
==== Front
JCEM Case Rep
JCEM Case Rep
jcemcr
JCEM Case Reports
2755-1520
Oxford University Press US

39263278
10.1210/jcemcr/luae147
luae147
Case Report
AcademicSubjects/MED00010
AcademicSubjects/MED00160
AcademicSubjects/MED00250
AcademicSubjects/MED00300
AcademicSubjects/MED00905
Hematologic Malignancies: Two Cases of a Rare Cause of Hypopituitarism
https://orcid.org/0000-0002-3883-3724
Lauzon Brian Department of Medicine, Division of Endocrinology & Metabolism, McMaster University, Hamilton L8S 4L8, Ontario, Canada

Abu-Hijleh Tala Department of Medicine, Division of Endocrinology & Metabolism, McMaster University, Hamilton L8S 4L8, Ontario, Canada

https://orcid.org/0000-0003-1495-3825
McInnes Natalia Department of Medicine, Division of Endocrinology & Metabolism, McMaster University, Hamilton L8S 4L8, Ontario, Canada

https://orcid.org/0000-0001-6767-7313
Prebtani Ally Department of Medicine, Division of Endocrinology & Metabolism, McMaster University, Hamilton L8S 4L8, Ontario, Canada

Correspondence: Ally Prebtani, BScPhm, MD, McMaster University, 237 Barton Street RM 411, Hamilton L8L 2X2, Ontario, Canada. Email: prebtani@mcmaster.ca.
9 2024
11 9 2024
11 9 2024
2 9 luae14705 2 2024
29 7 2024
11 9 2024
© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society.
2024
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Abstract

Hematologic malignancies are rare causes of sellar masses and hypopituitarism. We report 2 cases of hypopituitarism due to sellar masses from hematologic malignancies. The first patient was found to have hypopituitarism but initial non-gadolinium-enhanced magnetic resonance imaging (MRI) sella did not demonstrate a mass. Subsequent gadolinium-enhanced MRI and transsphenoidal biopsy confirmed a diagnosis of intravascular lymphoma. Treatment with systemic chemotherapy resulted in resolution of abnormalities on MRI. The second patient had a known diagnosis of chronic lymphocytic leukemia, and sellar involvement contributing to hypopituitarism was confirmed on biopsy. Treatment with ibrutinib, acalabrutinib, and stereotactic radiosurgery resulted in resolution of abnormalities on MRI. Both patients were treated with hormone replacement for hypopituitarism. These cases highlight that hematologic malignancies should be suspected as causes of sellar masses/hypopituitarism in patients with concurrent symptoms atypical for a pituitary adenoma (eg, constitutional symptoms), known diagnoses of hematologic malignancies, or rapid tumor growth and invasion on imaging. Gadolinium-enhanced MRI should be pursued if nonenhanced MRI is nondiagnostic. Transsphenoidal biopsy can be considered for diagnosis. Malignancy-directed systemic therapy may improve hypopituitarism and radiographic abnormalities on MRI.

hypopituitarism
sellar mass
lymphoma
leukemia
==== Body
pmcIntroduction

Hypopituitarism is characterized by diminished or absent secretion or production of one or more pituitary gland hormones (1). It is relatively uncommon with an estimated prevalence between 300 and 455 cases per million (1). Hypopituitarism can result from various insults affecting the hypothalamus, pituitary gland, or both (1). Common causes include pituitary adenomas, other mass lesions, sellar surgery, radiation, or trauma (1-3). Infectious, inflammatory, or infiltrative conditions can rarely cause hypopituitarism (1-3). Newly diagnosed hypopituitarism should be investigated with magnetic resonance imaging (MRI) of the sella to rule out hypothalamic or pituitary masses (1).

The most common cause of a sellar mass on MRI is a benign pituitary adenoma (4). Other masses, such as meningioma or craniopharyngioma, may also be implicated (Table 1) (4). Rarely, a primary neoplasm or metastatic malignancy will be the cause (4). Malignancies include metastatic breast and lung cancer and hematological malignancies, including lymphoma (Table 1) (4). Less than 1% of operated pituitary masses are secondary to metastases (5, 7).

