BENIGN PROSTATIC HYPERPLASIA I: HISTOLOGY
Benign prostatic hyperplasia (BPH) is a benign condition of advancing years affecting one-third of men age 50, more than half of men at age 65, and 80% of men in their ninth decade. It may or may not result in voiding symptoms, generally obstructive in nature. In about 15% of cases, symptoms are sufficiently severe or obstructive uropathy ensues that requires surgical intervention. A clear association between BPH and prostate cancer has not been demonstrated and the former is not considered a risk factor for development of the latter.
The term benign prostatic hyperplasia (often termed hypertrophy)
is currently used to designate a constellation of voiding symptoms that occurs
with age, regardless of prostatic histopathology. These symptoms include
decreased force of stream, hesitancy, straining, incomplete bladder emptying,
and nocturia. Such symptoms are generally referred to as “obstructive” in
nature. Irritative symptoms can also be associated with BPH and include urinary
frequency, urgency, and occasionally dysuria. BPH has been used synonymously
with “prostatism” and “bladder outlet obstruction,” implying that obstruction
to urinary outflow from prostatic enlargement is the etiology. More recently, it
has been recognized that prostatic enlargement is not necessary for such
symptoms. Furthermore, women may experience similar symptoms with age. Thus, lower
urinary tract symptoms is currently the preferred term to describe the
complex of urinary symptoms that occur with age.
Histologically confirmed BPH has a neoplastic character, with nodular
lesions located throughout the transition zone of the prostate that may grow
without limit. These nodules consist of distinct tissue types and do not
represent diffuse hyperplasia or hypertrophy of preexisting prostatic glands. Early
lesions consist of fibromyomas that represent proliferation of smooth muscle and
connective tissue surrounding the ducts of the urethral and submucosal glands.
The fibromyomatous structure is similar to that of uterine myomas (see Plate
8-25), except that prostate nodules usually contain epithelial elements arising
from invasion of epithelial buds from adjacent prostatic ducts. Early nodules
may vary from pure fibromuscular tissue with little or no epithelial component
to adenomas in which epithelial elements are profusely found. The fibromuscular
stroma lacks the elastic tissue present in the normal prostate. The epithelial
elements are composed of hyperplastic columnar cells that form numerous
enfolding papillae and are morphologically similar to those of the normal
prostate, except with reduced secretory activity. The vast majority of nodules
arise in a well- defined area in periductal tissue of the short urethral and
submucosal glands within the transition zone. However, adenomas may also
originate in the fibromuscular stroma surrounding the acini of the central and,
rarely, the anterior zone of the prostate rather than the usual periurethral
site. Hyperplasia is highly unusual in the posterior zone.
As the nodules grow, they compress the normal acini of the peripheral
zone into a thin rim of tissue between the growing hyperplastic nodule and the
prostatic capsule. These compressed “normal” glands, sometimes only 1 mm thick,
comprise the so-called surgical (false) capsule, which is not the same as the
true fibrous capsule that surrounds the entire prostate. On microscopic examination, the ducts and acini of the peripheral zone are flattened and
compressed.
Benign prostatic hyperplasia can adopt a number of different
configurations that result in urinary symptoms. One variety that presents with
the early onset of voiding symptoms is median bar or bladder neck hyperplasia,
which consists of exuberant growth of fibromuscular tissue near the bladder
outlet. The tissue may be more fibrotic than muscular and may contain hyperplastic epithelial elements originating from the suburethral glands
of Albarrán (see Plate 4-2) beneath the bladder outlet. The obstructing median
bar is not palpable on rectal examination but is suspected from obstructive
symptomatology. The diagnosis is confirmed by direct visualization through the
cystoscope. Depending on symptom severity, treatment can begin with daily
alpha-blockers or with t ansurethral endoscopic incision of the bladder neck.
