Pituitary Metastases from Follicular Thyroid Carcinoma

Abstract

Background:

Metastatic carcinomas to the pituitary gland are uncommon, occurring in only 1% of the pituitary masses. They often originate from breast or lung carcinomas and may resemble a nonfunctioning pituitary adenoma both clinically and radiologically. Here we describe a patient with pituitary metastasis from follicular thyroid carcinoma and discuss the unique features of these lesions.

Summary:

A 45-year-old woman was admitted to the emergency rescue room of our hospital with a 2-month history of progressive headache and blurred vision. Evaluation revealed right eye amaurosis, with a mild abducens and oculomotor palsy. Pituitary magnetic resonance imaging showed a mass that was hypo-intense in T1-weighted and hyper-intense in T2-weighted-images, located from the sphenoid sinus up to chiasmatic cisterns, raising and deflecting the optic chiasm, down to hypopharynx region, and distorting the cavernous sinuses. No evidence of anterior or posterior hypopituitarism was recorded. The immediate trans-sphenoidal surgery was uncomplicated with partial improvement of the visual fields and headache. Histopathology revealed a metastasis with well-differentiated follicular thyroid architecture. Total thyroidectomy and lymph node dissection was performed with a final histopathological diagnosis of follicular thyroid carcinoma. Subsequently, her headache became more severe. 131-I ablation treatments were performed 15 days and 12 months after thyroidectomy with decrease in headache and a decline in serum thyroglobulin levels.

Conclusions:

Pituitary metastases from thyroid carcinoma are very uncommon. As this patient illustrates, they tend to produce symptoms relating to space-occupying expansion in the parasellar region rather than to those due to destruction of the pituitary gland. Although rare, pituitary metastases caused by thyroid malignancy should be considered in patients with expanding parasellar lesions if they have thyroid cancer or uncharacterized thyroid diseases. They are unlikely to be amenable to complete resection and should be considered for 131-I treatment, perhaps avoiding the need for extensive neurological surgery.

Introduction

P ituitary metastases (PMs) are uncommon, representing only 1% of pituitary masses (1). PMs usually derive from epithelial carcinoma, particularly lungs in men and breast in women (1,2). They are mostly located in the posterior lobe with its preferential exposure to the systemic circulation (3). The most common clinical condition associated with PMs at the time of diagnosis is diabetes insipidus. Its prevalence is as much as 70%. A recent article, however, indicates that the prevalence of visual impairment and anterior hypopituitarism at presentation could be similarly high (4). The diagnosis of a PM at presentation is challenging. They may mimic the clinical and radiological features of other, far more common, pituitary lesions such as pituitary adenomas. Nonetheless, they must be evaluated in a timely fashion to provide the best outcome for neurosurgery (4).

Systemic metastases of thyroid cancers usually go to lung and bone. There are only about 13 reported cases of metastatic thyroid carcinomas to the sella turcica and/or pituitary (5). Here we describe a patient with PMs from an unsuspected follicular thyroid carcinoma. She was initially thought to have a hemorrhagic pituitary adenoma or clivus cordoma.

Patient

A 45-year-old woman with a 2-month history of progressive headache and blurred vision in the right eye was referred through the emergency room to the Neurosurgery Division of our hospital. On admission, she was afebrile with stable vital signs. She was not anemic, and her white blood cell count was normal as were electrolytes and tests for renal and hepatic dysfunction. Ophthalmological examination revealed amaurosis of the right eye and a mild quadrantopsia in the left eye, pale optic discs, and mild right abducens and oculomotor palsy. The medical history was positive for a diagnosis of multinodular goiter 10 years previously, which was treated with L-thyroxine. Seven years before presentation a fine-needle aspiration was performed for a 4.5 cm right medio-basal thyroid nodule. Cytology showed cystic-hemorrhagic changes and was negative for cellular atypia. The patient refused a thyroidectomy. One year before presentation thyroid ultrasonography showed a goiter with partial intrathoracic extension. She developed a headache at least 8 months before presentation that did not respond to common acetylsalicylic acid, paracetamol, or nimesulide.

