Pituitary T-lymphoblastic lymphoma combined with pituitary adenoma: A rare case report

Pituitary T-lymphoblastic lymphoma combined with pituitary adenoma: A rare case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Pituitary T-lymphoblastic lymphoma combined with pituitary adenoma: A rare case report Xiaoyu Chen, Long Cheng, Guowei Li This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8492951/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 6 You are reading this latest preprint version Abstract Background: T-cell lymphoblastic lymphoma (T-LBL) is a highly aggressive malignancy that originates from immature precursor T lymphocytes and is characterized by rapid progression. The typical clinical manifestations of T-LBL include superior vena cava syndrome and respiratory compression symptoms such as cough and dyspnea caused by large anterior mediastinal masses. Primary pituitary T-LBL is exceptionally rare, with only seven cases reported worldwide (including the case described in this study). Case presentation : This article presents the case of an elderly female patient who presented with headaches and progressive visual deterioration. Brain MRI revealed a sellar/suprasellar mass, while whole-body PET/CT imaging revealed a tumor confined to the central nervous system. Laboratory tests for blood parameters and pituitary hormone levels were normal. Following neuroendoscopic tumor resection, pathological examination and immunohistochemical analysis confirmed a diagnosis of pituitary T-LBL coexisting with pituitary adenoma. The patient’s headaches and visual impairment were resolved postoperatively. Subsequent chemotherapy with high-dose methotrexate, temozolomide, and liposomal doxorubicin effectively controlled the disease. Conclusions : This case highlights the rarity of concurrent sellar lymphoma and pituitary adenoma and summarizes previously reported cases of primary pituitary T-LBL to provide clinical diagnostic and therapeutic insights into this rare disease. T lymphoblastic lymphoma Pituitary Central nervous system lymphoma Case report Figures Figure 1 Figure 2 Figure 3 Background T-cell lymphoblastic lymphoma (T-LBL) is a highly aggressive malignant tumor that originates from immature precursor T lymphocytes. Classically, the disease primarily manifests as a large anterior mediastinal solid mass (accounting for approximately 70%-94% of cases), while clinical manifestations typically take the form of compression effects such as superior vena cava syndrome, dyspnea, and chest tightness caused by the mediastinal mass. Among all pituitary tumors, pituitary lymphoma is exceptionally rare, consisting of less than 0.1% of sellar region tumors. As of April 2025, nearly 40 cases of primary pituitary lymphoma (PPL) have been reported worldwide, with the vast majority derived from B lymphocytes. T-cell-origin pituitary lymphomas are exceedingly uncommon, with only 9 documented cases to date, including 7 cases of primary pituitary T-LBL and 2 cases of NK/T-cell lineage [ 1 ]. Notably, some patients develop pituitary lymphoma either simultaneously with pituitary adenoma resection or following adenoma removal (ranging from 4 to 25 years postresection) [ 2 ]. According to previous studies, the average age of onset of pituitary lymphoma among adults is 58 years, with a male-to-female ratio of 1.12:1. Most patients with pituitary lymphoma in the sellar/parasellar region present with pituitary insufficiency (72%), headache (56%), diplopia (39%), diabetes insipidus (DI) (39%), visual loss (28%), and fever (22%) [ 3 ]. All previously reported cases of pituitary T-cell lymphoma also presented with aggressive radiological features accompanied by visual loss or cranial nerve palsy. Given the clinical and radiological similarities between pituitary lymphoma and pituitary adenoma, the diagnosis cannot be based solely on clinical manifestations or imaging findings; cytological examinations and immunohistochemistry (IHC) are essential for confirming the lymphoid origin and evaluating the underlying pituitary cellular background. This case reports only the seventh reported instance of primary pituitary T-lymphoblastic lymphoma. The mass was initially misdiagnosed as a pituitary adenoma on imaging, but postoperative immunohistochemical staining and a detailed cytological examination confirmed a diagnosis of primary pituitary lymphoma. Pituitary T-LBL is exceedingly rare and has a highly aggressive clinical course, necessitating highly intensive therapeutic approaches. Thus, clarifying the clinical manifestations, radiological features, and immunohistochemical findings of pituitary T-LBL is critical for the early diagnosis and effective treatment of this rare disease. Case presentation Clinical data The patient was a 61-year-old female with a history of hypertension. She presented with intermittent headaches for six months and progressive visual decline over the prior two months. She denied a history of fever, weight loss, night sweats, limb weakness, or diplopia. A prior cranial magnetic resonance imaging (MRI) scan at an outside hospital revealed a "sellar and suprasellar mass," prompting admission to Huizhou Central People’s Hospital for further evaluation and management. Physical examination on admission revealed no palpable superficial lymph nodes, decreased left visual acuity on crude testing, unrestricted bilateral ocular movements, and no hepatosplenomegaly. Laboratory tests revealed normal blood counts, electrolytes, liver and kidney function, and urine osmolality but elevated lactate dehydrogenase (LDH; 260 U/L, reference range: 120–246 U/L). Hormone levels (sex hormones, thyroid hormones, cortisol) were within normal ranges. The levels of tumor markers (carcinoembryonic antigen [CEA], alpha-fetoprotein [AFP]) and immunological parameters (complements C3 and C4, immunoglobulin G [IgG], antinuclear antibody [ANA] profile) were unremarkable. The patient had no history of radiotherapy or chemotherapy. MRI revealed an irregular, slightly hyperintense mass in the sellar/suprasellar region and sphenoid sinus measuring approximately 40 mm × 34 mm × 46 mm (anteroposterior × transverse × craniocaudal). The mass exhibited well-defined but irregular margins, a homogeneous density, and nodular, hyperintense foci. The lesion was primarily located in the sellar region, obscuring the pituitary gland and stalk, and demonstrated a drill-like growth pattern, destruction of the sphenoid sinus wall and skull base, and upward displacement of the optic chiasm. No abnormal densities were observed in the brain parenchyma, ventricular system, or cisterns, and the midline structures remained central (Fig. 1 ). Positron emission tomography/computed tomography (PET/CT) imaging revealed increased fluorodeoxyglucose (FDG) uptake in the sellar/suprasellar region, sphenoid sinus, and right middle nasal meatus (SUVmax = 12.51), with a maximum cross-sectional dimension of 32 mm × 43 mm. An irregular soft tissue density and osteolytic destruction of the sphenoid sinus wall and clivus were noted, and no abnormal hypermetabolic activity was observed elsewhere ( Fig. 2 ) . Bone marrow flow cytometry revealed no abnormalities, and bone marrow biopsy pathology with IHC confirmed no evidence of T-lymphoma cell infiltration. Surgery and pathology The patient underwent neuroendoscopic transnasal-sphenoidal resection of the pituitary lesion (via a neuroendoscopic right nostril-sphenoidal approach for sellar pituitary tumor resection). Surgical procedure: Intraoperatively, the sellar floor appeared largely intact. The bone of the sellar floor was thinned with an eggshell technique, exposing the sellar dura. Upon incision of the latter, slightly reddish pituitary tissue was observed posteroinferior to the tumor. The tumor itself appeared yellowish and was firm in texture. Using a curette, the lesion was excised along the inner tumor capsule, starting from the right aspect and then proceeding to the left, posterior, and anterior aspects. Upon completing the anterior resection, the diaphragma sellae were visualized, and residual tissue was carefully curetted under the diaphragma. Exploration confirmed that there was no substantially residual abnormal tissue. The procedure concluded uneventfully. Postoperative pathological examination of the excised tissue revealed a sellar and suprasellar mass consistent with T-LBL coexisting with pituitary adenoma. Immunohistochemistry (IHC): Lymphoma component: CK(−), EMA(−), Vim(−), GFAP(−), CD3(+), CD5(+), CD20(−), PAX-5(−), CD30(−), CD99(+), TdT (focal weak+), CD34(−), CD4(+), CD8 (focally positive), GrB(−), CD56(-), and Ki-67 (90%); pituitary adenoma component: NSE(+), CgA(+), Syn(+). In situ hybridization: EBER (−) ( Figs. 3 ) . Treatment and follow-up The patient developed pituitary insufficiency postoperatively and was started on glucocorticoid replacement therapy. Concurrently, the patient underwent chemotherapy, consisting of