Dr.Joe's Data Base
MALE REPRODUCTIVE SYSTEM
Ed Friedlander, M.D., Chairman, Dept. of Pathology
University of Health Sciences, KC, MO -- Jan. 3, 1995
I used to pray, "Lord, give me chastity,
but not yet." -- St. Augustine, Confessions
While you are away, movie stars are taking
your women. Robert Redford is dating your
girlfriend. Tom Selleck is kissing your
lady. Bart Simpson is making love to your
wife.
-- "Baghdad Betty", Iraqui disk
jockey, during the Gulf War
QUIZBANK Disk 8: Men's problems (all)
HYPOSPADIAS: Abnormal opening of the urethra onto the ventral
surface of the penis or scrotum.
This results from failure of fusion of the urethral folds,
i.e., it is a form of feminization.
Wherever the opening occurs, a fibrous band (chordee) distal
to it will cause ventral curvature of the erect penis.
There is often associated cryptorchidism, ureterovesical
reflux, inguinal hernia, and/or other developmental problems
(J. Postgrad. Med. 37: 140, 1991).
EPISPADIAS: Abnormal opening of the urethra on the dorsal surface
of the penis.
Epispadias is actually a form of exstrophy of the urinary
bladder. There is usually an associated separation of the
pubic bones and inadequacy of the urinary sphincters.
Incontinence and bladder infections are usual. There are
many variants (J. Urol. 141: 903, 1989).
Epispadias is fortunately less common than hypospadias and
more difficult to correct surgically.
PHIMOSIS: Present when the prepuce cannot be retracted over the
corona.
Phimosis may be congenital, the orifice of the prepuce being
too small.
More often, phimosis is due to poor hygiene, resulting in
chronic inflammation and scarring, which sets up a vicious
cycle requiring circumcision.
Such an ongoing infection of the glans and prepuce is
called balanoposthitis. Many organisms may
participate. All about it: Urol. Clin. N.A. 19: 143,
1992. * Jogger's phimosis: Br. J. Ur. 63: 549, 1989.
{24987} balanitis
Paraphimosis results when a tight foreskin is forcibly
retracted, and edema of the glans prevents its replacement.
This can quickly lead to acute urinary retention and even
gangrene of the glans.
PRIAPISM: A persistent, non-pleasurable erection.
* "Priapus" was the classical-era Greek god of erections, but
priapism is no joke.
Most cases of priapism are probably due to obstruction of
the deep dorsal vein of the penis. Typically the corpus
spongiosum is uninvolved (i.e., the urethra and glans stay
limp).
Causes include sickle cell disease (J. Urol. 145: 65, 1991),
leukemia, metastatic cancer, papaverine treatment of
impotence (J. Urol. 142: 1323, 1989), and trauma (J. Urol.
148: 380, 1992); many cases are "idiopathic" (i.e.,
something is causing abnormal thrombosis). See Urology 26:
229 and 233, 1985.
URETHRITIS (dx & rx Med. Clin. N.A. 74: 1543, 1990)
Gonorrhea and "non-gonococcal urethritis" ("urethral
syndrome", due to chlamydia, mycoplasma, trichomonas,
perhaps others), are important sexually-transmitted
diseases.
Reiter's syndrome: the enigmatic triad of (1) arthritis
involving many joints, (2) conjunctivitis, and
(3) urethritis. It's a man's disease and lasts for several
months.
The urethritis is usually (if not always) chlamydia,
and one new study finds chlamydial RNA in the synovium
(Arth. Rheum. 35: 521, 1992); if the initial episode of
urethritis is treated appropriately, Reiter's is much
less likely to ensue (Arth. Rheum. 35: 190, 1992).
As with other "reactive arthropathies", there's an
impressive proliferation of T-cells specific for
chlamydia within the affected joints (Arth. Rheum. 34:
588, 1991).
Most patients are positive for HLA-B27.
* Patients with Reiter's syndrome are likely to have
circinate balanitis, keratoderma blennorrhagica of
soles, ulcers of the mouth, iritis, or even ankylosing
spondylitis ("poker-back").
Before assuring a guy his urethritis "must be due to
chlamydia" (because his gonococcal culture came back
negative), ask whether he eats lots of those little
Mexicanpeppers. The hot chemical in these can and does
cause a urethritis.
PEYRONIE'S DISEASE: Proliferation of dense fibrous tissue
involving a portion of the fascia. This leads to curvature of
erection. * Other names: "painful erection in the wrong
direction", "squint of the cock" (Osler).
This is one of several abnormal hyperplasias of fibrous
tissue which are sometimes called "fibromatoses": another
common one is palmar fibromatosis (Dupuytren's contracture
of the hand) which often occurs with Peyronie's disease.
* Metaplastic ossification and calcification are common
(J. Urol. 127: 52, 1982.)
Treatment for Peyronie's disease is not very satisfactory,
and many patients eventually require a penile prosthesis.
Natural history of Peyronie's: J. Urol. 144: 1376, 1990.
{25287} Peyronie's, histology
WARTS: There are two common "warts" involving the penis:
Condyloma acuminatum ("pointed knob"): a papillary,
keratinizing lesion caused by the sexually-transmitted
"human papilloma virus" (usually strain 6). In males, it
commonly occurs in the urethral meatus, which is a mess.
To spot HPV involvement, wet the man's external
genitalia with acetic acid ("* sheep dip") and involved
areas show white ("acetowhite", as on the uterine
cervix). It's now called "androscopy" (J.F.P. 29(3):
286, 1989). See J. Urol. 143: 920, 1990 for a
discussion on criteria for diagnosing HPV
histologically on biopsies of acetowhite areas. All
about the histopathology of HPV, warts and men: Arch.
Derm. 128: 495, 1992.
We have lots of ways of dealing with these warts,
ranging from electrocautery and lasers to interferon
and fluorouracil (Postgrad. Med. 86: 197, 1989, by my
friend Dr. Ila Peterson). It's important to treat both
partners, since this reduces reinfection.
* Believers in the "immune surveillance" theory of
tumorigenesis, or at least the immunity must be
suppressed locally to get a wart, will note that
Langerhans cells become few where warts grow, and grow
back when the wart is treated with 5-FU (J. Urol. 147:
1268, 1992). Surprised? (Or do you think perhaps the
wart suppresses the Langerhans cells instead?)
{24460} condyloma, gross
{25098} condyloma, histology; note HPV-effect
(shrunken, wrinkled nuclei, perinuclear
halo)
Condyloma latum ("flat knob"): groups of flat-topped lesions
which may ooze serous fluid; caused by secondary syphilis.
Typically occur in skin folds.
CANCER OF THE PENIS: Almost all are variations on squamous cell
carcinoma (histopathology: Urol. Clin. N.A. 19: 227, 1992; review
South. Med. J. 87: 848, 1994).
This is a disease of older men, and it originates on glans
and prepuce.
Only 1% of cancers among American men begin on the
penis; the figure is as high as 18% in the Orient.
