PDF herunterladen
CC BY-NC-ND 4.0 · Deutsche Zeitschrift für Onkologie 2019; 51(02): 74-80
DOI: 10.1055/a-0865-8464
Forschung
Eigentümer und Copyright ©Georg Thieme Verlag KG 2019

Der kausale Zusammenhang von Prostata-Hyperplasie, chronischer Prostatitis und Prostatakrebs

The Causal Relationship between Prostatic Hyperplasia, Chronic Prostatitis and Prostate Cancer
Ludwig Manfred Jacob
Weitere Informationen

Publikationsverlauf

Publikationsdatum:
24. Juni 2019 (online)

   Lizenzen und Reprints

Zusammenfassung

Die häufigsten Erkrankungen der Prostata sind Prostatitis, die benigne Prostata-Hyperplasie (BPH) und das Prostatakarzinom (PCa). Die westliche Ernährungs- und Lebensweise führt typischerweise zu einer Vermehrung von Bauchfett, erhöhten Spiegeln von Cholesterin, Östrogenen und Dihydrotestosteron (DHT) sowie Insulin und IGF-1, welche die Entwicklung von ProstataHyperplasie und -krebs fördern. Die vergrößerte Prostata begünstigt die Entwicklung einer chronischen Prostatitis, indem sie zu Urinrückfluss in die Prostata führt. Dies wirkt sich in der peripheren Zone der Prostata am schlimmsten aus, da sie ein schlechtes Ablaufsystem hat. Der proinflammatorischste Stoff im Urin ist kristalline Harnsäure, die sich bei pH 5,5 bildet. So sauer ist bei der heute typischen säurebildenden Ernährung häufig der Morgenurin, der insbesondere nachts (Nykturie) in die Prostata gelangt. Auch die Aktivität der 5-alpha-Reduktase ist bei saurem pH stark erhöht und prokanzerogenes DHT wird verstärkt gebildet. Die chronische Prostatitis fördert insbesondere durch den dauerhaft erhöhten oxidativen und nitrosativen Stress die Entstehung eines Prostatakarzinoms in der Randzone. Klassische Kanzerogene im Urin und im Enddarm verstärken den Prozess. Epidemiologisch passt dazu, dass die typischen „Säureerkrankungen“ Gicht und Nierensteine mit einem stark erhöhten Prostatakrebsrisiko einhergehen, während pflanzliche, basenbildende Ernährungsweisen das Risiko deutlich reduzieren und in klinischen Studien sogar bestehende Karzinome hemmen.

Abstract

The most common prostate diseases are prostatitis, benign prostatic hyperplasia (BPH) and prostate cancer (PCa). Western diets and lifestyles typically lead to an increase in abdominal fat, elevated levels of cholesterol, estrogens and dihydrotestosterone (DHT), as well as insulin and IGF-1, which promote the development of prostatic hyperplasia and cancer. The enlarged prostate favors the development of chronic prostatitis by causing intraprostatic reflux. This has the worst effect in the peripheral area of the prostate, as it has a poor drainage system. The most proinflammatory substance in urine is crystalline uric acid, which forms at pH 5.5. Eating the typical acid-forming diet of today, mens’ morning urine, which enters the prostate during the night (nycturia), is this acidic. The activity of 5-alpha reductase is also greatly increased at an acidic pH and more procarcinogenic DHT is formed. Chronic prostatitis promotes the development of prostate carcinoma in the peripheral zone, in particular due to the permanently increased oxidative and nitrosative stress. Classical carcinogens in the urine and rectum intensify this process. From an epidemiological point of view, the typical “acid diseases” gout and kidney stones are associated with a strongly increased risk of prostate cancer, while plant-based, alkaline diets significantly reduce the risk and even inhibit existing carcinomas in clinical studies.

Schlüsselwörter

Prostatakrebs - Hyperplasie - BPH - Prostatitis - intraprostatischer Reflux - pH - Harnsäure - Säure-Basen-Haushalt - Ernährung - 5-alpha-Reduktase - Haarverlust - DHT - Matrix-Metalloproteinasen

Key words

Prostate cancer - hyperplasia - BPH - prostatitis - reflux - pH - uric acid - acid-base balance - diet - nutrition - 5-alpha reductase - DHT - hair loss - MMP
 