high-dose methotrexate (3.5 g/m² on day 1), liposomal doxorubicin (40 mg/m² on day 2), and temozolomide (200 mg daily on days 1–5), which were administered every 28 days for a total of 6 cycles. Lumbar puncture with intrathecal injection was performed, revealing normal cerebrospinal fluid (CSF) pressure and unremarkable routine, biochemical, and flow cytometry CSF findings. Postoperative cranial MRI revealed no residual mass, and the patient reported resolution of her headaches and restored vision. Follow-up MRI after two chemotherapy cycles confirmed that there was no recurrent lesion in the pituitary region, while contrast imaging revealed short T1 and long T2 signal intensities at the surgical margins and no abnormal enhancement ( Fig. 1 d-f ) . As of Aug 2025, the patient has been followed for 10 months and remains in complete remission. Discussion Pituitary adenomas are the second most common type of primary brain tumor, with an estimated asymptomatic prevalence of approximately 10% in the general population [ 4 ]. The most common pituitary adenomas, in descending order, are prolactinomas, nonfunctioning adenomas, growth hormone-secreting adenomas, adrenocorticotropic hormone-secreting adenomas, and thyroid-stimulating hormone-secreting adenomas [ 4 ]. In contrast, pituitary lymphomas are exceedingly rare among all sellar tumors, accounting for less than 0.1% of all cases. Retrospective case analyses have reported a B-cell to T-cell origin ratio of 5.5:1 for pituitary lymphomas, mirroring the distribution observed in peripheral lymphomas [ 1 ]. Pituitary T-LBL, an even rarer subtype of central nervous system lymphoma, is clinically similar to pituitary adenoma but is more aggressive and has a poorer prognosis. To our knowledge, only 7 cases of primary pituitary T-LBL have been reported in the literature through 2025. This article synthesizes existing cases with the present case to provide a comprehensive summary of this rare entity. On the basis of existing data from the 7 reported cases of primary pituitary T-LBL, this entity has a marked female predominance (all 7 cases were female), which contrasts with the male predominance reported in the literature on general pituitary lymphomas. The age of onset ranges from 45 to 64 years (approximately middle to elderly ages), with a mean of 58.3 years ( Table 1 ) . This age distribution suggests a potential association with hormonal changes, such as postmenopausal elevation of gonadotropins and decreased estrogen level. Table 1 Summary of reported primary pituitary T-LBL cases Reference Sex Age (yrs) Symptoms Endocrine findings Radiology Treatment Follow-up Kuhn et al.[ 10 ] F 67 Oculomotor nerve palsy and amaurosis of the right side Hypopituitarism Suprasellar mass with homogeneous density and invasion of clivus Invasion of right cavernous sinus 6 months after surgery, followed by radiation to sellar region. Residual tumor after 5 months Romeike et al. [ 13 ] F 64 Left cranial nerve III paresis, double vision, left eye ptosis, bitemporal hemianopsia Pituitary insufficiency/hypopituitarism Contrast-enhancing intra- and suprasellar mass partially encasing left internal carotid artery, causing elevation of optic chiasm and involving left cavernous sinus. Post-operative methotrexate and external beam radiation. 19 months of stability Wiens et al. [ 19 ] F 58 Headache, right eye ptosis, cranial nerve III palsy Pituitary insufficiency/ hypopituitarism, DI Heterogeneously contrast-enhancing intra- and suprasellar mass displacing optic chiasm and extending into right cavernous sinus. Leptomeningeal dissemination. Post-operative intrathecal chemotherapy and craniospinal radiation. Death (meningeal spread) Gupta et al. [ 9 ] F 55 Headache, bilateral diminution of vision, altered sensorium Hypopituitarism (LH, TSH), and hyperpituitarism (prolactin, evening cortisol) Sellar/ suprasellar mass extending into suprasellar cistern, lateral ventricle, encasing Lt ICA, invading optic chiasm and infundibulam Surgery Death 2 months after surgery Sreedhara et al. [ 20 ] F 45 Headache, ptosis, diplopia, blurry vision CN III, IV, VI palsy, V1 numbness Secondary adrenal insufficiency, hyperprolactinemia, secondary hypothyroidism llar mass extending into sphenoid and cavernous sinuses and clivus, encasement of internal carotid artery (ICA) , abutment of optic chiasm transsphenoidal resection. high-dose methotrexate, regularly lumbar punctures with intrathecal chemo-therapy. alternating cyclophosphamide, vincristine sulfate, doxorubicin hydrochloride, and dexamethasone and methotrexate-cytarabine. Partial improvement Koga et al. [ 2 ] F 51 blurred vision and a visual field defect slightly elevated prolactin (PRL) and low insulin-like growth factor-1 levels a sellar mass extending to the suprasellar region, compressing the optic chiasma upward Two weeks postoperatively, leptomeningeal and pancreatic dissemination occurred. Treatment included cyclophosphamide, doxorubicin, vincristine, dexamethasone, methotrexate, and radiation. Paraplegia developed due to spinal dissemination. Death (10 months postop) Current case (2025) F 61 Headache, visual decline / mass in the sellar, suprasellar region and sphenoid sinus Surgery and high-dose methotrexate, liposomal doxorubicin, and temozolomide 10 months of remission The neurological manifestations of pituitary lymphoma resemble those of pituitary adenomas, as they depend on the location and extent of spread of the tumor. The most common clinical presentations include hypopituitarism, headache, and visual disturbances such as hemianopia or diplopia. Additional systemic symptoms may include fatigue, weight loss, fever, nausea, and vomiting [ 1 ]. If the lymphoma extends to the cavernous sinus or orbital apex, it may cause cranial nerve palsies (most frequently affecting cranial nerves II and III) and retro-orbital pain [ 5 ]. Notably, endocrine abnormalities such as hypopituitarism and DI are more prevalent in patients with pituitary lymphoma than in those with pituitary adenoma. Hypopituitarism in patients with pituitary lymphoma often manifests with diverse symptoms, including fatigue, muscle weakness, reduced libido, amenorrhea, thirst, and polyuria [ 3 ]. Among the 7 reported cases of pituitary T-LBL, the neurological symptoms primarily consisted of visual decline (85.7%), cranial nerve (CN) palsies (100%, most commonly involving CN III, IV, and VI), and headache (71.4%). Endocrine abnormalities predominantly included hypopituitarism (71.4%), and hyperprolactinemia (28.5%, 2 cases). Additional symptoms included diplopia, ptosis, and altered consciousness, the latter of which were likely associated with tumoral invasion or meningeal dissemination. The patient reported in this case report also exhibited visual decline and headache. Preoperative evaluations revealed normal pituitary function and no evidence of adrenal insufficiency or thyroid dysfunction. Postoperatively, her visual deficits and headaches improved significantly. However, secondary adrenal insufficiency developed after surgery, prompting the initiation of hydrocortisone replacement therapy. The radiological features of pituitary lymphoma include isointense lesions on T1-weighted imaging (T1WI), hypointense lesions on T2WI, and heterogeneous enhancement. All pituitary masses in these cases exhibited aggressive radiological characteristics, such as invasion of the clivus, sphenoid sinus, or cavernous sinus; erosion of the sellar floor; and encasement of the internal carotid artery. Given that the tumor frequently extended into the suprasellar region, cavernous sinus, and sphenoid sinus in most reported cases [ 6 – 13 ], some scholars have suggested that sphenoid sinus mucosal biopsies should be performed for patients whose pituitary masses display aggressive imaging features. Such an approach may help confirm the diagnosis while avoiding the surgical risks associated with pituitary resection[ 1 ].In our retrospective analysis of all reported cases of pituitary T-LBL, sellar masses were universally present, frequently invading the cavernous sinus (85.7%), sphenoid sinus (57%), and clivus (57%), and 57.1% of the masses encased the internal carotid artery. Two patients demonstrated meningeal or spinal dissemination, and one patient developed systemic metastasis (pancreatic involvement). On PET/CT imaging, some patients presented with hypermetabolic foci, although differentiation from adenoma remains challenging. In our case, the tumor extended to the suprasellar region, compressed the optic nerves (a previously reported manifestation), and invaded the sphenoid sinus, cavernous sinus, and even the clivus. While endocrine, neurological, and radiological assessments are crucial for diagnosing and managing primary pituitary lymphoma, alone, they are insufficient for distinguishing the disease from pituitary adenoma. The pathogenesis of primary pituitary lymphoma is poorly understood, but several hypotheses have