Hepatic metastases from prostatic adenocarcinoma
A 66 year old man that was diagnosed with prostate cancer underwent radical prostatectomy 2 years ago. Pathology result of the surgical specimen revealed poorly differentiated prostate carcinoma with positive surgical margins. He was treated with antiandrogens and adjuvant radiation therapy. Since the beginning of the last year and under hormonal monotherapy with Casodex his PSA levels doubled. PET CT of the abdomen and the pelvis revealed hepatic lesion. Ultrasound guided needle biopsy of this lesion diagnosed metastatic poorly differentiated prostatic carcinoma with a high proliferative index.
1. What therapy do you recommend?
2. Centers of excellence in Italy and/or abroad?
66 years old, male.
Type II diabetes mellitus
6 years ago an increase in PSA level (values till 10 ng) was noted. Repeated biopsies always gave negative outcome. 4 years ago the patient underwent TURP with laser. Last year, following a new increase in PSA level, a new prostate biopsy was carried out with result of Prostatic Adenocarcinoma Gleason Score 4 + 4.
Therefore, a radical prostatectomy was carried out whose histology examination confirmed: “Prostatic Adenocarcinoma with seminal vesicle invasion Gleason Score 5 + 4. Evidence of vascular invasion, evidence of lymphatic invasion, positive edges”.
At discharge, the patient, therefore, was treated with adjuvant therapy with Casodex 150 (continued till today) and radiotherapy for a total of 72 Gy.
Bone Scintigraphy negative for metastasis. Negative abdominal and chest CT scan. Stage pT3b N0 M0 Gleason Score 5 + 4 Grading 3.
For the last year was an increase in PSA level, taking Casodex: first value 13. 2 ng, new checkup 21 ng.
The patient, therefore, underwent oncological examination with finding of good general conditions, without any symptom. During that examination, it was deemed necessary to carry out a Choline PET scan without starting any new therapy different from the current ones in order to avoid distortion of results.
At the oncological follow-up, the PET scan was negative for disease at high metabolic activity; non-fixation area of the tracer at S8 level of the liver, therefore a diagnostic deepening with other methods is advised.
According to the oncologist, the negative PET scan excluded the presence of areas of fast evolutivity or of large volume, moreover he stated that the biochemical progression of the PSA level was undeniable. Therefore, an androgen block with LHRH agonists was suggested (Decapeptyl 3.75 1 intramuscular vial for 28 days), at first with Casodex and then only with PSA level monitoring. Following with Casodex alone has been deemed to be little justified, taking into consideration the PSA increasing and velocity. At the same time the specialist suggested a deepening of the nature of the hepatic area and of the prostate cavity disabled with MRI of the upper and lower abdomen with contrast medium.
New oncological follow-up, where the patient takes with him the MRI that reveals: “The liver shows increased size and not homogeneous MR structure since there are proofs of intraparenchymal nodule areas mainly placed in the right lobe, in S5 and S6 and at the passage between S8 and S5. In this second area there is the lesion of greater size with a diameter of 7 cm. The appearance of lesions is not homogeneously hyperintense in the T2 dependent sequences and appears hyperintense also in the sequences obtained in diffusion.
After intravenous administration of contrast medium the lesions show a not homogeneous impregnation, partially peripheral, surely not pathognomonic for the presence of angiomatous lesions. The medical report would seem to be ascribed likelihood to the presence of repetitive lesions. The Choline PET scan negative results leads to the suspect that the primitive lesion has not a prostate origin. The pancreas, the spleen, the suprarenal glands keep a MR normal appearance.
The kidneys show parenchyma of well preserved thickness: there is only evidence of a small cyst in the left mesorenal area. There are no images of adenopathy along the lomboaortic chains. As a result of radical postatectomy, the bladder’s walls are slightly thickened, especially at the back, but the medical report could still be compatible with a picture of hypertrophy of the tunica media.No abnormal expansive formations in the prostatectomy cavity are observed.
Sigma diverticulitis with no large signs of perivisceritis are observed.”
In the light of this medical report a therapy with Decapeptyl 3.75 1 vial every 28 days + Casodex already under way was decided. The patient decided however, for the moment, to put off continuing only with Casodex.
At the last oncological examination, the patient has taken with him the medical report of the ultrasound guided needle biopsy of the hepatic lesion: Histologal examination- HE: Hepatic metastasis of prostatic adenocarcinoma poorly differentiated. High Gleason Stage. Neuroendocrine: 1% Ki 67 65% PSA ++ TTFI neg, CEA neg.
The relevant oncological assessment is indicative of “Shown the prostate origin of the hepatic lesion, for the moment, the BAT (Decapeptyl + Casodex) is administered. Reccomended follow up in two months-PSA level, Hemochrome, AST (serum aspatate aminotransferase), ALT (alanine aminotransferase), ALP, GGT, Creatinine, Na, K, Testosterone.
Further follow-up only of the PSA level after a month + haepatic ultrasound scan and relevant therapeutic decisions based upon the answer.”
I have reviewed patient's past medical history and enclosed my opinion regarding the management of his prostate disease.
The patient is a 66 year old man that was diagnosed with prostate cancer. He underwent radical prostatectomy 2 years ago. Pathology result of the surgical specimen revealed poorly differentiated prostate carcinoma Gleason score 9(5+4) pT3b with positive surgical margins. He was treated with antiandrogens and adjuvant radiation therapy.
Since the beginning of the last year,under hormonal monotherapy with Casodex, his PSA levels doubled to 21ng/ml. PET CT of the abdomen and the pelvis revealed hepatic lesion but was non conclusive regarding it's nature. Ultrasound guided needle biopsy of this lesion diagnosed metastatic poorly differentiated prostatic carcinoma with a high proliferative index.
A single hepatic metastasis is a very rare manifestation of prostate cancer and should trigger further systemic workup. In spite of a normal bone scan and the above mentioned PET CT, I recommend repeating the last study using the (18)f-fluoride tracer. There is evidence in the literature that this kind of study is more sensitive for bone metastases which is the most common metastatic sight of prostate cancer.
The treatment of choice at this stage is total hormonal ablation with LHRH agonist (injection of Suprefact Depot 9.9mg or Zoladex 10.8mg every 12 weeks) combined with antiandrogen treatment–Casodex 50mg X1/day. The patient should be under careful onclogical follow up with serial imaging of the liver and monitoring of the PSA levels. Unfortunately the nature of his disease is not favorable and there is a high chance that the disease will go a transformation to a hormone refractory prostate cancer. At that stage Taxotere based chemotherapy should be considered.
I highly recommend to consult with Dr. Cora Sternberg at the department of Medical Oncology, San Camillo Forlanini Hospital, Rome ( [email protected]) regarding the future treatmrnt of this patient . Dr. Sternberg is a worldwide known oncologist participating and leading the treatment of patients with
uro-genital malignancies. I will be happy to answer any questions regarding the future treatment of the patient.