No 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.

Renal leiomyoma is a challenging diagnostic and therapeutic condition. It is clinically similar in presentation and radiographic appearance to its malignant counterpart, leiomyosarcoma. We review 30 cases of clinically diagnosed leiomyoma of the kidney from the literature, including 4 new cases with emphasis on the computerized tomography findings. Computerized tomography may locate a renal leiomyoma serendipitously in an asymptomatic patient. If the lesion is peripheral or in the parapelvic area and a plane can be seen between the tumor and kidney a capsular tumor, such as a leiomyoma of the kidney, might be considered in addition to the more common renal cell carcinoma. Renal leiomyomas have a variable radiographic pattern from that of a pure cystic to a mixed solid/cystic to an entirely solid lesion. Renal leiomyomas usually are sharply demarcated from the surroundings. Although computerized tomography cannot distinguish a renal leiomyoma from other benign or malignant renal processes the presence of invasion can virtually eliminate this benign tumor as a diagnosis. Since a preoperative diagnosis cannot be made, management involves renal exploration and radical nephrectomy in the larger lesions with a renal-sparing operation possible in selected cases. After treatment patients have a uniformly excellent prognosis.