Evolution of glycated haemoglobin in adults on growth hormone replacement therapy
Paola Andrea Parra R1, Beatriz Barquiel A1, Alberto Fernández M1
1Endocrinology Department, La Paz University Hospital, Paseo de La Castellana 261, 28046 Madrid, Spain.
Insights
Growth hormone replacement therapy (GHR) increased glycated haemoglobin (HbA1c) in patients with growth hormone deficiency (GHD) during the first two years. Patients without prior dysglycaemia showed a sustained HbA1c increase, while those with baseline dysglycaemia experienced no significant change.
Area of Science:
- Endocrinology
- Metabolic Disorders
- Clinical Research
Background:
- Adult growth hormone deficiency (GHD) impacts metabolic health.
- Glycated haemoglobin (HbA1c) is a key marker for glucose control.
- Understanding the long-term effects of GHR on glucose metabolism is crucial.
Purpose of the Study:
- To assess the 3-year impact of GH replacement therapy (GHR) on HbA1c.
- To evaluate the incidence of dysglycaemia during GHR in GHD patients.
- To analyze GHR effects based on baseline glycemic status.
Main Methods:
- Retrospective analysis of 41 adult GHD patients.
- Collected baseline and 3-year follow-up data on HbA1c.
- Defined dysglycaemia as fasting plasma glucose ≥ 100 mg/dl or HbA1c ≥ 5.7%.
Main Results:
- Mean HbA1c increased in the first two years of GHR (p<0.05).
- HbA1c levels stabilized in the third year.
- 68.2% of patients developed dysglycaemia; those without baseline dysglycaemia showed a sustained HbA1c rise.
Conclusions:
- GHR therapy leads to an initial increase in HbA1c over two years.
- Patients initiating GHR without dysglycaemia experience a progressive rise in HbA1c.
- GHR does not significantly alter HbA1c in patients with pre-existing dysglycaemia.
Objectives:
To evaluate the effects of GH replacement therapy (GHR) for 3 years on glycated haemoglobin (HbA1c) and on the presence of dysglycaemia at any time during follow-up in Spanish adult patients with growth hormone deficiency (GHD).
Study Design:
A retrospective study of 41 patients with GHD was conducted using baseline and long-term data. Changes in HbA1c values during the first 3 years of GHR were studied in both the overall population and patients with or without dysglycaemia during follow-up. Dysglycaemia was defined as FPG ≥ 100 mg/dl and/or HbA1c ≥ 5.7%.
Results:
Mean HbA1c value (5.4 ± 0.4% at baseline) increased during the first and second years of GHR (HbA1c 5.5 ± 0.4%, p=0.05, and 5.5 ± 0.4%, p=0.006 respectively). This increase was not maintained during the third year (HbA1c 5.4 ± 0.3%, p=0.107) of GHR. Twenty-eight patients (68.2%) had dysglycaemia during follow-up, 9 of them since baseline. In the 19 patients without baseline dysglycaemia, HbA1c increased during the first year and remained stable in the next 2 years (mean HbA1c 5.2 ± 0.4% at baseline; 5.5 ± 0.4% at 1 year, p<0.050; 5.4 ± 0.4% at 2 years, p=0.004, and 5.4 ± 0.4% at 3 years, p=0.016). In the 9 patients with baseline dysglycaemia, HbA1c did not significantly change during the 3 years of GHR therapy.
Conclusions:
HbA1c values increased during the first 2 years of GHR therapy. In patients with no dysglycaemia before treatment, HbA1c steadily increased over the 3 years. However, it did not change in patients with baseline dysglycaemia.
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