In:
Cardiovascular Therapeutics, Wiley, Vol. 35, No. 3 ( 2017-06)
Abstract:
Thrombosis and inflammation play an important role in pathophysiology of livedoid vasculopathy ( LV ). Plasminogen activator inhibitor‐1 ( PAI ‐1) is the main physiological inhibitor of fibrinolysis and is a pivotal modulator in a broad range of biological processes. Method The study specimens were retrospectively selected from archives of pathology department. We investigated PAI ‐1 mRNA expression in the paraffin blocks of patients with biopsy‐proven LV and controls. We analyzed the presence of thrombus, fibrinoid necrosis, ulcer, and epidermal atrophy in study samples. The correlation between histologic findings and PAI ‐1 expression was investigated. Results Analyses were performed in 14 LV patients (mean age 31±20, 79% female) and 4 controls (mean age 64±19, 50% female). PAI ‐1 gene expression was significantly higher in LV compared to the control group (median 7.74 (Iqr:13.94) vs 1.0 (0.31)), P =.011. Histological analysis displayed that fibrinoid necrosis was present on all patients with LV , 61.5% displayed thrombus, 46.2% displayed ulcer, and 15.4% displayed epidermal atrophy. Overall, we did not observe any discerning difference in PAI ‐1 expression between the LV blocks with or without thrombus, fibrinoid necrosis, or epidermal atrophy, yet the LV specimens that displayed ulcer histologically had higher PAI ‐1 mRNA expression compared to those without ulcer (median 13.98 (Iqr:19.21) vs 2.86 (5.59)), ( P =.046). Conclusion PAI ‐1 mRNA expression is significantly increased in cutaneous lesions of patients with LV . Histological finding of ulcer is associated with increased PAI ‐1 expression in LV specimen. In the current era of PAI ‐1 inhibitors, enhanced local PAI ‐1 expression can form a novel and local therapeutic target in LV .
Type of Medium:
Online Resource
ISSN:
1755-5914
,
1755-5922
DOI:
10.1111/cdr.2017.35.issue-3
DOI:
10.1111/1755-5922.12255
Language:
English
Publisher:
Wiley
Publication Date:
2017
detail.hit.zdb_id:
2417088-4
