ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2019) 63 P233 | DOI: 10.1530/endoabs.63.P233

Silent somatotropic adenoma: about a case

Sara Askaoui, Guizlane Lmghari, Sana Rafi & Nawal El Ansari


Departement of Endocrinology, Med VI, Marrakech, Morocco.


Introduction: Somatotropic adenomas are classically a source of hypersecretion of GH and consequently of IGF1 responsible for the clinical signs of acromegaly. Rarely, these adenomas remain ‘silent’, without any obvious clinical manifestation. They can then be detected on the basis of a routine determination of growth hormone under oral glucose tolerance test (GH/OGTT) and insulin growth factor 1 (IGF1) or be diagnosed only to immunohistochemical study as is the case of a patient we report.

Observation: Patient of 33-year-old, consult for secondary amenorrhea with galactorrhea. Clinical examination did not indicate a dysmorphic syndrome. A pituitogram was performed showing the presence of thyrotropic and corticotropic insufficiency, with a prolactin level of 153 ng/ml. The somatotropic axis has not been explored. A pituitary MRI revealed a hypophysary macroadenoma treated as prolactinoma by cabergoline with substitution of both deficits. The evolution at one year was marked by the increase (by 17%) of the tumor volume with a prolactin control at 0, 22 ng/with an altered visual field. An echo-heart was requested, revealing the presence of an average tricuspid insufficiency, the surgical indication was raised. Immunohistochemical analysis favors a somatotropic adenoma. A postoperative 3-month postoperative pituitary MRI showed constant tumor volume with some necrosis areas with IGF1 at 131 ug/l (112–300).

Discussion: Somatotropic adenomas are often identified because of their clinical consequences (dysmorphism); some cases of subclinical adenomas have been described in the literature, where only histopathological examination reveals a positive immuno-marking for GH. Their frequency is poorly studied: in the absence of an immunohistochemical study, a non-functional adenoma is concluded and IGF1 is not carried out as part of the follow-up; all this leads to a diagnostic delay giving later dysmorphism with the various complications of hypersecretion of GH. Treatment of this type of adenoma is initially based on surgery, then somatostatin analogues and lastly time on temozolamide and radiotherapy if signs of aggression.

Conclusion: Silent somatotropic adenoma is a distinct entity with respect to the usual cases of acromegaly, as it may be an onset of the disease, or a benign aspect of the disease?

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