Inconclusive Cytology and Non-Contributory Cyst Fluid Tumor Marker Analysis of Pancreatic Cystic Lesion: Is It the End of the Story?
Ming Zhang, Michael Carrozza, Yajue Huang. Temple University Hospital, Philadelphia, PA
Background: Pancreatic cystic lesions constitute a broad spectrum of entities ranging from non-mucinous to mucinous and benign to malignant cysts. Endoscopic ultrasound -guided fine needle aspiration (EUS-FNA) cytology is routinely utilized for pre-operative diagnosis. Cyst fluid obtained from EUS-FNA is commonly submitted for chemical analysis of tumor markers to aid in the diagnosis. However, the value of cytologic interpretation is frequently limited by low cellularity of aspirated fluid and the reliability of cyst fluid tumor marker is variable. Recently, molecular tests of cyst fluid have been applied and show high specificity in the differentiation of the pancreatic cystic lesions. In this study, we investigated the usefulness of molecular analysis of pancreatic cyst fluid in the setting of inconclusive cytology and non-contributory tumor markers test.
Design: We retrospectively reviewed pancreatic cystic lesions with EUS-FNA cytology, cyst fluid tumor markers (CEA and amylase) and molecular tests (K-ras mutation and loss of heterozygocity) from 2009-2011. The inconclusive cytology diagnosis was defined as “non-diagnostic” or “atypical cytology”. Non-contributory cyst fluid chemical analysis includes 2 situations: 1) amylase<250U/L and CEA <192 ng/ml or 2) amylase >250 U/L and CEA >192ng/ml. The molecular tests and the histopathologic results of the resection specimens were analyzed.
Results: The cohort consists of 32 pancreatic cyst EUS-FNA cytology cases, which shows 20 cases (62.5%) with non-diagnostic (34.4%) or atypical (28.1%) cytology. Among the 20 cases, non-contributory tumor marker analysis was found in 11 cases (55%). The molecular analysis shows K-ras mutation or loss of heterozygocity in 5 out of 11 cases (45%), which also indicates a mucinous cystic neoplasm with potential for neoplastic progression. Interestingly, 3 out of 4 pancreatic cyst resection specimens showed pancreatic intraepithelial neoplasias (PanIN)-1A or 1B with benign molecular features; while elevated cystic fluid CEA and amylase were identified in all the cases with PanIN-1A and 1B.
Conclusions: Inconclusive pancreatic cyst cytology and non-contributory cystic fluid tumor markers were frequently encountered, making accurate diagnosis challenging. Our study indicates that cyst fluid molecular tests for K-ras mutation and allelic imbalance provide extra information and may help with the diagnosis and clinical management. Our novel finding is that PanIN-1A and 1B might be related to both elevated cyst fluid CEA and amylase without K-ras mutation.
Wednesday, March 6, 2013 1:00 PM
Poster Session VI # 134, Wednesday Afternoon