been proposed: Hormone-Driven Hypothesis: Hormones secreted by pituitary adenomas (e.g., follicle-stimulating hormone [FSH] and adrenocorticotropic hormone [ACTH]) may promote lymphocyte proliferation via hormone receptor-mediated mechanisms. For example, in two reported cases of T-LBL coexisting with FSH-positive adenomas, FSH was hypothesized to activate proliferative signaling pathways through T-cell surface receptors [ 10 , 14 ]. Adhesion Molecule-Mediated Hypothesis: Lymphoma cells may express neural cell adhesion molecules (NCAMs) or integrins, allowing their specific colonization within the pituitary microenvironment [ 15 ]. Inflammatory Transformation Hypothesis: Chronic lymphocytic hypophysitis may undergo monoclonal transformation, particularly in immunosuppressed or genetically predisposed individuals [ 16 ]. Surgical or Radiotherapy-Induced Hypothesis: Some patients (e.g., one described in a 2024 case report) developed T-LBL years after pituitary adenoma resection, suggesting that surgical disruption of the blood‒brain barrier or localized inflammation may facilitate lymphomagenesis [ 2 ]. The gold standard for diagnosing this disease is pathology. Histologically, T-LBL is characterized by diffuse infiltration of small- to medium-sized lymphoblasts with abundant mitotic figures. Immunohistochemically, the tumor cells typically express CD3, CD4, CD8, and TdT and the Ki-67 index is elevated, while tests for B-cell markers (e.g., CD20) are negative. Molecular testing for T-cell receptor (TCR) gene rearrangement can confirm clonality[ 17 ]. Differential diagnoses include other pituitary neoplasms, such as pituitary adenoma, distinguished by positive immunohistochemical staining for pituitary hormones and, typically, reactive lymphocyte infiltration; lymphocytic hypophysitis, characterized pathologically by polymorphic inflammatory cell infiltration and a lack of clonality in lymphocytes; and metastatic lymphoma, which requires a thorough systemic evaluation to exclude secondary involvement[ 18 ]. Notably, a retrospective analysis revealed that among the 7 cases of pituitary T-LBL, 6 (85.7%) included confirmation of coexisting pituitary adenoma ( Table 2 ) . Three of these cases were identified simultaneously during surgery, whereas the remaining 3 cases were detected 9–25 years after pituitary adenoma resection and had often been misdiagnosed as recurrence of the adenoma. Among these 6 patients, 2 had gonadotropin-positive adenomas, 2 had nonfunctioning adenomas, and 2 had a combined ACTH-secreting adenoma. The coexistence of pituitary lymphoma and adenoma suggests that pituitary hormones may promote lymphocyte proliferation and contribute to lymphomagenesis. Table 2 Relationship between pituitary T-lymphoblastic lymphoma and pituitary adenoma Case source Lymphoma-adenoma relationship Adenoma characteristics (hormone secretion) Kuhn et al. [10] Lymphoma recurrence within a pituitary adenoma (25 years postresection) FSH-positive adenoma Romeike et al. [13] Lymphoma arising in a recurrent pituitary adenoma (17 years postresection) FSH-positive adenoma (5% cells expressed FSH) Wiens et al. [19] Coexisting lymphoma and adenoma (synchronous diagnosis) pituitary ACTH-cell hyperplasia (other hormones variably expressed Gupta et al. [9] Coexisting lymphoma and adenoma (synchronous diagnosis) ACTH/TSH-positive adenoma Koga et al. [2] Lymphoma developed 9 years postresection of pituitary adenoma Nonfunctioning adenoma Current Case (2025) Coexisting lymphoma and adenoma (synchronous diagnosis) Nonfunctioning adenoma Among the 7 reported cases of pituitary T-LBL, partial transsphenoidal resection was performed in most cases to alleviate the mass effect, whereas gross total resection was rarely achievable because the tumor had invaded the cavernous sinus or vascular encasement. Several patients received high-dose methotrexate (HD-MTX)-based central nervous system penetrating chemotherapy, often combined with cyclophosphamide, vincristine, and other agents (e.g., hyper-CVAD). Additionally, 71.4% of patients underwent whole-brain or sellar radiotherapy (45–50 Gy) to control local residual disease or leptomeningeal dissemination. To date, no evidence-based data support the use of targeted therapies or hematopoietic stem cell transplantation (HSCT), although these modalities represent potential investigational approaches. The outcomes of pituitary T-LBL patients remains poor, with a median survival of approximately 10 months (range: 2–19 months) among deceased patients. Causes of death include central dissemination (e.g., leptomeningeal spread, as exemplified by a patient described in a 2024 case report) and systemic metastasis (e.g., pancreatic involvement in a patient described in a 1999 case report). Early diagnosis combined with intensive chemotherapy may alleviate the patient’s symptoms; however, the high probability of recurrence persists, underscoring the need for novel therapeutic strategies. In summary, we present a case of primary pituitary T-LBL. Although pituitary lymphoma is rare, it should be considered in the differential diagnosis of sellar masses, particularly when neuroimaging suggests invasion of adjacent structures. While most sellar lesions originate from pituitary cells—making hormonal evaluation critical for a diagnosis of adenoma—a definitive diagnosis of pituitary lymphoma relies on immunohistochemical staining and microscopic identification of lymphoblastic tumor cells. In addition to endocrine, neurological, and radiological assessments, prompt immunohistochemical profiling and comprehensive cytogenetic analysis are essential for early diagnosis and improving outcomes. Notably, all reported pituitary T-LBLs occurred in middle-aged to elderly females, and the majority coexisted with pituitary adenomas. A subset of these adenomas were gonadotropin-secreting, suggesting that hormonally driven lymphocyte proliferation may contribute to lymphomagenesis—a hypothesis warranting further investigation. Pituitary T-LBL is a highly aggressive malignancy; while multimodal therapy (surgery, chemotherapy, and radiotherapy) may provide short-term disease control, novel targeted therapies must be explored to address its poor prognosis and high recurrence rates. Declarations Ethics approval and consent to participate The approval was obtained from the Clinical Research Ethics Committee of Huizhou Central People's Hospital. Consent for Publication Written informed consent was obtained from the patient for publication of this case report and any accompanying images. Availability of data and materials Original data generated and analyzed for this care report are included in this published article. Competing interests The authors declare no competing interests. Funding Nil. Authors' contributions Xiaoyu Chen and Guowei Li each made contributions to the manuscript. Xiaoyu Chen and Guowei Li were involved in the inpatient management of the patient. Long Cheng critically revised the intellectual content. Guowei Li was involved in the outpatient management of the patient. Acknowledgements None. References DUAN L, LIU J, ZHANG Y et al (2020) Primary Pituitary Lymphoma in Immunocompetent Patients: A Report on Two Case Studies and the Review of Literature [J]. Front Endocrinol (Lausanne) 11:562850 KOGA Y, AKAI T, SHIRO T et al (2024) Pituitary lymphoma appearing 9 years after pituitary adenoma resection [J]. Surg Neurol Int 15:262 LIU JK, SAYAMA C, CHIN SS et al (2007) Extranodal NK/T-cell lymphoma presenting as a pituitary mass. Case report and review of the literature [J]. J Neurosurg 107(3):660–665 MOLITCH M E (2017) Diagnosis and treatment of pituitary adenomas: a review [J]. JAMA 317(5):516–524 TARABAY A, COSSU G, BERHOUMA M et al (2016) Primary pituitary lymphoma: an update of the literature [J]. 