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Bone Abstracts (2019) 7 P153 | DOI: 10.1530/boneabs.7.P153


Long-term growth hormone treatment alters glucose metabolism in achondroplasia

Daisuke Harada, Hiroko Kashiwagi, Kaoru Ueyama, Kyoko Oriyama, Yuki Hanioka, Natsuko Sakamoto, Kawai Kondo Masafumi Izui, Yuiko Nagamatsu, Hiroyuki Yamada, Yoshiki Seino & Noriyuki Namba


Osaka Hospital, Japan Community Healthcare Organization (JCHO), Osaka, Japan.

Objective: To investigate the effect of growth hormone (GH) treatment on glucose metabolism in achondroplasia (ACH) patients.

Patients and methods: Twenty-five GH-treated (0.35 mg/kg/week) ACH patients (10 males and 15 females) were included in this study. Oral glucose tolerance test (OGTT) was performed at three time points; ‘pre-treatment’ (age: 4.0±1.9 years), ‘post short-term treatment’ (age: 6.5±3.0 years), and ‘post long-term treatment’ (age: 11.8±3.4 years). We evaluated homeostasis model assessment of insulin resistance (HOMA-IR, fasting insulin (μU/mL) × fasting glucose (mg/dL) / 405) and β cell function by calculating insulinogenic index (IGI, Δinsulin (μU/mL) / Δglucose (mg/dL)). Statistical analysis was performed with Mann-Whitney’s U test or analysis of variance (ANOVA) followed by multiple comparison using Tukey’s test.

Results and discussion: No patients were diagnosed as diabetes mellitus throughout the observation period. Prediabetes was detected at least one time point in 32% (8/25) of the patients before or after initiation of GH administration (prediabetes group). GH treatment increased both HOMA-IR (pre: 0.7±0.4, post short-term: 1.9±1.2, post long-term: 2.2±0.9, P<0.01) and IGI (pre: 0.25±0.19, post short-term: 0.98±0.42, post long-term: 1.02±0.51, P<0.05), although the increase was within normal range. There was no difference in HOMA-IR between the prediabetes and the normal groups at pre-treatment or post long-term GH treatment. However, in the prediabetes group, HOMA-IR was higher at post short-term GH treatment (2.6±1.5 vs 1.6±0.8, P<0.05). IGI was lower at pre-treatment in the prediabetes group than in the normal group (0.06±008 vs 0.38±0.05, P<0.01), but there was no significant difference during GH treatment.

Discussion and conclusion: Although residual β cell function sufficiently counteracts insulin resistance induced by GH, OGTT may demonstrate prediabetes in ACH patients with low β cell function. Since low IGI at pre-treatment and/or marked increase of HOMA-IR at post short-term GH treatment seems to be related to transient prediabetes, vigilant monitoring of glucose metabolism should be performed when administrating GH to ACH patients with these findings.

Disclosure: The authors declared no competing interests.

Volume 7

9th International Conference on Children's Bone Health


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