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  • Prostatitis

    K. G. Naber

    Urologic Clinic, Hospital St. Elisabeth, Straubing, Germany

    It has been estimated that up to half of all men sufferfrom symptoms of prostatitis at some time in their lives.In the early 1900s, prostatitis resulted in 2 millionoffice visits per year in USA, rivalling the number ofvisits for benign prostatic hypertrophy (BPH) at thetime. It is the most common urological diagnosis inmen younger than 50 years of age and the third mostcommon urological diagnosis in men older than50 years of age w1x. It has been clearly demonstratedthat patients diagnosed with chronic prostatitis havea qualitiy of life impact similar to patients sufferingfrom myocardial infarction, angina, or Crohns diseasew2x. Thus, prostatitis is a major health care issue, justas important as the other two major prostatic diseases,benign hyperplasia and carcinoma w3x. But ourknowledge of this subject is limited.

    Acute bacterial prostatitis

    The diagnosis of prostatitis suggests that this diseaseis of an inflammatory nature possibly caused by aninfective agent. This obviously holds true for patientswith acute bacterial prostatitis. These patients oftenpresent with a flu-like illness with systemic symptoms,indicating a tissue-invasive infection, in addition tourinary tract symptoms of bacteriuria, such as urinaryurgency, dysuria, frequency, etc. On physical exami-nation, the prostate can be tense and extremelytender. There are leukocytes in the prostatic fluid andmidstream urine. Culture demonstrates most fre-quently Escherichia coli, and less commonly, otherorganisms such as species of Klebsiella, Pseudomonas,Enterococcus, etc. Prostatic massage, however, shouldnot be performed in these patients because septicaemiacould be induced. The majority of these patients getbetter when treated with appropriate antibiotics.Occasionally patients develop complications such asurinary retention, septicaemia, prostatic abscess, andin rare cases metastatic infections such as pyogenicvertebral osteomyelitis. How often the acute status of

    infection is transformed into a chronic status, isunclear.

    Chronic prostatitis syndrome

    In contrast, the diagnosis of chronic prostatitisapparently represents a mixture of possibly differententities, which cannot be clearly separated with ourpresent knowledge. Therefore, this complex is bestdescribed as a syndrome consisting of various qualitiesof chronic pelvic pains, voiding disturbances andsexual dysfunctions, whereas the pelvic pains representthe most prominent urogenital symptoms as comparedto patients with benign hyperplasia of the prostate(BPH) and those with sexual dysfunctions w4x. Stressand psychological problems, particularly depression,are very commonly found in these patients. But itis not clear yet whether psychological dysfunctionsa priori are causing this syndrome, or if this syndromeitself causes the psychological dysfunctions.

    Classification of prostatitis syndrome

    In the past the classification according to Drach et al.w5x was most frequently used. It is based on the resultsof the bacteriological localization patterns obtained bythe four glass specimens w6x.

    Because of lack of knowledge concerning epidemi-ology, pathophysiology, diagnosis, and treatment ofprostatitis, the National Institutes of Health (NIH) ofthe USA started an international initiative. As a firststep, a new classification system w7x was suggested thatprovides uniform definitions of the various types ofprostatitis. The NIHuNIDDK (National Institute ofDiabetes and Digestive and Kidney Diseases) pro-posed this new classification system in 1995, whichwas reaffirmed in 1998 (Table 1).

    What pathogens cause chronic prostatitis?

    There is an ongoing debate on which bacteria can betaken as pathogens. In the most conservative approach

    Correspondence and offprint requests to: Kurt G. Naber, UrologischeKlinik, Klinikum St. Elisabeth, St. Elisabeth str. 23, D-94375,Straubing, Germany.

    Nephrol Dial Transplant (2001) 16 wSuppl 6x: 132134

    # 2001 European Renal AssociationEuropean Dialysis and Transplant Association

  • only those bacteria are considered pathogens, whichcan be localized in the prostatic secretion and causedocumented recurrent urinary tract infections w7x. Inthis view, pathogens other than E. coli, other membersof the Enterobacteriaceae family, such as Klebsiella,Enterobacter, Proteus and Serratia, and Pseudomonasaeruginosa can be considered as pathogens. Usingthis definition enterococci and staphylococci wouldbe outside of the scope even though these pathogensare often localized in the prostate and may also beassociated with chronic prostatitis syndrome.

    A number of other organisms have been reported tocause this syndrome: Trichomonas vaginalis, Chlamydiatrachomatis, genital mycoplasmas, difficult-to-cultureCoryneforms, and genital viruses, not to mention rarecases with mycobacterial, gonococcal, parasitic orfungal prostatitis. This subject has been carefullyreviewed elsewhere w8x. Evidence of the misclassifica-tion of at least some cases of non-bacterial prostatitisis accumulating w3x. Immunologic evidence, such asthe existence of antibodies to uropathogenic bacterialantigens, are detected in patients with negative culturesw9,10x, suggesting a non-culturable bacterial presence.This is further substantiated by evidence of bothbacterial DNA w11x and specifically cultured crypticbacteria w8x detected in prostate biopsies and prostaticfluids of patients with sterile cultures. As many as 50%of perineal biopsies in patients with prostatitis growbacteria w12x, presumably related to prostatic inflam-mation. Thus, the full impact of infection remainsunresolved in chronic inflammatory prostatitis anduntil now the mechanisms as well as alternativetreatment modalities are not well understood.