Risk factors include phimosis, smegma, and balanoposthitis
(Urology 24: 85, 1984). However, by far the strongest risk
is infection with HPV, notably HPV-16. The other risk
factors seem to create the fertile soil where Nowell's Law
can operate.
Good reading: Cancer of the penis is the second most-
common male cancer, and cancer of the cervix the most
common female cancer, on the island of Bali, where the
men are uncircumcised and unhygienic, and both cancers
are strongly HPV-linked (Cancer 64: 559, 1989).
We now know that the HPV-16 genome metastasizes right
along with the cancer of the penis (Cancer 70: 2143,
1992). Stay tuned for clarification of HPV in the
premalignant lesions of the penis.
Males circumcised as infants almost never get cancer of
the penis. The incidence is much lower in those
circumcised at a later age than among the
uncircumcised.
Carcinoma of the penis spreads to the inguinal lymph nodes.
Five year survival is around 50% overall.
{46450} squamous cancer of the penis
{46451} squamous cancer of the penis, with
inguinal node metastasis
PREMALIGNANT LESIONS OF THE PENIS
Erythroplasia of Queyrat: A raised, velvety plaque on the
uncircumcised glans or prepuce.
Histologic study shows dysplasia of the squamous
epithelium. * Treatment is with topical 5-fluorouracil
(Am. Fam. Phys. 29(4): 186, 1984).
A minority of cases (5-10%) develop into squamous cell
carcinoma if not removed.
{25095} erythroplasia of Queyrat, gross
{25096} erythroplasia of Queyrat, histology
Bowen's disease: Carcinoma in situ of the skin, most often
on the penis or scrotum in men.
Some cases (maybe 10%) develop into invasive squamous
cell carcinoma.
In many cases, the appearance of Bowen's disease on the
skin heralds the growth of another malignancy
internally.
Bowenoid papulosis: Multifocal carcinoma in situ, caused by
HPV-16.
Giant condyloma of Busck‚-Lowenstein, or verrucous
carcinoma: Another HPV-related, very ugly cauliflower-like
lesion. (See Arch. Derm. 126: 1208, 1990; J. Urol. 141:
950, 1989). Invasive cancer can breed here.
{25101} verrucous carcinoma, gross
{25102} verrucous carcinoma, histology
MALE INFERTILITY
Leave the pathology of these problems to specialists. Male
infertility (i.e., she's fertile, and they've been trying
without success for a year) has a variety of causes, known
(Down's, Klinefelter's, old torsion, old mumps,
cryptorchidism, some cases of old age, after radiation,
after some kinds of chemotherapy -- all will give a
"Sertoli-only" histology) and unknown.
Spermatogenesis can be temporarily diminished or even
stopped by a host of factors ranging from heavy
drinking to anabolic steroid abuse to alcoholism to
bicycling.
Obstruction of the sperm passages (can you think of
etiologies?) may be more amenable than the above to surgical
help.
{ 86} testicular atrophy, no sperms
{25154} testicular feminization (no sperms,
hyperplasia of useless Leydig cells,
why?)
* Evaluation of the azoospermic patient, by a friend of your
lecturer: J. Urol. 142: 62, 1989. He's also reviewed
anabolic-steroid induced hypogonadotropic hypogonadism: Am.
J. Sports Med. 18: 429, 1990.
CRYPTORCHIDISM (cryptorchism): Incomplete descent of the testis
into the scrotal sac.
Unilateral or bilateral cryptorchidism occurs in around 4%
of prepubertal boys. Cryptorchid testes may be found
anywhere along the normal route of descent (abdomen,
inguinal canal, prepubic).
The epididymis is likely to be malformed or at least
elongated. See J. Urol. 143: 340, 1990.
Ectopic testis is less common; it may stray into the
superficial inguinal region, penis, or femoral sheath.
Failure of the testes to descend into the scrotum causes
problems:
-- The tubules will undergo atrophy and fibrosis,
beginning in infancy (J. Urol. 128: 782, 1982) and
hopelessly advanced around puberty.
-- There is an increased risk of torsion of the spermatic
cord and gangrene of the testis.
-- The risk of germ cell cancer in undescended testes is
around 30x greater than normal. Review Mayo Clin.
Proc. 66: 372, 1991. The risk is also higher in
previously-undescended testes.
In 1989, 300 brave Danish men who had been treated
for cryptorchidism consented to needle biopsy; 5
had carcinoma in situ and 2 other had already been
treated for testicular cancer (J. Urol. 142: 998,
1989).
Most cryptorchidism is idiopathic. It may be associated
with other developmental abnormalities, diethyl-stilbestrol
exposure (J. Urol. 128: 1332, 1982), and poorly-understood
anatomic and hormonal problems.
EPIDIDYMITIS AND ORCHITIS: Ouch!
Nonspecific infections of the contents of the scrotum are
usually complications of urinary tract infection,
instrumentation (for example, clean-intermittent
catheterization: Eur. Ur. 22: 53, 1992), or prostate
surgery.
Gonorrhea: the infection often spreads to the epididymis,
less often the testis.
{40116} abscess of the epididymis, gonococcal
I'd bet; the tan structure with the
white rim is a cross-section of testis
Mumps: orchitis is common in adolescents and adults. It
usually follows the onset of parotitis by a week or so, and
may cause atrophy of the germinal epithelium and
infertility. The Leydig cells are spared.
Tuberculosis: granulomas involving the epididymis; may
spread to the testis. * BCG epididymitis and orchitis: J.
Urol. 148: 1534, 1992.
{25221} tuberculosis of epididymis
Syphilis: gummas involving the testis; may spread to the
epididymis.
TORSION OF SPERMATIC CORD ("torsion of the testis")
Twisting of the spermatic cord is likely to result in venous
infarction and gangrene in a few hours. This is quite
common, especially in children and adolescents.
The involved testis is painful and elevated; the cord is
typically twisted 540ø.
There may or may not be a history of trauma (often
minor, as in baseball or break dancing; see JAMA 256:
3366, 1984).
The underlying problem may be abnormal fixation of the
testis or cryptorchidism. Ask a urologist about the
"bell clapper" deformity, which supposedly results in
torsion after intermittent episodes of testicular pain
(J. Urol. 148: 134, 1992). Current thinking also
suggests spasm of the cremaster muscle plays a role.
An old infarcted (hyalinized) testis is a common
surprise finding in autopsy series -- suggesting that
the diagnosis of torsion is often missed.
More seriously, unilateral spermatic cord torsion can
somehow damage the opposite testis. Nobody knows how
this happens (J. Urol. 144: 366, 1990); reflex
vasoconstriction?
* Despite everything you've heard about "reperfusion injury
being caused by free radicals", superoxide dismutase
administration before detorsion failed to improve recovery,
at least in rats (J. Urol. 148: 639, 1992).
Torsion of the appendices of the testis and epididymis are
painful but not so serious.
A person can also suffer loss of one testis by catching it
in a hernia. (There's no room here to talk about hernias!)
{10892} torsion, gross
{25208} torsion, gross
{10898} testes: normal vs. "atrophic" (could
have been old torsion, old mumps, or
whatever)
GERM CELL TUMORS (cancer of the testis): Cancer of the germinal
epithelium. These tumors are among the commonest solid tumors of
young men. (Overall incidence is around 2/100,000 men.)