Table 1. Sellar and parasellar mass and mass-like lesions causing hypopituitarism and their relative frequency

Etiology [1, 4-6]	Frequency (%) [2, 3, 5, 7]	
Pituitary tumorsPituitary adenoma (common)

Pituitary carcinoma (rare)

	44%-61%	
Nonpituitary tumorsCraniopharyngioma

Chordoma

Chondroma

Germinoma

Meningioma

Astrocytoma

Primary third ventricle tumor

	7%-10%	
Metastatic solid tumorsBreast cancer

Lung cancer

Melanoma

Renal cell carcinoma

Colorectal cancer

Prostate cancer

Thyroid cancer

Pancreatic cancer

Unknown primary

	< 1%	
Hematologic malignanciesLymphoma

∘ Diffuse large B-cell lymphoma

∘ Intravascular lymphoma

∘ Burkitt lymphoma

∘ T-cell lymphoma

∘ NK/T-cell lymphoma

∘ Mucosa-associated lymphoid-tissue (MALT) lymphoma

∘ Hodgkin lymphoma

Multiple myeloma

∘ Plasmacytoma

Leukemia

∘ CLL

∘ Acute myeloid leukemia

∘ Acute lymphoblastic leukemia

	< 1%	
NontumorInfiltrative

∘ Sarcoidosis

∘ Hemochromatosis

∘ Langerhans cell histiocytosis

∘ Amyloidosis

Immunologic

∘ Hypophysitis

∘ Immunotherapy-induced hypophysitis

Infection

∘ Tuberculosis

∘ Abscess

	19%-39%	
Abbreviation: CLL, chronic lymphocytic leukemia.

We describe 2 cases of hypopituitarism as a result of sellar masses from lymphoproliferative malignancies, which have rarely been described in the literature. These patients developed hypopituitarism due to intravascular lymphoma and sellar chronic lymphocytic leukemia (CLL), respectively.

Case Presentation

Case #1 is a 64-year-old woman with a history of fibromyalgia, gastroesophageal reflux disease, and obstructive sleep apnea. Home medications included duloxetine and pantoprazole. She was investigated by a neurologist as an outpatient for headaches with MRI sella in 2021 demonstrating a prominent pituitary gland without a discrete lesion. She presented to the Emergency Department later that year with generalized weakness, body aches, decreased appetite, and 4-kg weight loss. She was admitted for further investigation.

Case #2 is a 69-year-old man with a history of coronary artery disease, hypertension, dyslipidemia, osteoarthritis, depression, and psoriasis. He was diagnosed with CLL in 2018 and followed by a hematologist for surveillance. Home medications included paroxetine, rosuvastatin, ramipril, metoprolol, pantoprazole, and aspirin. In 2019, he presented to hospital due to a fall in the context of worsening fatigue.

Diagnostic Assessment

Case #1 was found to have hypopituitarism with central hypothyroidism, hypogonadism, and hypoadrenalism (Table 2). There was no evidence of diabetes insipidus. MRI sella without contrast demonstrated a slightly enlarged pituitary gland measuring 1.5 × 1.5 × 1.0 cm (AP × CC × TD) with no discrete lesion. There was no optic chiasm compression. Levothyroxine and hydrocortisone were initiated with symptom improvement, and she was discharged home with a diagnosis of “hypopituitarism.” A repeat MRI with gadolinium as an outpatient was planned.

Table 2. Relevant laboratory investigations for Case #1 and Case #2

Test	Result	Reference range	
Case #1	
 TSH	0.24 mIU/L (0.24 mIU/mL)	0.47-4.68 mIU/L (0.47-4.68 mIU/mL)	
 Free T4	3.6 pmol/L (0.3 ng/dL)	10.8-28.2 pmol/L (0.8-2.2 ng/dL)	
 8 Am cortisol	< 28 nmol/L (< 1.0 µg/dL)	200-600 nmol/L (7.3-21.8 µg/dL)	
 ACTH	3.4 pmol/L (0.9 pg/mL)	< 10.3 pmol/L (< 2.8 pg/mL)	
 FSH	3.7 IU/L (3.7 mIU/mL)	21.5-31.0 IU/L (21.5-31.0 mIU/mL)	
 Prolactin	169.1 nmol/L (61.3 µg/L)	8.3-73.1 nmol/L (3.0-26.5 µg/L)	
Case #2	
 TSH	1.83 mIU/L (1.83 mIU/L)	0.47-4.68 mIU/L (0.47-4.68 mIU/L)	
 Free T4	6.7 pmol/L (0.52 ng/dL)	10.8-28.2 pmol/L (0.8-2.2 ng/dL)	
 8 AM cortisol	48 nmol/L (1.7 µg/dL)	200-600 nmol/L (7.3-21.8 µg/dL)	
 ACTH	1.7 pmol/L (0.5 pg/mL)	< 10.3 pmol/L (< 2.8 pg/mL)	
 FSH	0.4 IU/L (0.4 mIU/mL)	1.0-12.0 IU/L (1.0-12.0 mIU/mL)	
 LH	< 0.1 IU/L (< 0.1 mIU/mL)	0.6-12.1 IU/L (0.6-12.1 mIU/mL)	
 Total testosterone	< 0.7 nmol/L (< 20.2 ng/dL)	4.5-26.6 nmol/L (129.8-767.2 ng/dL)	
Abbreviations: ACTH, adrenocorticotropic hormone; FSH, follicle-stimulating hormone; LH, luteinizing hormone; T4, thyroxine; TSH, thyroid-stimulating hormone.

