Cases reported "Pseudolymphoma"

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1/12. Conjunctival lymphocytic infiltrates associated with Epstein-Barr virus.

    PURPOSE: To describe the clinicopathologic features of two patients with Epstein-Barr virus (EBV) associated conjunctival lymphocytic infiltrates. DESIGN: Two case reports. methods: The clinical histories and pathologic findings of two patients with salmon-colored conjunctival infiltrates are described. MAIN OUTCOME MEASUREMENTS: Clinical observation and pathologic examination of conjunctival biopsy specimens with accompanying immunohistochemical staining, flow cytometric immunophenotyping, and polymerase chain reaction analysis when appropriate. RESULTS: One patient had ipsilateral preauricular lymphadenopathy, elevated serum EBV titers, and a unilateral reactive lymphocytic infiltrate resulting in a conjunctival mass. The other patient had bilateral conjunctival lymphocytic infiltrates causing conjunctival masses. There was an expanded clonal population of B lymphocytes in the conjunctival mass in the second patient. Both patients had EBV antigen in their conjunctival lymphocytic infiltrates. CONCLUSIONS: Conjunctival lymphocytic lesions associated with EBV represent a spectrum of reactive infiltrates to monoclonal populations.
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2/12. sodium valproate-induced cutaneous pseudolymphoma followed by recurrence with carbamazepine.

    We report a patient with a sodium valproate-induced cutaneous pseudolymphoma, presenting with an erythematous papule, histologically mimicking a non-epidermotropic T-cell lymphoma. polymerase chain reaction study of the skin biopsy revealed monoclonal rearrangement of the T-cell receptor gamma gene. Withdrawal of sodium valproate was followed by regression of the lesion, but 5 months after substitution by carbamazepine, two further papules appeared, with similar histological features and a T-cell clone identical to the initial one. carbamazepine was stopped and the lesions disappeared without relapse over a 4-year follow-up. sodium valproate is very rarely responsible for a hypersensitivity syndrome, and our case is the first report of sodium valproate-induced cutaneous pseudolymphoma. The recurrence with carbamazepine may be due to a common effect on T-cell lymphocyte function. The return of the same monoclonal population shows that the recurrence of monoclonal T cells may be observed in benign conditions and is not an exclusive hallmark of cutaneous lymphoma.
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3/12. borrelia burgdorferi-associated lymphocytoma cutis simulating a primary cutaneous large B-cell lymphoma.

    The distinction between primary cutaneous B-cell lymphoma and B-cell pseudolymphoma on a histologic basis may be difficult, particularly in some cases of borrelia burgdorferi-associated lymphoid proliferations. We report two cases of B. burgdorferi-associated pseudolymphoma that showed a dense infiltrate with a predominance of large atypical B cells. Because of this misleading histologic feature, a diagnosis of primary cutaneous large B-cell lymphoma was first suspected in both cases. In one case, successive recurrences led to aggressive therapies before the B. burgdorferi infection was recognized. However, a detailed review of histologic and immunohistochemical features was finally suggestive of a B. burgdorferi-associated pseudolymphoma in both cases. The etiologic role of B. burgdorferi was confirmed by serology, polymerase chain reaction analysis of B. burgdorferi dna within the lesional skin, and response to antibiotic therapy. Because the distinction between B. burgdorferi-associated pseudolymphoma and primary cutaneous B-cell lymphomas may be difficult and true B. burgdorferi-associated B-cell lymphomas have been described, we suggest that antibiotic therapy should be considered as a first-line treatment in suspected or confirmed cases of primary cutaneous B-cell lymphoma in regions with endemic B. burgdorferi infection.
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4/12. Progression of cutaneous B-cell pseudolymphoma to cutaneous B-cell lymphoma.

