Is there a relationship between adenomyosis and nabothian cyst?

Purpose: The aim of this study was to investigate whether there is a relationship between adenomyosis and nabothian cyst (NC) in a large patient series. Material and methods: The patient's data were scanned retrospectively and patients with a junctional zone thickness of 12 mm and above on magnetic resonance imaging were accepted as group adenomyosis (group A). Patients with a junctional zone thickness of less than 12 mm were not admitted as adenomyosis (control group). Both groups were compared for NC. Results: In group A, 176 (69.8%) patients had NC (n = 250), while in the control group (n = 202), 57 (28.2%) patients had NC. NC was significantly higher in group A than in the control group (p < 0.001). Conclusions: The aetiology of NC is still unclear. According to our results, similar factors may affect adenomyosis and NC aetiopathogenesis

Syndecan 1 may slow the progression of subclinical atherosclerosis in patients with ankylosing spondylitis

Background Subclinical atherosclerosis may be seen at an early age of ankylosing spondylitis (AS). Syndecan 1 (S1) expression is increased in response to proinflammatory cytokine and inflammation. High S1 may reduce carotid atherosclerosis progression. We aimed to investigate the relationship between S1 levels and subclinical atherosclerosis in patients with AS. Methods Fifty-eight patients diagnosed with AS and 58 age-, sex-, and body mass index-matched controls were included in the study. S1 level and carotid intima-media thickness (cIMT) were evaluated using appropriate methods. Results AS patients’ cIMT (0.53 ± 0.1 vs 0.45 ± 0.1 mm, p = .008), S1 (6.0 [1.7–149.2] vs 5.5 [1.0–29.8] ng/ml, p = .020), CRP (C-reactive protein) (2.1 [0.1–19.7] vs 1.1 [0.3–9.6] mg/dl, p = .012), fibrinogen (330.2 ± 87.0 vs 278.0 ± 54.5 mg/dl, p < .001) values were significantly higher than the values of the control group. There was a negative correlation between cIMT and CRP (p = .034), age (p < .001), disease duration (p = .005), BASDAI (p = .048) and fibrinogen (p = .009) in AS patients. There was a negative correlation between cIMT and S1 (p = .029). In multivariate analysis, an independent relationship was found between cIMT and age (β = 0.611, p < .001) and syndecan (β = −0.196, p = .046). Conclusion S1 level may rise in AS patients to suppress the inverse effects of proinflammatory cytokines and inflammation. A negative relationship between the cIMT values of AS patients and S1 level may reveal that S1 has a protective effect on the development of atherosclerosis in AS patients, independent of disease activity

Proprotein convertase subtilisin/kexin type 9 is associated with atherosclerosis in patients with Behcet’s disease

Objectives The incidence of cardiovascular disease is increased in patients with Behcet’s disease (BD). Proprotein convertase subtilisin/kexin type 9 (PCSK9) causes the acceleration of atherosclerosis. We aimed to investigate whether there is a relationship between PCSK9 with carotid artery intima-media thickness (cIMT), a marker of subclinical atherosclerosis, and BD disease activity. Methods Fifty-eight patients with BD and 58 age-, gender-, and body mass index (BMI)-matched healthy control subjects were included in the study. The disease activity of the patients was estimated. Individuals’ cIMT values were measured, and PCSK9 levels were studied. Results Patients with BD’ cIMT (0.51 ± 0.1 vs 0.41 ± 0.1 mm, p < .001) and PCSK9 (623.2 ± 101.7 ± 10.1 vs 528.3 ± 242.7 ng/ml, p = .007), values were significantly higher than the control group. In stepwise regression analysis, there was an independent relationship between cIMT with PCSK9 (β = 0.179, p < .050). There was no independent relationship between disease activities with PCSK9. Based on the ROC curve analysis, the PCSK9 optimal cutoff value for cIMT was 595.1 ng/ml, sensitivity 66.7%, specificity 64.7% (AUC = 0.672; 95% CI: 0.530–0.815, p = .040). Conclusion There is a strong independent association between subclinical atherosclerosis and PCSK9 in patients with BD. There may be no independent association between PCSK9 and disease activity