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Neuroradiology Case of
the Week
Case 244
Jeremy Duda, BA,
Ajay Malhotra, MD,
and P-L Westesson, MD, PhD, DDS
Clinical
Presentation: A
57-year-old female initially presented with jaundice and was found to have diffuse large B cell lymphoma of the pancreatic head. Staging PET scan showed a hypermetabolic region posterior to the mandible near the parotid gland, and further imaging was requested.
Imaging Findings: Post-contrast axial CT images demonstrate a well circumscribed, nodular homogeneously enhancing lesion measuring approximately 1.4 x 1.0 cm in the superficial left parotid gland. There was no necrosis or calcification on imaging. Adjacent fascial planes were preserved. There was no evidence of cervical lymphadenopathy. The nodular enhancing lesion corresponded to the area of increased FDG uptake on the PET scan.
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Figure 1: Post-contrast CT image demonstrates left parotid mass.
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| Figure 2: Close up of left parotid mass. |
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| Figure 3: PET scan showing hypermetabolic area. |
Diagnosis: Papillary cystadenoma lymphomatosum (Warthin’s tumor)
Discussion: Warthin’s tumor, or papillary cystademona lymphomatosum, is the second most common salivary gland neoplasm after pleomorphic adenoma, and accounts for 6-30% of parotid tumors. It usually arises in ages 50-70, more often in men. There is an eightfold increase in incidence of Warthin’s tumor among tobacco users.
It usually presents as a mass measuring 2-4 cm arising within the parotid glands with rare exceptions. Microscopically it has elements of epithelial cells characteristic of salivary glands along with a lymphocytic infiltrate. Ten percent of the tumors are bilateral, and 10% are multifocal. The lymphocyte population is polyclonal and expresses normal B and T cell markers. Recent studies have been unable to identify abnormalities of tumor suppressor genes (p53, p16) commonly mutated in neoplasms.
The identity of Warthin’s has changed over the years. Although originally defined as a neoplasm, it has since been proposed to be an immune reaction to either heterotopic or metaplastic tissue. The parotid gland forms late in embryonic development and it was suggested that Warthin’s tumor arises when periparotid lymphoid tissue is aberrantly incorporated into the capsule of the organ. Alternatively, based on the similarities of the lymphocytic infiltrate of Warthin’s to that of immune mediated diseases like Hashimoto’s, it was proposed that some of the epithelial tissue undergoes metaplasia and induces a delayed hypersensitivity reaction. In either theory, the mass of the included lymphocytes increases and expands the tumor.
Clinical symptoms can be attributed to enlargement of the lesion, and often there is nothing more than a painless mass in the region of the parotid gland. Facial weakness may occur due to compression of the seventh cranial nerve. In rare instances inflammation of the mass causes patients to present acutely with local pain and swelling.
On ultrasound Warthin’s tumor appears as a rounded or lobulated heterogeneous mass that may have cystic changes with hyperechoic internal septation. On MR the lesion is again heterogeneous, with intermediate intensity on T1 and internal high intensity on T2 representing cystic change. The lesion does not enhance, which is helpful in differentiating it from pleomorphic adenoma and primary carcinoma. Cells within Warthin’s tumors have a high mitochondrial content and preferentially take up Tc-99m pertechnetate, appearing as a hot spot on radionucleotide scintigraphy. Fine needle aspiration helps establish the diagnosis, but pathologic specimen obtained during surgery is definitive.
Warthin’s tumor is a benign disease, with no primary malignant potential. Therefore observation is the preferred management in patients with contraindications for surgery. Excision is considered curative – there is a 2% chance of recurrence which is attributed to incomplete resection or multifocal disease that was not initially recognized.
The treatment of choice is superficial parotidectomy with preservation of the seventh cranial nerve. Total conservative parotidectomy may be indicated with recurrences or deep lesions.
References:
- Howlett DC, Kesse KW, Hughes DV, Sallomi DF. The role of imaging in the evaluation of parotid disease. Clin Radiol. 2002 Aug;57(8):692-701. [Medline]
- Arida M, Barnes EL, Hunt JL. Molecular assessment of allelic loss in Warthin tumors. Mod Pathol. 2005 Jul;18(7):964-8. [Medline]
- Cadier M, Watkin G, Hobsley M. Smoking predisposes to parotid adenolymphoma. Br J Surg. 1992 Sep;79(9):928-30. [Medline]
- Ebbs SR, Webb AJ. Adenolymphoma of the parotid: aetiology, diagnosis and treatment. Br J Surg. 1986 Aug;73(8):627-30. [Medline]
- Yoo GH, Eisele DW, Askin FB, Driben JS, Johns ME. Warthin's tumor: a 40-year experience at The Johns Hopkins Hospital. Laryngoscope. 1994 Jul;104(7):799-803. [Medline]
- Chapnik JS. The controversy of Warthin's tumor. Laryngoscope. 1983 Jun; 93(6):695-716. [Medline]
- Kumar: Robbins and Cotran: Pathologic Basis of Disease, 7th ed., Elsevier, 2007.
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