Thyroid Hormone Inactivation in Gastrointestinal Stromal Tumors
Open accessAbstract
Gastrointestinal stromal tumors (GISTs) are resistant to traditional chemotherapy but are responsive to the tyrosine kinase inhibitors imatinib and sunitinib. The use of these agents has improved the outcome for patients but is associated with adverse effects, including hypothyroidism. Multiple mechanisms of this effect have been proposed, including decreased iodine organification and glandular capillary regression. Here we report the finding of consumptive hypothyroidism caused by marked overexpression of the thyroid hormone-inactivating enzyme type 3 iodothyronine deiodinase (D3) within the tumor. Affected patients warrant increased monitoring and may require supernormal thyroid hormone supplementation.
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Consumptive hypothyroidism may also affect adult patients with hemangiomas and non-vascular tumors such as GIST and malignant fibrous tumors, though less frequently.
“Less frequently, consumptive hypothyroidism may also affect adult patients with hemangiomas but also non-vascular tumors such as gastrointestinal stromal tumor (GIST) and malignant fibrous tumors (63, 64).”
From Unusual causes of hyperthyrotropinemia and differential diagnosis of primary hypothyroidism: a revised diagnostic flowchart (2023) · cites this paper as [64]
The Discussion (page not provided) reports only three previous adult cases involving vascular or fibroblastic tumors and presents GIST as another cause of consumptive hypothyroidism. It does not identify the adult vascular tumors as hemangiomas or the fibroblastic tumors as malignant fibrous tumors; it also says the incidence in GIST is unknown. (LLM, conf=0.82)
Experimental — accuracy not yet measuredD3 mRNA expression directly correlates with serum TSH levels and the development of hypothyroidism.
“In particular, D3 mRNA expression directly correlated with serum TSH levels and the development of hypothyroidism.”
From Unusual causes of hyperthyrotropinemia and differential diagnosis of primary hypothyroidism: a revised diagnostic flowchart (2023) · cites this paper as [64]
The Results (Deiodinase Expression in GIST; page unavailable) report that four additional patients with hypothyroidism were positive for tumoral D3 activity. The Results (Endogenous D3 Activity in GIST Cells; page unavailable) separately report increased D3 mRNA in drug-exposed cells. Neither passage establishes a direct correlation between D3 mRNA expression and serum TSH levels or the development of hypothyroidism. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIn GIST, D3 overexpression can be induced by tyrosine kinase inhibitors such as sunitinib.
“In GIST, D3 overexpression can be also induced by the administration of tyrosine kinase inhibitor (TKI) such as sunitinib.”
From Unusual causes of hyperthyrotropinemia and differential diagnosis of primary hypothyroidism: a revised diagnostic flowchart (2023) · cites this paper as [64]
The Results (Endogenous D3 Activity in GIST Cells) report increased D3 activity and messenger RNA after cultured GIST-T1 cells were exposed to sunitinib or imatinib. The Discussion says tumor-biopsy studies before and during treatment are still needed, so the paper does not establish that administering sunitinib induces D3 overexpression in patients’ tumors. (LLM, conf=0.86)
Experimental — accuracy not yet measuredVascular tumors, fibroblastic tumors, and gastrointestinal stromal tumors may overexpress D3 and result in a need for increased LT4 dose.
“Vascular tumors (198), fibroblastic tumors (199), and gastrointestinal stromal tumors (200) may each overexpress D3 and result in a need for an increased dose of LT 4 .”
From Guidelines for the Treatment of Hypothyroidism: Prepared by the American Thyroid Association Task Force on Thyroid Hormone Replacement (2014) · cites this paper as [200]
Consumptive hypothyroidism may contribute to the etiopathogenesis of thyroid dysfunction induced by TKIs, although TKI-induced thyroid dysfunction is multifactorial.
“Although thyroid dysfunction induced by TKIs is multifactorial, consumptive hypothyroidism may contribute to its etiopathogenesis (63, 64).”
