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.
Key words: TSHoma, thyroid hormone resistance, central hyperthyroidism, diagnostic dilemmas
Highlights
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Dual pathology of thyroid-stimulating hormone (TSH)-secreting pituitary adenoma and RTHβ can mimic isolated central hyperthyroidism
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Dynamic testing and thyroid hormone receptor beta sequencing are essential to avoid misdiagnosis
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Normal α-subunit and sex hormone–binding globulin levels support resistance over autonomous secretion
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Pituitary incidentalomas may be functional, requiring postoperative reassessment
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RTHβ does not always exclude the presence of a functional TSH-secreting tumor
Clinical Relevance
This case underscores the need for genetic and hormonal evaluation in central hyperthyroidism, as the coexistence of RTHβ and a functional thyroid-stimulating hormone-secreting pituitary adenoma may complicate diagnosis and management.
Introduction
Central hyperthyroidism, defined by elevated circulating thyroid hormones (T3 and T4) with an inappropriately normal or nonsuppressed thyroid-stimulating hormone (TSH), is rare. It is chiefly caused by either a TSH-secreting pituitary adenoma (TSHoma) or resistance to thyroid hormone (RTH).1,2 TSHomas account for <1% of all pituitary tumors (prevalence of 1–2 per million) and produce autonomous TSH secretion leading to thyrotoxicosis.1,2 RTH (formerly “Refetoff syndrome”), first described in 1967,3 typically results from heterozygous mutations in the thyroid hormone receptor beta (THRB) gene (often autosomal dominant, occurring in ∼75 to 80% of cases).2,4 This causes reduced end-organ sensitivity to thyroid hormone and a biochemical profile of elevated T3/T4 with an inappropriately normal or elevated TSH.
Although RTH and TSHoma produce similar laboratory findings of central hyperthyroidism, they have distinct diagnostic criteria (Table 1). TSHoma is usually confirmed by evidence of a pituitary tumor on imaging together with autonomous TSH secretion: classically, TSH shows a blunted or absent rise in a thyrotropin-releasing hormone (TRH) stimulation test and fails to suppress with exogenous T3.1 Approximately 70% to 80% of TSHomas secrete excess α-subunit or have an elevated α-subunit-to-TSH molar ratio, and patients often exhibit pituitary mass effects or cosecretion of other pituitary hormones.2,4 RTH, in contrast, typically features a normal or exaggerated TSH rise with TRH and only partial suppression of TSH during a high-dose T3 suppression test.2,4 Supporting findings favoring RTH include normal sex hormone–binding globulin (SHBG) and α-subunit levels (which are usually elevated in TSHomas). Ultimately, identification of a pathogenic THRB gene mutation confirms the diagnosis of RTHβ. Distinguishing these entities is essential because their management differs markedly. Misdiagnosis can lead to inappropriate therapy—for example, unwarranted thyroid ablation for a TSHoma or unnecessary pituitary surgery for RTH.1
Table 1.
Key Clinical and Laboratory Distinctions Between RTH and TSHoma
| Feature | TSH-secreting adenoma | Thyroid hormone resistance |
|---|---|---|
| Thyroid hormones | ↑ FT4/FT3; TSH inappropriately normal or ↑2 | ↑ FT4/FT3; TSH inappropriately normal or ↑2 |
| Familial occurrence | Very rare | Often familial (∼70–85%)4 |
| THRB gene mutation | None (somatic mutations rare) | Present in ∼75–80% (dominant)2,4 |
| Pituitary MRI | Pituitary mass in ∼99% (macroadenoma)1 | Pituitary lesion in ∼20–25% (incidental)5,6 |
| α-Subunit/TSH ratio | Elevated (∼70–80% cases)1 | Normal (exceptional 1–3%) |
| SHBG | Elevated (reflecting true thyrotoxicosis)2,4 | Normal |
| TRH test | Blunted or no TSH rise4,7 | Normal/increased TSH rise4,7 |
| T3 suppression test | No suppression of TSH4 | Partial suppression of TSH4 |
| Treatment | Surgery ± somatostatin analogs4,8, 9, 10 | Conservative (β-blockers; avoid thyroidectomy)2 |
Abbreviations: MRI = magnetic resonance imaging; SHBG = sex hormone–binding globulin; THRB = thyroid hormone receptor beta; TRH = thyrotropin-releasing hormone; TSH = thyroid-stimulating hormone; TSHoma = TSH-secreting pituitary adenoma.
