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Testicular regression syndrome — a pathological study of 77 cases
Author(s) -
SMITH N.M.,
BYARD R.W.,
BOURNE A.J.
Publication year - 1991
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1111/j.1365-2559.1991.tb00033.x
Subject(s) - spermatic cord , calcification , pathological , pathology , medicine , epididymis , in utero , testicular artery , dystrophic calcification , testicle , anatomy , fetus , biology , artery , andrology , pregnancy , sperm , genetics
Testicular regression syndrome is characterized by a rudimentary epididymis and spermatic cord with absence of testicular tissue. Although it has been well‐described in the surgical literature, few pathological studies have been performed. We report 77 cases of the syndrome, deriving from a 26‐year retrospective review. Typical gross descriptions described several cm of spermatic cord with a small mass of firm, fibrotic tissue at one end; elements of the vas deferens, spermatic artery and venous plexuses were usually present. Histologically, the distal expansion of most of the specimens was composed of dense fibrovascular tissue with no evidence of seminiferous tubules or normal testicular elements. Instead, scattered foci of calcification and brown pigment were present. The finding of dystrophic calcification and haemosiderin deposition, with no evidence of viable testicular tissue, in the presence of relatively normal spermatic cord elements, supports the concept of generally unilateral and occasionally bilateral anorchia secondary to remote infarction. The young age of the patients, coupled with the history of an absent testis from birth, is supportive of in utero damage. These histopathological findings provide support for the concept of in utero torsion of the testis as the basis for the testicular regression syndrome.