DermKnowledgeBASE: Cherry Angioma

Cherry Angioma

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The text is the summary of recent articles on Cherry Angioma at 75 thresold from National Library of Medicine (NLM). This information is subject to NCBI's Disclaimer and Copyright notice.


The pathogenesis of abnormal angiogenesis in cherry angioma is not well known but the role of Inflammatory mediators and certain hormones, including prolactin, in the regulation of angiogenesis in other diseases has been reported [1]. Alterations in serum levels of prolactin and chemokines in SM-exposed victims and the impact on angiogenesis are indications of the role in SM-induced cherry angioma [2]. There was no significant difference in the serum levels of IL-8, RANTES and CX3L1 between the exposed subgroups with cherry angioma and without cherry angioma [3]. The most common Chronic skin lesions are mustard scars, xerosis, eczema, seborrheic dermatitis, cherry angioma and Hyperpigmentation [4]. We describe a 62-year-old Caucasian Woman with early formation of segmental cherry angiomas after Pregnancy, which are superimposed on non-segmental lesions of later onset after menopause [5].

In this pattern, segmental cherry angiomas could be taken as a further example of superimposed segmental manifestation of a polygenic skin disorder [6]. The patient returned 5 weeks later complaining of bleeding from the treatment site, which on examination showed a 23 x 23-mm Friable Nodular Lesion with the typical appearance of a pyogenic granuloma [7]. Histopathological examination confirmed the diagnosis of pyogenic granuloma [8]. The histopathologic findings of a cherry angioma are consistent with a true capillary hemangioma, which is formed by numerous, newly developed capillaries with narrow lumens and prominent endothelial Cells arranged in a Lobular fashion in the papillary Dermis [9]. The Medical records and radiotherapy charts were reviewed to determine if the patient developed a secondary neoplasm after treatment for malignancy [10].

Although some cytokines have been thought to be angiogenic factors, a nitric oxide (NO) synthase-dependent effector mechanism is reported to be involved in macrophage-derived angiogenesis in humans [11]. Other Vascular lesions, such as telangiectasia, venous lake, angiofibroma, lymphangioma, and cherry angioma, were also treated with success [12]. Five were macular: mat telangiectasia of scleroderma, Generalized essential telangiectasia, nevus flammeus, and 2 Macular types not previously described [13]. Three were papular: cherry angioma, angiokeratoma (Fabry), and angiokeratoma (Fordyce) [14]. The macular telangiectases were produced by dilatation of postcapillary venules of the upper horizontal plexus [15].

Thus, the Papular Telangiectases also arose by alterations of the existing microvasculature rather than by proliferation of new vessels with random anastomoses [16]. Reconstruction of the upper horizontal plexus from normal skin showed an undulating network of arterioles and their accompanying postcapillary venules [17].

References: 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 ,

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