From Unusual causes of hyperthyrotropinemia and differential diagnosis of primary hypothyroidism: a revised diagnostic flowchart (2023) · cites this paper as [64]
Consumptive hypothyroidism results from excess D3 produced by vascular, fibroblastic, and gastrointestinal stromal tumors, causing thyroid hormone elimination to exceed the thyroid gland's synthetic capacity.
“Consumptive hypothyroidism arises due to an excess of D3 produced by vascular, fibroblastic, and gastrointestinal stromal tumors, leading to an increased elimination of thyroid hormones that exceeds the synthetic capability of the physiologically stimulated thyroid gland.1,[72][73][74]”
From Refractory hypothyroidism: unraveling the complexities of diagnosis and management (2023) · cites this paper as [72]
Consumptive hypothyroidism diagnosis requires evidence of increased thyroid hormone inactivation, shown by high serum rT3 or excess LT4 demand.
“The diagnostic process for consumptive hypothyroidism requires evidence of augmented thyroid hormone inactivation, which is indicated by either heightened serum rT3 concentrations or an excess demand for LT4.”
From Refractory hypothyroidism: unraveling the complexities of diagnosis and management (2023) · cites this paper as [72]
Elevated serum thyroglobulin and increased thyroid radioactive iodine uptake support normal thyroid stimulation.
“Elevated serum thyroglobulin levels and augmented thyroid radioactive iodine uptake corroborate the normal thyroid stimulation.72”
From Refractory hypothyroidism: unraveling the complexities of diagnosis and management (2023) · cites this paper as [72]
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“Consumptive hypothyroidism caused by marked overexpression of the thyroid hormone-inactivating enzyme type 3 iodothyronine deiodinase (D3) within GISTs has been reported [10].”
BackgroundGastrointestinal Stromal Tumors
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Disorders of Thyroid Hormone Transporters and Receptors
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Angell, T. E., Huang, S. A., & Alexander, E. K. (2016) · Endocrinology · doi:10.1007/978-3-319-27318-1_14-1 · Cited by 1 · see citing works
Self-citationTsvetkova, E. V., Marginean, E. C., Nessim, C., & Verma, S. (2015) · touchREVIEWS in Oncology & Haematology · doi:10.17925/ohr.2015.11.01.74 · Cited by 1 · see citing works
Hipotiroidismo consuntivo en paciente con hipotiroidismo primario previo
Modino, S. C., Delgado, M. S. P., Muñoz, J. A. M.-P., Minchot, E. C., Molina, G. C., & Robles, A. R. (2020) · Endocrinología Diabetes y Nutrición · doi:10.1016/j.endinu.2019.10.009 · Cited by 1 · see citing works
Imatinib-Resistant Gastrointestinal Stromal Tumor Presenting as a Large Abdominal Mass
Haider, A., Mehershahi, S., Siddiqa, A., Sharma, M. D., & Patel, H. K. (2021) · Case Reports in Gastroenterology · doi:10.1159/000518122 · Cited by 1 · see citing works
Nakamura, H. K., Hanai, T., Mizukusa, T., Hatakeyama, H., & Nishiwaki, S. (2021) · Kanzo · doi:10.2957/kanzo.62.756 · Cited by 1 · see citing works
Angell, T. E., Huang, S. A., & Alexander, E. K. (2018) · Endocrinology · doi:10.1007/978-3-319-44675-2_14 · Cited by 1 · see citing works
Self-citationHuang, S. A. (2013) · Humana Press eBooks · doi:10.1007/978-1-60761-395-4_16
Self-citationType 3 deiodinase and consumptive hypothyroidism
Yen, P. M., & Salvatore, D. (2014) · Translational gastrointestinal cancer
