A case of invasive pituitary prolactinoma misdiagnosed as nasopharyngeal carcinoma: diagnostic lessons and management

Invasive pituitary adenomas with infrasellar extension can present with epistaxis and nasal obstruction, mimicking nasopharyngeal carcinoma (NPC) and leading to misdiagnosis. A 32‑year‑old male was initially misdiagnosed with NPC and received chemoradiotherapy. Multidisciplinary assessment revealed an invasive sellar mass, prolactin >2,000 ng/mL, and PIT‑1 positivity, establishing a diagnosis of invasive prolactinoma. Bromocriptine induced significant tumor reduction but was complicated by cerebrospinal fluid (CSF) leakage and intracranial infection. Surgical resection and leak repair led to favorable recovery with normalized prolactin levels. This case highlights the need for routine hormonal screening, nasopharyngeal mucosal integrity assessment, and multidisciplinary collaboration.

Introduction
Pituitary adenomas are common benign neoplasms; prolactinomas are the most frequent functional subtype. About 30–40% exhibit invasive growth. When tumors extend inferiorly into the nasopharynx, symptoms like epistaxis and nasal obstruction can mimic NPC, a prevalent head and neck malignancy in regions such as China. Both entities can cause skull base destruction, creating diagnostic challenges. This report details a case of invasive prolactinoma initially misdiagnosed as NPC and treated with chemoradiotherapy, analyzing reasons for misdiagnosis and key diagnostic points.

Case Presentation
History and initial management
A 32‑year‑old male presented with one year of blood‑stained nasal discharge, hemoptysis, and left orbital pain. CT showed a nasopharyngeal mass with skull base destruction. After nasal mass resection, pathology reported “squamous cell carcinoma.” He received radiotherapy and cisplatin chemotherapy. Symptoms did not improve. Pathological review then suggested “low‑grade neuroendocrine tumor, pituitary origin cannot be excluded.” Our hospital’s pathology consultation confirmed a PIT1‑lineage pituitary neuroendocrine tumor.

Re‑evaluation and treatment
On admission, paranasal sinus CT showed a soft tissue lesion in the sphenoid sinus and sella with clival destruction. MRI revealed a 47×39×44 mm enhancing mass encasing both cavernous sinuses and internal carotid arteries. Endocrine evaluation: prolactin >2,000 ng/mL, low testosterone and estradiol. Multidisciplinary discussion noted intact nasopharyngeal mucosa (against primary NPC), PIT‑1 positivity, and markedly elevated prolactin, diagnosing invasive prolactinoma. Bromocriptine 2.5 mg/day was started.

After one month, MRI showed significant tumor regression, but the patient developed CSF rhinorrhea, then fever and meningeal signs (intracranial infection). He received meropenem and lumbar drainage. After infection control, he underwent endoscopic transsphenoidal tumor resection and CSF leak repair. Postoperatively, a second intracranial infection occurred (fever, neck stiffness) and was treated with meropenem, vancomycin, lumbar drainage, and intrathecal vancomycin. CSF improved, and fever resolved. Pathology confirmed a PIT1‑lineage, densely granulated prolactin‑secreting adenoma (Ki‑67 <5%). At three‑month follow‑up, MRI showed satisfactory tumor removal, and prolactin levels were normal on continued bromocriptine.

Discussion
Diagnostic challenges arose from overlapping clinical presentations (epistaxis, nasal obstruction), misleading radiology (skull base destruction), and pathological misinterpretation (superficial biopsy). Key differentiating points: NPC typically shows nasopharyngeal mucosal irregularity, while pituitary adenomas maintain mucosal integrity even with skull base invasion. Other sellar lesions have characteristic features (craniopharyngiomas with calcifications, meningiomas with dural tail, chordomas with T2 hyperintensity). Routine hormonal screening (especially prolactin) is critical. A multidisciplinary team (MDT) approach integrating radiology, pathology, endocrinology, and surgery is essential to avoid diagnostic anchoring.

Management complexities: Rapid tumor shrinkage with dopamine agonists can expose pre‑existing dural and bony defects, leading to CSF leakage and infection. High‑risk patients require close monitoring for rhinorrhea, headache, or fever. Surgical repair is recommended for dopamine agonist‑induced rhinorrhea.

Limitations: single case report, retrospective design, short follow‑up (3 months). Future prospective studies are needed.

Conclusions
Pituitary tumors should be included in the differential diagnosis of lesions with nasopharyngeal symptoms and skull base destruction, even when imaging suggests extensive invasion. Routine preoperative hormonal screening for skull base lesions is essential. Avoid anchoring diagnosis solely on initial pathology. The MDT approach enhances diagnostic accuracy. Clinicians must anticipate and manage complications such as CSF leakage and intracranial infection during medical treatment of invasive prolactinomas.

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The study was recently published in the Neurosurgical Subspecialties.

Neurosurgical Subspecialties (NSSS) is the official scientific journal of the Department of Neurosurgery at Union Hospital of Tongji Medical College, Huazhong University of Science and Technology. NSSS aims to provide a forum for clinicians and scientists in the field, dedicated to publishing high-quality and peer-reviewed original research, reviews, opinions, commentaries, case reports, and letters across all neurosurgical subspecialties. These include but are not limited to traumatic brain injury, spinal and spinal cord neurosurgery, cerebrovascular disease, stereotactic radiosurgery, neuro-oncology, neurocritical care, neurosurgical nursing, neuroendoscopy, pediatric neurosurgery, peripheral neuropathy, and functional neurosurgery.

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