OBJECTIVE: It remains uncertain whether there is any disadvantage imposed upon women with pituitary disease who are GH-deficient and become pregnant. The aim of this study was to determine whether maternal GH deficiency adversely affects the outcome of pregnancy. DESIGN: Retrospective study. METHODS: The case notes of 77 female patients with known GH deficiency were examined. Sixteen patients (a total of 25 pregnancies) were identified who had been pregnant whilst known to be GH-deficient. Peak GH response to provocative testing prior to pregnancy, length of gestation, birth weight, maternal well-being and the incidence of maternal and fetal complications of pregnancy were documented. RESULTS: Peak GH response to insulin tolerance test (n = 21 ) or glucagon stimulation test (n = 4) prior to pregnancy was 8.7 (< 1 to 17.3)mU/l (peak < or =9 mU/l in 14 cases). There were 25 pregnancies resulting in 26 live births (including one set of twins and one set of quins) and 4 spontaneous first trimester abortions. Eight pregnancies were achieved by ovulation induction. Median gestation of live births was 39 (33 to 42) weeks. Median birth weight excluding multiple births (n = 19), uncorrected for gestational age, was 3.09 (1.64 to 4.19) kg, and the numbers with birth weights below the 10th, between the 10th and 90th, and above the 90th centiles were five, nine and five respectively. Preeclampsia occurred in two pregnancies and post-partum haemorrhage after one pregnancy. There were three minor congenital abnormalities. CONCLUSIONS: Our data suggest that pregnancy in GH-deficient females is not detrimental to the fetus and the incidence of maternal morbidity is low. We conclude that GH replacement therapy is probably not essential for GH-deficient females during pregnancy.
OBJECTIVE: It remains uncertain whether there is any disadvantage imposed upon women with pituitary disease who are GH-deficient and become pregnant. The aim of this study was to determine whether maternal GH deficiency adversely affects the outcome of pregnancy. DESIGN: Retrospective study. METHODS: The case notes of 77 female patients with known GH deficiency were examined. Sixteen patients (a total of 25 pregnancies) were identified who had been pregnant whilst known to be GH-deficient. Peak GH response to provocative testing prior to pregnancy, length of gestation, birth weight, maternal well-being and the incidence of maternal and fetal complications of pregnancy were documented. RESULTS: Peak GH response to insulin tolerance test (n = 21 ) or glucagon stimulation test (n = 4) prior to pregnancy was 8.7 (< 1 to 17.3)mU/l (peak < or =9 mU/l in 14 cases). There were 25 pregnancies resulting in 26 live births (including one set of twins and one set of quins) and 4 spontaneous first trimester abortions. Eight pregnancies were achieved by ovulation induction. Median gestation of live births was 39 (33 to 42) weeks. Median birth weight excluding multiple births (n = 19), uncorrected for gestational age, was 3.09 (1.64 to 4.19) kg, and the numbers with birth weights below the 10th, between the 10th and 90th, and above the 90th centiles were five, nine and five respectively. Preeclampsia occurred in two pregnancies and post-partum haemorrhage after one pregnancy. There were three minor congenital abnormalities. CONCLUSIONS: Our data suggest that pregnancy in GH-deficient females is not detrimental to the fetus and the incidence of maternal morbidity is low. We conclude that GH replacement therapy is probably not essential for GH-deficient females during pregnancy.