Here, we present the case of a 56-year-old man referred for management of presumed RTH who was found to have a pituitary microadenoma. This case underscores the importance of comprehensive hormonal testing and genetic confirmation in patients with central hyperthyroidism, and we review the literature to formulate a management approach for concurrent RTH and pituitary lesions.
Case Presentation
A 56-year-old man with a history of atrial fibrillation (on anticoagulation), obesity (body mass index 34 kg/m2), obstructive sleep apnea (on continuous positive airway pressure), and hypertension (on lisinopril and amlodipine) was referred for the evaluation of abnormal thyroid function. He had been diagnosed with RTH at an outside facility. Historical labs from 2012 to 2024 consistently showed elevated free T4 and free T3 levels with nonsuppressed TSH (eg, in 2024: TSH 3.2 μIU/mL, free T4 2.1 ng/dL, free T3 9.4 pmol/L). The SHBG level was 41 nmol/L (reference 18–114 nmol/L), within the normal range.
He had no known family history of thyroid disease (his son tested negative for RTH, and his daughter was lost to follow-up). On physical examination, he was obese but alert and clinically euthyroid in appearance. He had a mild goiter without nodules or stigmata of Graves’ disease. There were no visual field defects or other neurological signs to suggest a large pituitary mass.
Recent laboratory tests (Table 2) confirmed the picture of central hyperthyroidism: free T4 28.4 pmol/L (elevated), total T3 234 ng/dL (elevated), and TSH 3.1 μIU/mL (inappropriately normal). TSH receptor antibody was negative, and thyroid ultrasound showed a diffusely heterogeneous gland without any dominant nodule. Radioactive iodine uptake measured 16% at 24 hours (laboratory reference 10% to 30%), consistent with nonfocal uptake; this did not by itself distinguish RTH from a TSH-secreting adenoma.
Table 2.
Thyroid Function and Related Tests During Evaluation
| Timepoint | TSH (μIU/mL) | FT4 (ng/dL) | FT3 (pg/mL) | Notes |
|---|---|---|---|---|
| Baseline (wk 0) | 2.5 (0.4–4.0) | 5.6 (0.78–1.79) | 11.7 (1.95–4.88) | High TH, nonsuppressed TSH |
| TRH stim (wk 4) | ↑ to 7.8 | – | – | Normal TRH response (TSH ↑)4,7 |
| T3 suppr (wk 5) | 2.0 | – | – | Partial suppression of TSH4,7 |
| Methimazole trial (wk 6) | 48.0 | 0.78 (↓) | 2.6 (↓) | FT4/FT3 normalized, TSH markedly ↑ |
| Postgenetic (wk 8) | 48.0 | 1.16 | 3.3 | RTH confirmed; continued β-blocker |
| Postoperative (wk 10) | 0.04 | 0.70 | - | Marked suppression of FT4 and TSH postsurgery |
| Last week (wk 11) | 0.6 | 0.9 | - | Partial normalization indicates recovery of the axis or dual pathology |
Abbreviations: RTH = resistance to thyroid hormone; TH = thyroid hormone; TRH = thyrotropin-releasing hormone; TSH = thyroid-stimulating hormone.