Over 95% of tumors of the testis are malignant germ cell
tumors. All about them (for pathologists): Am. J. Surg.
Path. 17: 1075, 1993.
Current thinking about the histogenesis of cancers of the
testis emphasizes their common origin from germ cells:
--- GERM CELL -------¿
/
/ TOTIPOTENTIAL CELL
Seminoma (40%) <--/
Embryonal Cell Carcinoma (25%)
Extra-Embryonic Embryonic Tissues
Tissues ³ ³
Trophoblast Yolk Sac Three Germ
Layers
³ ³ ³
Choriocarcinoma (2%) Yolk Sac Teratocarcinoma
(25%)
Carcinoma
* Carcinoma in situ can usually be identified in nearby
seminiferous tubules (Arch. Pathol. Lab. Med. 109: 555,
1985 for pictures). Microinvasive carcinoma: Cancer
70: 659, 1992. See below.
All present as painless, non-tender masses in the testis.
The primary may be occult, especially pure
choriocarcinomas.
Many cause gynecomastia (after puberty) or precocious
puberty (children.)
Risk factors for this disease are poorly understood. They
include cryptorchidism and some intersex malformations
(Arch. Path. Lab. Med. 114: 679, 1990). Familial cases:
Mayo Clin. Proc. 65: 804, 1990. * Maternal DES exposure may
be a factor.
Other risk factors are earlier puberty, and lack of
exercise as a kid. Today's boys have both, compared to
us men who are now middle-aged, and this is probably
why cancer of the testis is becoming significantly more
common: Br. Med. J. 308: 1393, 1994.
Seminoma (Cancer 64: 1608, 1989): cancer that closely resembles
young spermatocytes.
Grossly these tumors are homogeneously soft and yellowish.
Tumor cells have "fried egg" appearance; arranged in masses
separated by fibrous septa with a lymphocytic infiltrate,
may have syncytiotrophoblast and/or granuloma formation.
Variant: spermatocytic seminoma of older men has
somewhat different histology, even better prognosis
(i.e., it almost never metastasizes).
Chorionic gonadotropin (hCG) is a tumor marker for the
50% or so of seminomas that contain syncytiotrophoblast
(i.e., the man has a positive pregnancy test). * You
may be told this is a bad prognostic indicator but this
is probably not important (Br. J. Urol. 57: 750, 1985;
J. Urol. 151: 67, 1994).
Seminomas typically metastasize to the retroperitoneal lymph
nodes and then to the lungs.
Seminomas are remarkable for their good response to
radiation or chemotherapy as appropriate, and even
widespread disease can usually be treated with five-year
survivals of 95% or better.
* Two years following complete remission, the patient can
probably consider himself cured. Later recurrence of
seminoma is very unusual; Cancer 52: 1957, 1983.)
Tumors with histology and response to therapy like
testicular seminomas (or other germ cell tumors) also arise
in other midline structures including the retroperitoneum,
thymus, and pineal ("germinomas"), as well as in the ovary
("dysgerminoma").
{25352} seminoma, gross
{25353} seminoma, histology
{ 8863} seminoma, histology
{40217} seminoma, histology
{ 8862} seminoma in situ in the tubular
epithelium
{25355} spermatocytic seminoma, gross
{25173} spermatocytic seminoma, histology
Embryonal cell carcinoma: a very primitive cancer that arises in
the testis.
Grossly these are grayish-white masses with hemorrhage and
necrosis. Microscopically, the tumor cells grow in sheets,
knobs, etc.
{23954} embryonal cell carcinoma, lumen of some
kind and some wilder stuff
{23956} embryonal cell carcinoma; cartilage and
erectile tissue
Many embryonal cell carcinomas also contain
differentiated structures of a teratoma. (Teratoma +
embryonal cell carcinoma = teratocarcinoma).
{25401} teratocarcinoma
{25402} teratocarcinoma
Tumor markers for common mixtures that include embryonal
cell carcinoma include hCG (from trophoblast areas),
alpha-fetoprotein (AFP, from yolk-sac areas), and * lactate
dehydrogenase (LD, LDH).
Tumors with an embryonal cell carcinoma component
metastasize to the retroperitoneum and everywhere else.
Metastases may mature into benign teratomas during
treatment (Cancer 50: 1629, 1982; Cancer 51: 408,
1983). * Whether these are really "benign" is unclear,
since there's aneuploidy, tumor marker production, and
proliferative antigens (J. Urol. 147: 82, 1992). But
they behave as benign tissue.
Or the cured metastases may turn into scar tissue, or
just plain necrotic debris (J. Urol. 142: 1239, 1989).
* Or curative chemotherapy can unmask a lethal sarcoma
component or other cancer (Cancer 54: 1824, 1984).
The response to newer chemotherapy protocols is very good,
with around 85% apparent cures even when metastatic disease
is widespread (Cancer 56: 2411, 1985).
* Most protocols are now based on bleomycin, etoposide,
and cisplatinum. (Formerly vinblastine took the place
of etoposide.)
* Chemotherapy for metastatic disease is so successful
that some oncologists now prefer to monitor patients
after surgery and give chemotherapy only if metastases
appear (J. Urol. 131: 491, 1984; Lancet 1: 8, 1985).
The most infamous after-effect of the traditional
retroperitoneal lymph node dissection is the loss of
the ability to ejaculate (why?); see J. Urol. 142:
1487, 1989 and Cancer 64: 2399, 1989 for psychological
well-being after testicular cancer. (I think I might
just opt for chemotherapy instead, and Mayo's seems to
think this is the right idea... Mayo Clin. Proc. 70:
821 & 911, 1995).
* Again, a two-year disease-free survival probably
indicates cure. For more on chemotherapy and survival,
see Cancer 67: 28, 1991.
Choriocarcinoma:
The bloodiest tumor in pathology; solid areas may be hard to
find.
The malignant cells resemble placenta, and the pathologist
must identify cytotrophoblast and syncytiotrophoblast.
There are no villi.
HCG levels are always very elevated (serum, urine.)
Choriocarcinoma most often is a component in a
teratocarcinoma, but may be pure or mixed with any
other germ cell tumor components.
Until recently, choriocarcinoma arising in the testis was
always lethal.
Today the prognosis is not much worse than for
embryonal cell carcinoma, even if the tumor is "pure
choriocarcinoma" (Cancer 51: 2121, 1983.)
* Yolk sac tumor ("endodermal sinus tumor", "orchioblastoma",
"infantile embryonal cell carcinoma"):
The commonest testicular tumor of children (but still quite
rare), usually occurs "pure" rather than mixed with other
germ cell tumor types.
It is composed of papillary structures (Schiller-Duval
bodies) with extracellular globs of alpha-fetoprotein and
alpha-1-protease inhibitor.
This carcinoma is also unusual because it metastasizes
hematogenously.