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Endocr J 52(5):543–549 INTERMESOLI T, WEBER A, LEONCIN M et al (2022) Lymphoblastic Lymphoma: a Concise Review [J]. Curr Oncol Rep 24(1):1–12 BĂLINIŞTEANU B, CEAUŞU R A, CîMPEAN AM et al (2011) Conventional examination versus immunohistochemistry in the prediction of hormone profile of pituitary adenomas. An analysis on 142 cases [J]. Rom J Morphol Embryol 52(3 Suppl):1041–1045 WIENS A L, HAGEN M C, BONNIN JM et al (2012) T-cell lymphoblastic lymphoma/leukemia presenting as a pituitary mass lesion: a case report and review of the literature [J]. Neuropathology 32(6):668–674 SREEDHARA P, CZERWINSKI V (2023) T-cell Lymphoblastic Lymphoma Presenting as a Pituitary Mass [J]. JCEM Case Rep 1(5):luad097 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 17 May, 2026 Reviewers agreed at journal 14 May, 2026 Reviewers invited by journal 04 Mar, 2026 Editor assigned by journal 30 Jan, 2026 Submission checks completed at journal 30 Jan, 2026 First submitted to journal 31 Dec, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8492951","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":600668349,"identity":"e614ab08-72eb-4391-a2eb-c53aa0aa621e","order_by":0,"name":"Xiaoyu Chen","email":"","orcid":"","institution":"Huizhou Central People's Hospital","correspondingAuthor":false,"prefix":"","firstName":"Xiaoyu","middleName":"","lastName":"Chen","suffix":""},{"id":600668351,"identity":"2f178c3b-0754-4105-b06a-3e2f0cc1ccaf","order_by":1,"name":"Long Cheng","email":"","orcid":"","institution":"The Affiliated Huizhou Hospital, Guangzhou Medical University","correspondingAuthor":false,"prefix":"","firstName":"Long","middleName":"","lastName":"Cheng","suffix":""},{"id":600668353,"identity":"a2b46d2d-34c3-4154-96f5-e21c102388df","order_by":2,"name":"Guowei Li","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAsUlEQVRIie3RMQqDMBSA4YRAp1cyB9o7ZBNB2qsIhU49xBPBM9iLOOcR6CR6AC9hhoJTqfEEz63Q/Mtb8pGEJ0Qq9YNZodAJUYDWyCYykvvJtG4HWYcvLJZMkmmq6N2MYIWTc3gwSI6E/txMkClU5tlxHkYVetNNkKM7qCOLeBnJANaVXPKSSKFze0i/3iI/NzAt1cy/jN6Hpb9cta5pDhwSU7CNbUHM5MI/m0qlUv/YFx+ePH4kPGgoAAAAAElFTkSuQmCC","orcid":"","institution":"Huizhou Central People's Hospital","correspondingAuthor":true,"prefix":"","firstName":"Guowei","middleName":"","lastName":"Li","suffix":""}],"badges":[],"createdAt":"2026-01-01 03:38:15","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8492951/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8492951/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":104405203,"identity":"7bedce2b-615d-4042-bdef-f69c26a92143","added_by":"auto","created_at":"2026-03-11 12:22:06","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":751406,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eComparison of preoperative and postoperative contrast-enhanced MRI scans of the brain.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePreoperative MRI demonstrated a well-defined, irregular mass within the sellar/suprasellar regions and sphenoid sinus. T1-weighted images showed a homogeneous isointense mass with internal nodular hyperintense foci. The lesion was primarily located within the sellar region, obscuring the pituitary gland and pituitary stalk. It exhibited a drill-like growth pattern, accompanied by osteolytic destruction of the sphenoid sinus wall and skull base. The optic chiasm was displaced superiorly due to compression from the mass (Figures 1a-c).\u003c/p\u003e\n\u003cp\u003eSeven months after surgery and chemotherapy, brain MRI revealed no tumor (Figures 1d-f).\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8492951/v1/902a5c0920a1eeae5c9b8d3b.png"},{"id":104321708,"identity":"eff4b278-c10f-4977-9928-71158aae556c","added_by":"auto","created_at":"2026-03-10 13:22:57","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":227740,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003ePostoperative PET/CT\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePET/CT findings: Increased FDG uptake (SUVmax=12.51) in the sellar region with sphenoid/clival destruction.\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-8492951/v1/7a1a2834c0b8cbc9989fc984.png"},{"id":104321711,"identity":"c4abe7c9-5a72-4f14-bc69-a84f615d582b","added_by":"auto","created_at":"2026-03-10 13:22:57","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":1673573,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eImmunohistochemistry of the lymphoma and pituitary adenoma\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e(a: H\u0026amp;E staining; b–i: CD3, CD4, CD8, TdT, CD20, CgA, Syn, NSE). Tumor cells are positive for T-cell markers (CD3, CD4, CD8, and TdT)，and negative for B-cell markers (CD20). Pituitary adenoma cells express neuroendocrine markers (CgA, Syn, and NSE).\u003c/p\u003e","description":"","filename":"3.png","url":"https://assets-eu.researchsquare.com/files/rs-8492951/v1/ac1528844a26e55b1404b8e3.png"},{"id":104409503,"identity":"786c33c3-94bd-473e-af67-d7fd0d595324","added_by":"auto","created_at":"2026-03-11 12:45:23","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":3733414,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8492951/v1/a34bcbe3-0799-4ee9-9863-129e0ad99e69.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Pituitary T-lymphoblastic lymphoma combined with pituitary adenoma: A rare case report","fulltext":[{"header":"Background","content":"\u003cp\u003eT-cell lymphoblastic lymphoma (T-LBL) is a highly aggressive malignant tumor that originates from immature precursor T lymphocytes. Classically, the disease primarily manifests as a large anterior mediastinal solid mass (accounting for approximately 70%-94% of cases), while clinical manifestations typically take the form of compression effects such as superior vena cava syndrome, dyspnea, and chest tightness caused by the mediastinal mass. Among all pituitary tumors, pituitary lymphoma is exceptionally rare, consisting of less than 0.1% of sellar region tumors. As of April 2025, nearly 40 cases of primary pituitary lymphoma (PPL) have been reported worldwide, with the vast majority derived from B lymphocytes. T-cell-origin pituitary lymphomas are exceedingly uncommon, with only 9 documented cases to date, including 7 cases of primary pituitary T-LBL and 2 cases of NK/T-cell lineage [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Notably, some patients develop pituitary lymphoma either simultaneously with pituitary adenoma resection or following adenoma removal (ranging from 4 to 25 years postresection) [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAccording to previous studies, the average age of onset of pituitary lymphoma among adults is 58 years, with a male-to-female ratio of 1.12:1. Most patients with pituitary lymphoma in the sellar/parasellar region present with pituitary insufficiency (72%), headache (56%), diplopia (39%), diabetes insipidus (DI) (39%), visual loss (28%), and fever (22%) [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. All previously reported cases of pituitary T-cell lymphoma also presented with aggressive radiological features accompanied by visual loss or cranial nerve palsy. Given the clinical and radiological similarities between pituitary lymphoma and pituitary adenoma, the diagnosis cannot be based solely on clinical manifestations or imaging findings; cytological examinations and immunohistochemistry (IHC) are essential for confirming the lymphoid origin and evaluating the underlying pituitary cellular background.\u003c/p\u003e \u003cp\u003eThis case reports only the seventh reported instance of primary pituitary T-lymphoblastic lymphoma. The mass was initially misdiagnosed as a pituitary adenoma on imaging, but postoperative immunohistochemical staining and a detailed cytological examination confirmed a diagnosis of primary pituitary lymphoma. Pituitary T-LBL is exceedingly rare and has a highly aggressive clinical course, necessitating highly intensive therapeutic approaches. Thus, clarifying the clinical manifestations, radiological features, and immunohistochemical findings of pituitary T-LBL is critical for the early diagnosis and effective treatment of this rare disease.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eClinical data\u003c/h2\u003e \u003cp\u003eThe patient was a 61-year-old female with a history of hypertension. She presented with intermittent headaches for six months and progressive visual decline over the prior two months. She denied a history of fever, weight loss, night sweats, limb weakness, or diplopia. A prior cranial magnetic resonance imaging (MRI) scan at an outside hospital revealed a \"sellar and suprasellar mass,\" prompting admission to Huizhou Central People\u0026rsquo;s Hospital for further evaluation and management.\u003c/p\u003e \u003cp\u003ePhysical examination on admission revealed no palpable superficial lymph nodes, decreased left visual acuity on crude testing, unrestricted bilateral ocular movements, and no hepatosplenomegaly. Laboratory tests revealed normal blood counts, electrolytes, liver and kidney function, and urine osmolality but elevated lactate dehydrogenase (LDH; 260 U/L, reference range: 120\u0026ndash;246 U/L). Hormone levels (sex hormones, thyroid hormones, cortisol) were within normal ranges. The levels of tumor markers (carcinoembryonic antigen [CEA], alpha-fetoprotein [AFP]) and immunological parameters (complements C3 and C4, immunoglobulin G [IgG], antinuclear antibody [ANA] profile) were unremarkable. The patient had no history of radiotherapy or chemotherapy.