Given the biochemical evidence of central hyperthyroidism, further evaluations were performed to distinguish RTH from TSHoma. A pituitary magnetic resonance imaging (MRI) revealed a 6 × 9 × 9 mm sellar lesion, consistent with a pituitary microadenoma. Dynamic endocrine testing was then performed. We performed a TRH stimulation test using 200 μg TRH IV, sampling TSH at 0, 20, 30, and 60 minutes. TSH rose from 2.5 μIU/mL at baseline to 7.8 μIU/mL at 20 minutes (3.1-fold), indicating a preserved pituitary response and atypical for TSHoma. Conversely, a high-dose T3 suppression test (oral liothyronine ∼80 μg daily for 7 days) resulted in only a partial reduction of TSH (nadir ∼2.0 μIU/mL from a baseline around 3 μIU/mL). This incomplete suppression of TSH indicates that exogenous T3 failed to fully suppress the thyrotrophs, a finding consistent with RTH (in normal individuals TSH would be nearly undetectable, whereas in TSHomas, TSH is typically unsuppressible). The patient’s serum glycoprotein α-subunit (α-GSU) level and the α-GSU/TSH molar ratio were within normal ranges, arguing against a TSHoma (TSH-producing adenomas often secrete excess free α-subunit).1 Similarly, SHBG was in the normal range (TSHomas often cause elevated SHBG due to true thyroid hormone excess).4 These biochemical findings collectively favored RTH over TSHoma. Accordingly, genetic testing for RTH was undertaken: Targeted sequencing of THRB revealed a heterozygous pathogenic missense mutation (in this patient, a glycine-to-arginine substitution in exon 9 of THRB), confirming the diagnosis of RTH-β.
Despite the weight of evidence for RTH, there remained some uncertainty regarding the clinical significance of the pituitary lesion. Although RTH alone can cause elevated thyroid hormones with nonsuppressed TSH, our patient’s persistent biochemical hyperthyroidism (inappropriate TSH secretion) and clinical symptoms (ongoing atrial fibrillation) suggested that an autonomous TSH-producing adenoma was contributing to her condition. A decision was made after multidisciplinary discussion to proceed with transsphenoidal surgery to resect the pituitary lesion. Intraoperatively, a small tumor was removed without complication.
Histopathological examination revealed a plurihormonal Pit-1 lineage pituitary adenoma with immunopositivity for TSH, growth hormone, and prolactin, confirming that the tumor was a TSH-secreting adenoma (albeit with co-expression of growth hormone and prolactin). Postoperative labs showed a dramatic decline in thyroid hormone levels: TSH dropped to 0.04 μIU/mL immediately after surgery (with free T4 0.7 ng/dL), followed by a slight recovery of TSH to 0.6 μIU/mL with free T4 0.9 ng/dL over the next week. This partial normalization of the thyroid function tests suggested that removal of the adenoma corrected at least part of the central hyperthyroidism. The patient’s atrial fibrillation and other symptoms improved as his thyroid function moved toward normal ranges. He recovered well from surgery and was discharged home without complications.
Final Diagnosis
RTH-β (heterozygous THRB mutation) with a coexisting TSH-secreting pituitary microadenoma (plurihormonal Pit-1 lineage adenoma).
Discussion
This case illustrates the challenge of differentiating RTH from TSHoma in a patient who exhibits features of both. Both conditions can present with elevated thyroid hormones and an inappropriately normal or elevated TSH (central hyperthyroidism). In RTH, reduced tissue sensitivity to thyroid hormone (most often due to THRB mutations) leads to feedback resistance, whereas TSHomas are true pituitary neoplasms that autonomously secrete TSH.2,7,11 TSHomas are often macroadenomas at diagnosis and may cause symptoms of tumor mass effect or co-secrete other pituitary hormones.1 However, small sellar lesions can coincidentally occur in patients with RTH—prior studies estimate that up to 20% to 25% of RTH cases have an incidental pituitary adenoma identified.1 In our patient, the pituitary lesion was initially presumed incidental given the classic RTH biochemical profile, but the postoperative normalization of thyroid indices indicated that the adenoma was at least partially functional. This scenario suggests dual pathology: a TSHoma coexisting with RTH.
Our patient’s dynamic testing strongly favored RTH. He demonstrated a normal TSH rise with TRH stimulation and only partial TSH suppression with T3, which is the pattern expected in RTH and only rarely seen in TSHomas (Table 3). Additionally, normal SHBG and α-subunit levels further supported RTH over TSHoma. Genetic confirmation of a THRB mutation ultimately established the diagnosis of RTHβ. Taken together, these investigations minimized diagnostic ambiguity. Pappa and Refetoff summarize that a TSHoma is suggested by failure of TSH to suppress with T3, failure to rise with TRH, elevated SHBG, and elevated α/TSH ratio, whereas RTH behaves oppositely.5 Importantly, if RTHβ is confirmed by genetic testing, invasive treatments directed at a presumed TSHoma (surgery or thyroid ablation) can usually be avoided.5
Table 3.
