Basal and stimulated inhibin B in pubertal disorders

Abstract

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.

Keywords: Constitutional delay in growth and puberty; Delayed puberty; FSH stimulated inhibin B; GnRH agonist stimulated inhibin B; Hypogonadotropic hypogonadism; Inhibin B; Precocious puberty.