Response to chemotherapy is very good (J. Urol. 128: 785,
1982.) * However, differentiation of an adult's embryonal
cell carcinoma toward an endodermal sinus tumor remains an
unfavorable prognostic sign (Cancer 53: 122, 1984; J. Urol
133: 219, 1985).
{25175} yolk sac cancer, gross
{11551} yolk sac cancer, histology
Teratomas:
Cystic teratoma of testis is rare (but common in ovary) and
is mostly composed of skin, hair, sebaceous glands, teeth.
Solid teratomas are of two types:
Mature solid teratoma is benign, usually occurs in
children.
Immature solid teratoma is malignant, usually contains
embryonal cell carcinoma (teratocarcinoma) or sometimes
squamous cell carcinoma.
* Even if an adult's teratoma appears altogether benign,
there is likely to be nearby intratubular carcinoma in
situ (Cancer 64: 715, 1989).
WARNING: Any tumor of germ cell origin may be mixed with any
other tumor of germ cell origin.
Further, any tumor of germ cell origin may metastasize as
another histologic type of germ cell tumor. (Recently a
seminoma turning into a yolk-sac tumor generated some
surprise: Am. J. Clin. Path. 97: 468, 1992).
We now know both in-situ and microinvasive testicular
cancer. See Cancer 70: 659, 1992; Urol. Clin. N.A. 20: 127,
1993; Cancer 64: 715, 1989. A monoclonal antibody that
stains carcinoma in situ: Cancer 65: 1135, 1990.
*Currently, the trend seems to be to remove microinvasive
cancer and radiate in-situ lesions. Detecting aneuploidy in
the ejaculate using a probe for chromosome 1: Am. J. Path.
136: 497, 1990 (want to screen us all, Hilary?)
Lymphoma arises in the testes of older men with some
frequency. Adenomatoid tumor is a benign nubbin derived
from mesothelium.
Germ-cell tumors (seminomas, embryonal cell tumors,
teratocarcinomas, choriocarcinomas, and the usual mixtures)
can and do arise in the retroperitoneum, mediastinum, and
pineal "because they are midline structures" (?!). Their
behavior is similar to testicular tumors. Review Chest 103-
S4: 331-S, 1993.
STROMAL TUMORS
Leydig cell tumors: occur at any age, are usually benign,
can produce precocious puberty or gynecomastia (Am. J. Surg.
Path. 9: 177, 1985).
The gross and microscopic appearances are typical for
endocrine tumors. Sometimes, the pathologist can make
the diagnosis easy by identifying a Reinke crystalloid!
Sertoli cell tumors ("androblastomas"; Urology 25: 1985; Am.
J. Clin. Path. 96: 717, 1991), etc. Animal model Am. J.
Path. 144: 454, 1994.
HYDROCELE: Fluid in the tunica vaginalis. Usually idiopathic, a
hydrocele may contain 100 cc or more of serous fluid.
If ascites is present and the patient has a patent processus
vaginalis, a hydrocele will appear and disappear as the
patient changes position.
You can distinguish a hydrocele from a tumor mass by trans-
illuminating it with a bright flashlight in a dark room.
{24589} hydrocele, gross
Hematocele: Blood in the tunica vaginalis. May follow
trauma (J. Urol. 127: 1195, 1982), or warn of an underlying
testicular cancer.
{25191} hematocele (guy got kicked probably)
VARICOCELE: Varicosities of the pampiniform plexus, usually on
the left side (why?)
This is common in young men, may cause fertility problems by
warming the testes.
A new varicocele in an old man often indicates
occlusion of the vein by renal cell carcinoma,
especially if the veins do not collapse when the
patient lies down.
Spermatocele: a cystic lesion up to 1 cm or so in the area
of the rete testis, filled with fluid and dead sperms.
PROSTATITIS (review: Urology 25: 439, 1985)
Acute and chronic prostatitis are uncomfortable problems,
and are common in men who catch sexually-transmitted
urethritis or lower urinary tract infections.
E. coli is the most common etiologic agent of both
acute and chronic prostatitis.
The diagnosis depends on physical and lab exams.
In acute prostatitis the gland is exquisitely tender.
You should probably not attempt to express fluid!
Gonorrhea is an important cause of acute
prostatitis (secondary to urethritis; remember it
can also cause epididymitis).
{25212} acute prostatitis, gross
{25213} acute prostatitis, histology
In chronic prostatitis the gland is somewhat tender and
the prostatic fluid you express contains WBC's and
grows bacteria.
Treatment is very difficult because of problems
getting antibiotics to the bacteria.
{25214} chronic prostatitis, histology
{25215} chronic prostatitis, histology
In "non-bacterial prostatitis", the findings are as in
chronic prostatitis, but no organisms grow. (Probably
chlamydia cause some of these infections. See J. Urol.
134: 711, 1985; J. Urol. 142: 1006, 1989; dissent J.
Urol. 141: 328 & 332, 1989.) Trichomonas is another
candidate (Am. Fam. Phys. 39: 177, Feb. 1989).
Autoimmunity is yet another: J. Urol. 152: 247, 1994).
"Prostatodynia" is a stress-related pain syndrome in
which there are no WBC's in the prostatic fluid. Other
exacerbating factors include constipation, smoking,
coffee, and spices (all of which make an infected
prostate hurt more, too. See Urology 26: 320, 1985.)
* "Prostatosis" is an old term for both non-bacterial
prostatitis and prostatodynia.
Granulomatous prostatitis may be due to TB (hematogenous
spread from the lungs), "idiopathic" (no TB, no caseation,
no clues as to the etiology) or * exotic (J. Urol. 143: 365,
1990). * The histiocytes may resemble cancer cells.
{23968} granulomatous prostatitis
PROSTATIC HYPERPLASIA ("benign prostatic hypertrophy or
hyperplasia", "BPH"). Review: Disease-a-Month 41: 437, 1995;
Urol. Clin. N.A. May 1995.
This is something that happens to most intact men over about
age 50; 10% of men living to age 80 will need prostate
surgery.
The normal prostate weighs around 20 gm. Old men's
prostates enlarge to 60-200+ gm.
The increased tissue is nodular overgrowth of
periurethral glands and stroma. The hyperplasia most
often involves the lateral and median lobes.
Future pathologists: Look for expanded glands,
often with papillary infoldings, and dense,
stroma. The low-power view proves that the
overall architecture of the gland is preserved.
All about the histopathology: Urol. Clin. N.A. 17:
477, 1990.
The site where the hyperplasia arises ("the
transition zone") is well-characterized (Urol.
Clin. N.A. 17: 477, 1990).
By contrast, "the posterior lobe is the most
common site for the development of prostatic
adenocarcinoma". (* Do you think that this might
simply reflect the fact that cancers here are
easier to detect early?)
Median lobe hyperplasia by itself produces a
"median bar", obstruction without an enlarged
gland. Don't be fooled.
The etiology of prostatic hyperplasia is obscure. It
probably has something to do with sex hormones and their
receptors. Heroic abstinence is also rumored to be a risk
factor.