Yan, L., Mo, X., Qin, Y., Wang, C., Chen, Z.-N., Lin, Y., & Chen, J. (2015)
Gastrointestinal Stromal Tumors: An Update for the General Surgeon
Trochsler, M., & Kanhere, H. A. (2019) · Springer eBooks · doi:10.1007/978-3-319-92768-8_22
Camandaroba, M. P. G. (2021) · Gastroenterology Medicine & Research · doi:10.31031/gmr.2021.05.000619
Ahmad, K. S., Essa, M. S., & Alenazi, N. A. (2020) · doi:10.21203/rs.2.19935/v1
Consumptive hypothyroidism in patient with previous primary hypothyroidism
Modino, S. C., Delgado, M. S. P., Muñoz, J. A. M.-P., Minchot, E. C., Molina, G. C., & Robles, A. R. (2021) · Endocrinología Diabetes y Nutrición (English ed ) · doi:10.1016/j.endien.2021.02.001
Unusual presentation of a large GIST: a challenging diagnostic dilemma
Tumpa, R. R., Chowdhury, A. Q., & Ali, M. O. (2023) · Bangladesh Critical Care Journal · doi:10.3329/bccj.v11i1.66052
Kolcsár, M., Zeces, I.-A., Kövecsi, A., Kovács, Z., & Gáll, Z. (2024) · Cureus · doi:10.7759/cureus.67426
“This type of hypothyroidism, namely consumptive hypothyroidism, was described after the use of TKIs in the treatment of GISTs, such as sorafenib, imatinib, or sunitinib [38,39].”
BackgroundRanjbarian, T., Antkowiak, M., Doherty, T. M., Jee, Y., & Sicklick, J. K. (2024) · Surgical Oncology Insight · doi:10.1016/j.soi.2024.100117
Cherella, C. E., & Smith, J. R. (2024) · Springer eBooks · doi:10.1007/978-3-031-66296-6_15
Refractory hypothyroidism: Diagnostic evaluation and management strategies
Mavromati, M., Jarlborg, P., Demarchi, M. S., & Leboulleux, S. (2026) · Annales d Endocrinologie · doi:10.1016/j.ando.2026.102489
Piao, L., Ma, J. F., Zhao, N., Liu, C., Hou, Y., & Wang, T. (2026) · Therapeutics and Clinical Risk Management · doi:10.2147/tcrm.s581042
- Authors
- Maynard, M. A., Marino-Enriquez, A., Fletcher, J. A., Dorfman, D. M., Raut, C. P., Yassa, L., Guo, C., Wang, Y., Dorfman, C., Feldman, H. A., Frates, M. C., Song, H., Jugo, R. H., Taguchi, T., Hershman, J. M., Larsen, P. R., & Huang, S. A.
- Affiliations
- Boston Children's Hospital (US)
- Dana-Farber Cancer Institute (US)
- Brigham and Women's Hospital (US)
- VA Greater Los Angeles Healthcare System (US)
- ORCID
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 2014-04-03
- Volume
- 370
- Issue
- 14
- Pages
- 1327-1334
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- PMC
- PMC4186889
- OpenAlex
- W2007849722
- Cited by
- 70
- References
- 25
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 3 · 2023: 5 · 2022: 5 · 2021: 9 · 2020: 3 · 2019: 4 · 2018: 6 · 2017: 7 · 2016: 7 · 2015: 8 · 2014: 9 · 2013: 1
- FWCI
- 10.36
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR001102)
- National Cancer Institute (P50CA127003, U54CA168512, 1P50CA12703)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK076099, R01DK044128, DK044128, R01DK076099)
- National Center for Research Resources (UL1RR025758)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal Tumor Research and Treatment
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Keywords
- gastrointestinal stromal tumor, thyroid hormone inactivation, hypothyroidism, imatinib, sunitinib, tyrosine kinase inhibitors, adverse drug reactions, thyroid hormone replacement, tumor overexpression
- MeSH terms
- Gastrointestinal Neoplasms, Humans, Hypothyroidism, Iodide Peroxidase, Male, Middle Aged, Radiography, Abdominal, Thyroid Hormones, Gastrointestinal Stromal Tumors
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