Konofaos et al. Journal of Medical Case Reports 2011, 5:380 http://www.jmedicalcasereports.com/content/5/1/380 process. The initial event of this process may be a long- term stimulation of activating B cells by an inflamma- tory stimulus [15]. Hiltbrand et al [16] also suggested that MALT lymphomas arise from BLL, not from intra- parotid lymphoid aggregates. Association between MALT lymphoma and autoim- mune diseases such as systemic lupus erythematous [17,18] or inflammatory diseases such as Helicobacter pylori infection in the stomach has been discussed. In the present case, no gastric lesions were observed after stomach examination. According to Rosenstiel et al [19] in patients with Sjögren’s syndrome, the risk of develop- ing Non-Hodgkin’s lymphoma increases 44-fold and 80% of these lymphomas are of the MALT type. Our patient had no clinical evidence of Sjögren’s syndrome. According to Anacak et al [6] salivary gland MALT lymphoma is mainly a disease affecting women; in their study the ratio of females to males was 3/1. Kojima et al [20] reported a female-to-male ratio of 1.7/1.0 for pri- mary lymphomas of the salivary glands. Kalpadakis et al [21] reported a series of 76 patients with non-gastric extra-nodal marginal zone lymphomas in which two thirds of the patients were female. The reason for this female predominance is not clear. Radiological representation of MALT lymphomas of the parotid gland is scarce [22]. According to Corr et al [23] who presented a cohort of 10 HIV-infected children with MALT lymphomas of the parotid gland, the CT scan appearance of these lesions consisted of multiple hypoechoic solid nodules, which corresponded to hyper- plastic lymphoid tissue or lymphoma. Cystic lesions (from compression of terminal parotid ducts by contigu- ous hyperplastic or neoplastic lymphoid tissue) and punctuate calcification, both intracystic and parenchy- mal may coexist. This radiologic appearance has also been described in BLL encountered in patients with AIDS [24] or Sjögren’s syndrome [25]. Currently, there is controversy in the reported litera- ture regarding the accuracy of PET-CT scan in MALT lymphomas. Elstrom et al [26] evaluated the accuracy of PET-FDG in identifying various lymphomas subtypes. According to their results, PET-FDG detected 67% of marginal zone lymphoma. Hoffmann et al [27] reported increased FDG uptake in patients with nodal marginal zone lymphoma but not in those with extranodal dis- ease, suggesting that the FDG-avidity depends on tumor location and ⁄or the lymphoma subtype. Perry et al [28] suggested that PET -CT is a useful tool for both, initial staging and follow-up after treatment in patients with MALT lymphoma and its sensitivity depends on disease location and stage at initial diagnosis. Most non-gastric MALT lymphomas have been noted to be indolent. Disseminated disease is relatively slow to develop in affected patients. Up to 50% of the patients Page 3 of 5 with non-gastric MALT lymphoma have multiple involved sites [29]. Whether this phenomenon can be attributed to synchronous disease occurrence at multiple sites or to undetected sub-clinical disease, the mechan- ism of disease dissemination is unknown [30]. An association between hepatitis C virus (HCV) infec- tion and B-cell lymphomas has previously been reported, especially in countries in which the prevalence of HCV is relatively high [31,32]. Other researchers have not found this association [33,34]. Thus, further studies are needed to define the role of HCV infection in the pathogenesis of MALT lymphoma. Rosenstiel et al [19] suggested that any patient with a cystic parotid mass must be screened for HIV infection or for Sjogren dis- ease, because it is more likely that the cystic mass is derived from either one of these underlying diseases than to a MALT lymphoma. According to Klussmann et al [35] Epstein - Barr virus (EBV), Human herpetovirus (HHV) types -6 and -8, HCV and HIV infections have been involved in the etiology of salivary MALT lymphomas. In our practice, clinical examination, preoperative FNA of the suspicious lesion and radiological investiga- tion in certain cases, is part of the preoperative assess- ment of a suspicious parotid gland lesion. However, Ando et al [36] suggested that a parotid MALT lym- phoma is hard to diagnose by fine-needle aspiration cytology. Thieblemont et al [37] suggested that patients with localized disease generally were treated with surgery or radiotherapy. Surgery is strongly recommended as a diagnostic tool of malignant lymphoma of the parotid gland [38], since histological evaluation is essential for treatment of malignant lymphoma. Parotid surgery is positively recommended both in order to treat the tumor and to ensure histological diagnosis of the tumor for further follow-up planning. The prognosis is excel- lent for patients with MALT lymphoma of the parotid gland. Limited data indicate five-year survival rates of more than 80%. Once MALT lymphoma is diagnosed, an in-depth eva- luation for synchronous multi-sited involvement and disseminated disease should be undertaken before initia- tion of local therapy. Radiotherapy and chemotherapy should be considered in association with surgery in dis- seminated forms or after removal. Sarris et al suggested [38] irradiation in case of localized lesions in early stage and chemotherapy in those with advanced disease. Mar- ioni et al [15] suggested that radiotherapy and che- motherapy should be considered in association with surgery in disseminated forms or after incomplete removal. Isobe et al [39] treated 37 patients with Stage IE extragastric MALT lymphomas with radiotherapy only. Local control was obtained in 97.3% of the