The most interesting work right now focuses in a nerve-
growth factor-like protein produced by the stromal
cells which causes hyperplasia of both glands and
stroma (J. Urol. 147: 1444, 1992.)
There's now a mouse model -- a transgenic mouse with
its int-2 proto-oncogene (fibroblast growth factor #3)
revved up. It shows the same androgen dependency as do
old men's prostates (J. Urol. 149: 633, 1993).
Prostatic hyperplasia causes many problems (collectively
called "prostatism"), though most patients are asymptomatic.
-- frequency (i.e., only small amounts are voided at a
time), nocturia (urinating at night, same reason),
difficulty starting and stopping urination,
incontinence (dribbling), dysuria (painful urination),
hernias (from straining), acute urinary retention
(emergency)
-- hematuria (due to stretching of veins), bladder
hypertrophy and trabeculation (accentuation of the
normal muscles), bladder diverticula, bladder stones,
hydronephrosis, renal failure
-- Residual urine accumulates in an enlarged bladder
behind the prostate gland. This gets infected, etc.,
etc.
The treatment is surgical -- one favorite procedure is
trans-urethral resection (TURP), or try the new laser
approach (J. Urol. 154: 174, 1995). (I still think I'd opt
for surgery rather than some of the new, cute hormonal
manipulations. When I'm older, maybe I'll change my mind.)
* Hyperthermia: J. Urol. 144: 1390, 1990. How and when to
intervene: Urol. Clin. N.A. 17: 509, 1990. Treatment
guidelines from the Feds: Geriatrics 49: 25, 1994.
{10743} prostate hyperplasia, gross. Don't try
this paper clip trick at home.
{17007} prostate hyperplasia, gross cut surface
{15382} prostate hyperplasia, gross; both gland
and bladder have been opened anteriorly
{18766} prostate hyperplasia, gross
{24445} prostate hyperplasia, gross
{17458} prostate hyperplasia, good median bar
{ 8856} prostate hyperplasia, histology
{17457} prostate hyperplasia, histology
{17197} prostate hyperplasia, histology
{ 8857} prostate hyperplasia, histology
PROSTATE CANCER: Adenocarcinoma of the subcapsular glands. All
about the pathology: Cancer 70(S1): 235, 1992; Cancer 71(S3):
906, 1993 (deja vu); changes after androgen deprivation Cancer
68: 821, 1991; all about the disease Br. Med. J. 308: 780, 1994.
The second commonest cancer in men, and the third leading
cancer killer of men. There are around 132,000 new cases in
the US yearly, and 34,000 deaths (i.e., it's now our most
common men's cancer, but most of these men die of something
else; see Lancet 1: 799, 1989).
This doesn't include latent prostate cancer (i.e., you
found it only at autopsy, and it caused no problems),
and probably not all cases of incidental prostate
cancer (i.e., you found it on the turp chips). Occult
prostate cancer might pop up in bone marrow or lymph
node prior to becoming symptomatic. Nobody knows yet
exactly what to make of prostatic intraepithelial
neoplasia ("carcinoma in situ" or whatever).
Prostate cancer is a disease of men over age 50.
Prostate cancer is rare in Oriental folks in Asia, more
common in Asian-Americans, common in U.S. whites, and
most common in U.S. Blacks.
The majority, but not all, arise in the posterior
lobes.
In classic studies, serial sections of prostates at
autopsy show little adenocarcinomas in 10% or so of US
50-year-old men and nearly 100% of 100-year-old men.
Most are "occult", however. Some more recent studies
suggest that, after a man turns thirty, his percentage
chance of having a little histological cancer is about
the same as his age (J. Urol. 150: 37, 1993). All
about those little microcarcinomas: Cancer 71(S3): 933
& 984, 1993. Grade and volume determine metastatic
potential. Surprised? Of course not. And if the
gland is clinically benign, the rate of metastasis
seems to be extremely low (or maybe even zero, Arch.
Path. Lab. Med. 119: 731, 1995).
Occult prostate cancers are common "incidental"
findings in prostate chips obtained at turp.
* How many turp chips should the pathologist check?
-- All of them (Am. J. Surg. Path. 10: 165,
1986)
-- Twelve grams (Am. J. Surg. Path. 10: 170,
1986)
-- Five blocks (Hum. Path. 17: 285, 1986)
The etiology of prostate cancer is essentially unknown.
Androgens play some role; early castration prevents the
development of adenocarcinoma (* not worth it,
though....)
There is probably no link to infection or prostatic
hyperplasia, or to lack of sexual activity (but see
Urology 28: 159, 1986).
Industrial exposure to cadmium (i.e., battery
factories) is probably linked to increased prostate
cancer. (Everything bad about cadmium: Nature 361:
369, 1993).
* Your lecturer suspects the alleged "link" between
vasectomy and prostate cancer simply reflects the fact
that men who get vasectomies go to the doctor more
often, and get their prostates checked more often.
(See JAMA 269: 913, 1993).
* Molecular signatures remain elusive. There's supposed
to be an anti-oncogene deletion at 16q23.1 (J. Urol.
153: 249, 1995); as you'd expect for an adenocarcinoma,
a few (but by no means all) have activated ras (Cancer
69: 2293, 1992), and when p53 is lost, the cancer turns
mean (J. Urol. 147: 789, 1992). ras product present in
most cases of prostate cancer can be demonstrated on
immunostaining: NEJM 314: 133, 1986. This is not
specific: Arch. Path. Lab. Med. 113: 13 & 16, 1989.
The tumor loses epidermal growth factor receptors as it
develops (J. Urol. 149: 170, 1993). The tumor loses
its androgen sensitivity when (Nowell's law!) the
androgen receptor gene mutates (no surprise, NEJM 332:
1440, 1995).
* There is currently a hoopla over high-fat diet as a
very important risk factor for cancer of the prostate
(Ann. Int. Med. 118: 793, 1993). You remember the same
claim about breast cancer in the 1980's; it didn't hold
up.
* I was more impressed with J. Urol. 154: 153, 1995;
smokers don't have a higher rate of prostate cancer,
but the cancers are higher-grade and meaner.
* A characteristic chromosomal break, del (10)(q24) has
been reported (NEJM 312: 315, 1985). Nowell's law: J.
Urol. 143: 742, 1990; several others.
Cancer of the prostate presents as a painless lump in the
gland.
These tumors are easier to feel than to see; they are
firmer than hyperplastic nodules, poorly circumscribed,
and yellowish.
Diagnosis is by biopsy or fine-needle aspiration. Or
it may turn up in a routine prostatectomy specimen.
(If you're going to operate for obstruction anyway,
there's no reason to biopsy first.)
When given a metastasis from a suspected primary, the
pathologist stains for prostatic acid phosphatase
and/or prostate-specific antigen -- both are highly
sensitive and specific for prostatic origin (Am. J.
Path. 121: 451, 1985; Act. Path. Micr. Imm. Scand. A.
94: 7, 1986; JAMA 253: 3574, 1985; J. Urol. 133: 877,
1985).
