Basal and Stimulated Inhibin B in Pubertal Disorders

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 reassurance or intervention. Researchers have thus long been searching for a robust test to indicate whether 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. Entry into puberty is characterized by a rise in inhibin B levels in both genders. For the past 2 decades, researchers have been studying the role of inhibin B in the differential diagnosis of DP and PP. Initial studies showed promising results for using inhibin B to distinguish between constitutional (or self-limited) DP and congenital hypogonadotropic hypogonadism. However, diverse population studies have revealed varying cutoffs, 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 concentrations were found to be more reliable than basal levels for investigation of pubertal disorders. This review examines the current status of basal-iB in the differential diagnosis of DP and PP, addressing its main advantages and limitations, and shedding light on the role of stimulated inhibin B concentrations.