Objectives  To confirm the expression of prostate specific antigen (PSA) and prostatic acid phosphatase (PAP) in ductal carcinomas of the prostate, and to analyse p53, Ki67, oestrogen (ER) and androgen (AR) receptors in these tumours. Materials and methods  Paraffin‐embedded samples from 12 patients with ductal carcinoma of the prostate were assessed for pattern, mitotic count and the presence of a microacinar carcinoma component. There were six pure ductal and six mixed microacinar and ductal carcinomas. Sections were stained immunohistochemically for the expression of PSA, PAP, Ki67, p53, AR and ER. Clinical data were obtained from case notes. Results  Six of the ductal tumours had a papillary pattern whilst the others had a cribriform appearance. The mitotic rates in the ductal areas were high in the tumours from eight of the 12 patients. PSA and PAP immunohistochemistry were positive in all the cases. No ER immunoreactivity was found in any of the patients. Ten of the ductal tumours showed strong reactivity with AR, the other two were weakly positive; two of the tumours were strongly positive for p53 protein. All the ductal carcinomas expressed Ki67, three having >25% nuclear marking. One patient who was strongly positive for p53 and had a high Ki67 score survived only one year after diagnosis. Survival ranged from 1 to 13 years after diagnosis. Conclusion  This study confirms the expression of PSA and PAP in ductal carcinomas of the prostate. The percentage of tumours expressing p53 was similar to that published for high‐grade microacinar carcinomas. The results for Ki67 suggest that ductal tumours have higher scores than microacinar tumours, but further studies are required to ascertain if this is significantly different. As half the patients with ductal tumours had co‐existent microacinar tumours, we advise transrectal prostatic biopsies in patients diagnosed with pure ductal carcinomas on transurethral resection specimens, to exclude high‐grade microacinar carcinomas. The presence of AR and the lack of ER in all the ductal carcinomas confirms that these tumours are prostatic in origin and should be treated with anti‐androgen therapy.

Occupational exposure and cigarette smoking have been well documented as risk factors in the development of TCC of the bladder, as has slow acetylation status. There are very few studies linking bladder cancer with alcohol consumption. It is important to subdivide types of alcohol consumed when considering this factor in an epidemiological study. In the case of beer, methods used by different brewing processes may also contribute to differences found, were such a study to be performed on a national scale.

Prostate biopsies were taken and revealed 'undiCerenCase report tiated' carcinoma on initial histology. After counselling, he underwent staging investigations which revealed no A previously healthy 53-year-old man presented with a short history of lower urinary tract symptoms, dysuria, metastasis. However, a pre-operative histological assessment of deeper sections and PSA immunostaining intermittent frank haematuria and rigors. He was treated empirically with ciprofloxacin by his GP. On referral, his revealed no tumour but florid diCuse granulomatous prostatitis ( Fig. 1). At follow-up, he was asymptomatic symptoms were resolving; he had a firm, smooth, moderately enlarged non-tender prostate. Investigations, but had persistently elevated PSA levels of about 10 ng/mL. TRUS carried out at 6 and 12 months was including urine culture, cystoscopy and IVP, were normal apart from his PSA level, which was 12.5 ng/mL.reported as showing BPE. Biopsies at this stage revealed only hyperplasia; 15 months later, further biopsies revealed a focus of moderately diCerentiated adenocarcinoma. The patient opted for radical prostatectomy after this prolonged traumatic period. The operative specimen revealed small confined foci of adenocarcinoma (Gleason grade 2+3=5) with a total volume of <4 mL and surrounding fibrous hyperplasia (Fig. 2). He remains well with no evidence of recurrence after surgery. CommentThere can be clinical, histological and psychological pitfalls with diagnosing diCuse granulomatous prostatitis in patients with elevated PSA levels. The condition may mimic prostatic malignancy, both clinically and histologically [1]. PSA levels may rise but this increase is elevation must be followed up after appropriate counselling and only after careful assessment of the histology with appropriate immunohistochemistry. References