We read with great interest the article entitle Chronic lymp

We read with great interest the article entitle “Chronic lymphocytic lymphoma and concomitant renal cell carcinoma (Clear Cell Type): Review of the literature”, written by Uz et al. and published in a recent issue of your journal. Here, we would like to emphasize some points about this review of the literature. Previously, we also reported 3 cases with hematological malignancies and renal cell carcinoma (RCC) . In our series, all patients had lymphoproliferative malignancies. Other than as specified in this article, we presented a 82-year-old female patient with coincidence of chronic lymphocytic lymphoma (CLL) and RCC . Coincidence of CLL and RCC may be synchronous or asynchronous. Beisland et al.’s study showed an incidence of 3.7% of synchronous tumors with RCC. Our patient had synchronous malignencies. The other case was a 53-year-old male patient diagnosed with RCC 4 years prior to Hodgkin\'s disease (Ann-Arbor, stage II-B) . And, the third was 69-year-old male patient, diagnosed with multiple myeloma (IgG, κ, stage II-A) and RCC of left nephrectomy specimens, synchronously . Interestingly, unlike our patient, Choueiri et al. reported case series of MM and RCC on the right side with right renal involvement except for one .
Introduction Esophageal lymphoma occurs mostly secondary to cervical and mediastinal lymph node invasion or contiguous invasion from gastric lymphoma [1], and thus primary esophageal lymphoma (PEL) is extremely rare, comprising less than 1% of primary gastrointestinal lymphomas [2]. The etiology of PEL is unknown, although HIV infection is thought to be one probable risk factor because several papers reported that some PEL patients were infected with HIV. The pathological subtypes of PEL are MALT lymphoma or diffuse large B cell lymphoma in most cases and other B, T, or NK cell lymphoma and Hodgkin lymphoma in a few cases. PEL patients complain of non-specific symptoms, i.e., epigastric pain, dysphagia, and B symptoms. MALT lymphoma appears in association with chronic mCAP Supplier induced by persistent infection and autoimmune diseases such as Helicobacter pylori (HP) infection and Hashimoto\'s thyroiditis, respectively. Gastric MALT lymphomas are well known to be associated with HP infection, although there are very few cases of localized esophageal MALT lymphoma in HP-infected patients. Here, we present a patient with primary esophageal MALT lymphoma who achieved complete remission without anti-lymphoma treatment after HP eradication therapy and has remained in remission for more than 3 years. The literature on PEL is also reviewed to show the relationship between PEL and HP infection.
Case presentation A 76-year-old woman visited our hospital with complaints of chest tightness after eating and epigastric discomfort for more than 10days. Findings of physical examinations were completely normal, with no palpable swelling of the lymph nodes, liver, and spleen. Laboratory tests revealed slight leukocytosis and anemia, with normal levels of both serum lactate dehydrogenase and soluble interleukin-2 receptor. The level of anti-HP immunoglobulin G antibody was elevated. Her medical history included atrophic gastritis diagnosed by esophagogastroduodenoscopy (EGD) 5 years previously, although she had not received HP eradication therapy. EGD revealed a fur-coated 2cm mass negatively stained with iodine in the lower esophagus, 34cm from the incisors (Fig. 1A), and no lymphoma involvement of the stomach or Barrett\'s change at the esophageal-gastric junction. Standard endoscopic biopsies were performed, and the histological findings showed mid-sized lymphocyte invasion mainly under the squamous epithelium and partially in the squamous epithelium. There was no follicular dendritic cell meshwork and lymphocyte aggregation, showing that it was not a reactive germinal center. The dyskaryosis was not severe, and lymphocytes formed a lymphoepithelial lesion. No HP organisms were identified. These lymphocytes were immunohistochemically positive for CD20 and CD79a, and negative for CD5, CD10, and BCL2 (Fig. 2). Histological findings of infiltrating atypical lymphoid cells were consistent with MALT lymphoma. Fluorescence in situ hybridization analysis of formalin-fixed paraffin-embedded tissue sections showed no split signal for MALT1. 18F-fluorodeoxyglucose (FDG) positron-emission tomography/computed tomography (PET-CT) demonstrated increased FDG uptake in the middle and lower esophagus, corresponding with the MALT lymphoma detected, and there were no other positive findings (Fig. 3). On the basis of these findings, the patient was diagnosed with MALT lymphoma of the esophagus, stage IA.