  • Literatur

  • 1 Albini A, Sporn MB. The tumour microenvironment as a target for chemoprevention. Nat Rev Cancer 2007; 7: 139-147
    CrossrefPubMedGoogle Scholar
  • 2 Alcaraz A, Hammerer P, Tubaro A. et al. Is there evidence of a relationship between benign prostatic hyperplasia and prostate cancer? Findings of a literature review. Eur Urol 2009; 55: 864-873
    CrossrefPubMedGoogle Scholar
  • 3 Bell KJ, Del Mar C, Wright G. et al. Prevalence of incidental prostate cancer: A systematic review of autopsy studies. Int J Cancer 2015; 137: 1749-1757
    CrossrefPubMedGoogle Scholar
  • 4 Bostwick DG, Burke HB, Djakiew D. et al. Human prostate cancer risk factors. Cancer 2004; 101 (10 Suppl.): 2371-2490
    CrossrefPubMedGoogle Scholar
  • 5 Bostwick DG, Cooner WH, Denis L. et al. The association of benign prostatic hyperplasia and cancer of the prostate. Cancer 1992; 70 (1 Suppl.): 291-301
    CrossrefPubMedGoogle Scholar
  • 6 Chen CJ, Yen JH, Chang SJ. Gout patients have an increased risk of developing most cancers, especially urological cancers. Scand J Rheumatol 2014; 43: 385-390
    CrossrefPubMedGoogle Scholar
  • 7 Chung SD, Liu SP, Lin HC. Association between prostate cancer and urinary calculi: a population-based study. PLoS One 2013; 8: e57743
    CrossrefPubMedGoogle Scholar
  • 8 De Marzo AM, Meeker AK, Zha S. et al. Human prostate cancer precursors and pathobiology. Urology 2003; 62 (5 Suppl. 1): 55-62
    PubMedGoogle Scholar
  • 9 De Marzo AM, Platz EA, Sutcliffe S. et al. Inflammation in prostate carcinogenesis. Nat Rev Cancer 2007; 7: 256-269
    CrossrefPubMedGoogle Scholar
  • 10 Eaton NE, Reeves GK, Appleby PN, Key TJ. Endogenous sex hormones and prostate cancer: a quantitative review of prospective studies. Br J Cancer 1999; 80: 930-934
    CrossrefPubMedGoogle Scholar
  • 11 Egeblad M, Werb Z. New functions for the matrix metalloproteinases in cancer progression. Nat Rev Cancer 2002; 2: 161-174
    CrossrefPubMedGoogle Scholar
  • 12 Elkahwaji JE. The role of inflammatory mediators in the development of prostatic hyperplasia and prostate cancer. Res Rep Urol 2012; 5: 1-10
    PubMedGoogle Scholar
  • 13 Frattaroli J, Weidner G, Dnistrian AM. et al. Clinical events in prostate cancer lifestyle trial: Results from two years of follow-up. Urology 2008; 72: 1319-1323
    CrossrefPubMedGoogle Scholar
  • 14 Gu F. Epidemiological survey of benign prostatic hyperplasia and prostatic cancer in China. Chin Med J (Engl) 2000; 113: 299-302
    PubMedGoogle Scholar
  • 15 Guess HA. Benign prostatic hyperplasia and prostate cancer. Epidemiol Rev 2001; 23: 152-158
    CrossrefPubMedGoogle Scholar
  • 16 He H, Xie B, Xie L. Male pattern baldness and incidence of prostate cancer: A systematic review and meta-analysis. Medicine (Baltimore) 2018; 97 (28) e11379
    PubMedGoogle Scholar
  • 17 Isaacs JT. Prostatic structure and function in relation to the etiology of prostatic cancer. Prostate 1983; 4: 351-366
    CrossrefPubMedGoogle Scholar
  • 18 Jacob LM. Der Prostatakrebs-Kompass – Prävention und komplementäre Therapie mit der richtigen Ernährungs- und Lebensweise. Heidesheim am Rhein: Nutricamedia 2014
    PubMed
  • 19 Johnson LL, Pavlovsky AG, Johnson AR. et al. A rationalization of the acidic pH dependence for stromelysin-1 (Matrix metalloproteinase-3) catalysis and inhibition. J Biol Chem 2000; 275: 11026-11033
    CrossrefPubMedGoogle Scholar
  • 20 Kato Y, Lambert CA, Colige AC. et al. Acidic extracellular pH induces matrix metalloproteinase-9 expression in mouse metastatic melanoma cells through the phospholipase D-mitogen-activated protein kinase signaling. J Biol Chem 2005; 280: 10938-10944
    CrossrefPubMedGoogle Scholar
  • 21 Kirby RS, Lowe D, Bultitude MI, Shuttleworth KE. Intra-prostatic urinary reflux: An aetiological factor in abacterial prostatitis. Br J Urol 1982; 54: 729-731
    CrossrefPubMedGoogle Scholar
  • 22 Martillo MA, Nazzal L, Crittenden DB. The crystallization of monosodium urate. Curr Rheumatol Rep 2014; 16: 400
    CrossrefPubMedGoogle Scholar
  • 23 McNeal JE, Redwine EA, Freiha FS, Stamey TA. Zonal distribution of prostatic adenocarcinoma. Correlation with histologic pattern and direction of spread. Am J Surg Pathol 1988; 12: 897-906
    CrossrefPubMedGoogle Scholar