Differential Diagnosis: Biochemical and Genetic Tests
| Test | RTHβ |
|---|---|
| TRH stimulation test | In RTH, exogenous TRH typically causes a normal or exaggerated TSH rise, whereas most TSHomas show a blunted or absent response5,8 (Carvalho Cunha et al found a “normal TSH elevation” on TRH in RTH8; similarly, Kim et al12 demonstrated a normal TRH response in their RTH patient.) |
| T3 suppression test | High-dose T3 administration usually suppresses TSH in RTH but fails to suppress TSH in autonomous TSHomas.5,6 Sriphrapradang et al6 noted that TSH was suppressed by T3 in their patient, indicating incidental adenoma rather than a secretory tumor. |
| α-Glycoprotein subunit (α-GSU) | TSHomas often secrete excess α-subunit or have an increased α-subunit/TSH molar ratio; RTH patients generally have a normal ratio.5,6 For example, Kim et al reported a normal α subunit and α/TSH ratio in a boy with RTHβ, reinforcing a non-TSHoma diagnosis.6 |
| SHBG | SHBG tends to be elevated in TSHomas (reflecting true hyperthyroidism) but usually normal in RTH.5,6,8,12 |
| Genetic testing | A definitive THRB mutation establishes RTHβ. Many cases have identified pathogenic THRB variants (eg, G251V, G344R, Pro453Ser, His435Arg, Leu341Val, and R438H) in RTH patients with pituitary lesions.6,8, 9, 10,12 Liao et al (2024) emphasize that genetic testing was “pivotal”—their patient had a THRB His435Arg mutation discovered only after pituitary surgery had been attempted for presumed TSHoma.10 Family history can also be informative (most RTH is familial), though as Petolicchio et al9 noted, this is not always available (eg, an adopted patient). |
Abbreviations: RTH = resistance to thyroid hormone; SHBG = sex hormone–binding globulin; THRB = thyroid hormone receptor beta; TRH = thyrotropin-releasing hormone; TSH = thyroid-stimulating hormone; TSHoma = TSH-secreting pituitary adenoma.
In our case, the postoperative course provided insight that both RTH and a TSH-secreting pituitary adenoma were present concurrently. Such dual pathology is unusual but has been reported. The patient’s pituitary tumor was positive for TSH by immunostaining, and the partial biochemical correction after resection indicates that the adenoma was contributing to the excess TSH. Thus, this case likely represents a rare instance of a true TSHoma coexisting with RTHβ.
Several case reports in the literature have documented patients with coexistent RTH and pituitary lesions, underscoring potential diagnostic pitfalls (Table 4). For example, Sriphrapradang et al6 described a 41-year-old woman with high thyroid hormone levels and a 4 × 2 mm pituitary microadenoma; a T3 suppression test in that case showed that TSH could be suppressed, and THRB sequencing identified a G251V mutation, confirming RTHβ with an incidental nonfunctioning adenoma. Similarly, Carvalho Cunha et al reported a 23-year-old female with elevated T3/T4 and a 7.5 mm pituitary microadenoma; a TRH stimulation test demonstrated a normal TSH rise, and genetic testing found a THRB mutation (G344R), leading to a diagnosis of RTHβ—the pituitary lesion was deemed an incidentaloma, and no surgery was performed.8 In 2024, Petolicchio et al9 detailed a 31-year-old man with elevated thyroid hormones, borderline-high TSH, and a small pituitary microadenoma. An octreotide long-acting release test in that patient initially suppressed thyroid hormone levels (suggesting a TSHoma), but an “escape” phenomenon was observed with subsequent doses—this, along with a heterozygous THRB Pro453Ser variant, led to the diagnosis of RTHβ, and the patient was managed medically (avoiding surgery). Liao et al reported a cautionary case of a 54-year-old woman who had palpitations, goiter, markedly elevated free T4, and a 4 mm pituitary lesion on MRI. She was misdiagnosed with a TSHoma and underwent transsphenoidal surgery, but pathology revealed no tumor cells; only afterward was a THRB His435Arg mutation identified, establishing RTHβ.10 This emphasizes that even a very small pituitary “adenoma” on MRI can be incidental in the setting of RTH and that proceeding to surgery without a definitive biochemical diagnosis can lead to unnecessary procedures.
