Normal Pituitary Gland and Pregnancy

Abstract

The normal pituitary gland enlarges gradually during pregnancy because of estrogen-stimulated hyperplasia and hypertrophy of prolactin cells. In parallel, serum prolactin levels rise and can reach 40 ng/ml at the end of the first trimester, 150 ng/ml by the end of the second trimester, and 200 or even 400 ng/ml at term. MRI is considered safe to follow, if necessary, the changes of the pituitary gland during pregnancy. The precautionary principle dictates to avoid MRI in the first trimester. For the same reason, gadolinium injection is prohibited. The normal pituitary gland height increases linearly by 0.08–0.1 mm/week, i.e., by 3–4 mm at term. The upper surface of the gland becomes more convex superiorly (Fig. 7.1). The pituitary gland height can reach 10 mm during the last trimester and 12 mm in the immediate postpartum period, and approach the optic chiasm. This situation can be more sharply defined in the cases of small sella (Fig. 7.2). It has been said that the pituitary stalk width presents its highest value within the 3 days postpartum; if this is true, it could be related to some enlargement of the pars tuberalis of the anterior pituitary; more likely, this change of the infundibulum corresponds to a shortening of the pituitary stalk in relation to the upward bulging of the pituitary content—the reverse of what is observed in empty sella where the pituitary stalk attached to the hypoplastic pituitary gland is stretched. At the same time, T1 signal intensity of the pituitary gland increases, particularly during the last trimester; this is clear when comparing the T1 signal of the anterior pituitary with that of the temporal white matter on coronal views or with that of the pons on sagittal views. The mechanism of T1 shortening of the anterior pituitary gland during pregnancy has not been fully elucidated. It has been suggested that the mechanism may be related to high protein-synthesis activity, an increase in the bound fraction of water molecules, and/or an increase in the number of secretory granules. Visualization of the normally hyperintense posterior lobe on sagittal T1 view has previously been reported as much less frequent during pregnancy. In fact, by using axial T1 fat-saturation sequences, the posterior lobe is constantly demonstrated just as it is in young nonpregnant women. The reason explaining the poor rate of its visualization on sagittal T1WI during pregnancy in the literature is that the posterior lobe may be slightly compressed and thinned by the enlarged anterior pituitary and pressed against the dorsum sellae (Fig. 7.3). In this situation, the posterior lobe can be masked by the dorsum, especially if the dorsum is not aerated and contains fatty bone marrow; however, the compressed posterior lobe is routinely clearly defined on axial T1WI, preferentially with fat saturation. Another reason is that changes of serum osmolarity in pregnant women lead to an increase of vasopressin release and, consequently, to a decrease of the posterior lobe hyperintensity if compared with that of nonpregnant women of the same age group. In the postpartum period, shrinkage of the pituitary gland is initiated about 2 weeks after delivery (Fig. 7.4). The return of T1 signal of the anterior pituitary to that observed in the nonpregnant state is delayed if the mother is breast-feeding.