Adequacy of post-glucose gh nadir <1 μg/l to define biochemical and neuroradiological remission of acromegaly
CL Ronchi1, V Varca1, C Giavoli1, E Ferrante1, A Lania1, M Arosio2, P Beck-Peccoz1 & A Spada1
We previously demonstrated that acromegalic patients with normal IGF-I levels after surgery also met the current criteria for cure (i.e. postglucose GH nadir <1 μg/l) after long term monitoring. Since some Authors recently proposed to even lower the present GH nadir cut off value, the aim of this study was to confirm its adequacy to define long lasting disease remission. A group of 24 acromegalic patients (9 M&15 F, age 54.2±9.6 yrs) normal IGF-I levels and postglucose GH nadir <1 μg/l after 3 months from surgery were revaluated after a median period of 8.5 yrs (range: 419). In all patients, basal and postglucose GH nadir levels, IGF-I concentrations, symptoms score, metabolic parameters such as BMI, fasting and post-OGTT glucose and insulin levels, insulin resistance by HOMA-IR, lipid profile and blood pressure, antero-pituitary functions and magnetic resonance imaging were evaluated. An OGTT was also performed in 29 healthy controls to define the normal GH nadir limit (mean+2 S.D.=0.19 μg/l). In the long term follow-up, IGF-I levels remained in the normal range and postglucose GH nadir <1 μg/l in all the patients. In particular, GH nadir was <0.19 μg/l in 14 patients and above that limit in 10. The 2 groups showed similar interval from surgery (11.3±4.2 vs 8.3±4.3 yrs, P NS), IGF-I concentrations (−0.8±0.6 vs −0.2±1.1 SDS, P NS), metabolic parameters except for BMI (30±6 vs 26±4 Kg/m2, P=0.08), fasting insulin levels (12.4±6.3 vs 6.6±4.0 mU/l, P<0.05) and HOMA-IR (3.1±2.0 vs 1.5±0.9, P<0.05), number of patients with hypopituitarism and/or secondary empty sella. Finally, none of the patients showed any clinical or neuroradiological evidence of disease recurrence. In conclusion, the current GH nadir cut off is still adequate to define long lasting remission of acromegaly in postoperative patients. The occurrence of obesity and insulin resistance in patients with lower GH nadir might imply the presence of a relative GH deficiency in these subjects or suggest that postglucose GH levels are reduced by progressive BMI increase.