ESPE Abstracts

GH deficiency (GHD) associated hypoglycaemia in infancy is an indication for GH treatment, although it is described in GHD1in older children. At that time, GH is prescribed in GHD for short stature. Here, two children are described in whom hypoglycaemia is the main reason to treat with GH. Patient one had hypoglycaemic seizures due to GHD in infancy. GH treatment was stopped with 5.5 y for reassessment. Growth rate diminished and hypoglycaemias occurred. Treatment of GH was restarted and continuous glucose was monitored during GH. Patient two with partial monosomy 18q had hypoglycaemias up from 6 y. Pre-treatment continuous glucose was determined and GH started. Assessment for metabolic or endocrine disorder was performed in both patients. Both patients had only GHD. Patient one, borderline cortisol induced a substitution between 2 and 5.5 y. Then, normal cortisol (peak in diurnal profile 21 mg/dl) was encountered. Peak GH concentrations after stimulation were 8.8 ng/dl for patient one and 4.75 ng/dl for patient 2. Patient 1 had no GH above 6 ng/ml in spontaneous GH secretion – assessed due to continuing hypoglycaemias. Nadir glucose was 45 mg/dl in patient 1 and 48 mg/dl in patient two. Both had day and night time hypoglycaemias. During assessment, we noticed that patient one ate large amount of sucrose to counter regulate hypoglycaemia. Since GH reduced but did not stop this, we re-monitored glucose profile. Hypoglycaemias occurred in the morning and around 6 pm. We divided the GH dose into 1/5 am and 4/5 pm. Then, low blood glucose occurred only around 6 pm, which was managed by diet. In patient two, we therefore started with divided GH doses with no further hypoglycaemias. Hypoglycaemia may be the predominant feature of GHD beyond infancy. The management of day time hypoglycaemias must be considered in GHD.