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ODP359 Thyrotropin secreting pituitary microadenoma and lung adenocarcinoma treated with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) Erlotinib and Osimertinib: a case report

BACKGROUND: Thyrotropin secreting pituitary adenoma (TSHoma) of the pituitary specific transcription factor-1 (PIT-1) lineage, is the rarest subtype of pituitary neuroendocrine tumours (pitNETs). TSHomas must be discriminated from primary hyperthyroidism and can cause morbidity through thyrotoxicosi...

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Autores principales: Di Ieva, Antonio, Kim, See Yoon, Lewis, David, Poursoltan, Pirooz, Preda, Veronica
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9625395/
http://dx.doi.org/10.1210/jendso/bvac150.1068
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author Di Ieva, Antonio
Kim, See Yoon
Lewis, David
Poursoltan, Pirooz
Preda, Veronica
author_facet Di Ieva, Antonio
Kim, See Yoon
Lewis, David
Poursoltan, Pirooz
Preda, Veronica
author_sort Di Ieva, Antonio
collection PubMed
description BACKGROUND: Thyrotropin secreting pituitary adenoma (TSHoma) of the pituitary specific transcription factor-1 (PIT-1) lineage, is the rarest subtype of pituitary neuroendocrine tumours (pitNETs). TSHomas must be discriminated from primary hyperthyroidism and can cause morbidity through thyrotoxicosis or local mass effect. Serum alpha-subunit level may be used as a marker of tumour activity, as 50-85% of TSHoma patients have high serum alpha-subunit levels. First line treatment is surgical resection of the tumour. Medical therapy with somatostatin analogues or radiotherapy may be used for tumour control. Epidermal growth factor receptor (EGFR) expression has been demonstrated in pitNETs including corticotrophs, gonadotrophs, lactotrophs and somatotrophs. EGFR inhibiting agent, Lapatinib, has been investigated for treatment of prolactinomas and EGFR expression is implicated in tumorigenesis of corticotrophs. EGFR targeting tyrosine kinase inhibitors (TKIs) can be used first line to treat metastatic adenocarcinoma of the lung harbouring activating EGFR mutations. CASE REPORT: A non-smoking 53-year-old male of Middle Eastern heritage was seen in clinic with secondary hyperthyroidism on a background of metastatic adenocarcinoma of the lung and hypertension. The patient had no symptoms of hyperthyroidism and had no personal or family history of thyroid dysfunction. No new headaches or visual disturbance were reported. Physical exam showed brisk reflexes, no specific signs of hyperthyroidism or thyromegaly were seen. Thyroid function tests demonstrated a persistently elevated TSH 5.1mIU/L (0.4-4. 0), T4 21.8pmol/L (9-19) and T3 6.4pmol/L (2.6-6. 0) with negative anti- thyroid receptor, thyroperoxidase and thyroglobulin antibodies. Ultrasound of the thyroid was unremarkable. MRI revealed a well-circumscribed left anterior pituitary lesion of 5.4×6.8mm in size. Surgery was deferred as 3 months prior, he was diagnosed with stage 4 intrapulmonary adenocarcinoma of the lung with an exon-19 deletion mutation in the EGFR gene. He received stereotactic radiotherapy and EGFR targeted therapy using 100mg of Erlotinib daily, which increased to 200mg 6 months later. After 1 year of therapy, his adenocarcinoma progressed and he was transitioned to the 3 rd generation EGFR-TKI Osimertinib. Instead of undergoing the risk of pituitary surgery, a trial of EGFR therapy for its pleiotropic pituitary adenoma effects was decided. During the EGFR-TKI treatment period, alpha subunit levels have remained stable and serial MRI imaging at 1 year showed no interval pituitary adenoma growth. CONCLUSION: This is a rare case of TSHoma identified during treatment of lung cancer with EGFR-TKIs. EGFR signalling is implicated in prolactinomas and corticotrophs though there is a paucity of data regarding TSHomas. To date, our patient has achieved radiological and biochemical stability in his TSHoma, with hyperthyroidism control on EGFR-TKI therapy, suggestive of a therapeutic benefit from EGFR signal blockade. Further studies are needed in larger cohorts to quantify EGFR expression in TSHomas and evaluate its possible role in pathogenesis. Presentation: No date and time listed
