Evidence map›Paper›PMID 41641293›Full record

ArticleAACE endocrinology and diabetes

Coexistence of Resistance to Thyroid Hormone and a Thyroid Stimulating Hormone-Secreting Pituitary Adenoma.

Thai Hau Koo, Hossein Gharib

Abstract readCase Reports
In one paragraph

Article in AACE endocrinology and diabetes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

What it found

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Thai Hau KooDivision of Endocrinology, Department of Internal Medicine, Hospital Pakar Universiti Sains Malaysia, Kota Bharu, Kelantan, Malaysia.
Hossein GharibDivision of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic College of Medicine, Rochester, Minnesota.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background/Objective: Central hyperthyroidism, characterized by elevated thyroid hormone levels with a nonsuppressed thyroid-stimulating hormone (TSH), presents a diagnostic challenge in distinguishing thyroid hormone resistance (RTH) from a TSH-secreting pituitary adenoma (TSHoma). Case Report: We report a 56-year-old man with a history of atrial fibrillation, obesity, and obstructive sleep apnea who was referred to our center with a prior diagnosis of RTH made elsewhere. Laboratory testing revealed elevated free T4 (2.2 ng/dL) and total T3 (234 ng/dL) with an inappropriately normal TSH (3.1 μIU/mL). Thyrotropin receptor antibody was negative, and radioactive iodine uptake was diffusely elevated. Pituitary magnetic resonance imaging demonstrated a 6 × 9 × 9 mm pituitary microadenoma, initially raising suspicion for TSHoma. However, a preserved TSH response to thyrotropin-releasing hormone stimulation, partial TSH suppression with high-dose T3, normal TSH α-subunit and sex hormone-binding globulin levels, and a pathogenic thyroid hormone receptor beta gene mutation all supported the diagnosis of RTH. Despite these findings, the patient underwent transsphenoidal pituitary surgery, and histopathology confirmed a plurihormonal PIT-1 lineage adenoma positive for TSH, growth hormone, and prolactin. Postoperatively, the patient recovered well and was discharged home. Discussion: With postoperative normalization of TSH and free T4, it is conceivable that the pituitary tumor contributed to the TSH elevation, suggesting the possibility of dual pathology-concomitant TSHoma and RTH. Conclusion: This case highlights the diagnostic dilemmas and overlapping features of RTH and TSHoma, emphasizing the need for comprehensive hormonal testing and genetic confirmation to avoid unnecessary surgery.

Indexed as

central hyperthyroidismdiagnostic dilemmasthyroid hormone resistanceTSHoma

Identifiers

PMID41641293
PMCPMC12866151

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