Darsha Adrija K, Cohen Philip R
School of Medicine, University of California San Diego, San Diego, USA.
Dermatology, University of California Davis Medical Center, Sacramento, USA.
Cureus. 2021 Nov 14;13(11):e19581. doi: 10.7759/cureus.19581. eCollection 2021 Nov.
Sticky skin is a dermatologic phenomenon in which the skin may cause objects to adhere to it on contact or adhere to itself or both. The entire skin can be affected in patients with sticky skin. Alternatively, just acral sites, such as the hand, can be involved. The acquisition of sticky skin has been described in patients treated with certain medications. These drugs include retinoids, proton pump inhibitors, and antifungals; they also include combination therapy utilizing an antineoplastic agent and an antifungal drug in patients with hormone-resistant prostate cancer. The pathogenesis of acquired cutaneous adherence in patients with androgen-independent prostate cancer was postulated to be the result of therapy-induced elevation of endogenous retinoids. Retinoids have multiple biological effects on epidermal differentiation that may contribute to the pathogenesis of acquired cutaneous adherence. These include the induction of fine, granular, mucus-like deposits within and between the keratinocytes in the upper stratum spinosum and stratum corneum, modulation of lipid composition in keratinocytes, prevention of cross-linked, cornified envelope formation in keratinocytes by the inhibition of epidermal transglutaminase, and altered and decreased content of keratin within the epidermis. We describe an older man who developed non-medication acquired sticky skin (NoMasts). His acquired cutaneous adherence was considered to be idiopathic. We postulate that aging may be associated with elevated endogenous retinoid levels in older individuals and may have resulted in his sticky skin. Further investigation into these retinoid-induced effects and to what extent they promote acquired cutaneous adherence is still needed.
粘性皮肤是一种皮肤学现象,即皮肤在接触时可能导致物体粘附其上,或自身相互粘附,或两者皆有。粘性皮肤患者的全身皮肤都可能受到影响。或者,仅累及手部等肢端部位。在接受某些药物治疗的患者中曾有粘性皮肤的报道。这些药物包括维甲酸、质子泵抑制剂和抗真菌药;还包括在激素抵抗性前列腺癌患者中使用抗肿瘤药和抗真菌药的联合治疗。雄激素非依赖性前列腺癌患者获得性皮肤粘连的发病机制被推测是治疗引起内源性维甲酸水平升高所致。维甲酸对表皮分化具有多种生物学效应,这可能有助于获得性皮肤粘连的发病机制。这些效应包括在上层棘层和角质层的角质形成细胞内及之间诱导形成细小的、颗粒状的、粘液样沉积物,调节角质形成细胞中的脂质组成,通过抑制表皮转谷氨酰胺酶防止角质形成细胞中交联的、角化包膜的形成,以及改变和降低表皮内角蛋白的含量。我们描述了一名老年男性,他出现了非药物性获得性粘性皮肤(NoMasts)。他的获得性皮肤粘连被认为是特发性的。我们推测衰老可能与老年个体内源性维甲酸水平升高有关,可能导致了他的粘性皮肤。仍需要进一步研究这些维甲酸诱导的效应以及它们在多大程度上促进获得性皮肤粘连。