Early postnatal testicular maldevelopment in cryptorchidism.
It has been previously postulated that many cases of cryptorchidism are manifestations of a forme fruste of hypogonadotropic hypogonadism. In support of this theory the earliest postnatal histological abnormality in cryptorchid testes demonstrated by this morphometric study of semithin microscopic sections of testicular biopsies was hypoplasia of the Leydig cells, which was obvious from the first month of life. The second abnormality, defective transformation of gonocytes into adult dark spermatogonia, was significant from early in life. No reduction in the mean number of germ cells was detected in the first 7 months of life. The abnormal persistence of the untransformed gonocytes resulted in a total germ cell count that was similar to normal controls until the seventh month, when secondary degeneration of untransformed gonocytes led to a decrease in the total germ cell count. These findings are compatible with the hypothesis that the blunted neonatal surge of gonadotropins previously demonstrated in cryptorchid boys triggers a cascade of hormonal and secondary histological abnormalities that may culminate in a reduced fertility potential in adults. Early replacement hormonal therapy deserves further investigation as a rational approach to the treatment of germ cell maldevelopment and reduced fertility potential associated with cryptorchidism.
Division of Urology, Children's Hospital of Philadelphia, Pennsylvania.
D S
DS
Huff
F
F
Hadziselimović
H M
HM
Snyder
B
B
Blyth
J W
JW
Duckett
D001706:Biopsy; D003456:Cryptorchidism / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D005854:Germ Cells; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D007985:Leydig Cells / Q000473:pathology / Q000502:physiology; D008297:Male; D013091:Spermatogenesis / Q000502:physiology; D013093:Spermatogonia; D013737:Testis / Q000254:growth & development* / Q000473:pathology / Q000503:physiopathology