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Mesenteric Adenopathy in Patients with Prostate Cancer

Frequency and Etiology

¹ Department of Radiology, Memorial Sloan-Kettering Cancer Center, 1275 York Ave., New York, NY 10021.
² Present address: Department of Radiology, University of California, San Francisco, Box 0628, M-372, 505 Parnassus Ave., San Francisco, CA 94143-0628.

Received June 18, 2001; accepted after revision July 20, 2001.

 
Address correspondence to F. V. Coakley.

Abstract

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OBJECTIVE. This study was undertaken to determine the frequency and etiology of mesenteric adenopathy revealed at initial-staging CT in patients with prostate cancer.

CONCLUSION. Mesenteric adenopathy is a rare finding at initial-staging CT in patients with prostate cancer and is more often due to coexistent lymphoma than to metastatic disease, particularly in the absence of associated pelvic adenopathy and a markedly elevated serum prostate-specific antigen level. Appropriate radiologic interpretation of the finding prevents overstaging of prostate cancer.

Introduction

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Prostate cancer is the most common noncutaneous cancer and the second most common cause of cancer death in American men [1]. Patients with cancer confined to the prostate are considered curable by radical prostatectomy, but up to 16% of patients with prostate cancer who are being considered for radical prostatectomy have nodal metastases [2]. Iliac and retroperitoneal nodes are the usual sites of adenopathy. The visualization of even minimally enlarged or asymmetric pelvic nodes at CT is suggestive of metastatic involvement [3]. The clinical relevance of adenopathy at other sites in patients with prostate cancer has been less extensively studied. We recently encountered a patient with mesenteric adenopathy visible on a CT scan obtained for staging prostate cancer; biopsy of a mesenteric node found non-Hodgkin's lymphoma. Because of this anecdotal experience and the lack of pertinent published research, we undertook this study to systematically examine the frequency and etiology of mesenteric adenopathy found at initial-staging CT for prostate cancer.

Materials and Methods

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We retrospectively identified all patients with prostate cancer who underwent CT of the abdomen and pelvis in our institution between January 1992 and May 1997 by searching the computerized radiology information system. From the reports of the initial Ct examinations in 1,429 patients, we identified seven patients with reported mesenteric adenopathy. The medical records and imaging findings in these seven patients were reviewed to determine the etiology of the mesenteric adenopathy. Adenopathy was defined as the presence of any node with a short-axis diameter larger than 1 cm or the presence of an abnormally increased number of nodes as subjectively assessed by the reviewing radiologist [4,5]. The presence or absence of retroperitoneal and pelvic adenopathy was noted, and the largest node size in all regions was recorded. The etiology was established by review of pathologic specimens. CT studies had been obtained on a HiLight Advantage nonhelical scanner (General Electric Medical Systems, Milwaukee, WI; n = 4) and a HiSpeed Advantage helical scanner (General Electric Medical Systems; n = 3) using a 10-mm slice thickness, pitch of 1, and 10-mm reconstruction interval after the administration of oral contrast material and 150 mL of IV iodinated contrast medium.

Results

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Seven (0.5%) of 1,429 initial abdominopelvic CT scans revealed mesenteric adenopathy, the form of which varied from an increased number of small nodes with surrounding mesenteric infiltration (n = 1) to discrete nodal masses with maximum short-axis diameters as large as 5 cm (n = 6). The mean age of these seven men was 65 years (age range, 56-72 years). The mean serum level was 29.3 ng/L (range, 5.0-86.2 ng/L). The median Gleason score was 6 (range, 5-9). Three patients had organ-confined disease and 4 patients had extracapsular spread, as determined by digital rectal examination (n = 4) or radical prostatectomy (n = 3).

The etiology of the mesenteric adenopathy was non-Hodgkin's lymphoma in four patients and prostate cancer in two. The etiology of mesenteric adenopathy was confirmed by direct mesenteric node biopsy in two patients with non-Hodgkin's lymphoma and confirmed by concurrent progression of mesenteric adenopathy with biopsy-proven disease at another metastatic site in two patients with prostate cancer and in two patients with non-Hodgkin's lymphoma. In the remaining patient, the etiology could not be determined because the patient transferred to another facility. Both patients with mesenteric adenopathy attributable to metastatic prostate cancer had associated pelvic adenopathy and a serum prostate-specific antigen level of 50 ng/L or more. Pelvic adenopathy was detected in only one of the four patients with lymphomatous mesenteric adenopathy. The serum prostate-specific antigen level in these four patients ranged from 5 to 14.6 ng/L. Patients with representative cases are illustrated in Figures 1 and 2.

