INFLAMACION Y CÁNCER DE PRÓSTATA

Dr. Julio César Potenziani Bigelli-Especialista Urólogo Hospital Privado Centro Médico de Caracas.
Dra Silvia D. Potenziani Pradella- Escuela de Medicina “Luis Razetti” UCV. Caracas-Venezuela.


Liu (2000) reveló que la expresión de VEGF fue significativamente infrarregulada al dársele inhibidores COX-2. Los resultados demostraron que los inhibidores selectivos COX-2 suprimen el crecimiento de células PC-3 in vivo. La supresión del crecimiento es alcanzada por una combinación de inducción directa de la apoptosis celular tumoral y la infrarregulación del VEGF tumoral con disminución de la angiogénesis. Desde que Virchow (1863) mencionó que el cáncer se originaba en los sitios de inflamación crónica muchos han sido los estudios que se han desarrollado al respecto (Balkwill 2001, Platz 2004).

Scott (2004) y Lucia (2004) entre otros desarrollaron el tema de la inflamación prostática como un parámetro para los fines de la quimioprevención. Referían que la inflamación podría contribuir a la carcinogénesis de tres maneras: elaborando citoquinas y factores de crecimiento que harán propenso el crecimiento de células tumorales, en segundo lugar induciendo la ciclooxigenasa-2 (COX-2) en macrófagos y células epiteliales y por ultimo en la generación de especies mutagénicas oxigeno reactivas (ROS) y especies de nitrógeno reactivas (RNS).

El TNF-alfa (Factor de necrosis tumoral alfa), es una citoquina proinflamatoria que dirige los eventos inflamatorios, originando la aparición de otras citoquinas y de otros factores de crecimiento. Actúa como promotor tumoral consiguiéndose en cantidades elevadas en varios tipos de cáncer entre los cuales destaca el cáncer prostático. Inducirá COX-2 y otros factores angiogénicos, matriz metaloproteasa, quimioquininas, todos ellos, factores pro-carcinogenéticos.

El factor de crecimiento vascular endotelial (VEGF) es un estimulante miogénico en las células endoteliales, ocasionando angiogénesis y regulando la permeabilidad vascular. Su producción es inducida por las prostaglandinas E2 y por la TNF-alfa previamente mencionada.

El MIF (Factor inhibitorio de migración) es una citoquina proinflamatoria ubicada en las células epiteliales de la próstata estimulando el crecimiento “in vitro”.

Myers (1999, 2000, 2001) refería que los medicamentos antiinflamatorios no esteroideos y sus derivados presentaban numerosos mecanismos de acción que podrían incluir la inhibición directa de la formación de eicosanoides, la inhibición indirecta de la formación de eicosanoides al inhibir la expresión de las enzimas involucradas en dicha síntesis o al interferir con la función de monofosfato cíclico de guanosina.

Refería Myers (2000) que el primer indicio que los eicosanoides podrían jugar un rol en el desarrollo del cáncer de próstata es el enlace epidemiológico entre dieta alta en carnes rojas y productos animales y el riesgo de desarrollar cáncer prostático metastásico. Las carnes rojas tienen acido araquidónico. El producto de araquidonato 12-lipooxigenasa (12-LOX), 12-HETE, parecieran promocionar la diseminación metastásica del cáncer de próstata.

Los inhibidores de la ciclo-oxigenasa y de la lipo-oxigenasa productores y mediadores de la obtención de las prostaglandinas, favorecedoras éstas del crecimiento tumoral, se están utilizando como argumentos Quimioterapéuticos en cáncer de próstata y tenemos que se están utilizando fármacos como antiinflamatorios no esteroideos (inhibidores COX-2), curcumin, té, silimarin, resveratrol (Cuendet 2000). Los inhibidores de la lipo-oxigenasa (LOX) se están utilizando también para tratar asma, artritis y psoriasis (Steele 1999).

Los inhibidores COX-2 afectarán el crecimiento de células tumorales PC-3 a través de mecanismos que incluyen inducción de apoptosis, infrarregulación de factores de crecimiento vascular endotelial y reduciendo la angiogénesis (Hernández 2004), Liu (2000).