Almost all are "prostate type" adenocarcinomas. To diagnose
prostate cancer, you want to see one of the following:
-- prominent nucleoli in large (>3æ) nuclei with
marginated chromatin (best; see Cancer 65: 1017, 1990)
-- invasion (especially perineural invasion; at least loss
of the normal gland-stroma interaction)
-- obvious distortion of the architecture
Beware: As in breast, several benign lesions exist that
are easily mistaken for cancer. Let us pathologists
worry about these. Good reading: Am. J. Clin. Path.
101: 48, 1994.
Grading of prostate cancer is now performed on the Gleason
I-V system, based on low-power H&E pattern of tumor.
Oversimplified Gleason's:
I: Glands with some stroma between
II: Glands that are very crowded
III: Nests / cribriform pattern
IV: You can still tell it's of glandular origin
V: You can't really tell it's of glandular
origin
Grade correlates with stage and prognosis. Most
prostate cancers, even the ones that have metastasized,
are fairly well-differentiated adenocarcinomas.
Tissue prognostic indicators: Am. J. Clin. Path.
100: 256, 1993.
The in-situ lesion (formerly "prostatic dysplasia", now
"prostatic intra-epithelial neoplasia") is now well-
characterized as well (J. Urol. 149: 170, 1993; Am. J.
Cln. Path. 96: 628, 1991). There's always nuclear
enlargement and crowding, there are usually nucleoli
and some piling-up, and the nuclei are more
hyperchromatic as the grade increases. But there is
no invasion or architectural distortion. Low-grade
"PIN" is common in young men (J. Clin. Path. 42: 383,
1989; J. Urol. 150: 379, 1993), and it probably takes
decades to transform.
* Much of the work on this lesion was done by Mayo
pathologist Dave Bostwick; I was his "path
resident" when he was a med student in 1978.
Dave's latest: Mayo Clin. Proc. 70: 395, 1995.
I'm proud of you, Dave!
* Staging of course also affects prognosis.
For the TNM system --
Tx: occult tumor
T1: intracapsular, involves less than « prostate
T2: involves more than « prostate
T3: confined to prostate, but causes prostatic
enlargement
T4: extends beyond prostate
More familiar:
A1: well-differentiated carcinoma on 5 or fewer
turp chips / fewer than 3 foci / fewer than
5% of the chip mass (rules vary).
A2: still occult, but on more than 5 chips or
high-grade
B: palpable nodule
C: through the capsule or in the seminal
vesicles
D: metastases
Uncommon prostate cancers include squamous and
endometrioid (J. Roy. Soc. Med. 85: 394, 1992; Acta
Cytol. 35: 45, 1991).
Cancer of the prostate seldom causes problems (or is
diagnosed) unless it spreads.
Rectal exam is still the most effective method of
diagnosis (cost per life saved a mere $6300; see JAMA
252: 3261, 1984).
For more on "prostate specific antigen", see the
upcoming lecture on cancer screening and monitoring.
Prostate cancer is often indolent even when it has
metastasized, but some prostate cancers are very
aggressive.
You will care for many patients with metastatic prostate
cancer.
Prostate cancer typically metastasizes to the axial
skeleton, eventually causing miserable bone pain.
(Future radiologists: prostatic metastases are often
osteoblastic.)
{17012} prostate cancer in bone, x-ray
Serum acid phosphatase (* tartrate inhibited) is a
classic tumor marker for prostate cancer (see JAMA 253:
665, 1985). The best new tests measure only the
prostatic component.
Patterns of metastatic spread: Cancer 54: 3078, 1984.
Treating prostate cancer:
Surgery and/or radiation are useful for localized
disease. Conventional chemotherapy is of limited
usefulness in prostate cancer, but protocols do exist.
Prostate cancer is usually quite responsive to
endocrine manipulations.
Castration (orchiectomy -- oh no!) and/or estrogen
therapy (causes cardiovascular problems) were for
many years the standard treatments for patients
with symptomatic bony metastases. Now they are
being replaced with newer agents.
One important new agent is leuprolide, a GnRH
(gonadotropin releasing hormone) agonist.
* When large amounts of leuprolide are present
for a while, the pituitary stops making GnRH
receptors and thus stops making
gonadotropins. (Seems paradoxical, doesn't
it?) The patient soon has stopped making
androgens, and the prostate cancer cells
undergo apoptosis.
* The histopathology of leuprolide response is
sufficiently distinctive to be recognizable
by a good pathologist: Cancer 73: 1472, 1994.
Another approach is the non-steroidal
anti-androgen Flutamide, which shrinks prostate
cancer supposedly "without causing impotence".
The anti-fungal agent ketoconazole blocks
synthesis of androgens and has also proved useful
as an anti-prostatic cancer drug.
* Future oncologists: Etidronate is a new drug treatment
for refractory bone pain -- it seems to work by
preventing formation of new bone.
* A recombinant cancer vaccine works for the rat model:
J. Urol. 151: 622, 1994. Deep stuff.
With the focus on early detection, it's worth
remembering that low-grade, low-stage prostate cancer,
treated very conservatively, doesn't seem to shorten
life expectancy (JAMA 274: 626, 1995).
Nowadays, of course, you can follow the course of
treated prostate cancer with serum prostate specific
antigen, the same stuff as you use for screening: Mayo
Clin. Proc. 69: 69, 1994.
{11188} prostate cancer in "turp" chips (tends
to be yellow)
{21031} prostate cancer, gross
{18767} prostate cancer, gross; looks yellowish
{ 3236} hydroureter in prostate cancer
{ 8865} well-differentiated prostate cancer
{23979} well-differentiated prostate cancer,
Gleason 2
{ 8866} prostate cancer, cribriform, Gleason 3
{ 8864} prostate cancer, Gleason 3
{23980} well-differentiated prostate cancer,
Gleason 4-5
{23975} atrophy of the prostate, as, after
removal of androgens
{23969} irradiated prostate; note radiation
changes in vessel to right of center
* We've already cited the work of the Hopkins group, which (as
in AIDS, renal disease, and coronary disease) found that
black men with prostate cancer get worse care and do worse
than their matched white counterparts. It turns out that
another group (NCI, not Hopkins) found that if the same
doctors treat both groups, the racial difference vanishes
(JAMA 274: 1599, 1995; "I told you so....")
A FEW ADDITIONAL IDEAS:
Despite "conventional wisdom", impotence is often organic,
even in younger men without obvious disease. Ask the guy if he
gets erections out of bed, or try the famous low-tech "postage-
stamp coil" test. Even tiny prolactinomas are notorious anti-
aphrodisiacs. See JAMA 249: 1736, 1983. Injection therapy
(phentolamine, prostaglandin E1, papaverine) for the guy to use
when he wants an erection: Arch. Phys. Med. Rehab. 75: 276, 1994.
Blunt trauma to the shaft during masturbation or intercourse can
crack the side of the dorsal vein, allowing blood to drain in
easily and causing impotence. How to fix it: J. Urol. 148: 1171,
1992.
