Nodular hyperplasia (the use of the term benign prostatic hyperplasia
is discouraged as hyperplasia by definition is a benign process) is a very
common condition associated with advancing age being uncommon below 40 years
of age but extremely common and increasing in frequency with age after age
50 years. It is seen at autopsy in over 95% of males, 70 years or older but
the prevalence of clinically significant disease (symptomatic nodular hyperplasia)
is much less, in the region of 5 to 10%. The condition is more common in blacks
than in whites.
The cause of nodular hyperplasia is unknown. There is evidence that the disease
is related to an imbalance of estrogen/testosterone/dihydrotestosterone created
by advancing age. Prepubertal castration prevents subsequent development of
nodular hyperplasia. In individuals with 5a
-reductase deficiency, the enzyme that converts testosterone to dihydrotestosterone,
the growth of the prostate is impaired. Administration of 5a
-reductase inhibitors is associated with reduction in size of the gland in
many cases of nodular hyperplasia. There is some experimental evidence in
dogs that estrogens may also play a role in nodular hyperplasia. In aging
men estradiol levels increase and may possibly be involved in the etiopathogenesis
of this disease.
Symptoms of nodular hyperplasia are related to its secondary effects. The
enlarged gland projects into the bladder impeding flow of urine by raising
the internal urethral orifice, compressing and stretching and distorting the
prostatic urethra. In some cases the enlargement involves mainly the median
lobe, which forms a valve-like mechanism at the internal urethral orifice.
As a result, the obstruction of the internal orifice increases as the patient
strains. Patients present with frequency, nocturia, difficulty in initiating
urination and stopping, overflow incontinence, dysuria and acute retention
of urine. The enlargement involves mainly the central submucosal region of
the gland. On cut surface, individual nodules are well defined each surrounded
by a fibrous pseudocapsule. The main peripheral tissue is compressed to form
a thin rim beneath the prostatic capsule. Focal areas of infarction may be
seen in larger nodules.
Nodular hyperplasia.
Microscopically, there is proliferation of epithelial cells of the glands
and ductules, smooth muscle cells and stromal fibroblasts in variable proportions
producing nodules of differing compositions. Glandular hyperplasia takes the
form of small to large to cystically dilated glands, arranged back-to-back
and lined by an inner layer of tall columnar and an outer cuboidal or flattened
cells. Numerous papillary projections and infoldings are present in the glands.
Areas of infarction accompanied by foci of squamous metaplasia of duct epithelium
may be present. Intraglandular and stromal chronic inflammatory cell infiltrates
are common.
Low magnification view of nodular hyperplasia of the prostate showing crowded
glands separated by stroma.
Medium power view showing back-to-back arrangement of glands with papillary
intraglandular projections. Two corpora amylacea are present.
High power magnification. The two-layer epithelium is obvious and there is
a lack of cellular pleomorphism. Nucleoli are indistinct unlike in PIN (see
under neoplasm) where they are prominent.
Low power view of an area of stromal hyperplasia. No glands are present.
High power view of the same area showing bundles of smooth muscle.
Nodular hyperplasia is an entirely benign condition with no relationship
to prostatic adenocarcinoma. Chronic retention of urine leads to distention
and hypertrophy of the urinary bladder and urinary stasis and urinary tract
infection. Prolonged, severe urinary obstruction causes backpressure, hydroureter,
hydronephrosis and ultimately renal failure and death.
