Endocrine Abstracts

GH deficiency (GHD) in adults is characterized by a tendency towards fat mass gain and may predispose to type 2 diabetes mellitus.GH replacement (GHR) is associated with impaired insulin sensitivity shortly after starting therapy, reflected by increased fasting glucose and insulin levels. Available evidence suggests that concerns regarding glucose intolerance in patients receiving long-term GHR have not been substantiated. However, several environmental and lifestyle-related factors could influence glucose abnormalities in patients with GHD, and no study has specifically addressed this issue in spanish patients. Thus, we aimed to describe the evolution of carbohydrate metabolism (fasting glucose (FG) and HbA1c) and ascertain possible risk factors for developing glucose abnormalities in adult patients receiving GHR.

We analyzed retrospectively 34 GDH adults (mean age 40.4 years; 16 females) from our centre who received GHR for at least 2 years (mean duration of treatment was 7.4 years). FG, HbA1c and anthropometric parameters were measured before starting treatment and at the end of the follow-up. Associations were tested by Mann–Whitney U test between baseline variables (age, BMI, total body fat, total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides, mean maintenance dose of GH, and glucocorticoid replacement) and these metabolic variables.

None were diabetic at baseline. FG and HbA1c were significantly higher at the end of follow-up when compared to baseline (+6.7 ( S.D.11.08) mg/dl P=0.001 and +0.2 (S.D.0.4) % P=0.014 respectively). Average HbA1c increase was 0.23%. No significant changes were observed in BMI or body composition. Six patients had dysglucosis, 4 (11.7%) developed diabetes and 2 (5.7%) impaired fasting glucose. However, no predefined baseline traits were significantly related to the metabolic derangements, including glucocorticoid replacement.

In conclusion, our results indicate that long-term GHR mildly increases FG and HbA1c. Current hydrocortisone replacement regime was not associated with dysglucosis in our series.