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      Thyrotoxicosis with absence of clinical features of acromegaly in a TSH- and GH-secreting, invasive pituitary macroadenoma

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          Summary

          A 54-year-old woman presented with bi-temporal hemianopia, palpitations, and diaphoresis. An invasive pituitary macroadenoma was discovered. The patient had biochemical evidence of secondary hyperthyroidism and GH excess; however, she did not appear to be acromegalic. Surgical removal of the pituitary mass revealed a plurihormonal TSH/GH co-secreting pituitary adenoma. TSH-secreting adenomas can co-secrete other hormones including GH, prolactin, and gonadotropins; conversely, co-secretion of TSH from a pituitary adenoma in acromegaly is infrequent.

          Learning points

          • This case highlights an unusual patient with a rare TSH/GH co-secreting pituitary adenoma with absence of the clinical features of acromegaly.

          • Plurihormonality does not always translate into the clinical features of hormonal excess.

          • There appears to be a clinical and immunohistochemical spectrum present in plurihormonal tumors.

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          Most cited references14

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          Thyrotropin-secreting pituitary tumors.

          H. Beck, R Smallridge, B Weintraub … (1996)
          Article 0 comments Cited 54 times – based on 0 reviews     Review now
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            Pituitary cell phenotypes involve cell-specific Pit-1 mRNA translation and synergistic interactions with other classes of transcription factors.

            D M Simmons, J W Voss, H A Ingraham … (1990)
            Development of the anterior pituitary gland involves proliferation and differentiation of ectodermal cells in Rathke's pouch to generate five distinct cell types that are defined by the trophic hormones they produce. A detailed ontogenetic analysis of specific gene expression has revealed novel aspects of organogenesis in this model system. The expression of transcripts encoding the alpha-subunit common to three pituitary glycoprotein hormones in the single layer of somatic ectoderm on embryonic day 11 established that primordial pituitary cell commitment occurs prior to formation of a definitive Rathke's pouch. Activation of Pit-1 gene expression occurs as an organ-specific event, with Pit-1 transcripts initially detected in anterior pituitary cells on embryonic day 15. Levels of Pit-1 protein closely parallel those of Pit-1 transcripts without a significant lag. Unexpectedly, Pit-1 transcripts remain highly expressed in all five cell types of the mature pituitary gland, but the Pit-1 protein is detected in only three cell types--lactotrophs, somatotrophs, and thyrotrophs and not in gonadotrophs or corticotrophs. The presence of Pit-1 protein in thyrotrophs suggests that combinatorial actions of specific activating and restricting factors act to confine prolactin and growth hormone gene expression to lactotrophs and somatotrophs, respectively. A linkage between the initial appearance of Pit-1 protein and the surprising coactivation of prolactin and growth hormone gene expression is consistent with the model that Pit-1 is responsible for the initial transcriptional activation of both genes. The estrogen receptor, which has been reported to be activated in a stereotypic fashion subsequent to the appearance of Pit-1, appears to be capable, in part, of mediating the progressive increase in prolactin gene expression characteristic of the mature lactotroph phenotype. This is a consequence of synergistic transcriptional effects with Pit-1, on the basis of binding of the estrogen receptor to a response element in the prolactin gene distal enhancer. These data imply that both transcriptional and post-transcriptional regulation of Pit-1 gene expression and combinatorial actions with other classes of transcription factors activated in distinct temporal patterns, are required for the mature physiological patterns of gene expression that define distinct cell types within the anterior pituitary gland.
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              Thyrotropin-secreting pituitary adenomas: outcome of pituitary surgery and irradiation.

              V. Campi, Juan E. Sala, Andrea Lania … (2014)
              Our objective was to describe the effects of surgery and radiotherapy on hormonal control and tumor mass in short- and long-term follow-up of TSH-secreting pituitary adenomas (TSHomas). This was a retrospective multicenter study. We collected data of 70 TSHomas (70% macroadenomas). The mean follow-up was 64.4 (range 3-324) months. Overall, 97% of patients were treated with surgery; in 27% of them radiotherapy was associated. After surgery, 75% of patients normalized thyroid function, 58% normalized both pituitary imaging and hormonal profile, 9% developed pituitary deficiencies, and 3% had tumor or hormonal recurrence, all within the first 2 years after surgery. Presurgical medical treatment did not significantly improve surgical outcome (63% vs 57%). Radiotherapy controlled hypersecretion in 37% of patients within 2 years, whereas 32% of patients developed new pituitary deficiencies from 18 to 96 months from treatment. At last follow-up, 80% of patients normalized thyroid function, whereas 20% were currently on medical treatment: 85% with somatostatin analog (SSA) alone and 15% with SSA combined with methimazole. Subjects who achieved disease control had surgery as the only treatment in 80% of cases and surgery combined with irradiation in 20%. Surgery remains the first-choice treatment for TSHoma. If surgery is successful, recurrence is rare. When surgery is unsuccessful or contraindicated, SSA and radiotherapy are effective in controlling hyperthyroidism and tumor growth in the majority of patients. The effects of radiotherapy on TSH secretion and tumor mass are greater within the first years after treatment, whereas pituitary deficiencies may occur several years later.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Endocrinol Diabetes Metab Case Rep
                Journal ID (iso-abbrev): Endocrinol Diabetes Metab Case Rep
                Journal ID (pmc): edm
                Journal ID (publisher-id): EDM Case Reports
                Title: Endocrinology, Diabetes & Metabolism Case Reports
                Publisher: Bioscientifica Ltd (Bristol )
                ISSN (Electronic): 2052-0573
                Publication date (Electronic): 1 January 2015
                Publication date (Print): 2015
                Volume: 2015
                Electronic Location Identifier: 140070
                Affiliations
                [1]Department of Endocrinology Diabetes and Metabolism, Cleveland Clinic Foundation , 9500 Euclid Avenue Desk F20, Cleveland, Ohio, 44195, USA
                [1 ]Patholgy and Laboratory Medicine Institute, Rose Ella Burkhardt Brain Tumor and Neuro-Oncology Center, Cleveland Clinic , Cleveland, Ohio, 44195, USA
                [2 ]Department of Neurosurgery and the Neurological Institute, Rose Ella Burkhardt Brain Tumor and Neuro-Oncology Center, Cleveland Clinic , Cleveland, Ohio, 44195, USA
                Author notes
                Correspondence should be addressed to P C Johnston Email: pcjohnston@ 123456doctors.org.uk
                Article
                Publisher ID: EDM140070
                DOI: 10.1530/EDM-14-0070
                PMC ID: 4285756
                SO-VID: 98bb6a48-90b8-41d3-9576-e4bf27822320
                Copyright © © 2015 The authors
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.

                History
                Date received : 10 September 2014
                Date accepted : 11 December 2014
                Categories
                Subject: Unique/Unexpected Symptoms or Presentations of a Disease

                Data availability:

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