For premature ejaculation, if the guy doesn't get good
results from the squeeze technique (which is fun), try
clomipramine or paroxetine (Am. J. Psych. 151: 1377, 1994; dudes:
these'll improve an anal-retentive outlook on life, too). Some
men cannot ejaculate; for the electronic gadget that helps, see
J. Urol. 152: 1034, 1994. Retrograde ejaculation results from
failure of one of those little bands of muscle to relax; think of
thioridazine therapy, or an anatomic cause (J. Urol. 151: 1017,
1994).
* Very rapid overfilling of the prostate and seminal vesicles
(i.e., prolonged arousal in a young male) results in pain
referred to the testes which can be severe ("blue balls",
"lovers' nuts", etc.) The cure is ejaculation by any means.
Your instructor suspects the mechanism is pressure of the seminal
vesicles on the genitofemoral nerves.
* Hey dudes! Are we being un-masculinized by rampant estrogen
pollution (diethylstilbestrol cattle-fattener, women's oral
contraceptive pill components excreted unchanged, other
substances)? In a widely-publicized paper, researchers presented
evidence that the average sperm count has declined by half over
the 1900's (Lancet 341: 1392, 1993, totally unconvincing graph
Science 265: 308, 1994). There is exactly no evidence that male
infertility is increasing: NEJM 332: 327, 1995. And if un-
masculinization were really at work, your lecturer believes we
modern men would have less body hair, less baldness, less B.O.,
and less belligerence. Nuh-uh! Your lecturer thinks that
modern-day dudes simply ejaculate more often (figure out "why?"
yourself, Doc) and therefore resorb less fluid between
ejaculations, concentrating the sperms less. The authors of the
paper apparently didn't think of this; and the NEJM article above
thought that "duration of abstinence" was probably the
explanation too. Since this paper, there has been a silly media
hype and even sillier discussion on the floor of the U.S. senate.
* Some men have had accidents. See J. Emerg. Med. 8: 305,
1990 (caught in the zipper), Acta. Urol. Jap. 34: 514, 1988
abstract 88267069 (caught in a milk bottle for seventeen hours),
J. Urol. 147: 1265, 1992 (all about bites), J. Urol. 133: 1046,
1985 (etiology of "sclerosing lipogranuloma", you would enjoy
reading this one), Plast. Rec. Surg. 91: 352, 1993 (review of
sclerosing granuloma, with a case study of a guy who injected
himself with transmission oil in the hopes of having a permanent
erection; bad idea, fellow) J. Urol. 134: 274, 1985 (fractures),
Urology 24: 18, 1984 (rings), Plast. Rec. Surg. 87: 771, 1991
(electrical injury), J. Emerg. Med. 8: 419, 1990 (young
skateboarder impales scrotum on a metal rod), Br. Med. J. 281:
26, 1980; Br. Med. J. 281: 591, 1980; JAMA 224: 630, 1973;
Urology 25: 41, 1985 & Indiana Med. 81: 252, 1988 (vacuum
cleaners; there are several other articles on the same subject),
Urology 26: 12, 1985 (foreign bodies), Urology 26: 50, 1985 (pet
rattlesnake), Urology 26: 81, 1985 (necklace), Am. J. For. Med.
Path. 7: 254, 1986 ("Eddie Spaghetti"), Genit. Med. 68: 334, 1992
(penicillin bottle under an enormous foreskin), electric cable,
paper clip, tweezers, etc., (Br. J. Urol. 68: 510, 1991), Int.
Ur. Neph. 25: 77, 1993 (uses high-tech term "SFB" for self-
inserted foreign body), guy self-injecting olive oil into his
scrotum to make it bigger gets fat embolus (Chest 107: 875,
1995), romantic love between a man and his hydraulic tractor ends
in death (J. For. Sci. 38: 359, 1993), Med. Asp. Hum. Sex. July
1991 (guy in love with a sander belt loses a testis and repairs
himself on-the-job with his handy staple gun). "Alcock syndrome"
is insensitivity of the penis (lasting up to several weeks)
resulting from pressure on the pudendal nerve (which runs through
"Alcock's canal") during bicycling. A "cultural practice" in
some Asian communities is attempting suicide by cutting off the
penis and bleeding to death (Am. J. Psych. 150: 350, 1993). Less
amusing: In past wars, when a captured man was being tortured
either for information or fun, mutilating the genitals was
commonplace. This was fairly common as recently as the Vietnam
era, and surfaced again in Bosnia. Stay tuned. Sexual torture:
Lancet 345: 1307, 1995. Injury to the vas deferens from torture:
Br. J. Urol. 72: 515, 1993. Reconstructing a youngster's penis
using microsurgery, so that it works: J. Urol. 149: 1521, 1993.
A grown-up's amputated penis is re-attached and still works: J.
Urol. 147: 1628, 1992. Another Arch. Sex. Behav. 19: 343, 1990.
We await publication of the full details of John Wayne B....
* A penis which, when stretched to its maximum flaccid length
(which is pretty much the same as its fully-erect length), is
shorter than 2« SD below the mean for the guy's age is an
official "micropenis". For a grown man:
11 cm 10th percentile
13 cm 50th percentile
15« cm 90th percentile.
Among a group of men 4-10 cm, the consensus was, indeed, that
"it's not what you've got, it's what you do with it." (Not
stated in exactly these terms, of course, and partners were not
surveyed by the tactful researchers; see J. Urol. 142: 569,
1989). The cause is probably androgenic deprivation for some
reason during embryogenesis (Arch. Dis. Child. 66: 1033, 1991).
* Agenesis of the penis: J. Urol. 143: 338, 1990. Two of
them (diphallus): J. Urol. 142: 356, 1989.
* Your lecturer predicts male circumcision will remain popular
for newborns (though the current fad in pediatrics is to oppose
it), as well as a popular choice for older people. Circumcision
in infancy prevents cancer of the penis quite effectively, and it
seems to greatly reduce urinary tract infections in little boys
(Pediatrics 83: 1011, 1989; good review). Hygiene is much
easier, the risk of catching AIDS from a woman during normal
lovemaking is much less (NEJM 319: 274, 1988, Lancet 2: 403,
1989, Urol. Clin. N.A. 22: 57, 1995), and what's more, many
people like it. Opponents cite "unnatural", "a male's right to
make the decisions affecting his own body", "religious freedom",
"problems of the uncircumcised are treatable" (except HIV and
gangrene, of course; the latter can happen to an unwashed little
boy). The best decision isn't "clear-cut" (ha-ha). Ask about an
anesthetic, even for a baby.
* Squamous metaplasia in prostate epithelium occurs at the
edges of infarcts, or in men treated with estrogens.
* Men with endometriosis (I always believed in the coelomic
metaplasia theory rather than the reverse menstruation theory,
anyway): Eur. J. Surg. 158: 7, 1992; Am. J. Ob. Gyn. 165: 214,
1991, others.
* When we get old, we men will probably get hormone
replacement, just as many women do. This is probably a good idea
(NEJM 334: 707, 1996).
The British found no link between vasectomy and testicular
cancer, prostate cancer, or any other of the common diseases for
which they sought a connection: Br. Med. J. 304: 743, 1992.
Surprised? Of course not. Full of disclaimers about
insufficient duration, insufficient patient numbers, etc.
