Intravesical BCG therapy-induced granulomatous prostatitis in a patient with non-muscle invasive bladder cancer and prostate adenocarcinoma

Abstract

Granulomatous prostatitis (GP) is a rare inflammatory condition that may mimic prostate cancer (PC) progression. We present the case of a 64-year-old man with low-risk PC on active surveillance who developed Bacillus Calmette-Guérin (BCG)-induced GP following intravesical therapy for non-muscle invasive bladder cancer. Clinical and imaging findings suggested PC progression, but biopsy confirmed granulomatous inflammation without malignancy upstaging. This case underscores the similarities in clinical presentation, as well as the importance of histopathological evaluation in differentiating GP from PC.

1 Introduction

Granulomatous prostatitis (GP) is an uncommon prostate condition characterized by inflammatory granulomatous lesions. Epstein and Hutchins classified GP into nonspecific, specific, post-surgical, and secondary to systemic granulomatous diseases with causes including infections and allergic reactions to surgical interventions. Systemic or genitourinary tuberculosis is a well-documented infectious cause of GP. Studies have also pointed to intravesical Bacillus Calmette-Guerin (BCG) treatment for non-muscle invasive bladder cancer (NMIBC) as a source of GP. Additionally, BCG-related GP has been associated with reduced malignancy risk in lesions classified as PI-RADS 3, 4, or 5 on MRI, complicating prostate cancer (PC) risk assessments.

The clinical presentations of GP often mimic those of prostate cancer, making differentiation difficult without histopathological examination. Common findings include a hard, fixed nodule on digital rectal exam (DRE), elevated serum prostate-specific antigen (PSA) levels, and MRI abnormalities similar to those seen with PC. Here, we present a case of intravesical BCG therapy-induced GP in a patient with existing PC, highlighting diagnostic and therapeutic challenges.

2 Case presentation

A 64-year-old man with a medical history of coronary artery disease, hyperlipidemia, and hypertension was initially diagnosed with localized PC with a Gleason Score (GS) of 6 (3 + 3) and an associated PSA of 3.6 ng/mL. The patient underwent active surveillance (AS) over the next twelve years comprised of serial MRIs, PSA measurements, and biopsy. Repeat prostate biopsy at year four showed unchanged disease state (GS 3 + 3). Due to PSA increase (10.3 ng/mL), a magnetic resonance imaging (MRI) of the prostate was obtained at year twelve which showed three suspicious lesions including a 1.3 cm lesion in the right (R) mid gland, a 1.2 cm lesion in the left (L) anterior transition zone, and a 0.9 cm lesion in the L anterior/posterolateral peripheral zone mid-gland. A repeat biopsy up-staged the PC to GS 7 (3 + 4, corresponding to the R mid gland lesion seen on the MRI), indicating more aggressive disease. Potential treatment options discussed included AS, radiation therapy, and surgery. The patient opted to continue AS. PSA remained stable (8–11 ng/mL) and a repeat MRI in year thirteen showed stable prostate lesions (1.4 cm, 1.2 cm, and 0.9 cm respectively) ( Fig. 1 A and B).

In year fourteen, the patient developed hematuria. Computer tomography (CT) of the abdomen/pelvis and cystoscopy revealed a 2 cm bladder mass on the left lateral wall; a trans-urethral resection of bladder tumor revealed high grade, NMIBC. The patient underwent intravesical gemcitabine instillation followed by six weeks of intravesical BCG treatment, with negative surveillance cystoscopies post treatment.

However, an MRI of the prostate 5 months post BCG treatment showed significant increase in the R mid-gland (from 1.4 cm to 4.2 cm), with extension in the left peripheral zone and left apex. The lesions in the L mid-gland and left anterior transition zone remained stable ( Fig. 1 C and D), with a new, non-specific, 0.6 cm R pelvic sidewall lesion (not shown). Prostate MRI at 8 months post BCG installation showed improvement: shrinkage of the R mid-gland (from 4.2 cm to 3.4 cm), stable appearance of L anterior transition zone lesion and left mid-gland lesion, and resolution of the right pelvic side wall lesion ( Fig. 1 E and F). CT of the chest/abdomen/pelvis and bone scan were negative for distant metastasis. Subsequent prostate biopsy was not consistent with PC progression: only 1 out of 15 biopsy cores showed prostate adenocarcinoma, down-staged from GS 7 (3 + 4) to GS 6 (3 + 3, Fig. 2 A). All other targeted and random cores, including the large R mid-gland lesion, showed prostate tissue with necrosis, acute, chronic, and granulomatous inflammation ( Fig. 2 B–C). Acid-fast bacilli (AFB) staining was negative.

Based on BCG exposure, discordance between findings on MRI and prostate cancer grade, severe granulomatous inflammation on prostate biopsy, and improvement on subsequent MRIs without therapeutic intervention, we conclude the patient developed BCG-associated GP superimposed on his existing PC.

3 Discussion

Granulomatous prostatitis is rare, accounting for <1 % up to 6 % of benign lesions in the prostate. ^, ^, The coexistence of GP and PC is an even rarer, with most patients presenting as case reports and documented concurrent diagnoses. ^, ^, This patient offers a unique perspective with longstanding PC subsequently developing BCG-induced GP. Particularly, the case highlights several diagnostic and therapeutic challenges in the context of GP mimicking PC progression.

PC and GP are clinically indistinguishable, both manifesting with urinary symptoms, serum PSA changes, and abnormal and/or worsening prostate nodules on physical exam and MRI. Several large case series of GP are summarized in Table 1 ^, ^, A majority of patients present with clinical symptoms (83–100 %), abnormal DRE (77–100 %) and a PSA ranging from normal up to 28.8 ng/mL ( Table 1 ). In most studies, PC was high on the differential based on clinical and laboratory evaluations, but only 4 of the 336 evaluable patients had concurrent PC diagnosis. ^, ^, GP should be on the differential when evaluating prostate-related symptoms in patients with risk factors such as certain bacterial/fungal/parasitic/viral infections (i.e., urinary tract infections, tuberculosis, syphilis, coccididiomycosis, schistosomiasis, herpes simplex virus), recent surgical intervention (i.e., TURP or biopsy), systemic granulomatous diseases (i.e., sarcoidosis) and intravesical BCG therapy. If GP is confirmed, treating the underlying cause is usually sufficient.

Table 1

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