suprasellar mass (arrow). Note the layering of complex fluid within the mass, which was found during surgery to be hemorrhage.
(Used with permission from Dr. April Baily.) his is caused by excessive growth hormone, usually from an acidophilic or a chromophobic pituitary adenoma. In normal pregnancy, pituitary growth hormone levels decrease as placental epitopes are secreted. Diagnosis is confirmed by elevated IGF-1 serum levels (Katznelson, 2014). Fewer than 100 cases of acromegaly have been reported during pregnancy (Cheng, 2012; Dias, 2013; Motivala, 2011). Pregnancy is probably rare in women with acromegaly because half are hyperprolactinemic and anovulatory. During pregnancy, afected women are at marginally greater risk for gestational diabetes and hypertension (Caron, 2010; Dias, 20l3).
Management is similar to that for prolactinomas, with close monitoring for symptoms of tumor enlargement. Dopamine agonist therapy is less efective than for prolactinomas. And, transsphenoidal resection, generally considered irst-line treatment outside of pregnancy, may be necessary for symptomatic tumor enlargement during pregnancy (Motivala, 2011). Guven and associates (2006) reported a case of pituitary apoplexy necessitating emergent transsphenoidal adenoma resection and cesarean delivery at 34 weeks. Successful treatment of pregnant women with the somatostatin-receptor ligand octreotide and with the GH analogue pegvisomant has also been reported (Dias, 2013; Fleseriu, 2015).
The vasopressin deficiency evident in diabetes insipidus is usually due to agenesis or destruction of the neurophypophysis (Robertson, 2015). True diabetes insipidus is a rare complication of pregnancy.
Diabetes insipidus therapy is intranasal administration of a synthetic analogue of vasopressin, desmopressin, which is 1-deamino8-D-arginine vasopressin (DDA P). Ray (1998) reviewed 53 cases in which DDAP was used during pregnancy with no adverse sequelae. Most women require increased doses during pregnancy because of an increased metabolic clearance rate stimulated by placentl vasopressinase (Lindheimer, 1994). By this same mecha nism, subclinicaL diabetes inspidus may become symptomatic or cases of transient diabetes inspidus may be encountered during pregnancy (Bellastella, 2012; Robertson, 2015). he prevalence of vasopressinase-induced diabetes insipidus is estimated at 2 to 4 per 100,000 pregnancies (Wallia, 20l3).
In our experiences, as described in Chapter 55 (p. 1062), transient secondary diabetes insipidus is more likely encoun tered with acute atty Liver of pregnancy (Nelson, 20 l3). This probably is due to altered vasopressinase clearance because of hepatic dysfunction.