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*Lymphoma
The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 4 1470-1476
Copyright © 2001 by The Endocrine Society

Special Articles

Pituitary Lymphoma Presenting as Fever of Unknown Origin*

Rita E. Landman, Sharon L. Wardlaw, Robert J. McConnell, Alexander G. Khandji, Jeffrey N. Bruce and Pamela U. Freda

Departments of Medicine (R.E.L., S.L.W., R.J.M., P.U.F.), Radiology (A.G.K.), and Neurosurgery (J.N.B.), Columbia University College of Physicians and Surgeons, New York, New York 10032

Address correspondence and requests for reprints to: Dr. Pamela U. Freda, Department of Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032. * Supported in part by a grant from the Endocrine Fellows Foundation (to R.E.L.).


   Abstract
Top
 Abstract
Introduction
 Discussion
 References
 
An 86-yr-old woman presented with fever of unknown origin. When laboratory evaluation revealed partial hypopituitarism, a magnetic resonance imaging scan of the head was performed and revealed a sellar mass consistent with a pituitary adenoma. Only after other possible etiologies for fever were excluded did she undergo transsphenoidal resection of the sellar mass, which proved to be a B-cell lymphoma. Primary central nervous system lymphoma of the pituitary region is a rare cause of a sellar mass, and this is the first reported case of pituitary lymphoma whose presenting manifestation was fever of unknown origin. Several disease processes can manifest themselves as fever and a sellar mass, including lymphomas. In our case, only surgical biopsy could make a diagnosis and distinguish this process from the more common pituitary adenoma.


   Introduction
Top
 Abstract
 Introduction
Discussion
 References
 
AN 86-YEAR-OLD CAUCASIAN female was admitted to the hospital for evaluation of fever. She was well until 4 months before admission, when she developed fevers, shaking chills, night sweats, a 20-pound weight loss, and decreased energy levels. She was electively admitted to another hospital where she had an unremarkable physical examination, but persistent fever spikes every 3–5 days. She underwent an extensive evaluation including: cultures of blood, urine, and stool; chest radiograph; echocardiogram; purified protein derivative skin testing for tuberculosis; computed tomography (CT) of the head, chest, abdomen, and pelvis; hepatitis panel; rapid plasma reagin; lyme titers; serum protein electrophoresis; immunoelectrophoresis; lumbar puncture; and bone scan. All were unrevealing. Laboratory evaluation was notable for a sodium of 117 mmol/L, which normalized with fluid restriction; TSH <0.08 mU/L; initial morning cortisol of 120 nmol/L; repeat morning cortisol of 280 nmol/L increasing to 1080 nmol/L 60 min after stimulation with 250 µg iv Cortrosyn; and lactate dehydrogenase (LDH) of 1122 U/L. She was given the diagnosis of syndrome of inappropriate antidiuretic hormone secretion and central hypothyroidism and, with continued fevers, was discharged on 0.025 mg daily levothyroxine with plans for further workup as an outpatient. Prednisone (5 mg twice a day) was added empirically for the possibility of an underlying inflammatory disorder. A gallium scan and bone marrow biopsy done as an outpatient were both negative.

At home, she became afebrile after several weeks and stopped the prednisone. She restarted the prednisone when the fevers recurred, and, when they persisted, she was admitted to our hospital. Physical examination on presentation was notable for a normal appearance without periorbital edema. Skin texture was normal. Cranial nerve and visual field examinations were normal. There was no galactorrhea. There was no lymphadenopathy or hepatosplenomegaly. Deep tendon reflexes and proximal muscle strength were normal. Initial temperature was 35.0 C, which rose to 39.4 C within several days. Laboratory investigations (Table 1Go) were consistent with hyponatremia and partial hypopituitarism. Again, an elevated LDH was noted, as well as an elevated erythrocyte sedimentation rate.


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  		Table 1. Laboratory tests on admission to our hospital

 
The patient was continued on 0.025 mg daily levothyroxine and 5 mg by mouth twice a day prednisone; her sodium normalized with fluid restriction. Magnetic resonance imaging (MRI) of the head demonstrated a 1.2 x 1.0 x 1.25-cm mass within a minimally enlarged pituitary fossa. The mass extended superiorly into the suprasellar cistern without evidence of chiasmatic compression and showed homogeneous enhancement after gadolinium administration (Fig. 1Go). These radiographic findings were felt to be consistent with a pituitary adenoma, which was thought to be nonsecreting. With the lack of clinical evidence of hormone hypersecretion, visual, or neurological compromise, surgical excision was deferred in favor of observation. Subsequent fever work-up consisted of repeat cultures of blood, urine, and stool; CT scans of the chest, abdomen, and pelvis; transvaginal ultrasound; echocardiogram; purified protein derivative skin test for tuberculosis; and temporal artery biopsy. The tests proved to be unrevealing, and on hospital day 24 she underwent transsphenoidal subtotal resection of the pituitary lesion. Pathologic examination was consistent with large-cell B-cell lymphoma (Fig. 2Go). Repeat radiographic studies, bone marrow biopsy, and cerebrospinal fluid cytology revealed no evidence of systemic disease. A peripheral blood interleukin 6 level was elevated at 180 pg/mL. She received several cycles of chemotherapy but died 3 months after diagnosis.



