Isolated Non-ascitic Peritoneal Carcinomatosis from Metastatic Prostate Cancer.

Prostate cancer most commonly metastasizes to bone, lung and liver. Omental metastasis of prostate cancer is extremely rare, with only a few cases reported in the literature, many of which have associated ascites. We present a case of non-ascitic omental metastasis of prostate cancer without any bone metastases. Furthermore, this patient has had two negative measurements of circulating tumor cells (CTCs) in the blood, suggesting a non-hematogenous route of metastasis to the omentum.

Introduction

Peritoneal carcinomatosis secondary to prostate cancer (pCa) with no further metastases is very rare, with only four reported cases in the available literature, all presenting with ascites. Port-site metastasis after minimally invasive urological surgery is similarly rare despite the widespread use of laparoscopic techniques in the management of urological malignancies. We report a case of possible port-site metastasis and subsequent peritoneal carcinomatosis following robot-assisted radical prostatectomy.

Case report

A 60-year-old man presented with an elevated prostate-specific antigen (PSA) of 9.5 ng/mL in 2010. Transrectal biopsy of the prostate revealed Gleason 3 + 4 prostatic adenocarcinoma. Robotic prostatectomy was performed at an outside hospital in October 2010 and after surgery, the PSA never became undetectable. The patient subsequently received adjuvant hormone therapy and salvage radiation therapy in April 2011. A bone scan performed in October 2011 was negative for metastatic disease. In March 2012, the PSA nadir was 0.02; rising with a doubling time of 3.4 months to reach 5.6 before starting ADT.

Baseline scans in September 2013 were a bone scan negative for metastatic disease and a CT chest/abdomen/pelvis scan showing a 0.9 × 1.1 cm indeterminate omental nodule, located on the right side just proximal to the prostatectomy exit port above the umbilicus. In February 2014 he reached a new PSA nadir of 0.4. A repeat CT scan then showed that the soft tissue nodule in the omentum had decreased in size from 1.1 cm to 0.8 cm with the onset of ADT. In February 2015, PSA was 4.1, bone scan again was without evidence of metastatic disease, and CT scan showed the omental nodule increased to 1.4 cm with a new adjacent subcentimeter nodule. PSA continued to increase with a 2.2 month doubling time, reaching 11.4 on 5/21/15.

Patient underwent CT-guided omental biopsy in April 2015, which stained positive for racemase and PSA, consistent with metastatic poorly differentiated carcinoma of prostatic origin. The same month a circulating tumor cell (CTC) assay, involving immunomagnetic sample enrichment with fluorescent antibody staining, showed zero tumor cells in the blood. Repeat bone scan in May 2015 showed no evidence of metastatic disease to bone and CT chest/abdomen/pelvic showed the omental nodule that now measured 1.7 × 1.4 cm in size (Fig. 1).

Figure 1

CT scan from May 2015, before total omentectomy, shows the 1.7 × 1.4 cm omental nodule (white arrow at center top).

Patient subsequently underwent a total omentectomy in May 2015. Pathology of the resected omentum showed a 2.5 cm, firm nodule whose microscopic examination confirmed the histological appearance on the prior biopsy. PSA was 11.8 before surgery and following surgery, PSA decreased to 1.8 within 1 month. The PSA continued to rise with a 1.9 month doubling time, reaching 31 in March 2016. A choline-11 PET/CT scan at that time showed radiotracer avid peritoneal nodules and nodules within the prostatic bed. There were three radiotracer avid lymph nodes: one left external iliac (2 × 1.7 mm) and one on the right (4 × 5 mm), and a left obturator node (5 × 7 mm). Circulating tumor cells were measured in April and May 2016, again showing zero cells. Patient started abiraterone in May 2016 when his PSA was 89; PSA fell to 1.0 by end of July 2016, with tumor nodule dimensions reduced 25%-50%.

Discussion

Prostatic adenocarcinoma metastasizes 35% of the time, with an overwhelming predilection to involve the bone. The most frequent organ involved in metastatic pCa is bone (90%). Clinical involvement of visceral sites, such as lung (46%), liver (25%), pleura (21%) and adrenals (13%), is less common, even in patients with widespread castration-resistant disease. Prostatic adenocarcinoma with metastasis to the peritoneum is extremely rare, even more so in the absence of any bony involvement.

Our case is unique in several ways. First, there are only four reported cases in the literature of pCa with omentum as its only metastasis.2, 3, 4, 5 None of the previously reported cases have the frequent imaging and staging of our case. All four cases presented with gross ascites, suggesting that such presentations of metastatic pCa likely present late in illness course. Additionally, none of the previously reported cases presented after a laparoscopic prostatectomy, which raises the possibility of this peritoneal carcinomatosis resulting from port-site metastasis. In our case, the discovery of peritoneal metastasis approximately 30 months post-op without any major abdominal symptoms such as ascites, is unique. The patient has had several bone scans come back negative for metastatic disease while his treatment course has been complicated by isolated metastasis to the omentum. Our case is a case of potential port-site metastasis without bony metastases, without the presentation of ascites and without the involvement of other intraabdominal structures apart from the omentum.

The mechanism of metastatic pCa to the omentum in the absence of skeletal metastasis is unclear. Since our patient has had the circulating tumor cells in his blood measured twice, both times coming back negative, hematogenous spread of the cancer is highly unlikely. Kehinde et al suggested that the mucinous adenocarcinoma of the prostate is reported to be characterized by rarity of bone metastases, lesser degree of response to local radiation therapy and lack of hormone dependence. However, our patient did not have a mucinous adenocarcinoma and clearly showed response to first line and second line hormonal treatment. The lack of hematogenous spread and relative absence of lymphatic involvement, suggests that the tumor cells traveled directly through the peritoneum to reach the omentum. Further peritoneal dissemination could have occurred from the omental port-site metastasis. Ultimately, the possibility of discovering whether or not seeding from a port-site metastasis occurred is and will likely remain unclear. The positive margin after laparoscopic prostatectomy also suggests that the cancer could have metastasized shortly after the prostate removal before pelvic radiation 6 months later.

Our patient's PSA substantial decrease following omentectomy suggests that omentum was the first site of metastasis. Whether or not this is a port-site metastasis will likely remain unclear, but what is definitive is the fact that we have a case of isolated peritoneal carcinomatosis without ascites unlikely to have resulted from hematogenous spread.

Conflict of interest

None.