Mimicking Polycystic Liver Disease: A Novel Case of Multifocal Pancreatic Neuroendocrine Tumour-Induced Hepatic Metastases Diagnosed via Endoscopic Ultrasound – A Diagnostic Challenge and Treatment Opportunity” Keywords: – Polycystic Liver Disease – Pancreatic Neuroendocrine Tumour – Hepatic Metastases – Endoscopic Ultrasound – Multifocal Hepatic Cysts – Pancreatic Neuroendocrine Tumour Liver Metastasis – EUS in Hepatic Metastasis Diagnosis – Liver Metastasis from Pancreatic Tumours – Polycystic Liver Disease Diagnosis

Diagnostic Dilemmas in Rare Pancreatic Neuroendocrine Tumors

Neuroendocrine neoplasms represent rare growths originating from specialized cells, showing an incidence of roughly 8.8 per 100,000 residents in England, as reported by health data. Within this category, gastro-entero-pancreatic neuroendocrine tumors make up 55 to 70 percent of cases. Pancreatic neuroendocrine tumors represent 12 to 20 percent of those subsets, translating to a mere 1 to 2 percent of all pancreatic malignancies overall.

Clinicians divide these growths into functional varieties tied to hormone hypersecretion and nonfunctional forms that lack such syndromes. Nonfunctional types typically present with vague complaints like abdominal pain, unexpected weight loss, and jaundice, or they turn up incidentally during scans for unrelated conditions. In a complex case tracked over a year and a half, a 62-year-old patient with a prior history of chronic lymphocytic leukaemia in remission presented an unusual diagnostic hurdle when routine tracking revealed multiplying liver lesions that mimicked benign cysts.

Eighteen-Month Radiological Surveillance and Escalation

The patient’s clinical journey began during a routine surveillance computed tomography scan of his chest, abdomen, and pelvis, which revealed an incidental adrenal nodule. Subsequent imaging a year later showed that the adrenal finding had resolved, but it unexpectedly exposed new focal hepatic infiltrates that were completely absent on prior scans. Positron emission tomography scans performed two months afterward identified periduodenal lymphadenopathy, pancreatic duct enlargement, and bilobar hypoattenuating liver lesions that lacked fluorodeoxyglucose uptake.

Magnetic resonance cholangiopancreatography confirmed main pancreatic duct dilatation without any intrinsic obstructing lesions. Although initial ultrasound-guided liver biopsies failed to yield an aspirate, a subsequent magnetic resonance imaging session displayed benign-appearing cystic lesions. However, their rapid proliferation over a four-month span triggered significant clinical concern regarding an underlying malignancy, such as a mucinous tumor or neuroendocrine metastasis. By the ninth month, repeat imaging revealed more than 30 randomly distributed low-density hepatic lesions alongside gross main pancreatic duct dilatation extending to the ampulla and two large enhancing lymph nodes near the superior mesenteric vein.

Endoscopic Ultrasound and Histopathological Confirmation

Faced with escalating radiological findings, the hepato-pancreato-biliary multidisciplinary team recommended endoscopic ultrasound with tissue sampling. The patient underwent the procedure, which exposed tortuous main pancreatic duct dilatation with hyperechoic margins in the body and neck, accompanied by pancreatic body and tail atrophy and generalized hypoechogenicity in the head. Multiple hepatic cystic lesions containing internal septations were visualized alongside large peripancreatic lymph nodes measuring 25 to 30 millimeters.

Fine needle aspiration samples collected from the pancreatic head, liver lesions, and lymph nodes underwent cytological and histopathological evaluation. Analysis revealed monomorphous plasmacytoid cells consistent with a well-differentiated neuroendocrine tumor. Immunohistochemistry confirmed an intermediate grade neuroendocrine tumor with a Ki-67 proliferation index of 8 percent, staging the condition as T1N1M1a. A Gallium-68 DOTATOC positron emission tomography computed tomography scan subsequently verified a somatostatin receptor-avid lesion in the pancreatic head.

While standard gastrointestinal neuroendocrine tumors typically manifest as contrast-enhancing masses on cross-sectional scans, aberrant presentations involving cystic hepatic features remain exceptional. Medical literature indicates that only a small percentage of patients experience cystic liver metastases that can easily mimic benign conditions, necessitating rigorous investigation before mapping out therapeutic plans. For instance, separate clinical documentation details instances where gastric neuroendocrine tumors with cystic hepatic metastases were initially misdiagnosed as hepatic echinococcosis before surgical excision revealed the true pathology.

Following the definitive tissue diagnosis, the multidisciplinary team structured a management strategy around the patient’s metastatic staging. Because surgical resection serves as the primary curative intent typically reserved for localized or larger symptomatic growths, unresectable scenarios require systemic approaches. Consequently, the care team initiated treatment with somatostatin analogues utilizing four-weekly lanreotide injections delivered with palliative intent, paired with ongoing radiological surveillance by the oncology service.