\u003c/p\u003e \u003cp\u003eMRI revealed an irregular, slightly hyperintense mass in the sellar/suprasellar region and sphenoid sinus measuring approximately 40 mm \u0026times; 34 mm \u0026times; 46 mm (anteroposterior \u0026times; transverse \u0026times; craniocaudal). The mass exhibited well-defined but irregular margins, a homogeneous density, and nodular, hyperintense foci. The lesion was primarily located in the sellar region, obscuring the pituitary gland and stalk, and demonstrated a drill-like growth pattern, destruction of the sphenoid sinus wall and skull base, and upward displacement of the optic chiasm. No abnormal densities were observed in the brain parenchyma, ventricular system, or cisterns, and the midline structures remained central (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003ePositron emission tomography/computed tomography (PET/CT) imaging revealed increased fluorodeoxyglucose (FDG) uptake in the sellar/suprasellar region, sphenoid sinus, and right middle nasal meatus (SUVmax\u0026thinsp;=\u0026thinsp;12.51), with a maximum cross-sectional dimension of 32 mm \u0026times; 43 mm. An irregular soft tissue density and osteolytic destruction of the sphenoid sinus wall and clivus were noted, and no abnormal hypermetabolic activity was observed elsewhere \u003cb\u003e(\u003c/b\u003eFig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e\u003cb\u003e)\u003c/b\u003e. Bone marrow flow cytometry revealed no abnormalities, and bone marrow biopsy pathology with IHC confirmed no evidence of T-lymphoma cell infiltration.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eSurgery and pathology\u003c/h3\u003e\n\u003cp\u003eThe patient underwent neuroendoscopic transnasal-sphenoidal resection of the pituitary lesion (via a neuroendoscopic right nostril-sphenoidal approach for sellar pituitary tumor resection). Surgical procedure: Intraoperatively, the sellar floor appeared largely intact. The bone of the sellar floor was thinned with an eggshell technique, exposing the sellar dura. Upon incision of the latter, slightly reddish pituitary tissue was observed posteroinferior to the tumor. The tumor itself appeared yellowish and was firm in texture. Using a curette, the lesion was excised along the inner tumor capsule, starting from the right aspect and then proceeding to the left, posterior, and anterior aspects. Upon completing the anterior resection, the diaphragma sellae were visualized, and residual tissue was carefully curetted under the diaphragma. Exploration confirmed that there was no substantially residual abnormal tissue. The procedure concluded uneventfully. Postoperative pathological examination of the excised tissue revealed a sellar and suprasellar mass consistent with T-LBL coexisting with pituitary adenoma. Immunohistochemistry (IHC): Lymphoma component: CK(\u0026minus;), EMA(\u0026minus;), Vim(\u0026minus;), GFAP(\u0026minus;), CD3(+), CD5(+), CD20(\u0026minus;), PAX-5(\u0026minus;), CD30(\u0026minus;), CD99(+), TdT (focal weak+), CD34(\u0026minus;), CD4(+), CD8 (focally positive), GrB(\u0026minus;), CD56(-), and Ki-67 (90%); pituitary adenoma component: NSE(+), CgA(+), Syn(+). In situ hybridization: EBER (\u0026minus;) \u003cb\u003e(\u003c/b\u003eFigs.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e\u003cb\u003e)\u003c/b\u003e.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e\n\u003ch3\u003eTreatment and follow-up\u003c/h3\u003e\n\u003cp\u003eThe patient developed pituitary insufficiency postoperatively and was started on glucocorticoid replacement therapy. Concurrently, the patient underwent chemotherapy, consisting of high-dose methotrexate (3.5 g/m\u0026sup2; on day 1), liposomal doxorubicin (40 mg/m\u0026sup2; on day 2), and temozolomide (200 mg daily on days 1\u0026ndash;5), which were administered every 28 days for a total of 6 cycles. Lumbar puncture with intrathecal injection was performed, revealing normal cerebrospinal fluid (CSF) pressure and unremarkable routine, biochemical, and flow cytometry CSF findings. Postoperative cranial MRI revealed no residual mass, and the patient reported resolution of her headaches and restored vision. Follow-up MRI after two chemotherapy cycles confirmed that there was no recurrent lesion in the pituitary region, while contrast imaging revealed short T1 and long T2 signal intensities at the surgical margins and no abnormal enhancement \u003cb\u003e(\u003c/b\u003eFig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003ed-f\u003cb\u003e)\u003c/b\u003e. As of Aug 2025, the patient has been followed for 10 months and remains in complete remission.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003ePituitary adenomas are the second most common type of primary brain tumor, with an estimated asymptomatic prevalence of approximately 10% in the general population [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. The most common pituitary adenomas, in descending order, are prolactinomas, nonfunctioning adenomas, growth hormone-secreting adenomas, adrenocorticotropic hormone-secreting adenomas, and thyroid-stimulating hormone-secreting adenomas [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. In contrast, pituitary lymphomas are exceedingly rare among all sellar tumors, accounting for less than 0.1% of all cases. Retrospective case analyses have reported a B-cell to T-cell origin ratio of 5.5:1 for pituitary lymphomas, mirroring the distribution observed in peripheral lymphomas [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e].\u003c/p\u003e \u003cp\u003ePituitary T-LBL, an even rarer subtype of central nervous system lymphoma, is clinically similar to pituitary adenoma but is more aggressive and has a poorer prognosis. To our knowledge, only 7 cases of primary pituitary T-LBL have been reported in the literature through 2025. This article synthesizes existing cases with the present case to provide a comprehensive summary of this rare entity.\u003c/p\u003e \u003cp\u003eOn the basis of existing data from the 7 reported cases of primary pituitary T-LBL, this entity has a marked female predominance (all 7 cases were female), which contrasts with the male predominance reported in the literature on general pituitary lymphomas. The age of onset ranges from 45 to 64 years (approximately middle to elderly ages), with a mean of 58.3 years \u003cb\u003e(\u003c/b\u003eTable\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e\u003cb\u003e)\u003c/b\u003e. This age distribution suggests a potential association with hormonal changes, such as postmenopausal elevation of gonadotropins and decreased estrogen level.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eSummary of reported primary pituitary T-LBL cases\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"8\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c6\" colnum=\"6\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c7\" colnum=\"7\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c8\" colnum=\"8\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eReference\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSex\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eAge (yrs)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eSymptoms\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eEndocrine findings\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c6\"\u003e \u003cp\u003eRadiology\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c7\"\u003e \u003cp\u003eTreatment\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c8\"\u003e \u003cp\u003eFollow-up\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eKuhn et al.[\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eF\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e67\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eOculomotor nerve palsy and amaurosis of the right side\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eHypopituitarism\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eSuprasellar mass with homogeneous density and invasion of clivus\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003eInvasion of right cavernous sinus 6 months after surgery,\u003c/p\u003e \u003cp\u003efollowed by radiation to\u003c/p\u003e \u003cp\u003esellar region.\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003eResidual tumor after 5 months\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRomeike et al. [\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eF\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e64\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eLeft cranial nerve III paresis,\u003c/p\u003e \u003cp\u003edouble vision,\u003c/p\u003e \u003cp\u003eleft eye ptosis,\u003c/p\u003e \u003cp\u003ebitemporal hemianopsia\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003ePituitary insufficiency/hypopituitarism\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eContrast-enhancing intra- and suprasellar mass partially encasing left internal carotid artery, causing elevation of optic chiasm and involving left cavernous sinus.\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003ePost-operative methotrexate and external beam radiation.\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e19 months of stability\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWiens et al. [\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eF\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e58\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eHeadache, right eye ptosis, cranial nerve III palsy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003ePituitary insufficiency/\u003c/p\u003e \u003cp\u003ehypopituitarism,\u003c/p\u003e \u003cp\u003eDI\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eHeterogeneously contrast-enhancing intra- and suprasellar mass displacing optic chiasm and extending into right cavernous sinus.