ABSTRACT
Introduction: The treatment of hypertension with certain groups of drugs may be problematic, particularly because certain drugs are capable of potentiating carcinogenesis. The presence of various receptors or components of the renin – angiotensin system in the skin, and particularly in melanocytes, determines the possible influence on this tissue by the so-called angiotensin receptor blockers or sartans. Thiazide diuretics can further influence the processes of carcinogenesis in all forms of skin cancer – melanocytic and non-melanocytic.
Areas covered: We present a 67-year-old patient treated for a period of 3 years with a combined preparation containing Telmisartan/hydrochlorothiazide 80 mg/12.5 mg. Within 2 years, the patient observed the rapid development of a nevus that progressed to melanoma and was subsequently identified histopathologically as nevus-associated cutaneous melanoma with a 0.6 mm thickness, Clark IV. Following surgical treatment, no tumor progression has occurred to date. To our knowledge, this is the first reported case of a patient who developed a nevus-associated cutaneous melanoma after combination therapy with generic sartan and hydrochlorothiazide.
Expert opinion: We discuss the diverse but mutually potentiating pro-carcinogenic effects of this class of agents, potentially leading to the development of cutaneous melanoma.
Article highlights
A brief analysis of the available data in the medical literature leads to the conclusion that, whether the angiotensin receptor blockers used to treat hypertension are original or generic, their pro-carcinogenic effect on melanoma is likely due to the agent itself.
The theoretical presence of nitrosamines could be seen additionally as responsible for the development of different types of melanomas.
Thiazide diuretics could also contribute to the development of cutaneous melanomas.
Based upon the data shared by us and other authors in the world literature, the use of combinations of angiotensin receptor blockers and hydrochlorothiazide should be the subject of serious debate in some patient groups.
Irreversible changes in DNA as a result of UV damage, identified in the genome regulator-p53 and the cyclin-dependent kinase inhibitor gene, CDKN2A, could lead to their subsequent ineffectiveness in eliminating dysplastic and cancer cells, with consequent tumor development.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewer disclosures
Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.