Los agentes fitoterapéuticos poseen un efecto antiinflamatorio al interferir con el metabolismo de las prostaglandinas, producidas por las ciclo-oxigenasas (COX-1 y COX-2) las cuales son consideradas carcinógenos o promotores tumorales, por lo cual la inhibición de la COX-1 y COX-2 y de la Lipo-oxigenasa-LOX podrían considerarse un argumento quimiopreventivo (Cuendet 2000, Norrish 1998, Bassler 2004).

El ácido araquidónico será convertido en prostaglandinas con la acción de dos enzimas la COX-1 y la COX-2, La COX-1 ayudará al organismo a mantenerse en un estado de normalidad. La COX-2 causará inflamación en el organismo lo cual podría estimular el crecimiento de los procesos cancerosos.

Según Moyad (2000) la segunda conversión del acido araquidónico es vía la lipo-oxigenasa, creando leucotrienos los cuales pueden causar inflamación y potencialmente aumentar el crecimiento neoproliferativo, así como causar trastornos respiratorios tipo asma.

Fármacos como el celecoxib el primer COX-2 involucrado en la biología de numerosos cánceres, (ya retirado del mercado) no sólo inhibía el crecimiento del tumor primario pero impedía el desarrollo de lesiones metastásicas. También ocasionaba inhibición de la angiogénesis inducida por factores de crecimiento como el factor beta de crecimiento fibroblástico (TGF-beta), en estudios a largo plazo se estaban dando celecoxib 400 mg dos veces al dia.

El Exisulind tiene el mecanismo de acción de inhibir la guanosina monofosfato cíclico fosfodiesterasa (cGMP), activando la proteína-kinasa G en las células tumorales lo que llevará a una apoptosis asociada a caspasas a través de mecanismos como la reducción de los niveles intracelulares de cateninas beta libres y en segundo lugar la activación de Jun kinasas y posiblemente ERK, inducirá apoptosis en las líneas celulares PC3 y LNCaP.

El R-Flurbiprofen (MPC-7869) disminuye la expresión de los COX-2 a niveles del ARN mensajero.

Lim (1999) demostró que el Sulindac inhibía el crecimiento de las líneas celulares del cáncer prostático e igualmente induce apoptosis por un mecanismo independiente COX-1 y COX-2 y ocurre independiente de la sensibilidad androgénica o de la expresión incrementada de bcl-2.

Nelson (2003) refería que la inflamación crónica o recurrente probablemente tiene un rol en el desarrollo de muchos tipos de cáncer incluyendo el cáncer de próstata. La Prostatitis sintomática ocurre en el 9% de hombres entre 40 y 79 años y la mitad de ellos tendrán más de 1 episodio de prostatitis a los 80 años. La prevalencia de la prostatitis asintomática no es conocida. En la mayoría de los casos el agente infeccioso no podrá ser identificado, sin embargo un aumento del riesgo de cáncer prostático ha sido asociado con infecciones de transmisión sexual sin importar el agente sugiriendo que la inflamación más que la infección inicia la carcinogénesis prostática. La célula inflamada elabora oxidantes microbicidas que pueden causar daño celular o daño genómico. La disminución del riesgo de cáncer prostático al tomar antioxidantes y AINES es posible. Dos de los genes identificados susceptibles a cáncer prostático como el RNASEL y el MSR1 codifican proteínas con función crítica en la respuesta al huésped a las infecciones.

Llama la atención que la pieza anatomopatológica de las prostatectomías radicales casi siempre presenta el diagnostico histopatológico de inflamación aguda y crónica de la glándula (Prostatitis), lo que ha hecho que autores como Gerstenbluth (2002) afirmaran que en un estudio sobre 40 prostatectomías existía inflamación en el 57% lo cual hace pensar en que su presencia no es fortuita, sino posiblemente relacionada.

Los productos de la degradación inflamatoria, más que los productos derivados de la infección iniciarían el proceso carcinogenético. Las células inflamatorias elaborarán oxidantes microbicidas que causarían daño celular o genómico dentro de la próstata.

