ABSTRACT
Hodgkin's lymphoma is due to the clonal transformation of cells originating from B lymphocytes, generating the pathognomonic binucleate Reed-Sternberg cells. Hodgkin's lymphoma is a B cell disease with a bimodal distribution, with higher incidence in adolescence and the third decade of life, showing a second peak in people over 55 years of age. Classic Hodgkin lymphoma cells routinely undergo gene expression reprogramming, as they lose the expression of most of the typical B-cell genes and acquire the expression of multiple genes that are typical of other types of cells in the immune system. The treatment algorithm will depend on whether it is classic or predominantly lymphocytic HL, if it is early stage with unfavorable prognostic markers or not, the initial management regimen, and whether there is bulky disease, among the most relevant variables.
El linfoma de Hodgkin (LH) se debe a la transformación clonal de células originadas en los linfocitos B, lo que genera las células binucleadas patognomónicas de Reed-Sternberg. El LH es una enfermedad de células B con una distribución bimodal, con mayor incidencia en la adolescencia y la tercera década de la vida y un segundo pico en personas mayores de 55 años. Las células del LH clásico habitualmente sufren una reprogramación de la expresión génica, ya que pierden la expresión de la mayoría de los genes típicos de las células B y han adquirido la expresión de múltiples genes que son típicos de otros tipos de células del sistema inmunitario. El algoritmo de tratamiento dependerá si se trata de LH clásico o de predominio linfocítico, si es un estadio temprano con marcadores de pronóstico desfavorables o no, el esquema inicial de manejo y si existe enfermedad voluminosa, entre las variables más relevantes.
Subject(s)
Consensus , Hodgkin Disease , Reed-Sternberg Cells , Age Distribution , Algorithms , Antineoplastic Agents/therapeutic use , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Gene Expression , Hodgkin Disease/drug therapy , Hodgkin Disease/epidemiology , Hodgkin Disease/genetics , Hodgkin Disease/pathology , Humans , Mexico , Neoplasm Staging , Positron Emission Tomography Computed Tomography , Reed-Sternberg Cells/pathologyABSTRACT
El linfoma de Hodgkin (LH) se debe a la transformación clonal de células originadas en los linfocitos B, lo que genera las células binucleadas patognomónicas de Reed-Sternberg. El LH es una enfermedad de células B con una distribución bimodal, con mayor incidencia en la adolescencia y la tercera década de la vida y un segundo pico en personas mayores de 55 años. Las células del LH clásico habitualmente sufren una reprogramación de la expresión génica, ya que pierden la expresión de la mayoría de los genes típicos de las células B y han adquirido la expresión de múltiples genes que son típicos de otros tipos de células del sistema inmunitario. El algoritmo de tratamiento dependerá si se trata de LH clásico o de predominio linfocítico, si es un estadio temprano con marcadores de pronóstico desfavorables o no, el esquema inicial de manejo y si existe enfermedad voluminosa, entre las variables más relevantes.Hodgkin's lymphoma (HL) is due to the clonal transformation of cells originating from B lymphocytes, generating the pathognomonic binucleate Reed-Sternberg cells. HL is a B cell disease with a bimodal distribution, with higher incidence in adolescence and the third decade of life, showing a second peak in people over 55 years of age. Classic Hodgkin lymphoma cells routinely undergo gene expression reprogramming, as they lose the expression of most of the typical B-cell genes and acquire the expression of multiple genes that are typical of other types of cells in the immune system. The treatment algorithm will depend on whether it is classic or predominantly lymphocytic HL, if it is early stage with unfavorable prognostic markers or not, the initial management regimen, and whether there is bulky disease, among the most relevant variables.
Subject(s)
Consensus , Hodgkin Disease , Age Factors , Algorithms , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Cell Transformation, Neoplastic/pathology , Hodgkin Disease/genetics , Hodgkin Disease/pathology , Hodgkin Disease/therapy , Humans , Immunotherapy/methods , Lymphoma, AIDS-Related/etiology , Mexico , Neoplasm Staging , Positron Emission Tomography Computed Tomography , Prognosis , Reed-Sternberg Cells/pathologyABSTRACT
BACKGROUND: There is no epidemiological registry in Mexico. The information about the epidemiology in our country is obtained by these types of studies, such as multicentric studies. A lot of improvements in the survival in non-Hodgkin lymphoma patients had occurred in the last 20 years. The access to treatment in these types of pathology could change the prognostic factors in Mexican Mestizos patients. The primary objective of the study was to learn what the most frequent histological varieties of non-Hodgkin lymphoma in Mexico are. The secondary objectives included clinical characteristics, treatments used, treatment response, disease-free survival and overall survival. METHODS: A retrospective, descriptive study of consecutive cases was carried out in 14 hospitals across 14 Mexican states with patients diagnosed with non-Hodgkin lymphoma using the World Health Organization (WHO) 2008 criteria. Inclusion criteria included: ≥ 18 years of age, male or female, any clinical stage at diagnosis, who had received any chemotherapy regimen, with a known outcome. Descriptive statistics was performed for all variables, and survival was assessed using Kaplan-Meier curves. RESULTS: Totally, 609 patients were enrolled, of which 545 were B-cell lymphomas and 64 were T-cell lymphomas. Median ages were 61 and 50, respectively. B-cell lymphomas were more common in males with 52.1%, and 65.5% of T-cell lymphomas occurred in females. For B-cell lymphomas, the two most frequent histological subtypes were diffuse large B-cell lymphoma in 63.9%, followed by follicular lymphoma at 18%. Meanwhile, 50% of T-cell lymphomas were of the T/natural killer (NK) subtype, and 87.1% of the patients received a CHOP-like regimen. Radiotherapy was given to 31% of B-cell Lymphomas and 46.9% of T-cell lymphomas. Overall survival at 9 years was 84.6% for B-cell lymphomas, and 73.4% for T-cell lymphomas. CONCLUSIONS: Diffuse large B-cell lymphoma constitutes the most frequent subtype for B-cell lymphomas in Mexico. The most frequent T-cell lymphoma is the NK/T histological subtype.