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  		Figure 1. A, T1-weighted spin echo coronal (top) and sagittal (bottom) images precontrast through the sella turcica show a moderately enlarged pituitary gland isointense in signal to brain parenchyma with a midline stalk. No significant suprasellar extension is seen. There is no chiasmatic compression. B, T1-weighted spin echo coronal (top) and sagittal (bottom) images after iv gadolinium administration reveal a homogeneously enhancing pituitary gland measuring 1.1 cm in superior-inferior axis x 1.5 cm in right-left axis x 1.2 cm in anterior-posterior axis. There is no definite extension into the adjacent cavernous sinuses.

 


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  		Figure 2. Lymphoma, large B-cell-invading pituitary gland (left) and sphenoid sinus (right).

 

   Discussion
Top
 Abstract
 Introduction
 Discussion
References
 
Fever of unknown origin (FUO)

This case is an unusual presentation of FUO. The definition of FUO has been recently revised to include three prerequisites: 1) illness of more than 3 weeks duration; 2) fever higher than 38.3 C (101 F) on several occasions; and 3) no diagnosis established despite 1 week of intensive evaluation (1). The various causes and their distribution include infections (30–40%), neoplasms (20–30%), rheumatological diseases (10–20%), miscellaneous (15–20%), and undiagnosed (5–15%; Ref. 1). The most common neoplasm causing FUO is lymphoma, both Hodgkin’s and non-Hodgkin’s types (1). Lymphomas, as well as other hematologic malignancies and some solid tumors, cause fever via the production of pyrogenic cytokines (2). When lymphoma predominantly or exclusively involves nonnodal structures, as it did in this case, the diagnosis becomes more difficult. Fever can be the presenting manifestation of endocrine disorders, most commonly hyperthyroidism and subacute thyroiditis. Uncommonly, primary or secondary adrenocortical insufficiency can cause fever (1, 3).

This patient underwent a thorough investigation for the cause of fever, including a detailed history, physical examination, laboratory evaluation, and radiographic tests. The partial hypopituitarism led her physicians to obtain an MRI, revealing a sellar mass, which initially was not pursued because it was not thought to be causally related to her fevers.

Differential diagnosis of sellar mass and fever

The most common cause of a sellar mass is a pituitary adenoma. In a large series of 1120 patients undergoing transsphenoidal surgery for sellar masses between 1981 and 1998, 91% of cases were pituitary tumors (4). The differential diagnoses of the remaining 9% included cell rest tumors, primitive germ cell tumors, benign lesions (such as meningiomas), metastatic tumors, vascular lesions, granulomatous processes, infectious processes, and lymphocytic hypophysitis (4). In this series, nonpituitary etiologies were more likely to present with diabetes insipidus (extremely rare with pituitary adenoma) and with cranial neuropathies. The presence of headache, visual compromise, or symptoms suggestive of anterior pituitary failure was not helpful in distinguishing a pituitary from a nonpituitary etiology. Pituitary tumors rarely are associated with fever (see below). Because our patient had no evidence of cranial neuropathy or diabetes insipidus, there was no clear evidence pointing to a nonpituitary etiology of her sellar mass.

The differential diagnosis of a sellar mass in a patient presenting with fever is more limited (see Table 2Go). Rarely, pituitary adenomas and other benign tumors can present with fever. Pituitary apoplexy, which typically presents with headache, visual disturbance, cranial neuropathy, and transient or permanent endocrinopathies, can also present as a sudden onset of fever and sterile meningitis. Fever, believed to be due to the extrasellar leakage of blood or necrotic material, is seen in 2.4% of cases (5, 6, 7). In the acute setting, CT can aid in the diagnosis by revealing a high-density or inhomogenous gland, with or without evidence of subarachnoid blood (7). Recurrent fever with asceptic meningitis has been described in patients with craniopharyngiomas (8), dermoid cysts (9), and epidermoid tumors (10). The etiology is thought to be the leakage of cyst contents into the subarachnoid space. The aforementioned cases are characterized by symptoms of an acute nature, with fever most often accompanied by meningeal signs. Periodic fever without meningeal signs has been described as an unusual manifestation of a recurrent Rathke’s cleft cyst (11). The MRI appearance of these cystic lesions can be helpful in making a diagnosis and varies depending on the proportion of solid vs. cystic components, the amount of calicifications, and the content of the cyst fluid (10).


