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Published on: December 5, 2011
Impaired endothelial function irrespective of systemic inflammation or atherosclerosis in mastocytosis
Nida Öztop1, Pelin Karaca Özer2, Semra Demir1
1Division of Immunology and Allergic Diseases, Department of Internal Medicine, İstanbul Faculty of Medicine, İstanbul University, İstanbul, Turkey.
Insights
Mastocytosis patients exhibit endothelial dysfunction, characterized by reduced flow-mediated dilatation (FMD) and increased vascular endothelial growth factor (VEGF). This dysfunction is linked to disease severity, not systemic inflammation or atherosclerosis.
Area of Science:
- Cardiovascular Research
- Hematology
- Vascular Biology
Background:
- Limited knowledge exists regarding endothelial dysfunction and its association with atherosclerosis in mastocytosis.
- Mastocytosis, a rare disorder involving mast cell proliferation, can impact various organ systems, including the vasculature.
Purpose of the Study:
- To investigate endothelial function in mastocytosis patients using flow-mediated dilatation (FMD).
- To assess biomarkers related to vascular endothelium and subclinical atherosclerosis (carotid intima-media thickness, CIMT).
- To evaluate the relationship between endothelial dysfunction, biomarkers, and disease severity in mastocytosis.
Main Methods:
- A study involving 49 mastocytosis patients and 25 healthy controls (HCs).
- Measurements included FMD, CIMT, and serum biomarkers: endocan, endothelin-1, vascular endothelial growth factor (VEGF), tumor necrosis factor-alpha, interleukin 6, and high-sensitive C-reactive protein.
- Transthoracic echocardiography was used for FMD and CIMT assessment.
Main Results:
- Patients with mastocytosis showed significantly lower FMD compared to HCs (11.26% vs 17.84%, P < .001).
- Serum VEGF levels were significantly higher in mastocytosis patients (P = .001) and correlated inversely with FMD.
- No significant differences in CIMT or correlations with inflammatory markers were observed.
Conclusions:
- Endothelial dysfunction is evident in mastocytosis, indicated by decreased FMD and elevated VEGF.
- This dysfunction appears independent of subclinical atherosclerosis and systemic inflammation.
- The degree of endothelial dysfunction correlates with mastocytosis disease severity.
Background:
Knowledge on endothelial dysfunction and its relation to atherosclerosis in mastocytosis is limited.
Objective:
To investigate the endothelial function in mastocytosis by flow-mediated dilatation (FMD) and biomarkers related to vascular endothelia and to evaluate its relationship with the presence of subclinical atherosclerosis by carotid intima media thickness (CIMT).
Methods:
A total of 49 patients with mastocytosis and 25 healthy controls (HCs) were included. The FMD and CIMT during transthoracic echocardiography biomarkers including endocan, endothelin-1, and vascular endothelial growth factor (VEGF) were measured in the sera of participants. Tumor necrosis factor-alpha, interleukin 6, and high-sensitive C-reactive protein were determined as inflammatory biomarkers.
Results:
The mean FMD % was lower in the patients than HCs (11.26% ± 5.85% vs 17.84% ± 5.27% P < .001) and was the lowest in the advanced systemic mastocytosis and smoldering systemic mastocytosis group among the patients (P = .03). The median value of VEGF was considerably higher in patients than HCs (73.30 pg/mL; minimum-maximum 32.46-295.29 pg/mL vs 46.64 pg/mL; minimum-maximum, 11.09-99.86 pg/mL; P = .001) and it was the highest in the advanced systemic mastocytosis and smoldering systemic mastocytosis group (P = .01). The FMD was inversely correlated with endocan (r = -0.390; P = .006), endothelin-1 (r = -0.363; P = .01) and VEGF (r = -0.402; P = .004) but there were no correlations between FMD and tumor necrosis factor-alpha, interleukin 6, and high-sensitive C-reactive protein. No differences in CIMT values between patients and HCs and no correlation between CIMT and the biomarkers were observed.
Conclusion:
Endothelial dysfunction in mastocytosis becomes evident with decreased FMD and elevated serum VEGF in the absence of atherosclerosis or systemic inflammation and is related to disease severity.
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