Abstract

BackgroundTo study the diagnostic and therapeutic features of pituitary tumorous hyperplasia due to primary hypothyroidism.MethodsFifteen patients with pituitary tumorous hyperplasia were studied in clinical manifestation, pathologic, endocrinological, radiographic and therapeutic features retrospectively.ResultsAll of these patients suffered from primary hypothyroidism. Magnetic resonance imaging (MRI) scanning found that there were masses in the sellar region with equal T1 and little longer T2 signal, and which could be obviously enhanced by gadolinium EDTA injection. Diameters of these masses were between 1.1 and 2.5 cm. Thyroxine substitution therapy was ordered. Four months later, MRI scanning found that the masses disappeared and only normal pituitary gland left. Plasma thyroxine, thyroid-stimulating hormone (TSH), and prolactin (PRL) levels dropped to their normal ranges.ConclusionsThyroxine substitution therapy was the first choice of pituitary tumorous hyperplasia due to primary hypothyroidism. If they are followed by TSH adenoma, or the optic chiasma was pressed by the enlarged pituitary, transsphenoidal microsurgery could be applied.

Highlights

  • To study the diagnostic and therapeutic features of pituitary tumorous hyperplasia due to primary hypothyroidism

  • From January 1999 to January 2006, 15 patients with pituitary tumorous hyperplasia due to primary hypothyroidism were hospitalized in our department

  • The Magnetic resonance imaging (MRI) scans found a mass in the sellar region with equal T1 and little longer T2 signal, and the mass could be obviously enhanced with Gd-EDTA injection

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Summary

Results

All of these hospitalized patients were diagnosed to have primary hypothyroidism according to clinical symptoms, laboratory examinations, laboratory dynamic hormone-. If the results show that TSH level declined partially, but the thyroid function made no significant improvement, longterm increased secretion of anterior pituitary TSHsecreting cells should be considered [2]; and this may lead to the formation of adenoma on the basis of TSHsecreting cell hyperplasia. If this happened, microsurgical resection via a transsphenoidal approach could be ordered. If after more than 4– 6 months of thyroxine tablet substitute therapy, serum TSH level declined but serum PRL level remained high, and amenorrhea and lactorrhea continued, while enlarged pituitary did not shrink in MRI scan, in this case, we should consider whether there is a pituitary PRL adenoma or not

Conclusions
Results of laboratory examination
Discussion
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