\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003eLeptomeningeal dissemination.\u003c/p\u003e \u003cp\u003ePost-operative intrathecal chemotherapy and craniospinal radiation.\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003eDeath (meningeal spread)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGupta et al. [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eF\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e55\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eHeadache, bilateral diminution of vision, altered sensorium\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eHypopituitarism (LH, TSH), and hyperpituitarism (prolactin, evening cortisol)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003eSellar/\u003c/p\u003e \u003cp\u003esuprasellar mass extending into suprasellar cistern, lateral ventricle, encasing Lt ICA, invading optic chiasm and infundibulam\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003eSurgery\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003eDeath 2 months after surgery\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSreedhara et al. [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eF\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e45\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eHeadache, ptosis, diplopia, blurry vision CN III, IV, VI palsy, V1 numbness\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eSecondary adrenal insufficiency,\u003c/p\u003e \u003cp\u003ehyperprolactinemia, secondary hypothyroidism\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003ellar mass\u003c/p\u003e \u003cp\u003eextending into sphenoid and cavernous sinuses and\u003c/p\u003e \u003cp\u003eclivus, encasement of internal carotid artery (ICA) ,\u003c/p\u003e \u003cp\u003eabutment of optic chiasm\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003etranssphenoidal resection.\u003c/p\u003e \u003cp\u003ehigh-dose methotrexate,\u003c/p\u003e \u003cp\u003eregularly lumbar punctures with intrathecal chemo-therapy.\u003c/p\u003e \u003cp\u003ealternating cyclophosphamide, vincristine sulfate, doxorubicin hydrochloride, and dexamethasone and methotrexate-cytarabine.\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003ePartial improvement\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eKoga et al. [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eF\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e51\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eblurred vision and a visual field defect\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eslightly elevated prolactin (PRL) and low insulin-like growth factor-1\u0026nbsp;levels\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003ea sellar mass extending to the suprasellar region, compressing the optic chiasma upward\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003eTwo weeks postoperatively, leptomeningeal and pancreatic dissemination occurred.\u003c/p\u003e \u003cp\u003eTreatment included cyclophosphamide, doxorubicin, vincristine, dexamethasone, methotrexate, and radiation. Paraplegia developed due to spinal dissemination.\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003eDeath (10 months postop)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCurrent case (2025)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eF\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e61\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eHeadache, visual decline\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003e/\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c6\"\u003e \u003cp\u003emass in the sellar,\u003c/p\u003e \u003cp\u003esuprasellar region and sphenoid sinus\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c7\"\u003e \u003cp\u003eSurgery and high-dose methotrexate, liposomal doxorubicin, and temozolomide\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c8\"\u003e \u003cp\u003e10 months of remission\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eThe neurological manifestations of pituitary lymphoma resemble those of pituitary adenomas, as they depend on the location and extent of spread of the tumor. The most common clinical presentations include hypopituitarism, headache, and visual disturbances such as hemianopia or diplopia. Additional systemic symptoms may include fatigue, weight loss, fever, nausea, and vomiting [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. If the lymphoma extends to the cavernous sinus or orbital apex, it may cause cranial nerve palsies (most frequently affecting cranial nerves II and III) and retro-orbital pain [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Notably, endocrine abnormalities such as hypopituitarism and DI are more prevalent in patients with pituitary lymphoma than in those with pituitary adenoma. Hypopituitarism in patients with pituitary lymphoma often manifests with diverse symptoms, including fatigue, muscle weakness, reduced libido, amenorrhea, thirst, and polyuria [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAmong the 7 reported cases of pituitary T-LBL, the neurological symptoms primarily consisted of visual decline (85.7%), cranial nerve (CN) palsies (100%, most commonly involving CN III, IV, and VI), and headache (71.4%). Endocrine abnormalities predominantly included hypopituitarism (71.4%), and hyperprolactinemia (28.5%, 2 cases). Additional symptoms included diplopia, ptosis, and altered consciousness, the latter of which were likely associated with tumoral invasion or meningeal dissemination.\u003c/p\u003e \u003cp\u003eThe patient reported in this case report also exhibited visual decline and headache. Preoperative evaluations revealed normal pituitary function and no evidence of adrenal insufficiency or thyroid dysfunction. Postoperatively, her visual deficits and headaches improved significantly. However, secondary adrenal insufficiency developed after surgery, prompting the initiation of hydrocortisone replacement therapy.\u003c/p\u003e \u003cp\u003eThe radiological features of pituitary lymphoma include isointense lesions on T1-weighted imaging (T1WI), hypointense lesions on T2WI, and heterogeneous enhancement. All pituitary masses in these cases exhibited aggressive radiological characteristics, such as invasion of the clivus, sphenoid sinus, or cavernous sinus; erosion of the sellar floor; and encasement of the internal carotid artery. Given that the tumor frequently extended into the suprasellar region, cavernous sinus, and sphenoid sinus in most reported cases [\u003cspan additionalcitationids=\"CR7 CR8 CR9 CR10 CR11 CR12\" citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e], some scholars have suggested that sphenoid sinus mucosal biopsies should be performed for patients whose pituitary masses display aggressive imaging features. Such an approach may help confirm the diagnosis while avoiding the surgical risks associated with pituitary resection[\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e].In our retrospective analysis of all reported cases of pituitary T-LBL, sellar masses were universally present, frequently invading the cavernous sinus (85.7%), sphenoid sinus (57%), and clivus (57%), and 57.1% of the masses encased the internal carotid artery. Two patients demonstrated meningeal or spinal dissemination, and one patient developed systemic metastasis (pancreatic involvement). On PET/CT imaging, some patients presented with hypermetabolic foci, although differentiation from adenoma remains challenging. In our case, the tumor extended to the suprasellar region, compressed the optic nerves (a previously reported manifestation), and invaded the sphenoid sinus, cavernous sinus, and even the clivus. While endocrine, neurological, and radiological assessments are crucial for diagnosing and managing primary pituitary lymphoma, alone, they are insufficient for distinguishing the disease from pituitary adenoma.\u003c/p\u003e \u003cp\u003eThe pathogenesis of primary pituitary lymphoma is poorly understood, but several hypotheses have been proposed:\u003c/p\u003e \u003cp\u003e \u003col\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eHormone-Driven Hypothesis: Hormones secreted by pituitary adenomas (e.g., follicle-stimulating hormone [FSH] and adrenocorticotropic hormone [ACTH]) may promote lymphocyte proliferation via hormone receptor-mediated mechanisms. For example, in two reported cases of T-LBL coexisting with FSH-positive adenomas, FSH was hypothesized to activate proliferative signaling pathways through T-cell surface receptors [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e, \u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e].