She presented to the hospital 5 months later with recurrent headaches, right facial numbness, right-sided ptosis, and cranial nerve III palsy with diplopia. MRI with gadolinium demonstrated a 1.4 × 2.8 × 1.4 cm sellar mass with invasion into the right cavernous sinus and encasement of the right cavernous internal carotid artery (Fig. 1A and 1B). She was admitted for endoscopic transnasal biopsy of the mass. Biopsy findings were consistent with diffuse large B-cell lymphoma suspected to represent intravascular lymphoma. Subsequent fludeoxyglucose–positron emission tomography (FDG-PET) scan demonstrated uptake in the sella turcica in addition to the bilateral ethmoid and maxillary sinuses, cervical lymph nodes, spleen, right humeral head, and right proximal femur.

Figure 1. MRI sella before and after treatment for Case #1. A, Sagittal T1-weighted view from 2021 MRI sella demonstrating intrasellar mass (arrow) measuring approximately 1.4 × 2.8 × 1.4 cm with extension to the suprasellar cistern. B, Coronal T2-weighted view from 2021 MRI sella demonstrates invasion into the right cavernous sinus, encasement of the cavernous segment of the right internal carotid artery (arrow), and no mass effect on the optic chiasm. C, Sagittal T1-weighted view from 2023 MRI sella demonstrating heterogeneous enhancement on postcontrast images favored to be post-treatment changes with no discrete masses noted.

Case #2 laboratory investigations revealed severe hyponatremia with sodium of 114 mmol/L (114 mEq/L) (normal reference range: 135-145 mmol/L; 135-145 mEq/L) that was unresponsive to intravenous saline. He was found to have hypopituitarism with central hypothyroidism, hypogonadism, and hypoadrenalism (Table 2). MRI sella demonstrated a 2.0 × 1.8 × 1.6 cm lobulated sellar mass abutting the optic chiasm with partial encasement of the right internal carotid artery (Fig. 2A and 2B). Hydrocortisone and levothyroxine were initiated with symptom improvement and resolution of hyponatremia. He was referred to a neurosurgeon upon discharge. A transsphenoidal biopsy of the sellar mass was performed 4 months later. Pathology demonstrated results consistent with CLL.

Figure 2. MRI sella before and after treatment for Case #2. A, Sagittal T1-weighted FLAIR view from 2019 MRI sella demonstrating a lobulated pituitary mass (arrow) measuring 2.0 × 1.8 × 1.6 cm. B, Coronal T2-weighted view from 2019 MRI sella demonstrates mild displacement of the optic chiasm (white arrow) and partial encasement of the cavernous segment of the right internal carotid artery (black arrow). C, Sagittal T1-weighted view from 2022 MRI sella demonstrating post-treatment changes in the pituitary fossa with no residual mass identified.

Treatment

Case #1 was initiated on chemotherapy with rituximab, cyclophosphamide, daunorubicin, vincristine, and prednisone (R-CHOP). She was treated with high-dose methotrexate for central nervous system prophylaxis. Lumbar puncture did not reveal evidence of cerebrospinal fluid (CSF) involvement.

Case #2 was initiated on ibrutinib 420 mg daily in early 2020 after funding was obtained for CLL treatment. Repeat MRI of the sella 8 months later demonstrated reduction in size of the intrasellar mass to 1.3 × 0.7 cm with slight optic chiasm deformity persisting.

