Excess GH secretion has a well recognized association with McCune-Albright;
syndrome. Although there have been a number of reported pregnancies in unc
ontrolled acromegaly, none has been described in the McCune-Albright syndro
me. We have studied the GH and insulin-like growth factor I (IGF-I) profile
s in a patient with confirmed McCune-Albright syndrome and GH hypersecretio
n throughout a successful pregnancy and postpartum period.
Prepregnancy, IGF-I was 60.6 nmol/L (normal, 18.0-43.1), and the daytime GH
profile measured using assay A was 9.6-14.0 mU/L. At 13 weeks gestation th
ere was a decline of IGF-I to 33.9 nmol/L and in the daytime GH profile (as
say A) to 5.4-6.8 mU/L. At 24 weeks, IGF-I had risen to 51.6 nmol/L. A simu
ltaneous daytime GH profile at this time using assay A revealed levels betw
een 21.3-22.1 mU/L, but only 2.1-3.0 mU/L with assay B. Assay A has signifi
cant cross-reactivity with human placental lactogen (HPL), unlike assay B.
At 36 weeks, IGF-I was still elevated at 56.6 nmol/L, with a daytime GH pro
file of 16.6-11.7 mU/L using assay A. and 1.5-3.9 mU/L with assay B. At 12
weeks postpartum, IGF-I was 71.4 nmol/L, and the daytime GH profile with as
say B was 5.6-8.6 mU/L. These data support a picture of GH suppression duri
ng pregnancy in acromegaly associated with McCune-Albright syndrome, shown
best with assay B, which discriminates between GH and HPL.
These results contrast with previous reports of pregnancy in uncontrolled a
cromegalics, in whom pituitary GH levels were unaffected by pregnancy, and
total GH and IGF-I levels were noted to be elevated. These data suggest tha
t GH secretion in a pregnant acromegalic with the McCune-Albright syndrome
may not be entirely autonomous, as seen in classic acromegaly, but may be a
ssociated with a degree of negative feedback control that could be exerted
by a circulating factor of placental origin, probably HPL or placental GH.