View larger version (138K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1. —CT scan of 72-year-old man with recently diagnosed Gleason-6 prostate cancer and prostate-specific antigen level of 86.2 ng/L shows enlarged mesenteric (arrow) and retroperitoneal nodes. Endobiliary stent was placed because of obstructive periportal adenopathy. Pelvic adenopathy was also present (not illustrated). Biopsy of pulmonary nodule showed metastatic prostate cancer.

View larger version (162K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2. —Ct scan of 56-year-old man with recently diagnosed Gleason-9 prostate cancer and prostate-specific antigen level of 11.0 ng/L reveals enlarged mesenteric nodes (arrow). Mesenteric node biopsy showed non-Hodgkin's lymphoma.

Discussion

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The CT appearance of mesenteric lymphadenopathy varies from clusters of multiple small ovoid soft-tissue densities in the fat of the small-bowel mesentery to large irregular confluent soft-tissue masses [6,7]. This type of appearance is characteristic in patients in whom the masses are around the superior mesenteric vessels between the loops of small bowel anteriorly and the posterior abdominal wall posteriorly [8]. More peripherally located nodules or masses may be difficult to distinguish from peritoneal implants [7], though the signs of typical peritoneal disease elsewhere (e.g., omental caking or surface implants on the liver or spleen) may suggest the latter.

In a review of 30 cases of mesenteric masses, non-Hodgkin's lymphoma and metastases accounted for 23 and six cases, respectively [6]. In a similar review of 95 patients with mesenteric disease, the corresponding figures were 41 and 39 [7]. None of the cases in these two series were due to metastatic prostate cancer. It is likely that both previous studies included cases of peritoneal carcinomatosis in addition to true mesenteric lymphadenopathy. Nonetheless, non-Hodgkin's lymphoma is clearly the most common cause of mesenteric adenopathy. Other rare but reported causes include leukemia, idiopathic retroperitoneal fibrosis, Whipple's disease, cat-scratch disease, sarcoidosis, celiac sprue disease, and mastocytosis [8,9,10,11,12,13,14].

Nodal metastases from prostate cancer typically occur in the locoregional iliac, obturator, inguinal, and retroperitoneal nodes [15]. Mesenteric nodes do not lie in the lymphatic drainage pathway of the prostate; therefore, mesenteric adenopathy is an unlikely early manifestation of metastatic prostate cancer. For example, in an autopsy study of 144 patients who had prostate cancer, only one (0.7%) had metastases to mesenteric nodes [15]. Our study confirms this finding because only two of 1,429 patients with prostate cancer were found to have metastatic mesenteric adenopathy at staging CT. In our review, both patients with mesenteric adenopathy attributable to prostate cancer also had extensive metastatic disease elsewhere, and the adenopathy likely was a reflection of concordant widespread dissemination. In addition, a markedly elevated baseline serum prostate-specific antigen level was present in both patients.

Atypical sites of metastatic disease are a recognized finding in advanced disease. For example, 3.2% of patients with prostate cancer were found to have peritoneal tumor implants at autopsy [15]. Non-Hodgkin's lymphoma was the cause of mesenteric adenopathy in four of our patients, and pelvic adenopathy was present in only one of these cases. This finding contrasts with the findings in the patients who had mesenteric adenopathy due to metastatic prostate cancer: pelvic adenopathy was found in both patients. These findings suggest that lymphoma is the leading diagnosis to consider in patients in whom mesenteric adenopathy is revealed at initial-staging CT for prostate cancer, particularly in the absence of pelvic lymphadenopathy, widespread dissemination, or a very high serum prostate-specific antigen level.

Our study has a number of limitations. The identification of adenopathy on the basis of an abnormally increased number of nodes, even in the absence of any individual node with a shortaxis diameter larger than 1 cm, is partially subjective, but such identification is in accordance with standard practice. In addition, only one of the seven cases of mesenteric adenopathy in our study was identified using this subjective criterion. The study was conducted retrospectively, and cases of mesenteric adenopathy were identified by reading the radiology reports rather than by directly reviewing the CT images. The degree of interobserver variability in the identification of mesenteric adenopathy is therefore unknown, although mesenteric adenopathy was evident on direct review of the CT images in all seven patients reported as having mesenteric adenopathy. However, we cannot rule out the possibility that some cases of mesenteric adenopathy were excluded and that the true frequency of mesenteric adenopathy in the study population was underestimated.

In conclusion, the visualization of mesenteric adenopathy at initial-staging CT for prostate cancer should suggest causes other than metastatic prostate cancer, particularly lymphoma. This distinction is of critical clinical importance because it prevents overstaging of potentially curable prostate cancer and allows prompt initiation of therapy for coexistent lymphoma.

References

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