Metastasic Prostate Cancer: Predictive Factors of Earlier Progression to Castration-Resistance

Introduction: Prostate cancer (PCa) can progress to the lethal phenotype of metastatic castration resistance (mCRPC), either from initially localized disease or de novo metastatic cancer. New drugs improving overall survival are now the cornerstone of treatment. Nevertheless, there are no defined sequences or established timing to initiate or discontinue treatments; besides, not all patients end in CRPC or reach this stage at the same time. Objective: To evaluate characteristics of patients who progress to mCRPC and establish an association with time to mCRPC diagnosis. Material and Methods: Retrospective, descriptive and observational study of 35 mCRPC patients, performed from 2013 to 2017. Variables analyzed were age, Gleason score and prostate-specific antigen (PSA) at diagnosis, initial stage, response time to androgen deprivation therapy (ADT), PSA nadir on ADT and time until mCRPC progression. Statistical analysis comparing variables with time to mCRPC diagnosis was performed. Results: Average age at diagnosis was 68.9 years; PSA values were classified into 3 categories: <20 ng/ml, 20-50 and >50. Gleason score was 7 in 50%, and 8-9 in the rest. Tumor was initially localized in 46% of the patients and metastatic in the rest. PSA nadir on ADT was <1 ng/ml in 67%. Average time to androgen deprivation: 5.5 years, time to mCRPC diagnosis: 6.9 years. Significant associations between time to mCRPC and time of androgen deprivation, PSA nadir during ADT and stage at diagnosis were found. Conclusion: Response time to ADT <1 year, PSA nadir value >5 ng/ml during treatment and metastatic stage at diagnosis were associated with earlier progression to mCRPC (AU)

Introducción: El cáncer de próstata (CaP) puedeprogresar al fenotipo letal de resistencia a la castraciónmetastásica (CPRCm), ya sea por enfermedad inicialmentelocalizada o por cáncer metastásico de novo. Los nuevosmedicamentos que mejoran la supervivencia general sonahora la piedra angular del tratamiento. Sin embargo, nohay secuencias definidas ni tiempos establecidos para iniciar o suspender los tratamientos; además, no todos los pacientes terminan en CPRC o llegan a esta etapa al mismotiempo.Objetivo: Evaluar las características de los pacientesque progresan a CPRCm y establecer una asociación entreéstas y el tiempo hasta el diagnóstico de CPRCm.Material y Métodos: Estudio retrospectivo, descriptivo y observacional de 35 pacientes con CPRCm, realizado entre 2013 y 2017. Las variables analizadas fueronedad, puntaje de Gleason y antígeno prostático específico(PSA, por sus siglas en inglés) al diagnóstico, estadio inicial, tiempo de respuesta a la terapia de deprivación androgénica (TDA), Nadir de PSA en TDA y tiempo hastala progresión a CPRCm. Se realizó un análisis estadísticocomparando las variables con el tiempo hasta el diagnósticode CPRCm.Resultados: La edad promedio al diagnóstico fue de68,9 años; Los valores de PSA<20: 15% de los pacientes,PSA 20-50: 63% de los pacientes, y PSA>50 20%. La puntuación de Gleason fue de 7 en el 50% y de 8-9 en el resto.El tumor fue inicialmente localizado en el 46% de los pacientes y metastásico en el resto. El nadir de PSA en TDAfue <1 ng / ml en 67%. Tiempo medio de respuesta a TDA:5,5 años, tiempo hasta el diagnóstico de CPRCm: 6,9 años.Se encontraron asociaciones significativas entre el tiempohasta CPRCm y el tiempo de deprivación de andrógenos, elnadir de PSA durante el TDA y el estadio al momento deldiagnóstico.Conclusión: el tiempo de respuesta a TDA <1 año... (AU)

Enzalutamide as monotherapy for advanced prostate cancer: why not? / Enzalutamida como monoterapia para cáncer de próstata avanzado: ¿por qué no?

OBJECTIVES: Prostate cancer (PCa) is an androgen-dependent disease. In some cases, the tumor progresses despite castration levels of serum testosterone, turning into the lethal phenotype of castration-resistant prostate cancer (CRPC), still driven by androgens and requiring the androgen receptor as a driver and responsible for progression. Enzalutamide, an androgen receptor inhibitor, is indicated for the treatment of metastatic CRPC, asymptomatic or mildly symptomatic, after failure of androgen deprivation. In both clinical trials that led to its approval, Enzalutamide was administered with an LHRH analog, setting the "standard of care" for its use. In this article we evaluate the available evidence and theory on the use of Enzalutamide as monotherapy. METHODS: Androgen deprivation well-known adverse events, together with the fact that its clinical benefit is moderate and the evidence strength is weak, and the direct negative impact on the common chronic conditions affecting this age-group led to investigation of Enzalutamide without LHRH analogs. RESULTS: There are clinical trials on Enzalutamide monotherapy for hormone-sensitive prostate cancer with favourable outcomes, and there are also two ongoing studies in different advanced PCa scenarios, the PROSPER and EMBARK trials. It would be up to now a safe alternative, with less toxicity and lower costs. CONCLUSION: It is mandatory to validate these early results on the use on Enzalutamide monotherapy for advanced prostate cancer, hormone-sensitive or castration resistant, metastatic or not, but in the meantime, we wonder, why not?