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  		Table 2. Differential diagnosis of sellar mass and fever

 
Pituitary abscesses are rare. Organisms can reach the pituitary via hematogenous spread or from the direct extension of infection following sphenoid sinusitis, otitis media, peritonsillar abscess, cavernous sinus thrombosis, or meningitis (12, 13). In one third of cases, abscesses occur within preexisting lesions of the pituitary region (4, 14, 15, 16). Abscesses can also occur after surgical intervention in the area. The presentation of pituitary abscess can be indistinguishable from that of a pituitary adenoma, with symptoms of headache, visual disturbances (>75%), or pituitary insufficiency (13, 14, 17). These symptoms can occur in the absence of symptoms of infection, or with associated meningitis, with or without fever (14, 15, 17). Thus, in many cases, a preoperative diagnosis of abscess is not made (17). On precontrast images on MRI, abscesses appear similar to adenomas with a signal intensity that is isointense or moderately hypointense on T1-weighted images and hyperintense on T2-weighted images. In contrast to adenomas, abscesses characteristically demonstrate ring enhancement and a central cavity that is isointense to brain with contrast administration (4).

In a large number of cases, abscesses are found to be sterile. When organisms are isolated, the majority are Gram-positive cocci (17), although a range of other organisms have been demonstrated, including Neisseria, Citrobacter diversus, Diphtheroids, Escherichia coli, Klebsiella, Proteus, Salmonella typhi, and Brucella (12, 15, 17, 18). Many other fungal and parasitic organisms have been known to produce infection in the pituitary. Cases of Candida albicans (19), Aspergillus (20), Coccidioidomycosis (21), Cryptococcus (22), Cycsticercosis (23), Toxoplasmosis (24), and Echinococcus (25) have been described in the literature where the presentation is that of a sellar mass, mimicking pituitary adenoma with the diagnosis made only with tissue biopsy. Entamoeba histolytica and Pneumocystis carinii have been seen to invade the pituitary in the course of disseminated infection (26, 27). A syphilitic gumma in the sellar region can occur in acquired syphilis. In most cases, these are discovered on autopsy often with additional lesions present in the brain or elsewhere in the body (28).

Sellar tuberculoma without evidence of systemic disease is rare but has been reported (29). In a review of the English language literature from 1900 to 1984, Berger et al. (12) found only nine well-documented cases of pituitary tuberculosis. Headache, fever, and visual disturbance were described in most cases. In a more recent review of 13 existing cases, Ashkan et al. (29) found visual field defects in 46.7% of cases, pituitary dysfunction in 78.6%, and suprasellar extension of sellar tuberculoma in 86% of cases. Headache was present in all cases. On MRI, tuberculous lesions are usually isointense on T1-weighted images and isointense to hyperintense on T2-weighted images. Lesions enhance strongly after contrast administration and are often accompanied by thickening and enhancement of the stalk and dura (4). Here again, the clinical presentation and MRI appearance of sellar tuberculoma can be confused with that of pituitary adenoma such that only pathological examination can ultimately confirm the diagnosis (29, 30).

Sarcoidosis is a granulomatous disease that can involve virtually any organ. The incidence of central nervous system (CNS) disease is 5% (31). The onset of neurosarcoidosis may precede systemic manifestations in 31% of cases, and 29% may present with simultaneous disease (32). Five percent of patients with neurosarcoid do not have evidence of disease elsewhere (33). Neurosarcoidosis can involve virtually any part of the nervous system although parenchymal CNS disease has a predilection for the hypothalamus and the posterior pituitary (34, 35). These patients often present with a combination of selective hormone deficiencies with diabetes insipidus (34). Other neurological manifestations are typically also present with cranial neuropathies and aseptic meningitis being the most common (34). Isolated hypopituitarism, however, can be the only manifestation of CNS sarcoid (36). On MRI, the intraparenchymal or sellar lesions of sarcoidosis appear isointense on T1-weighted images and variable on T2-weighted images. After contrast administration these lesions typically enhance and are accompanied by leptomeningeal enhancement (4).

