Rare Prostatic Metastasis from Rectal Cancer Detected by ¹⁸F-FDG PET/CT

INTRODUCTION

Colorectal cancer (CRC) is the third most commonly diagnosed malignancy worldwide and a leading cause of cancer-related mortality.^[1] Metastatic spread most frequently involves the liver, lungs, bones, and peritoneum, whereas dissemination to atypical sites is rare. Prostatic metastases are exceptionally uncommon; most malignant prostatic tumors are primary adenocarcinomas, and secondary deposits from CRC have been described only in isolated case reports – this rarity persists despite the close anatomical proximity of the rectum to the prostate.^[2]

¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG PET/CT) is widely used for staging and restaging various nonprostatic malignancies. Although its positive predictive value for primary prostate cancer detection is relatively low, incidental intraprostatic FDG uptake is occasionally observed. Earlier systematic reviews estimated suchfindings at 1.8%,^[3] whereas a recent large single-center retrospective study^[4] reported a higher rate (3%) in men undergoing PET/CT for nonprostate-related indications; notably, nearly 30% of these cases were ultimately diagnosed with prostate cancer.^[4] These data underscore the importance of prompt evaluation of incidental prostatic uptake, unless contraindicated by severe comorbidity or limited life expectancy.

Against this backdrop, we report a rare case of prostatic metastasis from moderately differentiated rectal adenocarcinoma metastatic pattern seldom encountered in clinical practice. This case demonstrates how ¹⁸F-FDG PET/CT can reveal clinically significant metastases in unexpected locations before they are detectable on conventional anatomical imaging, thereby enabling earlier diagnosis, guiding targeted therapy, and potentially improving patient outcomes.

CASE REPORT

A 76-year-old male with no significant past medical history was referred to our hospital in July 2022 for the evaluation of abdominal pain and rectal bleeding. Colonoscopy revealed a rectal tumor located 6 cm from the anal verge. Histopathology confirmed moderately differentiated rectal adenocarcinoma. He underwent neoadjuvant chemoradiotherapy followed by surgical resection. Three years later, he developed hematuria, delayed urination, and urinary urgency. Color Doppler ultrasound of the prostate showed a normal-sized gland with regular contours and an intact capsule. Abdominopelvic CT revealed no significant abnormalities involving the prostate, bladder, or ureteropelvic junctions. Laboratory tests showed a prostate-specific antigen (PSA) level of 0.28 ng/mL, carcinoembryonic antigen of 1.73 ng/mL, and carbohydrate antigen 19-9 of 6.26 U/mL, all within the normal limits. The markedly low PSA argued strongly against primary prostatic adenocarcinoma and oriented the differential diagnosis toward a secondary malignancy, given the patient’s CRC history.

¹⁸F-FDG PET/CT maximim intensity projection(MIP) image demonstrated an incidental focal uptake within the prostate [Fig 1a]. On axial fused PET/CT images,pathological uptake was noted at the rectal surgical site(maximum standardized uptake value [SUVmax] = 5.9) [Fig 1b] and as a focal hypemetabolic lesion in the prostate (SUVmax = 7.4). The corresponding axial non contrast CT image showed no morphological abnormality in the prostate [Fig 1c and 1d].

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Fig 1:

(a) Maximum intensity projection 8F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) image demonstrating incidental focal uptake within the prostate (yellow arrow). (b) Axial fused ¹⁸F-FDG PET/computed tomography (CT) image showing intense focal FDG uptake in the primary rectal tumor (maximum standardized uptake value [SUVmax] = 5.9) (white arrow). (c) Corresponding axial noncontrast CT image demonstrating no morphological abnormality in the prostate. (d) Axial fused PET/CT image depicting a hypermetabolic focus in the left prostate (SUVmax = 7.4) (yellow arrow). PET acquisition was performed 60 min after intravenous administration of 200 MBq ¹⁸F-FDG; CT parameters: 120 kVp, 80 mAs, 3 mm slice thickness, standard reconstruction algorithm.

