Prevalence of Salivary Ductal Inclusions in Parotid Lymph Nodes of Patients with Warthin Tumor
W Cope, CT Naugler, T Vyas, MJ Bullock. Cambridge University, Cambridge, United Kingdom; Dalhousie University, Halifax, NS, Canada
Background: The histogenesis of Warthin tumor (WT) has long been debated. A predominant theory is that WT arises from heterotopic salivary ductal inclusions in intra/periparotid lymph nodes (LN); however, it is still unclear if WT is neoplastic. The prevalence of these inclusions in LN of patients with parotid WT has not previously been studied. We sought to determine this in comparison with parotids excised for pleomorphic adenoma (PA).
Design: Cases were chosen from the files of the QEII HSC, Halifax. 74 WT and 77 PA were initally selected (consecutively). H&E sections were reviewed, and cases with parotid LN were included. Aggregates of lymphoid tissue with a capsule and subcapsular sinus were defined as LN. An inclusion could be oncocytic or non-oncocytic, and was considered LN-included if completely surrounded by lymphocytes and not merging with hilar fat. Inclusions with acinar cells were excluded. Distinction between small WT and LN with oncocytic inclusions was made at 1 cm. We recorded the presence/absence of inclusions as well as the proportion of LN sections with inclusions.
Results: 46 WT and 52 PA met the above criteria (p=0.5). Among WT, the average age was 62.5 yrs (37.8-85.2); the M:F ratio was 1:1.3. Among PA, the average age was 50.2 yrs (16.4-82.3); the M:F ratio was 1:1.6. 33 WT (71.7%) and 17 PA (32.7%) had inclusions in any LN (p<0.01). A total of 383 and 270 LN sections were examined from WT and PA, respectively. Of these, 85 (22%) from WT and 30 (11%) from PA had inclusions (p=0.00024). Smoking status is available from 40 WT and 49 PA patients. 92.5% (37/40) of WT patients are smokers/ex-smokers, compared with 55.1% (27/49) PA patients(p<0.01). Among PA patients, 12 of 27 smokers (44%) had inclusions compared with 5 of 22 (22.7%) non-smokers (NS).
Conclusions: Salivary ductal inclusions are more frequent in parotid LN from patients with WT than from those with PA. The high proportion of smokers among WT patients is consistent with prior studies. The M:F ratio among WT patients is lower. The results support the hypothesis that WT arises from salivary ductal inclusions found in intra or periparotid LN. The lack of a statistically significant difference in the prevalence of inclusions in smokers and non-smokers with PA suggests that smoking does not cause inclusions. We hypothesize that smoking acts on pre-existing inclusions to create WT. The study was limited by an inability to examine parotid glands that are free of neoplasia.
Category: Head & Neck
Monday, March 9, 2009 1:00 PM
Poster Session II # 162, Monday Afternoon