Endocrine Abstracts

Introduction: Acromegaly increases morbidity and mortality and should be treated even in the asymptomatic phase. It is almost always caused by a GH-producing pituitary adenoma and although transsphenoidal surgery is the treatment of choice in most cases, in others, primary medical therapy is indicated.

Clinical case: A 36-year-old female with a family history of thyroid functional pathology and diagnosed with micronodular goiter was evaluated in February 2015 for a transient minimal galactorrhea, unrelated with drugs and without other associated symptoms or signs. In the biochemical tests the following was observed: IGF-I 640 ng/ml (100–330), GH 1.4 ng/ml (0–4.3). Prolactin, FSH, LH, estradiol, cortisol, T4-free and TSH, calcium, phosphorus, renal and hepatic functions were normal. Pituitary magnetic resonance (MR) detected an increase in pituitary size at the expense of a 20 × 12 × 15 mm-sized lesion, bilaterally predominantly left, minimally hyperintense in T2, with some microcyst, hypointense in T1 and hypocaptant with respect to the rest of the gland. It partially invaded the left cavernous sinus and slightly bulged the upper contour of the gland without compromising the suprasellar structures. The pituitary stalk was discreetly horizontal and somewhat lateralized to the right. Given the existence of a macroadenoma that did not compress the optic chiasma and impossible to eliminate completely due to the extension to the cavernous sinus, Sandostatin LAR IM was prescribed, initially 20 and then 30 mg/month. One year later, the patient remained asymptomatic but, given the absence of a biochemical (IGF-I 674 ng/ml, GH 3 ng/ml) and morphological response we agreed to suspend this therapy and reassess the results of IGF-I with another methodology and performing oral glucose overload (baseline GH 5.2 ng/ml, nadir 2 ng/ml). After confirming acromegaly, in July 2017, we started treatment with Pasireotide-LAR IM 40 mg/month and 3 months later the IGF-I was within normal range. The October 2018 pituitary MR showed a reduction in size of the adenoma to 12 × 9 × 8 mm and that it contacted the left internal carotid artery without extending to the walls of the cavernous sinus. To date, with this therapy, the patient maintains biochemical normality with no significant side effects.

Discussion: In this patient with pituitary macroadenoma without surgery indication and null response to first generation somatostatin analogues, it was not possible to personalize the initial medical therapy. Pasireotide-LAR, chosen as second option, produced a biochemical and morphological response.