    BACKGROUND: Debates regarding nosology and clonality surround the entity known as cutaneous pseudolymphoma and its questionable transformation to frank cutaneous lymphoma. The relevance of these arguments is important, not only from a diagnostic standpoint, but also for making inferences based upon behavior, prognosis, and treatment. OBJECTIVE: Our goal was to demonstrate further evidence of progression from cutaneous pseudolymphoma to malignant lymphoma while at the same time advocating a comprehensive plan for evaluation, treatment, and followup of these patients. methods: A retrospective review was conducted of four patients initially considered to have cutaneous B-cell pseudolymphoma (CBPL) and who were later treated for primary cutaneous B-cell lymphoma (CBCL). A review of the literature of cases suggesting progression to malignant lymphoma from precursor lesions was also performed. RESULTS: Four patients initially diagnosed with CBPL by a combination of histologic, immunophenotypic, and gene rearrangement criteria had a progressive clinical course that, over a range of 17-51 months, evolved into CBCL. All patients had a comprehensive systemic workup to rule out the possibility of extracutaneous disease and were treated with local radiation therapy and close followup. There has been no evidence of extracutaneous disease with an average followup of 14 months. CONCLUSION: The potential for certain cutaneous pseudolymphomas to progress to CBCL is real. The combination of histologic and immunophenotypic criteria, along with the clinical picture, remains the best way to judge the aggressiveness of the lesion. gene rearrangement studies, whether performed by Southern blot or polymerase chain reaction (PCR), are of limited value and should be used to support the overall clinicopathologic picture. radiation therapy of these patients should be thought of early in the management plan and is a very successful form of treatment when combined with close followup.
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5/12. Cutaneous pseudolymphoma in association with molluscum contagiosum in an elderly patient.

    BACKGROUND: molluscum contagiosum (MC) is a common cutaneous infection, which has been reported in association with cutaneous pseudolymphoma in few cases. methods: A 72-year-old woman with a nodule arising on the external canthus was reviewed. The lesion was surgically removed, and the histopathological study demonstrated an epidermal invagination filled by molluscum bodies and a diffuse infiltrate comprising atypical lymphocytes. RESULTS: Immunohistochemical stains disclosed predominance of T cells with positive CD30 labeling. polymerase chain reaction failed to demonstrate clonal rearrangement of the T-cell receptor. CONCLUSION: After ruling out systemic involvement, the patient was followed up for 2 years with no evidence of recurrence. We report this case to the best of our knowledge and discuss the literature about atypical clinical and histological presentations of MC.
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6/12. Massive hyperplasia of marginal zone B-cells with clear cytoplasm in the lymph node: a case report.

    An enlarged axillary lymph node from a 63-year-old woman showed proliferating marginal zone B-cells arranged in a vague nodular pattern or in band-forming aggregates throughout the cortex. Marginal zone B-cells, which also infiltrated the adjacent fatty tissue, had round or slightly indented nuclei of medium size and a moderate amount of clear cytoplasm. Immunohistochemically, these cells were CD20 , CD79a , Bcl-2 , sIgD-, CD5-, CD10-, CD21-, CD23-, CD45RO-, Bcl-6-, and cyclin d-. A portion of the cells were sIgM- and CD43-positive. The polytypic nature of these cells was demonstrated by immunohistochemistry and polymerase chain reaction. Systemic bacterial infection appears to be the cause of marginal zone B-cell hyperplasia. This unusual marginal zone B-cell hyperplasia should be differentiated from low-grade B cell lymphomas, and particularly from nodal marginal zone B-cell lymphomas.
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7/12. Bilateral benign lymphoid hyperplasia of the conjunctiva in a paediatric patient.

    A 14-year-old boy presented with a 6-month history of bilateral slowly enlarging conjunctival lesions. There was no associated ocular or systemic symptomatology. Examination revealed bilateral salmon-coloured nodular lesions of the bulbar conjunctiva. The remainder of his ophthalmic and general examinations were normal. Extensive investigation excluded regional or systemic involvement. Excision biopsy of the lesions showed a predominantly mature B lymphocyte infiltrate with immunohistochemistry and flow cytometry consistent with reactive lymphoid hyperplasia. polymerase chain reaction testing for Epstein-Barr virus was negative. At 2 years follow-up, the patient remained healthy and there was no evidence of recurrence. Benign lymphoid hyperplasia of the conjunctiva with bilateral involvement is extremely rare in children. Only a few case reports have been documented in the literature.
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8/12. Cutaneous lymphoid hyperplasia and other lymphoid infiltrates of the breast nipple: a retrospective clinicopathologic study of fifty-six patients.