Brain magnetic resonance imaging (MRI) disclosed a 3.5 cm pituitary mass that was hypo-intense in T1-weighted and hyper-intense in T2-weighted images. It was located on the anterior skull base from the sphenoid sinus up to chiasmatic cisterns, raising and deflecting the optic chiasm, and down to hypopharynx region; the cavernous sinuses were bilaterally distorted. The anterior and posterior pituitary were detected and enclosed in the dorsal profile of the lesion. The internal carotid was surrounded by the mass. The major differential diagnosis based on the imaging study was hemorrhagic pituitary adenoma, clivus cordoma, or sphenoidal mucocele (Fig. 1). A computed tomography scan revealed an intense and homogenous enhancement of the lesion with thinning of the enclosing bone structures (Fig. 2). An angiogram showed a hypervascular pituitary lesion.

FIG. 1.

Multiple magnetic resonance imaging (MRI) views with reference mark for bone and pituitary location. (A) Brain magnetic MRI T1-weighted: mass located on anterior skull base from the sphenoid sinus up to chiasmatic cisterns, raising and deflecting the optic chiasm. (B) Brain MRI T1-weighted (after the 131-I therapy): reduction in mass size, which raised right oculomotor nerve and ipsilateral cavernous sinus.

FIG. 2.

Computed tomography images showing the localized pituitary lesion that shaped and thinned the bone-closing structures.

Other than mild hyperprolactinemia with a serum prolactin of 31.5 ng/ml, there were no biochemical tests suggestive of hypopituitarism; however, these were performed while the patient was on thyroid hormone (Table 1). There were no clinical signs of overt diabetes insipidus, suggesting normal posterior pituitary function. As a precaution she was started on cortisone, and transsphenoidal surgery with removal of the pituitary mass was performed.

Table 1.

Results of Basal Anterior Pituitary Function Tests Performed Preoperatively (T0) and Postoperatively, 18 Months After the Diagnosis (T1)

Tests (units)	Results T0	Results T1	Normal range
Prolactin (ng/mL)	31.5	15.0	2.8–29.2
FSH (mIU/mL)	2.6	52.40	2.5–10.2
LH (mIU/mL)	0.90	46.90	1.9–12.5
TSH (μUI/mL)	0.083	0.001^a	0.350–5.500
Free thyroxine (ng/dL)	0.81	1.79^a	0.89–1.76
GH (ng/mL)	6.44	6.23	<10.0
IGF-I (ng/mL)	267.0	270.0	54.0–336.0
ACTH (pg/mL)	19.5	NE^b	5.0–50.0
Cortisol (μg/dL)	14.9	NE^b	5.0–25.0

Tests conducted few days before (T0) and 18 months after (T1) trans-sphenoidal resection of pituitary metastases. Assays—prolactin: IRMA (PRL-CTK, Sorin; Saluggia); FSH: IRMA (C.T.; Radim); LH: IRMA (C.T.; Radim); TSH: IRMA (C.T.; Biocode); free thyroxine: RIA (Techno Genetics, Cassina dé Pecchi); GH: IRMA (hGH-CTK, Sorin; Saluggia); IGF-I: radioimmunoassay (RIA) (Nicholls Institute); ACTH: IRMA (Allegro HS-ACTH; Nicholls Institute Diagnostic); Cortisol: RIA (CORT–CTK 125, DIA Sorin; Diasorin Diagnostics, Saluggia).

During l-thyroxine treatment (125 μg/day).

During cortisone acetate treatment (37.5 mg/day).

ACTH, adrenocorticotropic hormone; TSH, thyrotropin; FSH, follicle-stimulating hormone; GH, growth hormone; IGF-I, insulin-like growth factor-I; LH, luteinizing hormone; NE, not evaluated; IRMA, immunoradiometric assay.

On macroscopic examination the tumor appeared as a hemorrhagic mass; the sphenoidal sinus was downsized to a paper-thin plate. On microscopic analyses no pituitary cells were found. Instead, there was a well-differentiated follicular thyroid tumor. Immunohistochemical analysis revealed no chromogranin A or neuron-specific enolase expression. Rather there was diffuse expression of thyroglobulin (Tg) and cytokeratin-7 and a focal positive staining for cytokeratin-19 and thyroid transcription factor-1 (Fig. 3).

FIG. 3.

(A) Photomicrograph of the surgical specimen of the metastatic pituitary tumor, revealing well-differentiated thyroid cells. (B) Immunohistochemical analysis for thyroglobulin (Tg; formalin-fixed, paraffin-embedded thyroid pituitary metastases): pituitary cells expressed Tg with high intensity.

