Clinical study of carotid superb microvascular imaging in evaluating the activity of Takayasu's arteritis.

Objective: The goal of this study is to use superb microvascular imaging (SMI) to observe neovascularization in the carotid vessel wall to identify potential Takayasu's arteritis (TAK) inflammation markers. Methods: Bilateral carotid arteries from 96 patients with TAK were imaged by a Doppler ultrasound and SMI. The one-way analysis of variance (ANOVA) was used to document significant differences between the activity and inactivity stages of TAK and the factors closely related to its activity in the binary logistics regression equation. Clinical and laboratory data included age, gender, duration of disease, treatment history, NIH score, erythrocyte sedimentation rate (ESR), and high-sensitivity C-reactive protein. Imaging data included the arterial wall thickness, degree of lesion, SMI grade, and arterial aneurysm formation. Results: There were 45 patients in the active TAK stage and 51 in the inactive stage. The one-way ANOVA showed significant differences in SMI (p = 0.001) and ESR (p = 0.022) between the active and inactive groups. The binary logistics regression analysis showed that SMI was an independent risk factor for TAK activity (B = -1.505, S.E = 0.340, Wald = 19.528, OR = 0.222 95%, CI = 0.114-0.433, p < 0.01). Using SMI G1 or G2 as the cutoff values for the diagnosis of active TAK, the positive predictive value, sensitivity, and specificity were 60 and 86%, 84% and 56%, and 54% and 92%, respectively. Conclusion: The SMI grade is a potential marker of disease activity in patients with TAK.

IL-9-producing Th9 cells may participate in pathogenesis of Takayasu's arteritis.

Takayasu's arteritis (TAK) is a type of large vessel vasculitis which involves the aorta and its major branches. Interleukin (IL)-9 or IL-9-producing Th9 cells were found to be involved in pathogenesis of autoimmune arteritis such as giant cell arteritis, but IL-9 or Th9 cells in TAK were not well known. Here, this study aims to analyze the levels of serum IL-9 and their major source Th9 cells in TAK. With the help of cytometric bead array (CBA), a total of 21 patients with TAK were examined for serum levels of cytokines IL-4, IL-6, IL-8, IL-17, IL-10, TNF-α, IFN-γ, and IL-9. Flow cytometry techniques were used to examine the frequencies of Th9 cells from peripheral blood mononuclear cells (PBMCs) for 11 patients with active TAK and 10 healthy controls. Higher serum levels of serum IL-6 (P < 0.05), TNF-α (P < 0.05), and IL-9 level (P < 0.05) were observed in TAK patients compared to those of healthy controls. Higher frequencies of CD4+ IL-9+ T cells and CD4+ PU.1+ T cells in PBMCs and IL-9+ PU.1+ T cells in CD4+ T cells were observed in active TAK patients than those in healthy controls (all P < 0.01). The levels of IL-9 had a positive correlation with ESR (r = 0.975, P = 0.015) in these cases. Our data suggested that Th9 cells and IL-9 could possibly be involved in the pathogenesis of TAK.

[Study on polymorphic Hind III restriction site of the Y chromosome and essential hypertension in Tangshan district].

OBJECTIVE: Since males are at higher risk of cardiovascular diseases than females, the aim of the study was to examine whether there is an association between BP and a polymorphic Hind III biallelic marker in nonrecombining region of Y chromosome in essential hypertension in Tangshan district in China. METHODS: In the study, 225 patients with essential hypertension and 187 healthy people were enrolled into this study as control group. DNA was extracted from white blood cell. Segments of polymorphic Hind III restriction site of the Y chromosome were amplified from DNA by polymerase chain reaction (PCR). PCR products were restricted with 10 U of Hind III for a night at 37 degrees C. The digested products were subjected to electrophoresis in 3% agarose gels, and stained with ethidium bromide. RESULTS: We amplified 178 controls (95.2%) and 216 essential hypertensive patients (96.0%) successfully. Hind III(-) genotype was found in 45.8% of the men in essential hypertension and in 32.0% of the men in the controlled group. The Hind III(-) genotype was significantly higher than that in the controls (chi2 = 7.782, P = 0.007). However, the Hind III(+) genotype was lower in SBP (133.16 mm Hg +/- 21.60 mm Hg vs. 143.58 mm Hg +/- 24.16 mm Hg, P < 0.001), DBP (82.82 mm Hg +/- 11.72 mm Hg vs. 86.82 mm Hg +/- 12.65 mm Hg, P = 0.001), pulse pressure (50.34 mm Hg +/- 14.31 mm Hg vs. 56.76 mm Hg +/- 14.20 mm Hg, P < 0.001) and mean arterial pressure (99.59 mm Hg +/- 14.19 mm Hg vs. 105.74 mm Hg +/- 15.31 mm Hg, P < 0.001) than the Hind III(-) genotype. CONCLUSION: Polymorphic Hind III restriction site of the Y chromosome seemed to be associated with essential hypertension in Tangshan district in China.