\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eAdhesion Molecule-Mediated Hypothesis: Lymphoma cells may express neural cell adhesion molecules (NCAMs) or integrins, allowing their specific colonization within the pituitary microenvironment [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e].\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eInflammatory Transformation Hypothesis: Chronic lymphocytic hypophysitis may undergo monoclonal transformation, particularly in immunosuppressed or genetically predisposed individuals [\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e].\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003cspan\u003e \u003cli\u003e \u003cp\u003eSurgical or Radiotherapy-Induced Hypothesis: Some patients (e.g., one described in a 2024 case report) developed T-LBL years after pituitary adenoma resection, suggesting that surgical disruption of the blood‒brain barrier or localized inflammation may facilitate lymphomagenesis [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].\u003c/p\u003e \u003c/li\u003e \u003c/span\u003e \u003c/ol\u003e \u003c/p\u003e \u003cp\u003eThe gold standard for diagnosing this disease is pathology. Histologically, T-LBL is characterized by diffuse infiltration of small- to medium-sized lymphoblasts with abundant mitotic figures. Immunohistochemically, the tumor cells typically express CD3, CD4, CD8, and TdT and the Ki-67 index is elevated, while tests for B-cell markers (e.g., CD20) are negative. Molecular testing for T-cell receptor (TCR) gene rearrangement can confirm clonality[\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e]. Differential diagnoses include other pituitary neoplasms, such as pituitary adenoma, distinguished by positive immunohistochemical staining for pituitary hormones and, typically, reactive lymphocyte infiltration; lymphocytic hypophysitis, characterized pathologically by polymorphic inflammatory cell infiltration and a lack of clonality in lymphocytes; and metastatic lymphoma, which requires a thorough systemic evaluation to exclude secondary involvement[\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eNotably, a retrospective analysis revealed that among the 7 cases of pituitary T-LBL, 6 (85.7%) included confirmation of coexisting pituitary adenoma \u003cb\u003e(\u003c/b\u003eTable\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e\u003cb\u003e)\u003c/b\u003e. Three of these cases were identified simultaneously during surgery, whereas the remaining 3 cases were detected 9\u0026ndash;25 years after pituitary adenoma resection and had often been misdiagnosed as recurrence of the adenoma. Among these 6 patients, 2 had gonadotropin-positive adenomas, 2 had nonfunctioning adenomas, and 2 had a combined ACTH-secreting adenoma. The coexistence of pituitary lymphoma and adenoma suggests that pituitary hormones may promote lymphocyte proliferation and contribute to lymphomagenesis.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eRelationship between pituitary T-lymphoblastic lymphoma and pituitary adenoma\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"3\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCase source\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eLymphoma-adenoma relationship\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eAdenoma characteristics (hormone secretion)\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eKuhn et al. \u003csup\u003e[10]\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eLymphoma recurrence within a pituitary adenoma (25 years postresection)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eFSH-positive adenoma\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eRomeike et al. \u003csup\u003e[13]\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eLymphoma arising in a recurrent pituitary adenoma (17 years postresection)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eFSH-positive adenoma (5% cells expressed FSH)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eWiens et al.\u003csup\u003e[19]\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCoexisting lymphoma and adenoma (synchronous diagnosis)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003epituitary ACTH-cell hyperplasia (other hormones variably\u003c/p\u003e \u003cp\u003eexpressed\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGupta et al. \u003csup\u003e[9]\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCoexisting lymphoma and adenoma (synchronous diagnosis)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eACTH/TSH-positive adenoma\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eKoga et al. \u003csup\u003e[2]\u003c/sup\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eLymphoma developed 9 years postresection of pituitary adenoma\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNonfunctioning adenoma\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCurrent Case (2025)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCoexisting lymphoma and adenoma (synchronous diagnosis)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNonfunctioning adenoma\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eAmong the 7 reported cases of pituitary T-LBL, partial transsphenoidal resection was performed in most cases to alleviate the mass effect, whereas gross total resection was rarely achievable because the tumor had invaded the cavernous sinus or vascular encasement. Several patients received high-dose methotrexate (HD-MTX)-based central nervous system penetrating chemotherapy, often combined with cyclophosphamide, vincristine, and other agents (e.g., hyper-CVAD). Additionally, 71.4% of patients underwent whole-brain or sellar radiotherapy (45\u0026ndash;50 Gy) to control local residual disease or leptomeningeal dissemination. To date, no evidence-based data support the use of targeted therapies or hematopoietic stem cell transplantation (HSCT), although these modalities represent potential investigational approaches.\u003c/p\u003e \u003cp\u003eThe outcomes of pituitary T-LBL patients remains poor, with a median survival of approximately 10 months (range: 2\u0026ndash;19 months) among deceased patients. Causes of death include central dissemination (e.g., leptomeningeal spread, as exemplified by a patient described in a 2024 case report) and systemic metastasis (e.g., pancreatic involvement in a patient described in a 1999 case report). Early diagnosis combined with intensive chemotherapy may alleviate the patient\u0026rsquo;s symptoms; however, the high probability of recurrence persists, underscoring the need for novel therapeutic strategies.\u003c/p\u003e \u003cp\u003eIn summary, we present a case of primary pituitary T-LBL. Although pituitary lymphoma is rare, it should be considered in the differential diagnosis of sellar masses, particularly when neuroimaging suggests invasion of adjacent structures. While most sellar lesions originate from pituitary cells\u0026mdash;making hormonal evaluation critical for a diagnosis of adenoma\u0026mdash;a definitive diagnosis of pituitary lymphoma relies on immunohistochemical staining and microscopic identification of lymphoblastic tumor cells. In addition to endocrine, neurological, and radiological assessments, prompt immunohistochemical profiling and comprehensive cytogenetic analysis are essential for early diagnosis and improving outcomes.\u003c/p\u003e \u003cp\u003eNotably, all reported pituitary T-LBLs occurred in middle-aged to elderly females, and the majority coexisted with pituitary adenomas. A subset of these adenomas were gonadotropin-secreting, suggesting that hormonally driven lymphocyte proliferation may contribute to lymphomagenesis\u0026mdash;a hypothesis warranting further investigation. Pituitary T-LBL is a highly aggressive malignancy; while multimodal therapy (surgery, chemotherapy, and radiotherapy) may provide short-term disease control, novel targeted therapies must be explored to address its poor prognosis and high recurrence rates.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe approval was obtained from the Clinical Research Ethics Committee of Huizhou Central People\u0026apos;s Hospital.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for Publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for publication of this case report and any accompanying images.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eOriginal data generated and analyzed for this care report are included in this published article.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNil.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026apos; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eXiaoyu Chen and Guowei Li each made contributions to the manuscript. Xiaoyu Chen and Guowei Li were involved in the inpatient management of the patient.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eLong Cheng critically revised the intellectual content. Guowei Li was involved in the outpatient management of the patient.