correlation test was used to evaluate the relationship between variables. The diagnostic performance of quantitative methods for the ability to distinguish limited ILD from extensive ILD was calculated using ROC analysis. Results: Forty-four patients, 29 female and 15 male, were included in the study. A significant correlation was found between diffusion capacity of the lungs carbonmonoxide (DLCO) and total lung capacity (TLC), which are clinical markers, and both quantitative methods (p < 0.001). In terms of the performance of diagnostic tests, the power of Method 1 and Method 2 to distinguish limited and extensive disease classified based on semiquantitative scores was found to be strong (Method 1 AUC = 0.945, Method 2 AUC = 0.785 based on “ILD score”; Method 1 AUC = 0.911, Method 2 AUC = 0.700 based on “modified coarseness of reticular disease (MCRD) score”). Conclusion: This study demonstrates that quantitative methods (Method 1 [− 700 to − 200 HU] and Method 2 [− 800 to − 500 HU]) play a significant role in assessing the severity of RA-associated ILD (RA-ILD). Both methods showed significant correlations with pulmonary function tests (DLCO [r ₁ = − 0.338, p ₁ = 0.025; r ₂ = − 0.452, p ₂ = 0.002] and TLC [r ₁ = − 0.567, p ₁ < 0.001; r ₂ = − 0.576, p ₂ < 0.001), with Method 1 (AUC_ILD = 0.945 and AUC_MCRD = 0.911) demonstrating superior performance in distinguishing between limited and extensive ILD. Our findings suggest that Hounsfield unit threshold–based quantitative CT analysis may serve as a more objective and reproducible alternative to semiquantitative systems (e.g., Goh score) in the standard evaluation of RA-ILD. Specifically, Method 1 may enable early detection of progression by mechanism, e.g., “tracking subtle density changes.” However, further validation in multicenter prospective cohorts is needed to address limitations such as bias. Key Points• Interobserver and intraobserver variability poses a significant challenge in the objective assessment of rheumatoid arthritis–associated interstitial lung disease.• User independent quantitative methods can be used instead of user-dependent semiquantitative methods in assessing rheumatoid arthritis–associated interstitial lung disease.• Quantitative computed tomography analysis enables precise stratification of disease severity in rheumatoid arthritis-associated interstitial lung disease, distinguishing limited interstitial lung disease from extensive interstitial lung disease, which has a poor prognosis.

Castleman’s disease (CD) is a rare, systemic disease with histopathological features of angiofollicular lymph node hyperplasia. In the literature, there are case-level reports that mimic or coexist with systemic lupus erythematosus (SLE) clinically and in the laboratory. Is this condition two separate diseases or is it an imitation of each other? A 73-year-old female patient was admitted to our clinic with arthritis, lymphadenopathy, fever, weight loss, and malar rash. He had a history of idiopathic thrombocytopenic purpura and thrombosis in the right leg tibialis posterior and dorsalis pedis arteries. Excisional lymphadenopathy biopsy indicated a diagnosis of hyaline-vascular-type CD. She had anti-nuclear antibody >1/80 homogeneous pattern, anti-double stranded DNA (anti-dsDNA), Anti-Smith (Sm) antibody positivity, hypocomplementemia (C3 and C4), pleural effusion, and pericardial effusion. For this reason, the classification criteria of the European League Against Rheumatism/American College of Rheumatology were studied. Clinical findings, idiopathic thrombocytopenic purpura history, antibody positivity, malar rash, and arthritis led us to the diagnosis of SLE. She was treated with 1 mg/kg/day prednisolone and hydroxychloroquine 200 mg 2 × 1. Azathioprine 2.5 mg/kg daily was added to the patient whose complaints did not improve. In the follow-ups, she completely recovered clinically and laboratory. SLE and CD are systemic diseases that overlap in many ways. The literature review shows that these two diseases may mimic each other or may coexist. This situation may be a reflection of a pathophysiological process that has not yet been clarified. This confusing process also affects the treatment decision. This confusing process also affects the treatment decision.