Unfortunately, he developed bilateral pleural effusions later that year, thought to be secondary to ibrutinib. His dose was decreased to 280 mg daily, but his functional decline progressed despite adequate treatment of hypopituitarism. Ibrutinib was discontinued and acalabrutinib 100 mg twice daily was initiated. His symptoms did not improve, and he was referred to a radiation oncologist. He underwent fractionated stereotactic radiosurgery (25 Gy in 5 fractions) in late 2021. Acalabrutinib was discontinued afterwards.

Outcome and Follow-Up

Case #1 completed 6 cycles of R-CHOP and 3 cycles of high-dose methotrexate 5 months later without evidence of recurrence at most recent follow-up in 2023. Repeat MRI in 2023 demonstrated stable postsurgical changes with no residual sellar mass (Fig. 1C). Physiologic replacement of hydrocortisone and levothyroxine for hypopituitarism was continued with overall improvement in clinical status.

Case #2 remains on hormone replacement with dexamethasone and levothyroxine as of follow-up in 2023. Regarding CLL, his most recent lymphocyte count was 1.5 × 109/L (1500/uL) (normal reference range: 1.0-4.5 × 109/L; 1000-4500/uL). Testosterone replacement for hypogonadism was not pursued in light of his coronary artery disease. MRI sella from 2022 demonstrated stable post-treatment changes with no residual sellar mass (Fig. 2C).

Discussion

We report 2 cases of hypopituitarism secondary to sellar masses due to hematological malignancies. Review of the literature identified 17 previous cases of intravascular lymphoma and 5 cases of CLL resulting in hypopituitarism, summarized below.

Intravascular lymphoma is a rare subtype of large B-cell lymphoma characterized by proliferation of lymphoma cells in the lumina of small blood vessels (8). Disease phenotype is often clinically aggressive, with nonspecific symptoms and multisystem involvement (8). Hypopituitarism is rare and may be caused by vascular occlusion by lymphoid tumor cells in the hypothalamus and/or pituitary gland (9). Pituitary lymphoma is more common in immunocompromised hosts (5).

Review of the literature identified 17 cases of hypopituitarism secondary to intravascular lymphoma (8-23). Full-text reports were unavailable for 3 cases (10, 23). Symptoms at presentation were varied, including fever, neurologic symptoms, constitutional symptoms, pancytopenia, and respiratory failure (8, 9, 11-22). Varying degrees of hypopituitarism were described (8, 9, 11-22). No patients had vasopressin deficiency, but syndrome of inappropriate antidiuretic hormone (SIADH) was described in one case (16). MRI identified pituitary abnormalities in 12 of 14 patients, including pituitary gland thickening and discrete micro- and macrolesions (8, 11-13, 15-22). One patient did not have a lesion on MRI, but FDG-PET demonstrated uptake in the pituitary (13). Of the patients without radiographic sellar abnormalities, one patient was diagnosed with intravascular lymphoma on autopsy of the pituitary, and the other was diagnosed based on bone marrow biopsy and finding of lymphoma cells in the CSF on lumbar puncture (9, 14).

All patients reviewed were treated with some form of hormone replacement therapy. Three patients did not receive systemic treatment as diagnosis was made on autopsy (14, 16, 20). One patient was too critically ill to receive chemotherapy and later passed away (19). One patient was initially treated with chemotherapy but passed away from infectious complications (11). Nine patients completed treatment with systemic chemotherapy (8, 9, 12, 13, 15, 17, 18, 21, 22). Three patients had resolution of radiographic findings with therapy, while another 3 had improvement on imaging (12, 15, 17, 18, 21, 22). Hypopituitarism resolved in 2 cases with systemic treatment, and improved in 2 others (8, 9, 18, 22). The remaining patients had ongoing need for hormone replacement at last known follow-up.

CLL rarely causes pituitary dysfunction. In a retrospective review, Bower et al (1997) found central nervous system involvement in only 8 of 962 CLL patients reviewed, the majority of which was leptomeningeal involvement (24). Only 1 patient had pituitary involvement (24). A subsequent review of autopsy patients from 1958 to 1982 found evidence of pituitary involvement in 20 of 109 patients at autopsy, although it is unclear if these patients had hypopituitarism (25).