* Among adults, only fools and ideologues haven't figured out
that sexual behavior (broadly defined) has many purposes (good,
bad, indifferent) in addition to fertilization. As far as I
know, all durable societies have decided that a stable, lifelong,
committed, faithful relationship is the best setting for sex
(pseudo-anthropologist Margaret "Cultural Relativism" Mead was,
of course, the victim of a hoax by some teenagers.) People think
about sex a lot, and we know that making it a taboo subject or a
big dreadful mystery is asking for trouble. The wise adult
learns that setting limits is the key, and decides what limits to
set. Not everyone does this. Further, it is easier (and better
power-politics) to get up on a soap-box about sex than to try to
understand it. As a physician you must at least do the latter.
Male sexuality becomes a major concern for the pathologist when
it leads to death (i.e., homicide, in which sex is usually a
factor, suicide, in which sex is often a factor, and autoerotic
asphyxia, which is not rare) or when it involves someone who does
not, or cannot, consent. Almost every man realizes that to force
himself on another person (employee, family member, date,
stranger, child) is shameful, wrong, disgusting, and un-
masculine. Most men also feel entitled to "get their loving",
and for many men, self-esteem gets tied up with "getting it".
Most bright men figure out early that self-control, though
difficult, is muy macho. For some men, controlling the urge to
act-out sexually (which can take various forms, some of them
harmful for other people) is as hard as sticking to a weight-
reduction diet (see especially Psych. Clin. N.A. 15: 675, 1992).
Probably these men have a wiring problem, whatever else may have
gone wrong, and a psychiatrist can help (swallow your pride,
dude; major review Psych. Clin. N.A. 15: 703, 1992; clomipramine
fixes up a compulsive flasher Am. J. Psych. 149: 843, 1992;
fluoxetine cures a Peeping Tom: Am. J. Psych. 148: 950, 1991;
there's behavioral, insight, and pharmacological ways of helping
most problem guys, if they want to be helped, and for criminal-
justice cases, there's now stuff that works better than
saltpeter). Perhaps the most interesting article on male
sexuality that your lecturer has ever seen was a prison survey in
which 23% of prisoners admitted to having been forcibly raped by
a male bully, and those who could tell the interviewer about this
without becoming visibly and acutely upset were almost all sex
offenders. The conclusion is that at least a good number of sex
offenders come to terms with what's happened to them by acting
out "in a strange and cruel way" (Med. and Law 12: 181, 1993).
There's gotta be a better way of making sense of what's happened
to you; perhaps a family physician, talking sense and explaining
"you're still a man", etc., etc. could have made all the
difference. Your lecturer finds a Don Juan as baffling as a
gourmet, and a man with a pornography obsession as puzzling as
the "Food" section of the Kansas City Star. It is also very hard
for a man to defend against a false accusation of rape (in spite
of what you've been told by "women's advocates", this is all-too-
common; ask a cop, or stay tuned for the next few lectures), and
the forensic pathologist can make all the difference here. If
you are accused of rape or child molestation, dude, you can now
have your penis hooked up to a pressure sensor, get read dirty
stories and shown dirty pictures, and your erectile responses
used as evidence against you in a court of law ("phallometry"); I
am disturbed by the gross lack of scientific controls on this
kind of work (not to mention a certain misandrism; J. Con. Clin.
Psych. 58: 886, 1990; Arch. Sex. Behav. 20: 75, 1991; lots of
things are turn-ons for lots of dudes, even us well-behaved ones:
Arch. Sex. Behav. 20: 137, 1991. The right-wing-and-left-wing
stereotype of "the evil male criminal perpetrator and the
innocent female victim", while it sometimes corresponds to
reality, has placed the 1990's male at a grave disadvantage
before the law. You can cite your own examples. One way to
protect yourself is obtain specific and verbal permission prior
to each step of the lovemaking process (that's gentlemanly and
fun); however, she may still lie afterwards and claim you raped
her (permanently traumatized her emotionally, etc.) anyway.
Better not even to talk to a woman until you're sure she isn't
nuts, and absolutely never be alone with her. Contrary to the
media emphasis, moms are probably just as likely as
dads/boyfriends to physically and emotionally abuse children (go
get your own statistics; in the current political climate,
nobody's going to address this). Speaking of "links", in the one
recent massive study comparing normal men, rapists, and child
molesters, "frequency of adult use of sexually explicit material
does not differ significantly among groups". Nor did the
frequency of sex crimes increase in Sweden when they made the
even the most disgusting pornography as available as alcohol and
tobacco. See J. Sex. Marit. Ther. 19: 77, 1993. I'd like an
easy scapegoat, too, Mr. Bundy, but the roots of evil go much,
much deeper. The paraphilias: Psych. Clin. N.A. 15: 675, 1992.
"A review of sexual behavior in the United States": Am. J. Psych.
151: 330, 1994.
Retarded guy with large testes: Fragile X!
* One of the silliest quack theories of disease, which
persisted from ancient times up until the middle of this century,
was that masturbation (male, female) was a major risk factor for
everything. Pathologists and serious clinicians never believed
this nonsense, and it was primarily a political-churchy thing.
It would be difficult to find a control group. See Am. J.
Psychoth. 45: 9, 1991; Arch. Neurol. 51: 600, 1994.
Scrotal squamous cell carcinoma is the subject of the famous
chimney sweep story. Fournier's gangrene is a bacterial
infection that produces the dreaded "black sack" (no joke). Many
older men get a few angiokeratomas, especially on their scrotums,
and this doesn't mean Fabry's.
{ 9753} scabies
{11550} syphilis
{25537} chancre and gonorrhea both
{12598} lichen planus
{12600} lichen planus
{24988} lichen planus
{14133} herpes simplex
{14238} candida
{23958} epidermoid cyst of the testis
* {24988} lichen sclerosus
* {12188} lichen sclerosus
* {12189} balanitis xerotica
* {25049} balanitis xerotica, histology
{25116} Fabry's angiokeratomas
{25196} sperm granuloma after a vasectomy
*When I was one-and-twenty
I heard a wise man say,
"Give crowns and pounds and guineas
But not your heart away;
Give pearls away and rubies
But keep your fancy free."
But I was one-and-twenty,
No use to talk to me.
When I was one-and-twenty
I heard him say again,
"The heart out of the bosom
Was never given in vain;
'Tis paid with sighs a-plenty,
And sold for endless rue."
And I am two-and-twenty,
And oh, 'tis true, 'tis true.
-- A.E. Housman,
"A Shropshire Lad"
*When I was one-and-twenty,
My ills were in their prime,
With aches and pains aplenty,
And gout before my time;
I had the pyorrhea,
And fever turned me blue--
They said that I would be a
Dead man at twenty-two.
Now I am two-and-twenty,
The aches and pains I thought
Were miseries a-plenty,
Compared to these, are naught;
And even these are bubbles,
That scarce can worry me,
When I regard the troubles
I'll have at twenty-three.
-- Samuel Hoffenstein,
"The Shropshire Lad's Cousin"