SAT-226 - Physiologic Determinants of Blood Pressure Response during Arginine-Clonidine Growth Hormone Stimulation Testing in Children

Background: Arginine–clonidine growth hormone stimulation testing (GHST) is a pediatric standard that produces predictable hypotension via clonidine’s central sympatholytic effects. However, the physiologic determinants and inter-individual variability of blood pressure (BP) responses remain poorly characterized, limiting evidence-based risk stratification.

Objective: To characterize BP trajectories and identify clinical and endocrine predictors of BP decline during GHST.

Methods: We performed a retrospective analysis of 243 children undergoing standardized arginine–clonidine GHST. Serial BP measurements were obtained at 0, 30, 60, 90, and 120 minutes. Pubertal status was defined as Tanner stage ≥ 2. The primary outcome was baseline-to-nadir systolic BP change (ΔSBP). Secondary outcomes included diastolic BP change (ΔDBP), timing of BP nadir, and frequency of large BP declines (≥ 20% and ≥30% SBP reduction). Multivariable linear regression examined predictors of ΔSBP, adjusting for baseline BP, age, sex, pubertal status, BMI z-score, clonidine dose, and GH status (peak GH < 10 ng/mL).

Results: Participants were aged 11±3 years (74% male, 33% pubertal, 39% GH deficient). SBP declined from 108 ± 10 to 91 ± 10 mmHg and DBP from 68 ± 8 to 56 ± 8 mmHg (both p < 0.001). Mean ΔSBP was 23± 11 mmHg; 54% experienced ≥20% SBP decline and 18% experienced ≥30%. BP nadir occurred late at 90–120 minutes in 63% of cases. In multivariable analysis, baseline SBP was the strongest predictor of ΔSBP (β = 0.69 per 1 mmHg; p < 0.001). GH deficiency (β = -3.2; p = 0.012) and BMI z-score (β = -1.1; p = 0.028) showed modest independent associations. Age, sex, and clonidine dose were not associated with ΔSBP. Baseline SBP also predicted ≥30 SBP decline (OR 1.07; p < 0.001), with pubertal participants at higher risk (OR 2.5; p = 0.03). Adverse events occurred in 13%; severe hypotension or syncope was rare (1%) and self-limited.

Conclusion: BP decline during GHST is a reproducible, physiology-driven event primarily determined by baseline hemodynamic state. While GH deficiency and BMI affect the absolute magnitude of decline, they do not predict clinically significant drops. Crucially, the late occurrence of BP nadirs in most patients dictates that hemodynamic monitoring must be maintained through the very end of the test. The increased risk in pubertal children supports heightened vigilance in this subgroup, though the protocol remains overall safe.

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