Of the 5 previous cases of CLL causing hypopituitarism identified, all patients had sellar masses or pituitary enlargement on MRI (26-30). Only 2 patients were previously known to have CLL (29, 30). Clinical manifestations included fatigue, weight loss, dyspnea, and neurologic symptoms, including headache, decreased visual acuity, and ophthalmoplegia (26-30). The diagnosis of CLL was confirmed on pathology from sellar mass resection in 4 cases and was based on clonal lymphocyte population consistent with CLL in the CSF from lumbar puncture in the last (26-30). All patients were treated with hormone replacement (26-30). Only one patient was treated with ibrutinib and had radiographic resolution of MRI findings (pituitary stalk thickening) at follow-up (30). The long-term follow-up for these patients is unknown.

Hematologic malignancies are rare causes of sellar masses and hypopituitarism, often with varying clinical presentations and degrees of hypopituitarism, making the diagnosis challenging. Initial symptoms can include headaches, visual disturbances, cranial nerve deficits (eg, ophthalmoplegia), constitutional symptoms, or symptoms related to hypopituitarism (5). Specifically, sellar/pituitary metastases, including lymphoma, may cause central diabetes insipidus/vasopressin deficiency as the systemic circulation supplies the posterior pituitary directly (7). We report 2 cases of hypopituitarism secondary to hematologic malignancies. One patient had hypopituitarism and no mass on initial MRI imaging, later diagnosed with intravascular lymphoma, and the other patient had known CLL, new hypopituitarism, and a sellar mass, with biopsy demonstrating CLL.

These cases outline the importance of considering hematologic malignancies as potential etiologies for hypopituitarism, especially in patients with concurrent symptoms atypical for a pituitary adenoma or with known hematologic cancers. Other clues include elevated lactate dehydrogenase, erythrocyte sedimentation rate, or other abnormalities on complete blood count (5). Rapid tumor growth with invasion to surrounding structures or pituitary stalk thickening should also raise suspicion (5). Our case of intravascular lymphoma highlights that gadolinium-enhanced MRI can be helpful in establishing the diagnosis when a nonenhanced MRI is normal or demonstrates nonspecific findings. Hypopituitarism may predate the appearance of radiographic sellar abnormalities due to vascular occlusion by lymphoid tumor cells in the sella (9). If a hematologic malignancy is suspected, adjunctive diagnostic modalities may include FDG-PET or transsphenoidal biopsy (5).

Given the paucity of data available, the ideal treatment of these patients is unknown, although malignancy-directed systemic therapy has demonstrated success in reversing radiologic findings and correcting hypopituitarism in some cases. This is consistent with outcomes seen in our patients, who both improved clinically following systemic treatment and hormone replacement. Both patients had resolution of radiographic findings with treatment. However, more information is required to determine the optimal methods for diagnosis and treatment of this patient population.

Learning Points

Hematologic malignancies can rarely cause sellar masses and hypopituitarism.

Diagnosis should be suspected in patients with symptoms atypical for a pituitary adenoma (eg, constitutional symptoms), known hematologic malignancies, other laboratory abnormalities (eg, pancytopenia, elevated lactate dehydrogenase etc.), rapid tumor growth with invasion into surrounding structures, and/or central diabetes insipidus/vasopressin deficiency.

Gadolinium-enhanced MRI should be considered if nonenhanced MRI does not show evidence of a sellar mass.

PET-CT and transsphenoidal biopsy are options if the diagnosis remains unclear.

Malignancy-directed systemic therapy may improve both hypopituitarism and radiographic abnormalities on MRI.

Acknowledgments

We would like to acknowledge Dr. Arun Mensinkai, neuroradiologist at Hamilton Health Sciences, for his assistance with interpreting magnetic resonance images for this report.

Contributors

All authors made individual contributions to authorship. A.P. and B.L. were involved in the diagnosis and management of Case #1. T.A. and N.M. were involved in the diagnosis and management of Case #2. B.L. drafted the manuscript with input from the other authors. All authors reviewed and approved the final draft.

Funding

No public or commercial funding.

Disclosures

B.L., T.A., and A.P. have nothing to disclose. N.M. has received research grant support from AstraZeneca, Merck, and Sanofi, but perceives no conflicts of interest with the submitted work.

Informed Patient Consent for Publication

Signed informed consent obtained directly from the patients.

Data Availability Statement

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

Abbreviations

CLL chronic lymphocytic leukemia

CSF cerebrospinal fluid

FDG-PET fludeoxyglucose–positron emission tomography

MRI magnetic resonance imaging

R-CHOP rituximab, cyclophosphamide, daunorubicin, vincristine, and prednisone
==== Refs
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