After pituitary surgery, the patient developed transient diabetes insipidus. Her visual field defect improved partially and her headaches were less severe. Thyroid ultrasonography as well as neck and chest computed tomography scans showed thyroid enlargement with multiple nodules and marked retrosternal extension that dislocated vessels, trachea, and esophagus. Multiple areas were suggestive for neoplasm degeneration. Ultrasonography demonstrated laterocervical lymph node abnormality, suspicious for neoplastic involvement.

A total thyroidectomy with central and laterocervical lymph node dissection was performed. Histopathology showed a well-differentiated but widely invasive follicular thyroid carcinoma. It was partially encapsulated, but the margins were infiltrated and there was extensive vascular invasion. The structural features varied: there was follicular architecture combined with solid and trabecular areas. The histological characteristics of the thyroid lesion were different compared to the pituitary lesion (Fig. 3). Moreover, lymphonodal metastasis was found (pT2N1M1) (6).

Two weeks after thyroid surgery, the patient presented with deterioration of her clinical condition and sudden intensification of her headache. An MRI showed that the pituitary lesion had grown from 3.5 to 4.5 cm. Because of the concern for hemorrhage and postoperative edema, neurosurgery was considered to be contra-indicated. Therefore, 80 mCi 131-I was administered. The dosage for ablation was determined by quantitative dosimetry as the patient's serum creatinine had increased to 2.5 mg/dL (normal value in our lab: 1–1.5 mg/dL). The patient's pituitary lesion persisted on imaging studies (pituitary MRI), but her clinical status improved. Subsequently, L-thyroxine was temporarily stopped at which time the serum Tg became markedly elevated to 3000 ng/ml. Both whole-body scintigraphy with 131-I and positron emission tomography with flourine-18 fluorodeoxyglucose (FDG/PET) showed marked uptake in the pituitary level and the region of the pelvis (Fig. 4). Therefore, a second 131-I treatment with 80 mCi was performed. This was done 12 months after her thyroid surgery and 15 months after her pituitary surgery. Her last MRI, performed 9 months after the second 131-I treatment, revealed a reduction (RECIST criteria: class PR-30% from baseline in the sum of the individual measurements, confirmed after 4 weeks) (7) in the mass size that was still located on anterior skull base from the sphenoid sinus up to chiasmatic cisterns, raising the right oculomotor nerve and the omolateral cavernous sinus (Fig. 1). The patient's clinical condition improved without headache and bone pain, and with normal vitality and energy. Serum follicle-stimulating hormone, luteinizing hormone, and estradiol levels were in the menopausal range. Serum insulin-like growth factor-I was normal according to age (Table 1). Although there was no definitive evidence for anterior pituitary deficiency, glucocorticoid replacement was maintained as a precaution.

FIG. 4.

Comparison between PET (A) with FDG uptake and 131-I whole-body scintigraphy 131-I scans (B) at basal condition (after surgery) and after the second 131-I treatment.

After the second 131-I treatment there was a progressive reduction of serum Tg (Fig. 5). However, because a persistent pituitary uptake on the whole-body scintigraphy, a third 131-I treatment was planned if the patient's clinical and hematological tests permit this.

FIG. 5.

Serum thyroglobulin (HTg) levels in relation to thyroidectomy and 131-I treatment.

Discussion

PMs are an uncommon cause of sellar masses, but the 5% of patients with known malignancies should have a PM according to autopsy data (8). In about two-thirds of patients with PM, their pituitary is macroscopically normal and many are clinically asymptomatic. The prevalence of unsuspected PMs in autopsy examinations ranges up to 27% of all brain metastases (8). In patients with known cancer, a pituitary mass should be strongly considered as a PM from that cancer because the prevalence of pituitary adenomas in patients with a diagnosis of cancer is low, under 2%, according to some sources (1,9).

