The Complexity of Testicular Lesions in Arteriosclerosis

To understand the repercussions of arteriosclerosis on the testicular parenchyma, it must be born in mind that the testicle is both an exocrine and endocrine gland. As an exocrine gland, any alteration of the spermatic ducts, in this case due to a vascular lesion, leads to atrophy of the ducts, resulting in their partial or total obstruction and, consequently, to retrograde ectasia of the testicular fluid, which can affect the epididymis, rete testis (cystic transformation), and seminiferous tubules (tubular ectasia and subsequent atrophy of the seminiferous epithelium). As an endocrine gland, the seminiferous epithelium is very sensitive not only to hypoxia, but also to a gonadotrophin deficiency secondary to decreased blood flow caused by stenosis of the arterial vessels. To further complicate the correct interpretation of spermatogenesis lesions, the following must also be considered. Apart from advanced age, patients may also have pathology of other organs like the liver or kidney, the function of which directly interferes with testicular function. It should also not be forgotten that many patients are undergoing treatment with drugs that may be gonadotoxic. The term arteriosclerosis, which etymologically only refers to a hardening of the arterial wall, groups three different lesions together: atherosclerosis, arteriolosclerosis, and Mönckeberg medial calcific sclerosis. Peculiar forms of testicular artery involvement are arteriosclerosis obliterans and arteriolar hyalinosis.