ObjectivePsoriatic arthritis (PsA) has a genetic background. Approximately 40% of patients with psoriasis or PsA have a family history of psoriasis or PsA, which may affect disease features. The aim of this study was to assess the effects of family history of psoriasis and PsA on disease phenotypes.MethodsData from 1,393 patients recruited in the longitudinal, multicenter Psoriatic Arthritis International Database were analyzed. The effects of family history of psoriasis and/or PsA on characteristics of psoriasis and PsA were investigated using logistic regression.ResultsA total of 444 patients (31.9%) had a family history of psoriasis and/or PsA. These patients were more frequently women, had earlier onset of psoriasis, more frequent nail disease, enthesitis, and deformities, and less frequently achieved minimal disease activity. Among 444 patients, 335 only had psoriasis in their family, 74 had PsA, and 35 patients were not certain about having PsA and psoriasis in their family, so they were excluded from further analysis. In the multivariate analysis, family history of psoriasis was associated with younger age at onset of psoriasis (odds ratio [OR] 0.976) and presence of enthesitis (OR 1.931), whereas family history of PsA was associated with lower risk of plaque psoriasis (OR 0.417) and higher risk of deformities (OR 2.557). Family history of PsA versus psoriasis showed increased risk of deformities (OR 2.143) and lower risk of plaque psoriasis (OR 0.324).ConclusionFamily history of psoriasis and PsA impacts skin phenotypes, musculoskeletal features, and disease severity. The link between family history of psoriasis/PsA and pustular/plaque phenotypes may point to a different genetic background and pathogenic mechanisms in these subsets.

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Background/aim: Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation. The study aimed to assess serum 14-3-3eta, anti-CarP, and anti-Sa in seronegative RA (SNRA) patients who were treatment-naïve as well as in healthy subjects. This is the first study in the literature to examine these autoantibodies together in SNRA patients. Materials and methods: Forty-five treatment-naïve SNRA patients and 45 healthy subjects were recruited. Drugs change the levels of autoantibodies; therefore, patients who took any medication had been excluded from our study. Anti-carbamylated protein, anti-Sa, and 14-3-3eta were measured by using three different ELISA kits. Results: Median serum concentration of healthy controls in 14-3-3eta was 0.02 (0.02-0.27) ng/mL. Median serum concentration of SNRA patients in 14-3-3eta was 1.00 (0.48-1.28) ng/mL. Data were analyzed with Mann-Whitney U tests; the P-value was <0.001 in 14-3-3eta. Receiver operating characteristic (ROC) curve analysis showed that 14-3-3eta in SNR compared to healthy controls had a significant (P < 0.001) area under the curve (AUC) of 0.90 (95% confidence interval, 0.83-0.96). At a cutoff of ≥0.33 ng/mL, the ROC curve yielded a sensitivity of 88.9%, a specificity of 82.2%, a positive predictive value of 83.3%, and a negative predictive value of 88.1%. Conclusion: We found that 14-3-3eta can be used as a diagnostic marker in SNRA.

Background/aim: The distribution of Mediterranean fever (MEFV) gene mutations in Turkish familial Mediterranean fever (FMF) patients varies according to geographic area of Turkey. There is a need for highly representative data for Turkish FMF patients. The aim of our study was to investigate the distribution of the common MEFV mutations in Turkish FMF patients in a nationwide, multicenter study. Materials and methods: Data of the 2246 FMF patients, from 15 adult rheumatology clinics located in different parts of the country, were evaluated retrospectively. The following mutations have been tested in all patients: M694V, M680I, M694I, V726A, and E148Q. Results: There were 1719 FMF patients with available genetic testing. According to the genotyping, homozygous M694V, present in 413 patients (24%), was the most common mutation. One hundred and fifty-four (9%) of patients had no detectable mutations. Allele frequencies of common mutations were: M694V (n = 1529, 44.5%), M680I (n = 423, 12.3%), V726A (n = 315, 9.2%), E148Q (n = 214, 1%), and M694I (n = 12, <1%). Conclusion: In this large-scale multicenter study, we provided information about the frequencies of common MEFV gene mutations obtained from adult Turkish FMF patients. Nearly half of the patients were carrying at least one M694V mutations in their alleles.

Background This study aimed to examine fetomaternal outcomes in pregnant women in a large Turkish Takayasu arteritis (TAK) cohort and to evaluate the effects of pregnancy on the disease in those patients. Methods This is a cohort study involving 296 pregnancies of 112 TAK patients from 8 tertiary rheumatology centers in Turkey. Pregnancies were divided into 2 groups as pre‐d (before disease onset) and post‐d (after disease onset). In addition, post‐d pregnancies were further divided into 2 subgroups according to fetomaternal complications (FMC) development status. Finally, patients were grouped into those with and without a history of pregnancy after disease onset. Results In post‐d pregnancies, rates of worsening hypertension, new‐onset hypertension, and preeclampsia were higher than in pre‐d pregnancies (0.9% vs 16%, P < .001, 0.5% vs 5.3%, P = .012, and 0% vs 4%, P = .013, respectively). Patients with FMC were more likely to have renal artery involvement (65% vs 21%, P = .003). The patients who had post‐d were younger, had longer disease duration, and had more relapses number than other patients (P < .001, P = .028, P = .016, respectively). Vasculitis Damage Index (VDI) results were similar in patients with or without post‐d pregnancies. Conclusion Pregnancies after disease onset were found to be associated with HT and preeclampsia/eclampsia. HT‐related FMCs are increased in TAK, and patients with renal artery involvement are at higher risk. The number of relapses increases in patients who become pregnant after disease onset, but pregnancy was not an independent risk factor for relapse. Pregnancy after the onset of disease had no negative effect on VDI.