Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 164-196-Pituitary
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-185
Natalia Volkova*1, Maria Antonenko2 and Igor Reshetnikov3
1Rostov State Med Univ, Rostov on Don, Russia, 2Rostov State Med Univ, Rostov-on-don, Russia, 3Rostov State Medical University, Rostov-on-Don, Russia
Background:the result of surgical treatment of acromegaly is often accompanied with secondary hypothyroidism and adrenal insufficiency. Here we present a clinical case with developed concurrent Graves’ disease (GD) inspite of expected secondary hypothyroidism at surgically treated patient with acromegaly.

Clinical Case: the patient male 53 y.o. observed the first signs of acromegaly (increase of hands and feet, changed facial features) in 2003. In December 2005, the patient was seen by endocrinologist. Basing on increased IGF-1 level 1246 ng/ml (N 89-255ng/ml), brain MRI findings (pituitary lesion 11*8*7 mm with endosellar grow), there was diagnosed acromegaly (somatotropinoma). The was  performed transsphenoidal lesion resection. Postoperatively, IGF-1 was not in reference range. On brain MRI there was residual pituitary mass 6*7*6 mm. The patient  was offered a reoperation. Hovewer, he declined. In 2011, the patient noted new signs of acromegaly. Due to the deterioration, he applied to be reoperated again. Postoperativelly, there was only developed secondary adrenal insufficiency, and glucocorticoid replacement therapy was started, therefore. The levels of IGF-1 and results of GH supression test were consistent with surgical cure. After 3 months there was time to perform hormonal evaluation (the function of gonadal axis and thyroid function). Within a time of evaluation, there was developed significant weakness, appetite loss, weight loss (-18kg). At that time the patient was also seen by oncologist and there was supposed oncology disease. Hovewer, the signs were consistent with non-compensated adrenal insufficiency. Gonadal function was decreased. TSH was suppressed and free T4 was increased. Thus, in inspite of expected secondary hypothyroidism, there was presented hyperthyroidism. The level of TSH receptor antibody was 8.5IU/ml (<1.5IU/ml) allowed to set the diagnosis of GD. The dose of glucocorticoids was increased. Medical and than surgical treatment of GD was performed. The patient returned to initial glucocorticoid dose. Hormonal replacement therapy was also presented with thyroxin and testosteron. Nowadays, he is in remission state of acromegaly.

Conclusion: this clinical case presents an uncommon combination of acromegaly and concurrent GD. It also underlines the great importance of strictly guideline following that has helped to manage this difficult clinical situation and prevent unuseful diagnostics and treatment.


Nothing to Disclose: NV, MA, IR

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