Tchernev Georgi, Temelkova Ivanka
Medical Institute of the Ministry of Interior, Department of Dermatology, Venereology and Dermatologic Surgery, General Skobelev Nr 79, Sofia, Bulgaria.
Onkoderma, Policlinic for Dermatology and Dermatologic Surgery, General Skobelev 26, Sofia, Bulgaria.
Open Access Maced J Med Sci. 2019 Jan 9;7(1):121-123. doi: 10.3889/oamjms.2019.043. eCollection 2019 Jan 15.
Drug-induced melanoma is a topic, concept or "reality" becoming more and more popular as the list of drugs considered as potential inducers of cutaneous melanoma is constantly growing. Interesting and current at the moment is the question/dilemma of "Irbesartan induced melanomas" and "Valsartan induced melanomas"! The following questions are without answers: 1) the general risk which angiotensin receptor blockers contain for potentiating the carcinogenesis and cancer development (as a whole); 2) available officialized data for withdrawal from the market of products with valsartan and irbesartan due to detected potential carcinogens-NDMA/NDEA, and 3) the missing official information on the most likely forms of cancer potentiated by these drugs. That is precisely why many questions remain open, and the inevitable assumption arises for the key, although according to some conspiratorial role of so-called "pharmaceutical giants" in the concept of drug-induced malignancies.
We present a 72-year-old man with arterial hypertension in connection with which he is taking Irbesartan 300 mg (1-0-0), Amlodipine 5 mg (0-0-1) and Moxonidine 0.2 mg (0-0-1). The patient reported the presence of pigment lesion in the head area, which dates from many years and 3 years ago it was at the size of the nail plate on the index finger. Irbesartan therapy dates from 1.5-2 years, and according to the patient 1.5-2 years after the start of irbesartan therapy, the lesion grew sixfold, accompanied by sensitivity and discomfort in the area. Clinically and dermatoscopically the lesion had data on superficial spreading cutaneous melanoma. Tumour thickness ≤ 1 mm was measured preoperatively by ultrasound. The so-called one-step melanoma surgery (OSMS) was performed, and the lesion was removed by elliptical excision with an operative surgical margin of 1 cm in all directions within one operative session. The subsequent histological study (and screening staging) found that it was a superficial spreading melanoma stage IA (T1bN0M0).
Possible, but unlikely, in our opinion, is that the intake of angiotensin receptor blockers (in particular irbesartan), and the progression of benign precursor lesions to malignant do not have a direct relationship. The growing number of data in the literature for drug-induced melanoma and massive withdrawal of products with valsartan and irbesartan due to the content of probable carcinogens speaks, however in favour of the opposite, namely that it is more likely to speak about established dependence than of a sporadic association. Drug-induced melanoma-rather a reality than a myth.
药物性黑色素瘤是一个越来越受关注的话题、概念或“现实”,因为被认为可能诱发皮肤黑色素瘤的药物清单在不断增加。目前有趣且热门的问题是“厄贝沙坦诱发的黑色素瘤”和“缬沙坦诱发的黑色素瘤”!以下问题尚无答案:1)血管紧张素受体阻滞剂在促进致癌作用和癌症发展方面的总体风险(总体而言);2)由于检测到潜在致癌物NDMA/NDEA而从市场撤回缬沙坦和厄贝沙坦产品的现有官方数据;3)关于这些药物最可能诱发的癌症形式的缺失官方信息。这正是为什么许多问题仍然悬而未决,并且不可避免地会产生一种关键假设,尽管根据一些阴谋论的说法,所谓的“制药巨头”在药物性恶性肿瘤概念中扮演了某种角色。
我们介绍了一名72岁患有动脉高血压的男性,他正在服用300毫克厄贝沙坦(1-0-0)、5毫克氨氯地平(0-0-1)和0.2毫克莫索尼定(0-0-1)。患者报告头部区域存在色素性病变,该病变已存在多年,3年前其大小如食指指甲盖。厄贝沙坦治疗始于1.5至2年前,据患者称,在厄贝沙坦治疗开始后的1.5至2年,病变增大了六倍,同时该区域伴有敏感和不适感。临床及皮肤镜检查显示该病变具有浅表扩散性皮肤黑色素瘤的特征。术前通过超声测量肿瘤厚度≤1毫米。实施了所谓的一步式黑色素瘤手术(OSMS),在一次手术中通过椭圆形切除将病变切除,手术切缘在各个方向均为1厘米。随后的组织学研究(以及筛查分期)发现这是一例IA期浅表扩散性黑色素瘤(T1bN0M0)。
在我们看来,血管紧张素受体阻滞剂(特别是厄贝沙坦)的摄入与良性前驱病变向恶性病变的进展之间可能存在但不太可能存在直接关系。然而,文献中关于药物性黑色素瘤的数据不断增加,以及由于可能含有致癌物而大量撤回缬沙坦和厄贝沙坦产品,这表明情况恰恰相反,即更有可能存在既定的关联而非偶发的联系。药物性黑色素瘤——与其说是神话,不如说是现实。