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spelling pubmed-96253952022-11-14 ODP359 Thyrotropin secreting pituitary microadenoma and lung adenocarcinoma treated with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) Erlotinib and Osimertinib: a case report Di Ieva, Antonio Kim, See Yoon Lewis, David Poursoltan, Pirooz Preda, Veronica J Endocr Soc Neuroendocrinology and Pituitary BACKGROUND: Thyrotropin secreting pituitary adenoma (TSHoma) of the pituitary specific transcription factor-1 (PIT-1) lineage, is the rarest subtype of pituitary neuroendocrine tumours (pitNETs). TSHomas must be discriminated from primary hyperthyroidism and can cause morbidity through thyrotoxicosis or local mass effect. Serum alpha-subunit level may be used as a marker of tumour activity, as 50-85% of TSHoma patients have high serum alpha-subunit levels. First line treatment is surgical resection of the tumour. Medical therapy with somatostatin analogues or radiotherapy may be used for tumour control. Epidermal growth factor receptor (EGFR) expression has been demonstrated in pitNETs including corticotrophs, gonadotrophs, lactotrophs and somatotrophs. EGFR inhibiting agent, Lapatinib, has been investigated for treatment of prolactinomas and EGFR expression is implicated in tumorigenesis of corticotrophs. EGFR targeting tyrosine kinase inhibitors (TKIs) can be used first line to treat metastatic adenocarcinoma of the lung harbouring activating EGFR mutations. CASE REPORT: A non-smoking 53-year-old male of Middle Eastern heritage was seen in clinic with secondary hyperthyroidism on a background of metastatic adenocarcinoma of the lung and hypertension. The patient had no symptoms of hyperthyroidism and had no personal or family history of thyroid dysfunction. No new headaches or visual disturbance were reported. Physical exam showed brisk reflexes, no specific signs of hyperthyroidism or thyromegaly were seen. Thyroid function tests demonstrated a persistently elevated TSH 5.1mIU/L (0.4-4. 0), T4 21.8pmol/L (9-19) and T3 6.4pmol/L (2.6-6. 0) with negative anti- thyroid receptor, thyroperoxidase and thyroglobulin antibodies. Ultrasound of the thyroid was unremarkable. MRI revealed a well-circumscribed left anterior pituitary lesion of 5.4×6.8mm in size. Surgery was deferred as 3 months prior, he was diagnosed with stage 4 intrapulmonary adenocarcinoma of the lung with an exon-19 deletion mutation in the EGFR gene. He received stereotactic radiotherapy and EGFR targeted therapy using 100mg of Erlotinib daily, which increased to 200mg 6 months later. After 1 year of therapy, his adenocarcinoma progressed and he was transitioned to the 3 rd generation EGFR-TKI Osimertinib. Instead of undergoing the risk of pituitary surgery, a trial of EGFR therapy for its pleiotropic pituitary adenoma effects was decided. During the EGFR-TKI treatment period, alpha subunit levels have remained stable and serial MRI imaging at 1 year showed no interval pituitary adenoma growth. CONCLUSION: This is a rare case of TSHoma identified during treatment of lung cancer with EGFR-TKIs. EGFR signalling is implicated in prolactinomas and corticotrophs though there is a paucity of data regarding TSHomas. To date, our patient has achieved radiological and biochemical stability in his TSHoma, with hyperthyroidism control on EGFR-TKI therapy, suggestive of a therapeutic benefit from EGFR signal blockade. Further studies are needed in larger cohorts to quantify EGFR expression in TSHomas and evaluate its possible role in pathogenesis. Presentation: No date and time listed Oxford University Press 2022-11-01 /pmc/articles/PMC9625395/ http://dx.doi.org/10.1210/jendso/bvac150.1068 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle Neuroendocrinology and Pituitary
Di Ieva, Antonio
Kim, See Yoon
Lewis, David
Poursoltan, Pirooz
Preda, Veronica
ODP359 Thyrotropin secreting pituitary microadenoma and lung adenocarcinoma treated with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) Erlotinib and Osimertinib: a case report
title ODP359 Thyrotropin secreting pituitary microadenoma and lung adenocarcinoma treated with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) Erlotinib and Osimertinib: a case report
title_full ODP359 Thyrotropin secreting pituitary microadenoma and lung adenocarcinoma treated with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) Erlotinib and Osimertinib: a case report
title_fullStr ODP359 Thyrotropin secreting pituitary microadenoma and lung adenocarcinoma treated with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) Erlotinib and Osimertinib: a case report
title_full_unstemmed ODP359 Thyrotropin secreting pituitary microadenoma and lung adenocarcinoma treated with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) Erlotinib and Osimertinib: a case report
title_short ODP359 Thyrotropin secreting pituitary microadenoma and lung adenocarcinoma treated with epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) Erlotinib and Osimertinib: a case report
title_sort odp359 thyrotropin secreting pituitary microadenoma and lung adenocarcinoma treated with epidermal growth factor receptor (egfr)-tyrosine kinase inhibitors (tkis) erlotinib and osimertinib: a case report
topic Neuroendocrinology and Pituitary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9625395/
http://dx.doi.org/10.1210/jendso/bvac150.1068
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