Pleuropulmonary and Lymph Node Progression after Docetaxel – Benefits from Treatment with Cabazitaxel in Metastatic Prostate Cancer
A 74-year-old male with performance status 0 presented with a prostate specific antigen (PSA) level of 51.2 ng/ml in August 2001. After biopsy, computed axial tomography (CT) and bone scan, prostate adenocarcinoma T2bN0M0, Gleason 6 (2 + 4), was diagnosed and considered an intermediate risk. The patient was treated with radical prostate-bed radiotherapy and full androgenic block with oral (PO) bicalutamide 50 mg/24 h and subcutaneous goserelin 10.8 mg quarterly until March 2002, when it was decided to remove the blockade after reaching an almost undetectable PSA level.\nHe was asymptomatic with a stable PSA level less than 0.07 ng/ml until March 2003, when the PSA level started increasing until reaching its highest level (7.27 ng/ml) in May 2005. Because of this biochemical relapse, antiandrogenic treatment was initiated with PO tamoxifen 10 mg/12 h and PO bicalutamide 50 mg/24 h, progressively reducing the PSA level (reaching its nadir of 0.66 ng/ml in September 2006). The blockade was suspended and a quarterly subcutaneous treatment with leuprorelin acetate was initiated. In September 2009, the PSA level rose to 47.53 ng/ml along with a clinical picture of weakness of the lower limbs, ambulatory difficulty and mechanical lumbar pain.\nA thoracic-abdominal-pelvic CT scan was requested; it focused on adenopathies between 1 and 2 cm in the upper and middle mediastinum and the left infrarenal para-aortics, as well as diffuse bone lesions in the lumbar vertebral bodies. Abnormal deposits of diffuse-shaped tracer were detected in the bone scan. Magnetic resonance imaging showed a mass of soft tissue at the spinal level causing a spinal stenosis, maximum T7 level, without compromising the spinal cord, so it was treated with palliative intent radiotherapy (fig. ).\nDue to the hormonal refractoriness, first-line chemotherapy treatment was started with intravenous docetaxel 75 mg/m2 and PO prednisone 5 mg/12 h. The first cycle was given on October 21, 2009. The patient's PSA level at this time was 47.53 ng/ml. He completed 9 cycles of treatment (the last in April 2010) with excellent tolerance. His PSA analytical nadir reached 19.81 ng/ml after chemotherapy was completed. A further evaluation in May 2010 gave a partial response, continuing only with luteinizing hormone-releasing hormone analogues.\nIn April 2011, pulmonary progression with right pleural effusion and pathological size increase in paratracheal adenopathies and the aortopulmonary window were observed on a CT scan and histologically confirmed. Due to this situation and the good overall condition of the patient, it was decided to initiate intravenous treatment with cabazitaxel 25 mg/m2 and PO prednisone 10 mg continuously. At the beginning of the treatment, his PSA level was 120.62 ng/ml, reaching 64 ng/ml after the third cycle in June 2011.\nAfter 6 cycles of chemotherapy, a reduction of mediastinal adenopathies and infrarenal para-aortic stable bone involvement and an absence of pleural effusion were observed. The patient's PSA level was 48.58 ng/ml. Given the good response and the absence of toxicity, it was decided to continue with 2 more cycles. After 8 cycles, the last of which was in September 2011, treatment was discontinued as it was considered that the therapeutic plan had been fulfilled without having relevant toxicity at any time.\nIn February 2012, his PSA level increased to 94 ng/ml. A thoracic-abdominal-pelvic CT scan was requested, which showed stability of the infradiaphragmatic and supradiaphragmatic gland injuries, as well as diffuse bone metastasis. To date, the patient remains asymptomatic. Since February 2012, a progressive PSA increase without clinical deterioration has been noted. In January 2013, the PSA level was 191 ng/ml (fig. ). Should further symptoms occur, a new treatment will be proposed. The reintroduction of cabazitaxel treatment would be our first choice given the clinical benefit and the important targeted radiological and biochemical responses. Currently, there is a treatment-free interval following the end of the 16-month cabazitaxel treatment and a 6-month period free of biological progression.