RESUMO
Skin cancers occur more frequently in solid organ transplant recipients relative to the general population. Transplant recipients are at particularly high risk of squamous cell carcinoma, with up to a 100-fold increase in the relative risk when compared to the nontransplanted population. This compares with a 10- to 16-fold increase in basal cell carcinoma for renal transplant recipients. An increased incidence of melanoma in transplant patients has also been reported. Other types of skin cancer associated with immunosuppression in transplant patients include Kaposi sarcoma, Merkel cell carcinoma, and posttransplant lymphoproliferative disorder. This review discusses the epidemiology and pertinent pathologic features of each of these tumors. A brief clinical management strategy is outlined. In addition, the contribution of viral induced carcinogenesis with respect to Kaposi sarcoma, Merkel cell carcinoma, and posttransplant lymphoproliferative disorder is discussed.
Assuntos
Transplante de Rim/efeitos adversos , Transplante de Órgãos/efeitos adversos , Neoplasias Cutâneas/epidemiologia , Neoplasias Cutâneas/patologia , Pele/patologia , Carcinoma Basocelular/etiologia , Carcinoma de Célula de Merkel/etiologia , Carcinoma de Células Escamosas/epidemiologia , Carcinoma de Células Escamosas/etiologia , Humanos , Ceratose Actínica/etiologia , Transtornos Linfoproliferativos/etiologia , Poroceratose/epidemiologia , Poroceratose/etiologia , Medição de Risco , Sarcoma de Kaposi/epidemiologia , Neoplasias Cutâneas/etiologia , Neoplasias Cutâneas/terapiaRESUMO
Traumatic ulcerative granuloma with stromal eosinophilia (TUGSE) is an ulcerative lesion of the oral mucosa with unknown pathogenesis. A few recent case reports have demonstrated molecular evidence of T-cell clonality in TUGSE and CD30 immunoreactivity in the large atypical mononuclear cells, raising the possibility that a TUGSE subset may represent the oral counterpart of primary cutaneous CD30+ T-cell lymphoproliferative disorders. We examined the immunoreactivity for CD30 and T-cell receptor (TCR) gamma gene rearrangement in 37 TUGSE cases. Clonal TCR gene rearrangements were demonstrated in 7 (24%) of 29 cases with amplifiable DNA, and the morphologic features and CD30 immunoreactivity of these cases did not differ from those with polyclonal TCR gene rearrangements. Clinical follow-up was available for 5 of 7 TUGSE cases with clonal TCR gene rearrangement for an average period of 1.75 years after the initial biopsy or excision, and there was no evidence of local recurrence or development of systemic T-cell lymphoproliferative disorder. Without morphologic and/or clinical evidence of lymphoma, T-cell clonality and/or CD30 positivity in these lesions is not indicative of malignancy and should be interpreted with caution.
Assuntos
Eosinofilia/genética , Rearranjo Gênico do Linfócito T , Granuloma/genética , Antígeno Ki-1/biossíntese , Doenças da Boca/genética , Úlceras Orais/genética , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Criança , Células Clonais , Eosinofilia/metabolismo , Eosinofilia/patologia , Feminino , Genes Codificadores dos Receptores de Linfócitos T/genética , Granuloma/metabolismo , Granuloma/patologia , Humanos , Imuno-Histoquímica , Linfoma/genética , Linfoma/patologia , Masculino , Pessoa de Meia-Idade , Doenças da Boca/metabolismo , Doenças da Boca/patologia , Úlceras Orais/metabolismo , Úlceras Orais/patologia , Reação em Cadeia da PolimeraseRESUMO
We report a case of compound heterozygous hemoglobins S [beta6(A3)Glu6Val] and Korle-Bu [beta73(E17)Asp73Asn] in a 2-year-old girl. This hemoglobin genotype is associated with a benign clinical course, much like the sickle cell trait; however, its laboratory characteristics are very similar to compound heterozygous hemoglobin S and hemoglobin D-Los Angeles [beta121(GH4)Glu121Gln], which produces severe sickling hemolytic anemia. We describe laboratory data used to resolve this important differential diagnosis and review the interactions between hemoglobin S and the variant hemoglobins that may account for the different clinical phenotypes in compound heterozygotes.