ABSTRACT
Resumen El linfoma de Hodgkin (LH) se debe a la transformación clonal de células originadas en los linfocitos B, lo que genera las células binucleadas patognomónicas de Reed-Sternberg. El LH es una enfermedad de células B con una distribución bimodal, con mayor incidencia en la adolescencia y la tercera década de la vida y un segundo pico en personas mayores de 55 años. Las células del LH clásico habitualmente sufren una reprogramación de la expresión génica, ya que pierden la expresión de la mayoría de los genes típicos de las células B y han adquirido la expresión de múltiples genes que son típicos de otros tipos de células del sistema inmunitario. El algoritmo de tratamiento dependerá si se trata de LH clásico o de predominio linfocítico, si es un estadio temprano con marcadores de pronóstico desfavorables o no, el esquema inicial de manejo y si existe enfermedad voluminosa, entre las variables más relevantes.
Abstract Hodgkin's lymphoma is due to the clonal transformation of cells originating from B lymphocytes, generating the pathognomonic binucleate Reed-Sternberg cells. Hodgkin's lymphoma is a B cell disease with a bimodal distribution, with higher incidence in adolescence and the third decade of life, showing a second peak in people over 55 years of age. Classic Hodgkin lymphoma cells routinely undergo gene expression reprogramming, as they lose the expression of most of the typical B-cell genes and acquire the expression of multiple genes that are typical of other types of cells in the immune system. The treatment algorithm will depend on whether it is classic or predominantly lymphocytic HL, if it is early stage with unfavorable prognostic markers or not, the initial management regimen, and whether there is bulky disease, among the most relevant variables.
ABSTRACT
To identify this increasingly common pathology, known as multiple myeloma (MM), it is necessary to refer to the specific factors that characterize it; to this end, the classic criteria known as CRAB (hyperkalemia, renal failure, anemia, and lytic lesions) are available, in which renal failure is one of the most frequent complications. Recently, three indisputable biomarkers have been described for the diagnostic support for MM, which are: more than 10% of clonal plasma cells in bone marrow or, a biopsy that corroborates the presence of a plasmacytoma, light chain ratio ≥ 100 mg/dL and more than one focal lesion on magnetic resonance imaging. A differential diagnosis for plasma cell leukemia, solitary bone plasmacytoma, and extramedullary plasmacytoma should always be considered. Being this an incurable disease, a lot of research has been done regarding its therapeutic management, whose main objective is the disappearance of plasma cells and the patient clinical improvement. Melphalan was the first drug that showed a benefit in 1958 and afterward, with the addition of a steroid as a second drug, it was possible to improve response rates. Subsequently, different molecules were studied, forming multiple combinations, and achieving better rates of overall survival and progression-free survival. Years later, with the arrival of proteasome inhibitors such as bortezomib, and immunomodulators such as thalidomide and lenalidomide, an important turnaround in the disease has been seen, as deeper responses, more prolonged remissions, and improvement in the quality of life of patients have been achieved. This consensus has the purpose of integrating a group of Mexican specialists and promoting the updating of this pathology.
Para identificar una patología cada vez más común, conocida como mieloma múltiple, es necesario hacer alusión de los factores específicos que la caracterizan. Para ello existen los clásicos criterios conocidos como CRAB (hipercalcemia, insuficiencia renal, anemia y lesiones líticas), siendo la insuficiencia renal una de sus complicaciones más frecuentes. Recientemente se han descrito tres biomarcadores indiscutibles para el apoyo diagnóstico del mieloma múltiple, que son: más del 10% de células plasmáticas clonales en medula ósea o biopsia que corrobora la presencia de un plasmocitoma, relación de cadenas ligeras ≥ 100 mg/dl y más de una lesión focal en resonancia magnética. Se debe tomar siempre en cuenta el diagnóstico diferencial con leucemia de células plasmáticas, plasmocitoma óseo solitario y plasmocitoma extramedular. Al ser una enfermedad incurable, se ha investigado mucho en cuanto al manejo terapéutico, el cual tiene como objetivo principal la desaparición de las células plasmáticas y la mejoría clínica del paciente. El primer fármaco que demostró algún beneficio fue el melfalán en el año 1958 y posteriormente al adicionar un esteroide como segundo fármaco se logró mejorar las tasas de respuesta. Después se fueron estudiando diferentes moléculas, con las que se han realizado múltiples combinaciones, alcanzando mejores tasas de supervivencia global y supervivencia libre de progresión. Años más tarde, con la llegada de los inhibidores de proteosoma como el bortezomib, así como de los agentes inmunomoduladores como la talidomida y la lenalidomida, se presenta un giro importante en la enfermedad, ya que se logran respuestas más profundas, periodo de remisiones más prolongadas y mejoría en la calidad de vida de los pacientes. Este consenso tiene la finalidad de integrar a un grupo de especialistas mexicanos y promover la actualización de esta patología.