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNone.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eDUAN L, LIU J, ZHANG Y et al (2020) Primary Pituitary Lymphoma in Immunocompetent Patients: A Report on Two Case Studies and the Review of Literature [J]. Front Endocrinol (Lausanne) 11:562850\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKOGA Y, AKAI T, SHIRO T et al (2024) Pituitary lymphoma appearing 9 years after pituitary adenoma resection [J]. Surg Neurol Int 15:262\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLIU JK, SAYAMA C, CHIN SS et al (2007) Extranodal NK/T-cell lymphoma presenting as a pituitary mass. Case report and review of the literature [J]. J Neurosurg 107(3):660\u0026ndash;665\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMOLITCH M E (2017) Diagnosis and treatment of pituitary adenomas: a review [J]. JAMA 317(5):516\u0026ndash;524\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eTARABAY A, COSSU G, BERHOUMA M et al (2016) Primary pituitary lymphoma: an update of the literature [J]. J Neurooncol 130(3):383\u0026ndash;395\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGIUSTINA A, GOLA M, DOGA M et al (2001) Clinical review 136: primary lymphoma of the pituitary: an emerging clinical entity [J]. J Clin Endocrinol Metab 86(10):4567\u0026ndash;4575\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAU W Y, KWONG Y L, SHEK T W et al (2000) Diffuse large-cell B-cell lymphoma in a pituitary adenoma: an unusual cause of pituitary apoplexy [J]. Am J Hematol 63(4):231\u0026ndash;232\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCHAUDHARY B R BANVS, ALLINSON K et al (2017) Concomitant primary CNS lymphoma and FSH-pituitary adenoma arising within the sella. Entirely coincidental? [J] Neurosurg 80(1):E170\u0026ndash;E175\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGUPTA R K, SARAN R K, SRIVASTAVA A K et al (2017) T cell lymphoblastic lymphoma/leukemia within an adrenocorticotropic hormone and thyroid stimulating hormone positive pituitary adenoma: a cytohistological correlation emphasizing importance of intra-operative squash smear [J]. Neuropathology 37(4):358\u0026ndash;364\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKUHN D, BUCHFELDER M, BRABLETZ T et al (1999) Intrasellar malignant lymphoma developing within pituitary adenoma [J]. Acta Neuropathol 97(3):311\u0026ndash;316\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMARTINEZ J H, MARTINEZ M D, DE GORGOLA M M et al (2011) The coexistence of an intrasellar adenoma, lymphocytic hypophysitis, and primary pituitary lymphoma in a patient with acromegaly [J]. Case Rep Endocrinol 2011:941738\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMORITA K, NAKAMURA F, KAMIKUBO Y et al (2012) Pituitary lymphoma developing within pituitary adenoma [J]. Int J Hematol 95(6):721\u0026ndash;724\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eROMEIKE B F, JOELLENBECK B, STEIN H et al (2008) Precursor T-lymphoblastic lymphoma within a recurrent pituitary adenoma [J]. Acta Neurochir (Wien) 150(8):833\u0026ndash;836\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCOSTA O, BOUTHET C, SAUVAGE P et al (1990) Age-dependent LH and FSH effect on the proliferation of women's peripheral blood lymphocytes in vitro [J]. Int J Immunopharmacol 12(8):821\u0026ndash;829\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBRAESCH-ANDERSEN S, PAULIE S, STAMENKOVIC I (1992) Dopamine-induced lymphoma cell death by inhibition of hormone release [J]. Scand J Immunol 36(4):547\u0026ndash;553\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eHUANG Y Y, LIN S F, DUNN P et al (2005) Primary pituitary lymphoma presenting as hypophysitis [J]. Endocr J 52(5):543\u0026ndash;549\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eINTERMESOLI T, WEBER A, LEONCIN M et al (2022) Lymphoblastic Lymphoma: a Concise Review [J]. Curr Oncol Rep 24(1):1\u0026ndash;12\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBĂLINIŞTEANU B, CEAUŞU R A, C\u0026icirc;MPEAN AM et al (2011) Conventional examination versus immunohistochemistry in the prediction of hormone profile of pituitary adenomas. An analysis on 142 cases [J]. Rom J Morphol Embryol 52(3 Suppl):1041\u0026ndash;1045\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWIENS A L, HAGEN M C, BONNIN JM et al (2012) T-cell lymphoblastic lymphoma/leukemia presenting as a pituitary mass lesion: a case report and review of the literature [J]. Neuropathology 32(6):668\u0026ndash;674\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSREEDHARA P, CZERWINSKI V (2023) T-cell Lymphoblastic Lymphoma Presenting as a Pituitary Mass [J]. JCEM Case Rep 1(5):luad097\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"annals-of-hematology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"aohe","sideBox":"Learn more about [Annals of Hematology](http://link.springer.com/journal/277)","snPcode":"277","submissionUrl":"https://submission.nature.com/new-submission/277/3","title":"Annals of Hematology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false},"keywords":"T lymphoblastic lymphoma, Pituitary, Central nervous system lymphoma, Case report","lastPublishedDoi":"10.21203/rs.3.rs-8492951/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8492951/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground: \u003c/strong\u003eT-cell lymphoblastic lymphoma (T-LBL) is a highly aggressive malignancy that originates from immature precursor T lymphocytes and is characterized by rapid progression. The typical clinical manifestations of T-LBL include superior vena cava syndrome and respiratory compression symptoms such as cough and dyspnea caused by large anterior mediastinal masses. Primary pituitary T-LBL is exceptionally rare, with only seven cases reported worldwide (including the case described in this study).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase presentation\u003c/strong\u003e: This article presents the case of an elderly female patient who presented with headaches and progressive visual deterioration. Brain MRI revealed a sellar/suprasellar mass, while whole-body PET/CT imaging revealed a tumor confined to the central nervous system. Laboratory tests for blood parameters and pituitary hormone levels were normal. Following neuroendoscopic tumor resection, pathological examination and immunohistochemical analysis confirmed a diagnosis of pituitary T-LBL coexisting with pituitary adenoma. The patient’s headaches and visual impairment were resolved postoperatively. Subsequent chemotherapy with high-dose methotrexate, temozolomide, and liposomal doxorubicin effectively controlled the disease.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusions\u003c/strong\u003e: This case highlights the rarity of concurrent sellar lymphoma and pituitary adenoma and summarizes previously reported cases of primary pituitary T-LBL to provide clinical diagnostic and therapeutic insights into this rare disease.\u003c/p\u003e","manuscriptTitle":"Pituitary T-lymphoblastic lymphoma combined with pituitary adenoma: A rare case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-03-10 13:22:52","doi":"10.21203/rs.3.rs-8492951/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2026-05-17T15:51:03+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"39244198664655795160358877083672796150","date":"2026-05-14T14:58:05+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-03-04T13:40:29+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-01-30T09:39:30+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-01-30T09:34:34+00:00","index":"","fulltext":""},{"type":"submitted","content":"Annals of Hematology","date":"2026-01-01T03:31:46+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"annals-of-hematology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"aohe","sideBox":"Learn more about [Annals of Hematology](http://link.springer.com/journal/277)","snPcode":"277","submissionUrl":"https://submission.nature.com/new-submission/277/3","title":"Annals of Hematology","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Springer Hybrid","inReviewEnabled":true,"inReviewRevisionsEnabled":false}}],"origin":"","ownerIdentity":"9120e74c-8fef-43e4-8425-1ee304e5e689","owner":[],"postedDate":"March 10th, 2026","published":true,"recentEditorialEvents":[{"type":"editorInvitedReview","content":"","date":"2026-05-17T15:51:03+00:00","index":16,"fulltext":""},{"type":"reviewerAgreed","content":"39244198664655795160358877083672796150","date":"2026-05-14T14:58:05+00:00","index":15,"fulltext":""}],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-03-10T13:22:53+00:00","versionOfRecord":[],"versionCreatedAt":"2026-03-10 13:22:52","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8492951","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8492951","identity":"rs-8492951","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}