Table 4.
Published Cases of Coexisting RTH and Pituitary Adenomas—Clinical Features, Diagnostics, and Outcomes
| Case | Patient | THRB mutation | Pituitary lesion | Key test findings | Treatment and outcome |
|---|---|---|---|---|---|
| Sriphrapradang et al,6 2016 | 41 F | c.1037G>T (p.G251V) | 4 × 2 mm microadenoma (incidental) | TSH suppressed by T3 (normal feedback); TRH test not done | No pituitary surgery; RTH confirmed by genetic testing; incidental adenoma observed. |
| Carvalho Cunha et al, 20198 | 23 F | c.1030G>A (p.G344R) | 7.5 mm microadenoma (incidental) | Normal TSH rise on TRH stimulation; T3 test not performed | No surgery or ablation; THRB mutation confirmed (RTHβ); managed conservatively (no antithyroid drugs). |
| Petolicchio et al,9 2024 | 31 M | c.1358C>T (p.Pro453Ser) | 3–4 mm microadenoma (incidental) | T3 suppression test contraindicated (AF); Octreotide LAR test showed initial TSH/TH reduction then escape | No surgery; RTHβ confirmed by genetics; treated with triiodothyroacetic acid (Triac) for thyrotoxicosis; pituitary lesion monitored. |
| Liao et al, 202410 | 54 F | c.1304A>G (p.His435Arg) | 4 mm microadenoma (misdiagnosed as TSHoma) | TRH/T3 tests not done prior to surgery (assumed TSHoma); surgery yielded no tumor | Underwent unnecessary transsphenoidal surgery (pathology negative); THRB mutation discovered afterward, confirming RTHβ; no further tumor treatment (managed as RTH). |
| Akiyoshi et al,13 1996 | 33 F | (None reported) | 2 mm microadenoma (TSHoma) | Significant TSH rise with TRH; T3 administration suppressed TSH (partial autonomy) | Transsphenoidal resection of microadenoma; pathology: TSHβ-positive adenoma; postoperative thyroid levels normalized without medication. |
| Kim et al,12 2024 | 13 M | c.1021C>G (p.Leu341Val) | 3 mm microadenoma (incidental, nonfunctioning) | Normal TRH stimulation test; normal α-GSU level and α/TSH ratio; T3 suppression test not performed (pediatric) | No pituitary surgery; initial misdiagnosis as hyperthyroidism was corrected—methimazole was stopped once RTHβ was confirmed. Symptoms improved with β-blocker; pituitary microadenoma managed by observation. |
Abbreviations: α-GSU = alpha glycoprotein subunit of TSH; AF = atrial fibrillation; F = female; LAR = long-acting release; M = male; RTH = resistance to thyroid hormone; T3 = triiodothyronine; TH = thyroid hormone; THRB = thyroid hormone receptor beta; TRH = thyrotropin-releasing hormone; TSH = thyroid-stimulating hormone; TSHoma = TSH-secreting pituitary adenoma.
Previous reports generally advocate for conservative management once RTH is confirmed: for instance, neither Sriphrapradang et al’s nor Carvalho Cunha et al’s patient underwent pituitary surgery or thyroid ablation, given that test results pointed to RTH.6,8 In contrast, an older report by Akiyoshi et al13 described a 33-year-old woman with central hyperthyroidism and a 2 mm pituitary microadenoma. In that case, dynamic tests actually favored RTH (TSH responded to TRH and suppressed with T3), yet the microadenoma was resected “because the adenoma could become large and intractable.” Postoperatively, her thyroid function normalized without medication, suggesting that the tiny tumor had indeed been contributing to her hyperthyroidism. This case illustrates that clinical judgment may sometimes favor surgical intervention if a pituitary lesion is present and thought likely to progress or cause harm.