Primary CNS lymphoma

Our patient was found to have primary pituitary lymphoma as the etiology of her sellar mass and presumably accounting for her presenting manifestation of fever. Once considered a rare neoplasm, the incidence of primary CNS lymphoma (PCNSL) has been increasing since the 1970s both in immunocompetent and immunocompromised individuals (37, 38). Although the risk in an immunocompetent individual is low, the absolute risk in AIDS patients is 2–6% (39, 40, 41). The overwhelming majority (98%) of PCNSLs are B-cell non-Hodgkin’s lymphomas (37), as was the case in our patient.

Most tumors are periventricular in location, typically involving the corpus callosum, basal ganglia, or thalamus (41). Leptomeningeal involvement occurs in 12% of cases, and pure leptomeningeal PCNSL without involvement of the brain parenchyma is rare (40, 42). This is in contrast to secondary lymphoma, which has a propensity to involve the extracranial space and both the spinal epidural and subarachnoid spaces (42, 43).

Despite the more common location of PCNSL in the supratentorial space (41, 44), involvement of the sellar region is rare (4, 45). Hypothalamic involvement in PCNSL has been described in several series and multiple case reports (44, 46, 47, 48, 49, 50, 51), but cases involving the pituitary are few (4, 52, 53, 54, 55, 56, 57).

In addition to our case, eight cases of pituitary PCNSL have been reported in the English language literature (described in detail in Table 3Go). The median age at presentation for this group of nine patients is 65, a decade older than that reported in the literature for PCNSL, where the median age is 55 in immunocompetent patients and 31 in AIDS patients (41).


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  		Table 3. Pituitary lymphoma: summary of cases reported in the English language literature

 
We notice that a majority of patients with PCNSL of the pituitary presented with headache, cranial nerve abnormalities, and evidence of pituitary insufficiency. Six of nine patients presented with headache, five of nine patients exhibited cranial nerve abnormalities, and four of nine patients had evidence of visual impairment. In the five patients in whom endocrine testing was performed, evidence of anterior pituitary dysfunction was present. Four patients had panhypopituitarism whereas only our patient had hypogonadotropic hypogonadism and central hypothyroidism. One patient had evidence of diabetes insipidus, and one patient was noted to have an elevated PRL attributed to stalk deviation. These presentations are clearly different from those of patients with PCNSL elsewhere, where symptoms include specific neurological defects in more than 50% of patients, as well as altered mental status, seizures, and symptoms of increasing intracranial pressure such as headache, nausea, and vomiting (41, 58). Due to the sellar location of the tumor, and the proximity of the tumor to the cranial nerves traversing the cavernous sinuses, patients with PCNSL more frequently demonstrated hypopituitarism and cranial nerve abnormalities. Among all cases of PCNSL, symptoms and signs of systemic lymphoma are typically absent at the time of first presentation (40). This finding was observed in the group of nine patients with pituitary PCNSL where our patient was the only one to present with systemic symptoms of lymphoma. In fact, these were her most prominent symptoms.

Details of the MRI findings in pituitary PCNSL, although not available in all previously reported cases, when noted describe an isointense lesion on T1- and T2-weighted images that enhances after gadolinium administration. Six of the nine cases demonstrate invasion of the cavernous and/or sphenoid sinuses. These findings are consistent with the appearance of PCNSL, in general, described in the literature where tumors appear hypodense to isodense on T1- and T2-weighted images and enhance after gadolinium injection; less commonly they are hyperintense relative to gray matter on T2-weighted images (40, 42, 43). On noncontrast CT, lesions appear isodense or hyperdense and show enhancement with contrast (41, 42). The appearance of primary and secondary lymphoma within the brain is similar (43). The signal intensity of PCNSL varies from the appearance of pituitary adenomas, which are typically hypointense on T1-weighted images, hyperintense on T2-weighted images in up to one half of cases, and show delayed enhancement with contrast administration, compared with the normal pituitary gland (4).

Summary

To our knowledge, this is the first case of pituitary lymphoma presenting as a case of FUO. It demonstrates that lymphoma should be listed as a cause of sellar mass and fever. Although this differential remains large, radiographic and clinical presentation can help in the diagnosis. This is particularly true when systemic evidence of disease is present, as often occurs with sarcoidosis or tuberculosis. However, the processes listed in Table 2Go can also occur in the absence of disease elsewhere, and without all of their classic symptoms and signs. In these instances, as in our case, a diagnosis can be made only with surgical biopsy.


   Acknowledgments
 
We are indebted to Dr. Steven Chin for assistance in preparation and interpretation of the pathological findings.

Received October 27, 2000.

Revised December 18, 2000.

Accepted December 27, 2000.


   References
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 Introduction
 Discussion
 References
 

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Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals