Basal and stimulated inhibin B in pubertal disorders.

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Pubertal disorders in the form of delayed puberty (DP) or precocious puberty (PP) can cause considerable anxiety to both children and parents. Since the clinical and biochemical signatures of self-limiting and permanent conditions overlap considerably, it can be hard to determine whether to offer them reassurance or intervention. Researchers have thus long been searching for a robust test to indicate that the process of endogenous puberty is underway and is likely to proceed to completion. Although existing tests are available, such as basal gonadotropins, gonadotropin-releasing hormone (GnRH)-stimulated luteinizing hormone, and basal and human chorionic gonadotropin-stimulated testosterone, their diagnostic specificity is inadequate. Inhibin B, a glycoprotein hormone, is secreted by Sertoli cells in males and small antral follicles in females. The entry into puberty is characterized by a rise in inhibin B levels in both genders. For the past two decades, researchers have been studying the role of inhibin B in the differential diagnosis of DP as well as PP. Initial studies showed promising results for using inhibin B to distinguish between constitutional (or self-limited) DP (SLDP) and congenital hypogonadotropic-hypogonadism (CHH). However, diverse population studies have revealed varying cut-offs, limiting the use of basal inhibin B(basal-iB) in routine clinical practice. Recently, the concept of stimulated inhibin B has been introduced, using either follicle-stimulating hormone (FSH) or GnRH-analogs. Both FSH- and GnRH-analog-stimulated inhibin B concentration were found to be more reliable than basal levels in the investigation of pubertal disorders. This review examines the current status of basal-iB in the differential diagnosis of delayed and precocious puberty, addressing its main advantages and limitations, and shedding light on the role of stimulated inhibin B concentrations.