Chawla Nitika, Kataria Sant Prakash, Aggarwal Kamal, Chauhan Pardeep, Kumar Dinesh
Department of Pathology, BPS GMC, Sonepat, Haryana, India.
Departments of Pathology, Venereology and Leprology, Postgraduate Institute of Medical Sciences, Rohtak, Haryana, India.
Indian J Pathol Microbiol. 2017 Apr-Jun;60(2):189-195. doi: 10.4103/IJPM.IJPM_862_15.
Pathogenesis of psoriasis is a debated issue. Several mechanisms have been proposed to identify the etiology and pathogenesis so that specific treatments can be given to patients with psoriasis.
(1) To compare pattern and distribution of vascular endothelial growth factor (VEGF) and CD31 in patients with psoriasis and other psoriasiform lesions of skin. (2) To study the correlation between VEGF and CD31 expression, clinical severity, and histopathology of psoriasiform lesions of skin. (3) Evaluation of microvessel density (MVD) by using computer-assisted quantitative image analysis in psoriatic skin lesions.
This study was conducted on eighty cases, out of which forty were diagnosed cases of psoriasis and forty cases of clinically suspected psoriasiform lesions, submitted in the Department of Pathology, Pt. B.D. Sharma, University of Health Sciences, Rohtak, for histopathological examination. Histopathological sections were stained by routine hematoxylin and eosin staining, and these biopsies were further subjected to immunohistochemical staining with VEGF and CD31 as per standard technique.
Assessment of various histopathological features revealed strong correlation between epidermal hyperplasia, suprapapillary thinning, and elongation of rete ridges. Suprabasilar keratinocytes in psoriatic lesions stained intensely for VEGF. The difference for number of microvessels and MVD in psoriasis and psoriasiform lesions was statistically significant. Correlation between intensity of VEGF staining by suprabasilar keratinocytes and MVD was found to be highly significant in psoriatic lesions.
The present study concluded that psoriatic lesions exhibit potent angiogenic activity. Early lesions show increased MVD along with other histomorphological parameters such as hypogranulosis, parakeratosis and Munro's microabscesses. Overexpression of VEGF by suprabasilar keratinocytes correlated with increased MVD in papillary dermis.
银屑病的发病机制是一个有争议的问题。已经提出了几种机制来确定病因和发病机制，以便能够为银屑病患者提供特定的治疗。
（1）比较银屑病患者和其他皮肤银屑病样病变中血管内皮生长因子（VEGF）和CD31的模式及分布。（2）研究VEGF和CD31表达、临床严重程度以及皮肤银屑病样病变组织病理学之间的相关性。（3）通过计算机辅助定量图像分析评估银屑病皮肤病变中的微血管密度（MVD）。
本研究对80例病例进行，其中40例为银屑病确诊病例，40例为临床疑似银屑病样病变病例，提交至罗塔克健康科学大学Pt. B.D. Sharma病理学系进行组织病理学检查。组织病理学切片采用常规苏木精和伊红染色，这些活检标本按照标准技术进一步用VEGF和CD31进行免疫组织化学染色。
对各种组织病理学特征的评估显示，表皮增生、乳头上方变薄和表皮嵴延长之间存在强相关性。银屑病病变中的基底上层角质形成细胞VEGF染色强烈。银屑病和银屑病样病变中微血管数量和MVD的差异具有统计学意义。在银屑病病变中发现基底上层角质形成细胞VEGF染色强度与MVD之间的相关性非常显著。
本研究得出结论，银屑病病变表现出强大的血管生成活性。早期病变显示MVD增加以及其他组织形态学参数，如颗粒层减少、角化不全和Munro微脓肿。基底上层角质形成细胞VEGF的过度表达与乳头真皮中MVD增加相关。