As noted, PMs from lung and breast cancers are not unusual, but only approximately 13 cases of metastatic thyroid carcinomas involving the sella turcica and/or the pituitary gland have been reported (10 –12). None of these patients had overt anterior or posterior pituitary dysfunction, differing from the situation that commonly occurs when PMs from other cancers occur and are detected ante mortum (4). PMs of thyroid carcinomas generally produce signs and symptoms related to mass effect such as blurred vision, ptosis, oculomotor and abducens nerves palsies, and headache. These symptoms suggest a parasellar lesion with relatively fast growth rather than an intrasellar lesion that destroys pituitary tissue or disconnects the pituitary stalk (11,12). This behavior is also characteristic of thyroid carcinoma in loco, which grows outwardly rather than invasively (13). The only cases of hypopituitarism or diabetes insipidus as first clinical condition at the diagnosis were displayed by a papillary but not follicular thyroid carcinoma (12,14) (Tables 2 and 3).

Table 2.

Characteristics of the 13 Published Cases of Pituitary Metastases by Thyroid Carcinoma

References	Histological type	Morphology	Clinical features	MRI radiological presentation	Treatment	Outcome
Santarpia et al. (18)	Medullary thyroid cancer	Bilobed mass infiltrating the clivus, invading the right cavernous sinus, and encasing the right internal carotid artery	Diabetes isipidus Hypopituitarism Optic chiasmatic compression	Inhomogeneous hyso-intense high-signal intensity on T2-weighted	Transsphenoidal resection	Death 2 months after surgery due to an intercurrent infection
Bhatoe et al. (19)	Medullary thyroid cancer	Sellar and suprasellar tumor with retrosellar extension	Decrease of libido-Gynecomastia Visual loss	A large solid mass enhancing contrast on T1-weighted T2-weighted not reported	Craniotomy and subfrontal resection Adjuvant radiotherapy	Follow-up for nearly 9 months
Chrisoulidou et al. (11)	Follicular thyroid carcinoma	Pituitary mass extending to cavernous sinuses and sparing the optic chiasma	Diplopia Ptosis of the right eye and paresis of the right oculomotor nerve	Not reported	Transsphenoidal resection Adjuvant radiotherapy	Follow-up, hormonal suppressive therapy, and hormonal replacement
Yilmazlar et al. (5)	Follicular thyroid carcinoma	Pituitary mass destroying the sella	Headache Nausea Visual loss Galactorrhea	Hypo-intense on T1-weighted and hyper-intense on T2 weighted	Transsphenoidal resection	Follow-up and 131-I ablation and hormonal suppressive therapy
Simon et al. (20)	Follicular thyroid carcinoma	Pituitary mass with calcifications in the area of the central skull base involving the clivus, filling the sphenoid sinus and sellar region, extending into the suprasellar cystern	Headache Diplopia	Hypo-intense on T1-weighted and hyper-intense on T2 weighted	Two 131-I ablations	Follow-up and hormonal suppressive therapy
Bell et al. (12)	Papillary thyroid carcinoma	Partial hemorrhagic mass that displaced anterior pituitary	Diabetes insipidus Amenorrhea Visual loss	MRI not reported	Transsphenoidal resection	Follow-up
Masiukiewicz et al. (21)	Papillary thyroid carcinoma (case 1)	Pituitary mass	Hypopituitarism Oculomotor nerve palsy	Homogenous enhancing mass	131-I ablation Adjuvant chemiotherapy (bone and lung metastases)	Follow-up
Masiukiewicz et al. (21)	Papillary thyroid carcinoma (case 2)	Pituitary mass extending to right cavernous sinus and right orbit	Hypopituitarism Right diplopia and palpebral ptosis left with optic and oculomotor nerve palsy	Homogenous enhancing mass	Stereotactic radiosurgery Adjuvant external radiotherapy	Death 2 months after refusing further interventions
Ochiai et al. (10)	Follicular thyroid carcinoma	Mass extending and destroying the left cavernous sinus, sphenoid sinus, and prepontine cistern	Diplopia and left retro-orbital pain with left abducens and oculomotor nerve paralyses	Hypo-intense tumor on T1-weighted and hyper-intense on the T2-weighted	Transsphenoidal resection Adjuvant irradiation using 131-I	Follow-up and hormonal replacement therapy
Sziklas et al. (14)	Papillary thyroid carcinoma	Not reported	Diabetes insipidus Hypopituitarism	MRI not performed. computed tomography scan revealed a large intrasellar pituitary tumor	Transsphenoidal resection	Death 13 months after the surgery due to massive intrathoracic hemorrhage
Kistler and Pribram (22)	Follicular thyroid carcinoma	Pituitary mass destroying the sella	Visual loss Paresis of the right oculomotor nerve	Not performed	Transsphenoidal resection	Not reported
Johnson and Atkins (23)	Papillary thyroid carcinoma	Erosion of the sella	Hypopituitarism Visual loss Optic, oculomotor, and trochlear nerve palsy	Not performed	Roentgen therapy Transsphenoidal resection Adjuvant irradiation using 131-I	Follow-up
Trunnel et al. (24)	Follicular thyroid carcinoma	Erosion of the sella	Visual loss Optic nerve palsy	Not performed	Two 131-I ablations	Not reported

