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Genetic susceptibility of benign prostatic hyperplasia.

Abstract

In an effort to provide new insight into the etiology of benign prostatic hyperplasia (BPH), an evaluation of genetic factors was performed. Recognizing that early age of onset is a marker for hereditary disease, we performed a case-control study of men with early onset of significant BPH. Men in the youngest quartile (less than 64 years old) with a large prostate (greater than 37 gm. resected tissue) who underwent surgery for BPH were identified as case probands from 909 consecutive prostatectomies for BPH. Control probands, selected because of the ability to distinguish treatment for benign prostate disease from treatment for malignant prostate disease, were women whose spouses underwent radical prostatectomy during the same interval. Male relatives of men with early onset of BPH had a 66% cumulative lifetime risk of prostatectomy for BPH, compared to a 17% cumulative risk among control relatives (p = 0.001). A 4-fold increase in age-specific risk of prostatectomy for BPH was present among relatives of men who had undergone prostatectomy for BPH (p = 0.0003), while brothers of these affected cases had a 6-fold increase in risk (p = 0.0089) compared to controls. To determine the likelihood that genetic factors account for this familial aggregation of BPH, segregation analysis was done. Although the small sample size prevented rigorous exclusion of nongenetic models, direct comparison of mendelian and nongenetic models showed that mendelian transmission provided the best overall explanation of the observed familial aggregation. The optimal model suggested mendelian dominant inheritance of a gene associated with early age at onset of BPH. These findings identify family history of BPH as a risk factor for clinical BPH and suggest the presence of a predisposing gene in patients with early onset BPH. Evidence of dominant mendelian transmission of this allele provides a framework for genetic studies to characterize this gene and elucidate the development of BPH in general.

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  • Authors+Show Affiliations

    ,

    Brady Urological Institute, School of Public Health, Baltimore, Maryland.

    , , ,

    Source

    The Journal of urology 152:1 1994 Jul pg 115-9

    MeSH

    Aged
    Case-Control Studies
    Cluster Analysis
    Disease Susceptibility
    Genes, Dominant
    Humans
    Male
    Middle Aged
    Pedigree
    Prostatectomy
    Prostatic Hyperplasia
    Risk Factors

    Pub Type(s)

    Journal Article
    Research Support, U.S. Gov't, P.H.S.

    Language

    eng

    PubMed ID

    7515446

    Citation

    Sanda, M G., et al. "Genetic Susceptibility of Benign Prostatic Hyperplasia." The Journal of Urology, vol. 152, no. 1, 1994, pp. 115-9.
    Sanda MG, Beaty TH, Stutzman RE, et al. Genetic susceptibility of benign prostatic hyperplasia. J Urol. 1994;152(1):115-9.
    Sanda, M. G., Beaty, T. H., Stutzman, R. E., Childs, B., & Walsh, P. C. (1994). Genetic susceptibility of benign prostatic hyperplasia. The Journal of Urology, 152(1), pp. 115-9.
    Sanda MG, et al. Genetic Susceptibility of Benign Prostatic Hyperplasia. J Urol. 1994;152(1):115-9. PubMed PMID: 7515446.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Genetic susceptibility of benign prostatic hyperplasia. AU - Sanda,M G, AU - Beaty,T H, AU - Stutzman,R E, AU - Childs,B, AU - Walsh,P C, PY - 1994/7/1/pubmed PY - 1994/7/1/medline PY - 1994/7/1/entrez SP - 115 EP - 9 JF - The Journal of urology JO - J. Urol. VL - 152 IS - 1 N2 - In an effort to provide new insight into the etiology of benign prostatic hyperplasia (BPH), an evaluation of genetic factors was performed. Recognizing that early age of onset is a marker for hereditary disease, we performed a case-control study of men with early onset of significant BPH. Men in the youngest quartile (less than 64 years old) with a large prostate (greater than 37 gm. resected tissue) who underwent surgery for BPH were identified as case probands from 909 consecutive prostatectomies for BPH. Control probands, selected because of the ability to distinguish treatment for benign prostate disease from treatment for malignant prostate disease, were women whose spouses underwent radical prostatectomy during the same interval. Male relatives of men with early onset of BPH had a 66% cumulative lifetime risk of prostatectomy for BPH, compared to a 17% cumulative risk among control relatives (p = 0.001). A 4-fold increase in age-specific risk of prostatectomy for BPH was present among relatives of men who had undergone prostatectomy for BPH (p = 0.0003), while brothers of these affected cases had a 6-fold increase in risk (p = 0.0089) compared to controls. To determine the likelihood that genetic factors account for this familial aggregation of BPH, segregation analysis was done. Although the small sample size prevented rigorous exclusion of nongenetic models, direct comparison of mendelian and nongenetic models showed that mendelian transmission provided the best overall explanation of the observed familial aggregation. The optimal model suggested mendelian dominant inheritance of a gene associated with early age at onset of BPH. These findings identify family history of BPH as a risk factor for clinical BPH and suggest the presence of a predisposing gene in patients with early onset BPH. Evidence of dominant mendelian transmission of this allele provides a framework for genetic studies to characterize this gene and elucidate the development of BPH in general. SN - 0022-5347 UR - https://www.unboundmedicine.com/medline/citation/7515446/full_citation L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-5347(17)32831-8 DB - PRIME DP - Unbound Medicine ER -