Low risk of impaired testicular Sertoli and Leydig cell functions in boys with isolated hypospadias

REY RA; CODNER E; IÑÍGUEZ G; BEDECARRÁS P; TRIGO R; OKUMA C; GOTTLIEB S; BERGADÁ, I; CAMPO SM; CASSORLA FG

JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM

ENDOCRINE SOC

Lugar: Chevy Chase; Año: 2005

0021-972X

Context: Isolated hypospadias may result from impaired testicularfunction or androgen end-organ defects or, alternatively, from hormone-independent abnormalities of morphogenetic events responsiblefor urethral seam.Objective: The objective was to evaluate the relative prevalence ofhormone-dependent etiologies in boys with isolated hypospadias.Design, Patients, and Main Outcome Measures: We studied endocrinetesticular capacity in 61 patients with isolated hypospadiasand 28 with hypospadias associated with micropenis, cryptorchidism,or ambiguous genitalia. Serum anti-Mu¨ llerian hormone and inhibinB were used as Sertoli cell markers. A human chorionic gonadotropintest was performed to evaluate Leydig cell function.Results: Testicular dysfunction was observed in 57.1% and androgenend-organ defects in 7.2% of patients with hypospadias associatedwith cryptorchidism, micropenis, or ambiguous genitalia. In the remaining35.7%, the disorder was idiopathic. The presence of ambiguousgenitalia predicted the existence of testicular or end-organ dysfunctionwith 81.8% specificity. Isolated hypospadias was associatedin 14.8% of patients with testicular dysfunction and in 6.5% of caseswith end-organ defects; in 78.7% of cases, the condition was idiopathic.The occurrence of isolated hypospadias ruled out the existenceof testicular or end-organ disorders with 80.0% sensitivity. Altogetherour data indicate that the risk for the existence of an underlyingtesticular or end-organ dysfunction is low in patients with isolatedhypospadias (odds ratio, 0.13; 95% confidence interval, 0.05?0.36; P0.001).Conclusions: Boys with isolated hypospadias are more likely to havenormal endocrine testicular and androgen end-organ functions, suggestingthat transient disruption of morphogenetic events in earlyfetal life may be the predominant underlying cause.