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¹⁸F-FDG PET/CT demonstrated pathological uptake at the rectal surgical site (maximum standardized uptake value [SUVmax] = 5.9) [Fig 1b] and an incidental focal FDG-avid lesion in the prostate (SUVmax = 7.4) [Fig 1d]. Pelvic magnetic resonance imaging (MRI) revealed a poorly defined 10 mm nodular lesion in the right lobe with extracapsular extension. Transurethral resection was performed for diagnostic confirmation. Histopathology revealed adenocarcinomatous proliferation in tubular and occasional cribriform patterns [Fig 2]. The tumor cells showed marked nuclear atypia, without vascular emboli. Immunohistochemistry demonstrated strong CK20 and CDX2 expression, preserved MLH1, and negativity for CK7, PAX8, and GATA3. This profile is typical of colorectal adenocarcinoma and distinct from primary prostatic adenocarcinoma, which expresses PSA, PAP, and NKX3.1 and lacks diffuse CK20/CDX2 expression. The complete absence of prostate-lineage markers with a definitive colorectal marker signature confirmed a secondary origin.

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Fig 2:

Histopathology (H and E stain, ×5) showing moderately differentiated rectal adenocarcinoma arranged in tubular structures with a cribriform pattern infiltrating prostatic tissue

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Based on clinicopathological and immunohistochemical findings, a diagnosis of metastatic moderately differentiated rectal adenocarcinoma to the prostate was established. The case was reviewed at a multidisciplinary tumor board, which recommended systemic chemotherapy. At a 3-month follow-up, the patient had partial symptom improvement and radiological disease stabilization, without new metastatic lesions.

DISCUSSION

Prostatic metastasis from CRC is exceedingly rare, with only a limited number of cases reported.^[2] Most patients, present several years after initial CRC treatment, have low or nonelevated PSA, and exhibit a CK20+/CDX2+/CK7– immunophenotype. As summarized in Table 1, this consistent profile supports the prompt investigation of metastasis when encountered in CRC survivors with a new prostatic lesion.^[5,6]

The metastatic pathway to the prostate remains incompletely understood and may involve multiple mechanisms. Hematogenous spread is plausible when tumor cells enter capillary venules, as in our case where postoperative pathology revealed serosal invasion. Mechanical factors, such as intraoperative tumor manipulation, increased peristalsis during obstruction, and postoperative inflammation, may facilitate dissemination.^[7] Disruption of the Denonvilliers fascia during colorectal surgery can also allow the direct extension to the prostate.^[8]

Accurate diagnosis of prostatic metastasis is crucial because it directly influences treatment planning and prognosis. In patients with a history of malignancy presenting with lower urinary tract symptoms, metastasis should be considered, particularly when PSA is low or only mildly elevated.^{[2] 18}F-FDG PET/CT offers whole-body metabolic imaging that can reveal hypermetabolic lesions in atypical metastatic sites, including the prostate.^[4] While FDG uptake is not specific and may occur in benign conditions,^[9] despite its limited sensitivity for primary prostate cancer (19%–64%),^[10] PET/CT remains valuable for identifying unexpected metastatic disease. Higher uptake in aggressive tumors is related to increased GLUT-1 expression, which correlates with tumor aggressiveness.^[9]

Histological differentiation between metastatic CRC and primary prostatic or bladder adenocarcinoma can be challenging due to shared enteric-type morphology.^[7] Immunohistochemistry is therefore essential: CRC typically expresses CK20 and CDX2 and is negative for CK7, while primary prostatic adenocarcinoma shows the opposite profile and expresses PSA, PAP, and NKX3.1.^[11,12] In our patient, the absence of prostate-lineage markers combined with strong colorectal marker expression confirmed the diagnosis of secondary involvement.

For advanced or unresectable metastatic CRC, treatment is primarily palliative, aiming to improve the quality of life through systemic chemotherapy, targeted agents, immunotherapy, or local interventions.^[8] Despite advances, prognosis remains poor, with stage IV CRC having a 5-year survival rate below 12%.^[13,14] In our case, early PET/CT detection, prior to anatomical changes visible on CT or MRI, enabled timely histological confirmation and initiation of systemic therapy, resulting in symptom improvement and short-term disease stabilization.

CONCLUSION

Prostatic metastasis from CRC is exceptionally rare and typically occurs in the advanced stages of the disease. It is often associated with atypical clinical presentations and poses diagnostic challenges. ¹⁸F-FDG PET/CT serves as a valuable imaging modality for detecting uncommon metastatic sites, while histopathological examination combined with immunohistochemical analysis remains essential for confirming the diagnosis and guiding therapeutic decisions. Despite advances in systemic therapies, the prognosis for patients with advanced metastatic CRC remains poor, highlighting the importance of early detection, accurate diagnosis, and personalized treatment strategies to optimize both survival and quality of life.