Outcome of radical prostatectomy in patients meeting criteria for active surveillance.

OBJECTIVES: Advances in diagnosis of prostate cancer (PCa)have led to an increased detection of these tumors, some of them with low-risk of progression, with the consequent risk of overdiagnosis and overt treatment. In consequence, there is a tendency to offer alternatives to active therapy, like active surveillance (AS)however, some patients under AS need definitive therapy and after surgery it becomes evident that they are not "low-risk" patients. We retrospectively reviewed the data of patients who met criteria for low-risk tumors treated with radical prostatectomy. METHODS: We selected 21 out of 190 patients treated with radical prostatectomy from January 2004 to December 2008 who met Epstein's criteria for low-risk tumors. We analyzed the number of organ-confined tumors,Gleason undergrading and understaging by biopsy, surgical margins and postoperative PSA. RESULTS: Mean age was 58.6 years; mean PSA was 6.6 ng/ml, predominant Gleason score was 6 (3+3), 76%were unilateral tumors and 90%were organ-confined, 10% had extracapsular extension, none had involvement of the seminal % vesicles, 15% of the patients had Gleason score >6 and surgical margins were positive in 30% of the specimens. Eighty five percent had their first postoperative PSA <0.10 ng/ml and 75% remain free of biochemical recurrence. According to the Johns Hopkins criteria for "incurable tumors ", our cohort had 28%. CONCLUSION: Patients with low-risk prostate cancer include cases that may have greater risk than estimated. In our series, we had 10% extracapsular disease, 15% understaging for Gleason score and 25% biochemical recurrence, which demonstrates that current criteria do not warrant good oncological results. Active surveillance offers good quality of life and acceptable oncological results, it can be proposed until definitive therapy, without seriously endangering the patient. Anyway, as a therapeutic tool, it still requires improvements. Technical advances are awaited so as to properly assess each patient's risk and to define the best therapeutic option for every case.

Tumor renal bilatareal asincrónico / Asinchronic renal bilateral tumor

Paciente de 61 años de edad a quien se le realizó nefrectomía derecha en 1991 por tumor de polo superior (carcinorna renal de células claras). Comienza con terapia inmunomoduladora con control durante 1.5 año perdiéndose el paciente hasta 1995 en que vuelve a la consulta por tumoración palpable en hipocondrio izquierdo. Los estudios revelaron tumor sólido de 6 cm en región media y polo inferior del riñón izquierdo. Se comenzó tratamiento con interleukina y 5-fluoracilo con los controles necesarios por T.A.C. que mostraban reducción del tamaño tumoral. Actualmente continúa con la misma terapia más ciclos de vimblastina observando disminución importante del tamaiío tumoral que permitiría en un futuro realizar nefrectomía parcial o tumorectomía

Duplicacion intestinal: informe de dos casos / Intestinal duplication: report of 2 cases

Las duplicaciones intestinales son infrecuentes y resultan de fallos embriológicos en la canalización normal del tubo digestivo. Este trabajo presenta un caso de duplicación intestinal en el ileon y su diagnóstico diferencial con el Divertículo de Meckel. A continuación se presenta un caso de duplicación de recto en un paciente de edad asintomático

Duplicacion intestinal: informe de dos casos / Intestinal duplication: report of 2 cases

Las duplicaciones intestinales son infrecuentes y resultan de fallos embriológicos en la canalización normal del tubo digestivo. Este trabajo presenta un caso de duplicación intestinal en el ileon y su diagnóstico diferencial con el Divertículo de Meckel. A continuación se presenta un caso de duplicación de recto en un paciente de edad asintomático (AU)

[Intestinal duplication. Report of 2 cases]. / Duplicación intestinal. Informe de dos casos.

Intestinal duplications are rare and they result from embryological failures in the canalization of the gastrointestinal tract. This paper presents a case of ileal intestinal duplication and its differential diagnosis from Meckel's diverticulum. Besides, a case of rectal duplication in an asymptomatic elder patient is presented.

Duplicación intestinal. Informe de dos casos. / [Intestinal duplication. Report of 2 cases]

Intestinal duplications are rare and they result from embryological failures in the canalization of the gastrointestinal tract. This paper presents a case of ileal intestinal duplication and its differential diagnosis from Meckels diverticulum. Besides, a case of rectal duplication in an asymptomatic elder patient is presented.

Duplicación intestinal. Informe de dos casos. / [Intestinal duplication. Report of 2 cases]

Intestinal duplications are rare and they result from embryological failures in the canalization of the gastrointestinal tract. This paper presents a case of ileal intestinal duplication and its differential diagnosis from Meckels diverticulum. Besides, a case of rectal duplication in an asymptomatic elder patient is presented.