Ayhan Kamanli

Objective: Behçet’s disease (BD) is a systemic vasculitis characterized by thrombo-inflammation. This cross-sectional study compared inflammatory indices obtained from complete blood counts (CBC), focusing particularly on red blood cell distribution width (RDW), with conventional acute-phase reactants (CRP, ESR). It examined phenotype-specific hematological patterns across clinical manifestations and the cross-sectional relationships of hematological parameters and vascular involvement with treatments. Subjects and Methods: A total of 100 BD patients (ISG criteria) and 42 age- and sex-comparable healthy controls were studied. RDW, MPV, PHR, and CBC-derived indices (NLR, PLR, MLR, SII, SIRI, AISI) were calculated. Disease activity (BDCAF), clinical manifestations (DVT, composite vascular complications, genital ulcer history, arthralgia, pathergy), and treatment regimens were recorded. Between-group comparisons used the Mann–Whitney U test; separation from controls was assessed by ROC analysis with Youden-derived cut-offs. The Benjamini–Hochberg procedure controlled the false discovery rate (FDR) across subgroup comparisons. Results: CRP (p = 0.299) and ESR (p = 0.184) did not differ between groups, whereas RDW (median 15.05% [IQR 13.57–16.32] vs. 13.45% [12.90–13.70], p < 0.001) and MPV (8.85 fL [8.38–10.00] vs. 10.05 fL [9.30–10.60], p < 0.001) did. RDW showed the highest observed AUC for separation from controls (AUC 0.77; cut-off > 13.95), followed by MPV (AUC 0.72); CRP (AUC 0.551) and NLR (AUC 0.49) were uninformative. PHR was nominally lower in DVT (median 17.08 [IQR 15.66–18.97] vs. 20.08 [16.54–25.64], p = 0.043) and composite vascular complications (17.16 [15.23–19.28] vs. 20.22 [16.66–26.26], p = 0.024), accompanied by higher hemoglobin (p = 0.013) and hematocrit (p = 0.006). RDW was lower in patients with a history of genital ulcers (13.65% [IQR 13.07–14.35] vs. 15.70% [14.17–16.45], p < 0.001). After Benjamini–Hochberg correction, the BD–control differences and the genital ulcer–RDW association remained significant, whereas marginal subgroup associations (DVT–PHR, pathergy–SIRI/AISI; p = 0.02–0.05) did not. Colchicine use was nominally associated with a lower DVT frequency (8.1% vs. 28.6%; OR 0.23, 95% CI 0.05–1.24), an unstable, exploratory finding based on only 14 non-users and substantially confounded by indication. Conclusions: In BD, CBC-derived indices, particularly RDW and MPV, separated BD patients from healthy controls even when conventional acute-phase reactants (CRP and ESR) remained normal, although this reflects separation from health rather than diagnostic accuracy for BD. RDW was lower in patients with a history of genital ulcers, while an exploratory PHR signal in deep vein thrombosis was inconclusive. These readily accessible indices may serve as complementary markers in BD, pending validation in disease-controlled prospective studies.

Background/Objectives: Although vitamin K has been implicated in osteoarthritis pathophysiology, the specific effects of vitamin K2 (menaquinone) on cartilage degeneration remain poorly characterized. This study aimed to investigate the effect of oral vitamin K2 supplementation in a monosodium iodoacetate-induced osteoarthritis model. Methods: Twenty-four male Sprague Dawley rats were included in the study and divided into 3 equal groups: sham group, control (osteoarthritis) group, and treatment group. Saline was applied to the right knee of the sham group, and MIA was applied intra-articularly to the right knee of the control and treatment groups to create an osteoarthritis model. Rats in the treatment group were given 8 micrograms (μg)/day of vitamin K2 orally in addition to the standard diet. After 28 days of follow-up, all rats were euthanized. The right knee articular cartilage was examined histologically with Hematoxylin–Eosin and Safranin O and immunohistochemically with type II collagen alpha 1 and Matrix Metalloproteinase-13. Results: Histological evaluation demonstrated significantly lower Mankin scores in the treatment group (4.25 ± 0.83) compared with the control group (11.10 ± 0.83). Immunohistochemical analysis showed more intense type II collagen staining and reduced matrix metalloproteinase-13 staining in the treatment group relative to the control group. Conclusions: Oral vitamin K2 administration was associated with reduced cartilage degeneration and improved matrix preservation at the 28-day endpoint in an induced MIA osteoarthritis rat model.