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内脏恶性肿瘤的皮肤表现

Author
Cindy Owen, MD
Section Editor
Jeffrey Callen, MD, FACP, FAAD
Deputy Editor
Abena O Ofori, MD
Translators
林麟, 主任医师

引言

内脏恶性肿瘤的皮肤表现包括与恶性肿瘤伴发的非恶性皮肤疾病(副肿瘤性皮肤病)，以及代表着由于疾病转移或局部扩散或者循环中的肿瘤细胞沉积(如皮肤白血病)导致的恶性肿瘤细胞浸润至皮肤的皮肤病变。多种类型的副肿瘤性皮肤病已有报道，包括增生性、炎症性、大疱性和其他类型的皮肤病[1,2]。当副肿瘤性皮肤病在发现内脏肿瘤之前发生时，识别这些皮肤病有助于恶性肿瘤的诊断。

Curth法则，即一套诊断标准，已经被一些作者用来判断一种皮肤疾病是否应该被分类为一种副肿瘤性皮肤病[1]。Curth法则见下表(表 1)。

最常见的副肿瘤性皮肤病将在此讨论，表现为肿瘤细胞浸润皮肤的疾病不在本专论的讨论范围。 (参见“Paget disease of the breast”和“急性髓系白血病的临床表现、病理特征和诊断”和“艾滋病相关Kaposi肉瘤：分期和治疗”和“蕈样肉芽肿的临床表现、病理特征和诊断”)

恶性肿瘤的代谢产物引起的皮肤病

异位Cushing综合征中的色素沉着过度 — 异位Cushing综合征是最常见与内脏恶性肿瘤相关的激素诱导的副肿瘤综合征。此综合征的特点是广泛的色素沉着过度(皮肤和黏膜)、肌萎缩、近端肌无力、低钾性代谢性碱中毒、糖耐量异常和高血压[3]。 (参见“库欣综合征的流行病学和临床表现”)

异位Cushing综合征是由于垂体外的肿瘤分泌过多的前阿片黑素皮质素原(proopiomelanocortin, POMC)引起的。POMC是促黑素细胞激素(melanocyte-stimulating hormone, MSH)和促肾上腺皮质激素(adrenocorticotropic hormone, ACTH)的激素原。MSH和ACTH都能够刺激黑色素合成，从而导致发生色素沉着过度[4]。 (参见“库欣综合征的病因和病理生理学”)

                                  

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Literature review current through: 2017-06 . | This topic last updated: 2017-01-11.
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