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We reported a rare case of pleomorphic TSH-producing pituitary adenoma with calcification and reviewed the literature. A 25-year-old female was admitted to our hospital with a complaint of anterior neck swelling. An endocrinological examination demonstrated elevated serum levels of free triiodothyronine (FT3: 5.6 pg/ml), free thyroxin (FT4: 2.2 ng/dl), TSH (5.85 microIU/ml), and TSH a-subunit (5.9 ng/ml), whereas a physical examination revealed no goiter. CT scan showed a suprasellar isodensity mass with dense calcification. Contrast-enhanced T1-weighted images revealed a less enhancing tumor extending from the left upper portion of pituitary fossa into suprasellar cistern. The patient underwent gross total removal of the tumor via the right pterional approach. Microscopically, medium-sized to enlarged tumor cells with marked pleomorphism and prominent calcification were observed. The tumor cells displayed positive reaction for TSH (beta-subunit). The MIB-1 index averaged 2.9%. The histological diagnosis was a pleomorphic TSH-producing pituitary adenoma. Postoperatively, the serum levels of FT3, FT4, TSH, and TSH alpha-subunit decreased to normal range. Follow-up MR images showed no evidence of recurrent tumor 3 years after the resection. All of six patients with densely calcified TSH-producing pituitary adenoma, previously reported in the literature, remained well without tumor recurrence. We suggest that this type of TSH-producing pituitary adenoma may be associated with favorable prognosis despite histologically pleomorphic appearance.

We investigated propofol pharmacokinetics in a patient with secondary hyperthyroidism caused by thyroid stimulating hormone (TSH) producing pituitary adenoma. Laboratory data indicated thyrotoxic state with elevated TSH, FT3 and FT4 levels. General anesthesia was maintained with a doubled propofol infusion rate (8-10 mg.kg-1.hr-1) compared to our standard procedure. During 370 min of infusion, propofol concentrations in arterial blood were kept within optimal ranges (2-4 micrograms.ml-1). Although the clearance of propofol was high (2.8 l.min-1) because of the thyrotoxic state, the patient showed delayed recovery from anesthesia. The half-life of blood propofol after the termination of infusion exceeded 30 minutes (normal: 10-15 minutes). We conclude that the delayed recovery was due to the accumulation of propofol in the adipose tissue during long-term infusion in spite of the increased propofol clearance.

The pituitary glycoprotein hormone, TSH, is synthesized and secreted by thyrotrophs in the anterior pituitary. Similarly to other pituitary glycoproteins, LH and FSH, it consists of two non-covalent subunits, alpha and beta. The alpha-subunit is common to all three hormones, while the beta-subunit is unique for each hormone. Both subunits are synthesized as separate peptides from distinct mRNA. T3 is the most important negative regulator of the TSH gene. The T3-T3 receptor complex binds to the specific promoter region, T3 response element (TRE), of its target genes and regulates the transcriptional activities. Although TREs have been studied in many genes, the TSH beta-TRE has not yet been fully identified. The mechanism how T3 suppresses TSH beta gene remains undetermined. Another important TSH gene regulator, TRH, is considered to stimulate the transcriptional activity by binding to the different promoter region of TSH beta gene. The interaction between TRH-response element and Pit-1/GHF-1, the pituitary specific factor, -response element is interesting. TRH affects TSH glycosylation, which is important to the biological activity. TSH in central hypothyroid patients is known to have a lower ratio of biological per immunological activity. Recently, in cases with congenital isolated TSH deficiency, a point mutation has been identified in the CAGY region of TSH beta gene, which is critical for dimer formation between alpha- and TSH beta-subunits.