Evaluation of the Effect of Alpha2-Adrenergic Receptor Stimulation on Prolactin Secretion Using the Clonidine Test in the Diagnosis of Children with Short Stature

TL;DR

This study examines how clonidine affects prolactin levels in children with short stature, finding differences between those with growth hormone deficiency and those with idiopathic short stature.

Contribution

The study reveals that clonidine suppresses prolactin in both groups but recovery occurs only in idiopathic short stature, suggesting GH signaling may regulate prolactin.

Findings

Clonidine suppresses prolactin in both ISS and GHD children.

Prolactin recovers in ISS but remains suppressed in GHD.

GH and PRL levels correlate at 90 and 120 minutes post-clonidine.

Abstract

Prolactin (PRL) and growth hormone (GH) originate from somatomammotropic cells and share regulatory mechanisms. Alpha2-adrenergic receptor stimulation with clonidine is routinely used in diagnosing GH deficiency (GHD), yet its effect on PRL secretion remains unclear. This study aimed to assess the impact of clonidine-induced α2-adrenergic receptor stimulation on PRL secretion and compare PRL dynamics between children with idiopathic short stature (ISS) and GHD. Forty-nine children with height < −2.0 SD (29 ISS, 20 GHD) underwent clonidine stimulation (0.15 mg/m2 administered orally). Serum GH and PRL were measured at 0, 30, 60, 90, and 120 min. Groups did not differ in chronological age, bone age, height SDS, or BMI SDS. Both groups exhibited a significant decrease in PRL at 30, 60, and 90 min compared to baseline. In ISS, PRL concentrations increased from 60 min onward, returning near baseline at 120 min. In GHD, PRL remained suppressed throughout the test. GH and PRL concentrations correlated positively at 90 (r = 0.35, p < 0.05) and 120 min (r = 0.35, p < 0.05). Clonidine-induced alpha2-adrenergic stimulation suppresses PRL in both ISS and GHD, but recovery is observed only in ISS, suggesting a potential involvement of GH signaling in PRL regulation.

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