Según Gann (1999,2002), Clark (1995,1996,1998), Heinonen (1998), Norrish (1998), la probabilidad de cáncer prostático disminuirá en la medida que se tomen antioxidantes o A.I.N.E.

Nelson, De Marzo, Epstein (2001, 2002, 2003, 2004) de la División de Patología Genitourinaria del Hospital Johns Hopkins de Baltimore en Estados Unidos de Norteamérica, descubren la relación entre inflamación y cáncer de próstata. Se propuso que una lesión llamada atrofia inflamatoria proliferativa es precursora de neoplasia intraepitelial prostática de alto grado (HGPIN) y del cáncer prostático como consecuencia de una proliferación regenerativa de las células epiteliales prostáticas en respuesta al daño causado por los oxidantes inflamatorios (De Marzo 1998,1999).

La inflamación crónica o recurrente probablemente tiene un rol en el desarrollo de muchos tipos de cáncer incluyendo el cáncer de próstata. La Prostatitis sintomática ocurre en el 9% de hombres entre 40 y 79 años y la mitad de ellos tendrán más de 1 episodio de prostatitis a los 80 años. La Prevalencia de la prostatitis asintomática no es conocida. En la mayoría de los casos el agente infeccioso no podrá ser identificado, sin embargo un aumento del riesgo de cáncer prostático ha sido asociado con infecciones de transmisión sexual sin importar el agente sugiriendo que la inflamación más que la infección inicia la carcinogénesis prostática. La célula inflamada elabora oxidantes microbicidas que pueden causar daño celular o daño genómico. La disminución del riesgo de cáncer prostático al tomar antioxidantes y AINES es posible. Dos de los genes identificados susceptibles a cáncer prostático como el RNASEL y el MSR1 codifican proteínas con función crítica en la respuesta al huésped a las infecciones.

En un trabajo conjunto australiano-norteamericano con el prestigioso Dr McNeal de Stanford University, Cohen (2005) se sugiere la participación de un agente infeccioso en la etiopatogenia del cáncer prostático. Acaban de publicar la presencia en el 35% de las biopsias prostáticas de 34 pacientes, en un estudio prospectivo, la presencia de una bacteria denominada propionibacterium acnés con alto grado de inflamación que podría originar a través de productos de degradación inflamatoria la aparición de cáncer prostático. Asemejándose a lo sucedido con el Helicobacter pylori en el estomago humano con la secuencia inflamación, atrofia gástrica y carcinoma gástrico.

PARA TERMINAR ESTE ASPECTO ES DIGNO DE MENCIONAR QUE CUANDO EL URÓLOGO RECIBE LAS MUESTRAS DE UNA GLÁNDULA PROSTÁTICA, BIEN SEA DE UNA HIPERPLASIA PROSTÁTICA BENIGNA O DE UN CÁNCER DE PRÓSTATA A TRAVÉS DE UNA PIEZA DE PROSTATECTOMÍA RADICAL O DE LAS REALIZACIÓN DE UNA BIOPSIA POR PISTOLA DE TRUCUT, LO QUE SIEMPRE ESTARÁ PRESENTE EN EL INFORME HISTOPATOLÓGICO SERA LA PROSTATITIS CRÓNICA, CON UNA PREVALENCIA DE PRÁCTICAMENTE 100%. ESTO DEBE ALERTAR A LOS INVESTIGADORES EN LA RELACIÓN SIN DUDA EXISTENTE ENTRE PROSTATITIS Y CÁNCER PROSTÁTICO.

LUEGO DE DÉCADAS DE INVESTIGACIONES SE ESTA LLEGANDO A LA CONFIRMACIÓN DE ESTA PREMISA, LO QUE A SU VEZ OCASIONARÁ UNA CAMBIO EN EL ENFOQUE Y TERAPÉUTICA DE LOS SÍNDROMES DE PROSTATITIS, ANTAÑO APARTADOS DEL TEMA DE CÁNCER Y HOY EN CAMBIO ÍNTIMAMENTE LIGADO.
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