  • 24 McVary KT. BPH: Epidemiology and comorbidities. Am J Manag Care 2006; 12 (5 Suppl.): S122-128
    PubMedGoogle Scholar
  • 25 Max Rubner-Institut. Nationale Verzehrsstudie II. Ergebnisbericht Teil 2. Die bundesweite Befragung zur Ernährung von Jugendlichen und Erwachsenen. 2008. https://www.bmel.de/SharedDocs/Downloads/Ernaehrung/NVS_ErgebnisberichtTeil2.pdf?__blob=publicationFile (abgerufen am 21.02.2018)
    PubMed
  • 26 Max Rubner-Institut. Kochsalzzufuhr der deutschen Bevölkerung. Max Rubner-Institut präsentiert aktuelle Zahlen. Pressemitteilung des Max Rubner-Instituts vom 26.03.2013
    PubMed
  • 27 Nelson WG, De Marzo AM, DeWeese TL, Isaacs WB. The role of inflammation in the pathogenesis of prostate cancer. J Urol 2004; 172 (5 Pt 2): S6–11; discussion S11-12
    PubMedGoogle Scholar
  • 28 Nickel JC. Inflammation and benign prostatic hyperplasia. Urol Clin North Am 2008; 35: 109-115; vii
    CrossrefPubMedGoogle Scholar
  • 29 Ornish D, Magbanua MJ, Weidner G. et al. Changes in prostate gene expression in men undergoing an intensive nutrition and lifestyle intervention. Proc Natl Acad Sci U S A 2008; 105: 8369-8374
    CrossrefPubMedGoogle Scholar
  • 30 Palapattu GS, Sutcliffe S, Bastian PJ, Platz EA. et al. Prostate carcinogenesis and inflammation: emerging insights. Carcinogenesis 2005; 26: 1170-1181
    CrossrefPubMedGoogle Scholar
  • 31 Pejler G, Hu Frisk JM, Sjostrom D. et al. Acidic pH is essential for maintaining mast cell secretory granule homeostasis. Cell Death Dis 2017; 8 (05) e2785
    CrossrefPubMedGoogle Scholar
  • 32 Pontari MA. Etiology of chronic prostatitis/chronic pelvic pain syndrome: psychoimmunoneurendocrine dysfunction (PINE syndrome) or just a really bad infection?. World J Urol 2013; 31: 725-732
    CrossrefPubMedGoogle Scholar
  • 33 Remer T, Manz F. Paleolithic diet, sweet potato eaters, and potential renal acid load. Am J Clin Nutr 2003; 78: 802-803 author reply 803–804
    CrossrefPubMedGoogle Scholar
  • 34 Rizzo NS, Jaceldo-Siegl K, Sabate J, Fraser GE. Nutrient profiles of vegetarian and nonvegetarian dietary patterns. J Acad Nutr Diet 2013; 113: 1610-1619
    CrossrefPubMedGoogle Scholar
  • 35 Ross RK, Bernstein L, Lobo RA, Shimizu H. et al. 5-alpha-reductase activity and risk of prostate cancer among Japanese and US white and black males. Lancet 1992; 339 (8798): 887-889
    CrossrefPubMedGoogle Scholar
  • 36 Sfanos K, Wilson B, De Marzo A, Isaacs W. Acute inflammatory proteins constitute the organic matrix of prostatic corpora amylacea and calculi in men with prostate cancer. Proc Natl Acad Sci U S A 2009; 106: 3443-3448
    CrossrefPubMedGoogle Scholar
  • 37 Suzuki M, Willcox B, Willcox C. The Okinawa Centenarian Study 2012. http://www.okicent.org/study.html (abgerufen am 25.05.2012)
    PubMed
  • 38 Tantamango-Bartley Y, Knutsen SF, Knutsen R. et al. Are strict vegetarians protected against prostate cancer?. Am J Clin Nutr 2016; 103: 153-160
    CrossrefPubMedGoogle Scholar
  • 39 van Doren SR. Matrix metalloproteinase interactions with collagen and elastin. Matrix Biol 2015; 44–46: 224-231
    PubMedGoogle Scholar
  • 40 Wang W, Xu D, Wang B et al. Increased risk of cancer in relation to gout: A review of three prospective cohort studies with 50,358 subjects. Mediators Inflamm 2015; 2015: 680853
    PubMed
  • 41 Willcox BJ, Willcox DC, Todoriki H. et al. Caloric restriction, the traditional Okinawan diet, and healthy aging: The diet of the world’s longest-lived people and its potential impact on morbidity and life span. Ann N Y Acad Sci 2007; 1114: 434-455
    CrossrefPubMedGoogle Scholar
  • 42 Willcox DC, Willcox BJ, Wang NC. et al. Life at the extreme limit: Phenotypic characteristics of supercentenarians in Okinawa. J Gerontol A Biol Sci Med Sci 2008; 63: 1201-1208
    CrossrefPubMedGoogle Scholar
  • 43 Zhou CK, Levine PH, Cleary SD. et al. Male pattern baldness in relation to prostate cancer-specific mortality: A prospective analysis in the NHANES I epidemiologic follow-up study. Am J Epidemiol 2016; 183: 210-217
    CrossrefPubMedGoogle Scholar
  • 44 Zhou CK, Pfeiffer RM, Cleary SD. et al. Relationship between male pattern baldness and the risk of aggressive prostate cancer: An analysis of the prostate, lung, colorectal, and ovarian cancer screening trial. J Clin Oncol 2015; 33: 419-425
    PubMedGoogle Scholar