MRI, magnetic resonance imaging.

Table 3.

Differences Between Pituitary Adenoma, Pituitary Metastases, and Pituitary Metastases of Thyroid Follicular Carcinoma at Magnetic Resonance Imaging

	Pituitary adenoma	Pituitary metastases	PM-T
Size/morphology	1. Micro/macro 2. Intra/extrasellar	1. Intrasellar (often < 1cm) 2. Small-lack of sella enlargement; dumb-bell morphology; often invasion of third ventricle	1. Macro 2. Extrasellar
Intensity on T1–T2-weighted images	Hyso-intense on T1 Hyper-intense on T2	Hyso-intense to brain parenchyma on T1 and T2	Hypo-intense on T1 Hyper-intense on T2
Growth characteristics	Slow growth of benign lesions	1. Invasive growth of malignant diseases 2. Localized growth in clinically asymptomatic	Rapid progression of symptoms with fast extensive growth
Signs/symptoms	1. Clinically asymptomatic 2. Headache 3. Chiasmatic syndrome 4. Sinus cavernous syndrome 5. Diabetes Insipidus 6. Hypopituitarism 7. Endocrine hypersecretion	1. Clinically asymptomatic 2. Visual impairment with trochlear, abducens, and oculomotor palsy (often) 3. Hypopituitarism 4. Diabetes insipidus	1. Optic, oculomotor and abducens palsy 2. Headache

PM-T, pituitary metastases of thyroid follicular carcinoma.

On MRI most PMs from cancers other than the thyroid are smaller than adenomas and tend to be hyso-intense characterized by brain parenchyma in T1- and T2-weighted images (3,15,16), lack of sella enlargement, a dumb-bell morphology, and occasional invasion of the third ventricle (2,15). In contrast, the PMs of differentiated thyroid carcinoma do not have these MRI features because they usually show hypo-intense in T1-weighted and hyper-intense in T2-weighted images, destroying the enclosing bone structures. Therefore, if these features are encountered in a PM, this could be a reason to perform thyroid ultrasonography before neurosurgery. However, it is unclear if neurosurgery should be considered as the first therapeutic approach for PMs due to well-differentiated thyroid cancer. This is because 131-I treatment is generally the first choice of therapy for metastatic follicular thyroid cancer (17).

Immunohistochemistry of the PM in our patient revealed diffuse staining for Tg, confirming the diagnosis of metastatic thyroid carcinoma. It was also positive for cytokeratin-7 and for focal staining of cytokeratin-19 and thyroid transcription factor-1. Normal thyroid follicular epithelium is often negative to cytokeratin-19, and the focal staining of this marker is usually distinctive for a follicular adenoma or carcinoma (13).

Conclusions

PMs from thyroid cancers are rare and have different MRI features compared with the far more common PMs that come from lung and breast cancers. They tend to produce signs and symptoms related to mass effect rather than to hypopituitarism. If a patient with a PM has these features, or a known thyroid cancer, the possibility that the PM is from thyroid cancer should be considered. If the patient has a thyroid lesion, this should be characterized in conjunction with the pituitary work-up to rule out PM from thyroid cancer. If there is good evidence that the PM is from thyroid cancer, the possibility of doing minimally invasive surgery to confirm this should be considered along with a consideration of 131-I as the first line of treatment.

Footnotes

Acknowledgments

This study was supported by Regione Piemonte (Ricerca Finalizzata 2008 bis, prot. n. 2133). The authors thank Bastiaan Arler for English revision.

Disclosure Statement

The authors declare that no conflicts of interest or competing financial interests exist.

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