These cases highlight that in patients with biochemical evidence of RTH, small pituitary lesions are often incidental. Aggressive treatment (surgery or radioablation) should be avoided unless there is compelling evidence of an autonomous TSH-secreting tumor.14 In our patient, despite confirming RTH, the decision to operate was influenced by the concern that the pituitary microadenoma was contributing to thyrotoxicosis (as supported by postoperative results). Indeed, this proved to be a dual pathology scenario. Managing such dual cases requires balancing the risks of untreated TSHoma (tumor growth and sustained hyperthyroidism) against the risks of unnecessary intervention in RTH.
Based on our experience and the literature, we propose the following framework for managing inappropriate TSH secretion when both RTH and a pituitary lesion are considerations.
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1.
Verify the laboratory abnormality: Exclude assay interference or other artifactual causes of elevated T4/T3 with normal TSH (eg, heterophile antibodies or familial dysalbuminemic hyperthyroxinemia). Also, rule out common causes like Graves’ disease (TSH receptor antibodies) or T4 ingestion.
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2.
Distinguish RTH vs TSHoma with targeted tests: Measure serum α-GSU and calculate the α-GSU/TSH molar ratio (elevated in ∼70 to 80% of TSHomas, but normal in RTH). Perform a TRH stimulation test—a normal or high TSH response favors RTH, whereas little or no TSH increase suggests TSHoma. Perform a T3 suppression test—any significant suppression of TSH suggests intact feedback (RTH), whereas failure to suppress is expected in TSHoma. In equivocal cases, a long-acting somatostatin analog trial (octreotide long-acting release test) may be considered, as TSHomas typically respond with a decrease in TSH and thyroid hormone levels, although caution is advised in interpreting results.
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3.
Obtain genetic testing for RTH: If clinical suspicion for RTH is high (family history and classical test results), perform sequencing of the THRB gene before pursuing any invasive therapy. A definitive mutation finding will confirm RTHβ and prevent unnecessary and potentially harmful treatments. In our patient and many reported cases, genetic confirmation was pivotal in management decisions.
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4.
Tailor the treatment to the confirmed diagnosis: If RTH is confirmed and there is no pressing evidence of a functional pituitary adenoma, manage conservatively. Treatment is typically symptomatic—for example, β-adrenergic blockers to control tachycardia or palpitations and thyroid hormone analogs (such as triiodothyroacetic acid, Triac) in select cases to reduce thyroid hormone levels by exploiting alternate receptor pathways. Importantly, avoid thyroidectomy or radioiodine ablation in RTH patients, as their thyroid gland is not the source of the dysregulation. If a bona fide TSHoma is diagnosed (or if dual pathology is strongly suspected, as in our case), indicate transsphenoidal surgery to remove the adenoma. Standard preoperative preparation for TSHoma may include achieving euthyroidism with somatostatin analogs or antithyroid drugs and β-blockers. Postoperatively, or if surgery is contraindicated, ongoing management options include somatostatin analogs, pituitary radiation, or thyroid ablation—but these should be reserved for true TSH-secreting tumors.
In conclusion, a meticulous, stepwise approach is essential when evaluating a patient with discordant thyroid function tests and a pituitary lesion. High clinical suspicion and appropriate use of biochemical testing (TRH stimulation, T3 suppression, and α-subunit measurement) combined with genetic analysis enable accurate differentiation of RTH from TSHoma. Our patient’s outcome was favorable, with improvement in thyroid levels and symptoms after surgery. The postoperative findings suggest that both pathologies contributed to his condition—a reminder that central hyperthyroidism can occasionally have dual causes. This case and the reviewed literature underscore the importance of thorough evaluation and cautious management to prevent unnecessary interventions in patients with inappropriate TSH secretion.
Disclosure
The authors have no conflicts of interest to disclose.
Acknowledgment
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Statement of Patient Consent
The patient provided consent for clinical information pertaining to this case to be used in a medical publication.
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