    This study characterizes the clinicopathological spectrum of lymphoproliferations involving the breast nipple and/or areola. Morphologic, immunohistochemical, molecular-genetic, and clinical features of 58 specimens from 56 patients were analyzed. They were re-diagnosed as cutaneous lymphoid hyperplasia (CLH, n = 44); other benign lymphoid infiltrates (OBLI, n = 8); peripheral T-cell lymphoma, not otherwise specified (n = 1); cases with overlapping features of CLH and B-cell lymphoma (n = 3), one of them composed of spindle cells. Cutaneous lymphoid hyperplasia infiltrates were dense, composed mainly of B cells forming follicles with germinal centers (GC). Cutaneous lymphoid hyperplasia frequently showed features suggesting a malignancy as coalescing follicles with non-polarized germinal centers lacking mantle zones, and smudged infiltrates of lymphoid cells spreading into collagen (often as "Indian files"), smooth muscle, vessel walls, and nerve sheaths. Only two cutaneous lymphoid hyperplasias recurred; otherwise all patients are without disease (mean follow-up 62 months). Monoclonal rearrangement of immunoglobulin heavy chain gene was detected in five, and of T-cell receptor gamma gene in two cutaneous lymphoid hyperplasias using polymerase chain reaction (PCR), but the patients fared well too. In 47% of cases borrelia burgdorferi was detected by polymerase chain reaction and/or serology, of which one was monoclonal. We conclude that cutaneous lymphoid hyperplasia is the most common lymphoproliferation of the breast nipple, rarely recognized clinically, and often overdiagnosed histologically as lymphoma.
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9/12. Varicella-zoster-virus folliculitis promoted clonal cutaneous lymphoid hyperplasia.

    Post herpes zoster (HZ) reactions have been associated with panoply of neoplastic, inflammatory, and fibro-inflammatory cutaneous disorders. Varicella zoster virus (VZV) dna has not been identified in most of these reports. After an episode of HZ, a healthy, active 90-year-old female developed ulcerative nodules in the affected trigeminal V1 dermatome and the contra-lateral trigeminal region over a 1-year period. Excision and/or biopsy of all these lesions showed similar pathologic changes that consisted of herpetic folliculitis, adjacent dense mixed nodular lymphocytic infiltrates with germinal centers (cutaneous lymphoid hyperplasia (CLH)), and in the deeper excision specimens, an obliterative vasculitis of a vessel with smooth muscle in its wall. Immunophenotype analysis revealed a mixed, predominate T- and B-cell population without loss of pan-T cell antigens or aberrant expression by B cells of T-cell antigens. polymerase chain reaction for herpetic dna was positive for VZV dna. Lymphocyte gene rearrangement analysis revealed 2 distinct, anatomically and chronologically, monoclonal B-cell populations and a monoclonal T-cell population in one nodule. Treatment with valacyclovir has lead to almost complete resolution of her cutaneous nodules after 6 months of therapy. In this case, it can be surmised that persistence of VZV infection and lack of effective cell-mediated immunity lead to development of both immunopathology (vasculitis) and excessive lymphoid cell proliferation (CLH).
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10/12. Reactive lymphoid hyperplasia of the liver in a patient with multiple carcinomas: a case report and brief review.

    A rare case of reactive lymphoid hyperplasia (RLH) of the liver in a 75-year-old woman admitted to hospital for surgical treatment of gastric, caecal and colon carcinomas is described here. Two nodular lesions in the left and right lobes of the liver were clinically diagnosed as metastatic tumours by computed tomography of the abdomen. A demarcating grey-white mass of size 1.4 cm was observed in a partially resected liver specimen. On examining the lesion microscopically, it was found to be composed of hyperplastic lymphoid follicles, lymphocytes, plasma cells, other inflammatory cells and interlaced hyalinised fibrous tissues. In the portal tracts around the lesion, chronic inflammatory cell infiltrates were seen, but no interface hepatitis or lymphoid follicle was observed. No evidence of monoclonality was observed by immunohistochemistry for B and T cell markers, in situ hybridisation for kappa and lambda light chains, and polymerase chain reaction analysis of immunoglobulin heavy chains or T cell receptor beta and gamma gene rearrangements. Bcl-2 immunoreactivity was not observed in the germinal centre. Epstein-Barr virus (EBV) antigen (latent membrane protein-1) and EBV-encoded small RNAs were not detected. A proliferation neither of myofibroblasts nor of cells positive for follicular dendritic cell markers was observed. RLH, formerly known as pseudolymphoma, has been reported of the liver in only 14 cases and is considered to be a differential diagnosis of small nodular lesions of the liver. That RLH has an inflammatory reactive nature, not a neoplastic disposition, and that EBV does not participate in the pathogenesis of RLH is supported by this case.
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