    The role of antimicrobial therapy inchronic prostatitis

    Despite reports that -0% of prostatitis cases arebacterial w13x a much higher proportion of men dia-gnosed with prostatitis receive antimicrobials. Anti-biotic therapy is recommended for acute bacterialprostatitis (ABP) and chronic bacterial prostatitis(CBP); it is debatable in patients with inflammatorychronic pelvic pain syndrome (CPPS) w14x.

    Because of their favourable pharmacokinetic prop-erties the fluoroquinolones can be considered drugs ofchoice. In the meantime, several clinical studies withquinolones have been published w15x. The results aredifficult to compare, however, because not all workersused the Meares and Stamey technique for diagnosis.

    The duration of treatment, which should last fora minimum of 24 weeks, and the follow-up periodgreatly differed. Only a few studies had a follow-upperiod of at least 4 weeks. Since in chronic prostatitisrelapse is the main problem, the follow-up period mustbe sufficiently long in order to state that the patient iscured. The first clinical results with fluoroquinolonesare promising, at least in patients with chronic bacterialprostatitis due to E. coli and other Enterobacteriaceae.The therapeutic role of these drugs, however, needs tobe defined by controlled studies. In order to achievecomparable results an internationally accepted proto-col should be utilized. Such a protocol was propagatedat the 3rd International Symposium on ClinicalEvaluation of Drug Efficacy in UTI w16x.

    Conclusion

    In contrast to acute bacterial prostatitis, the chronicprostatitis syndrome is caused by infection and needsantimicrobial therapy in only a minority of patients. Inthese cases, the fluoroquionolones can be considereddrugs of choice. But controlled clinical studies with asufficient long-term follow-up period are still neededto define the definitive role of antimicrobial therapy.

    References

    1. Collins MM, Stafford RS, OLary MP, Barry MJ. How commonis prostatitis? A national survey of physician visits. J Urol 1998;159: 12241228

    2. Wenninger K, Heiman JR, Rothman I, Berghuis JP, Berger RE.Sickness impact of chronic nonbacterial prostatitis and itscorrelates. J Urol 1996; 155: 965968

    3. Nickel JC. Effective office management of chronic prostatitis.Urol Clin North Am 1998; 25; 677684

    4. Krieger JN, Egan KJ, Ross SO, Jacobs R, Berger RE. Chronicpelvic pains represent the most prominent urological symptomsof chronic prostatitis. Urology 1996; 48: 715722

    5. Drach GW, Fair WR, Meares EM, Stamey TA. Classificationof benign diseases associated with prostatic pain: prostatitis orprostatodynia. J Urol 1978; 120: 266

    6. Meares EM, Stamey TA. Bacteriologic localisation patterns inbacterial prostatitis and urethritis. Invest Urol 1968; 5: 492518

    7. Schaeffer AJ. Prostatitis: US perspective. Int J AntimicrobialAgents 1999: 11; 205211

    8. Domingue GJ, Hellstrom WJG. Prostatitis. Clin Microbiol Rev1998; 11: 604613

    9. Shortliffe L, Elliot JK, Sellers RG. Measurement of urinaryantibodies to crude bacterial antigen in patients with chronicbacterial prostatitis. J Urol 1989; 141: 632636

    10. Kumon H. Detection of local prostatic immune response tobacterial prostatitis. Infection 1992; 20 wSuppl 3x: S236S238

    11. Krieger JN, Riley DE, Robers MC, Berger RE. ProkaryoticDNA sequences in patients with chronic idiopathic prostatitis.J Clin Microbiol 1996; 34: 31203128

    12. Nickel JC, Costerton JW. Bacterial localization inantibiotic-refractory chronic bacterial prostatitis. Prostate1993; 23: 107114

    13. Weidner W, Schiefer HG, Krauss H, Jantos Ch, Friedrich HJ,Altmannsberger M. Chronic prostatitis: A thorough search foretiologically involved microorganisms in 1461 patients. Infection1991; 19 wSuppl 3x: 119125

    Table 1. NIHuNIDDK classification of prostatitis (1995)

    Category I Acute bacterial prostatitisCategory II Chronic bacterial prostatitisCategory III Chronic pelvic pain syndrome (CPPS)

    IIIA CPPS: inflammatoryIIIB CPPS: non-inflammatory

    Category IV Asymptomatic inflammatory prostatitis

    133Prostatitis

  • 14. Bjerklund Johansen TE, Gruneberg RN, Guibert J et al. The roleof antibiotics in the treatment of chronic prostatitis: a consensusstatement. Eur Urol 1998; 34: 457466

    15. Naber KG, Weidner W. Prostatitis, epididymitis and orchitis.In: Armstrong D, Cohen J, eds. Infectious Diseases. Mosby,London, 1999b; 58.158.6

    16. Naber KG, Giamarellou H. Proposed study design in prostatitis.Infection 1994; 22 wSuppl 1x: S59S60

    17. Workshop Committee of the National Institute of Diabetes andDigestive and Kidney Disease (NIDDK). Chronic ProstatitisWorkshop, Bethesda, MD, Dec 78, 1995

    134 K. G. Naber