Transcript P. acnes - Red Sulfur

SEBACEOUS GLANDS
DISORDERS
Prof
IHAB YOUNIS
SEBACEOUS GLANDS
• Found on all areas of the skin except for the
palms, soles, and dorsa of the feet
• They are holocrine glands, i.e., their secretion is
formed by complete cell destruction
• Most sebaceous
glands have their
ducts opening into
hair follicles
(pilosebaceous
apparatus)
• Free sebaceous glands (not associated
with hair follicles) open directly to the
surface of the skin, e.g., Meibomian
glands of the eyelids, Tyson's glands of
the prepuce, and free glands in the female
genitalia and in the areola of nipples
Hormonal control
• Sebaceous gland development is an early
event in puberty, and the prime hormonal
stimulus for this glandular development is
androgen
• Although the sebaceous glands are very
small throughout the prepubertal period,
they are large at the time of birth, probably
as a result of androgen stimulation in
utero, and acne may be seen in the
neonatal period
• Sebum production is low in children
• Testicular androgen maintains sebum
production at a higher level in men than
women where androgens are produced by
the adrenals and ovaries
• In women sebum production decreases
significantly after the age of 50
• In both sexes, estrogen administration
decreases the size of the sebaceous
glands and the production of sebum
Composition and function
• Sebum is composed of triglycerides and
free fatty acids, wax esters, squalene, and
cholesterol
• Sebum controls moisture loss from the
epidermis. The water-holding power of
cornified epithelium depends on the
presence of lipids
• Sebum also protects against fungal and
bacterial infections of the skin due to its
contents of free fatty acids. Ringworm of
scalp becomes rare after puberty
ACNE VULGARIS
Etymology
• The word acne comes from the Greek
word "akme“ which means the highest
point. It was misspelled by the 6th century
author, Aëtius, into “acne”
Etiology
• Sex prevalence:
-It starts earlier in girls than boys due to
earlier onset of puberty
-It is more common in males than in
females during adolescence but more
common in women than in men during
adulthood
• Age prevalence:
- It may be present in the first few weeks of life
when a newborn is still under the influence of
maternal hormones and when the androgenproducing portion of the adrenal gland is
disproportionately large. This neonatal acne
resolves spontaneously
- Some degree of acne affects 95% of 16years old boys and girls but only 20% of
sufferers need medical help
-Adolescent acne usually begins prior to
the onset of puberty, when the adrenal
gland begins to produce and release more
androgen hormone
-Acne resolves slowly between the age of
20-25
-As many as 80% of patients have some
degree of acne by the age of 40 but only
1% of males and 5% of females have
significant lesions
• Genetic factors
-Acne was present in 45% of boys with a
history of affection of one or both parents
compared to 8% of boys without affected
parents
-Acne is more common in whites than in
blacks
• Four key factors are responsible for the
development of an acne lesion:
1- Comedone formation (comedogenesis)
2- Excess sebum
3- Presence & activity of Propionibacterium
acnes
4- Inflammation
1- Comedone
formation(comedogenesis)
The exact underlying cause is not known, 3
theories exist:
i.Androgen hormones
- Comedones begin to appear around
adrenarche
- The degree of comedonal acne in prepubertal
girls correlates with circulating levels of DHEAS -Androgen hormone receptors are present in
the portion of the follicle where the comedone
forms
- Sebaceous activity is predominantly
dependent on androgens, thus, abnormally
high levels of sebum secretion could result
from high overall androgen production, or
increased availability of free androgen,
because of a deficiency in sex-hormonebinding globulin (SHBG)
- Most men and women with acne have
normal circulating levels of androgen
hormones, thus an end-organ
hyperresponsiveness to androgen hormones
has been hypothesized
ii- Changes in lipid composition(see later)
iii- Inflammation(see later)
2- Excess sebum(seborrhea)
• Excess sebum may dilute the normal
epidermal lipids resulting in diminished
concentrations of linoleic acid. This
relative decrease in linoleic acid may be
what initiates comedone formation
3- P. acnes
• P. acnes is a microaerophilic organism
• It has not been shown to be present in
microcomedo, but its presence in later
lesions is almost certain
• P. acnes stimulates inflammation by
producing proinflammatory mediators that
diffuse through the follicle wall
• Recent studies have shown that P. acnes binds
to the toll-like receptor (receptors that recognize
abnormal organisms) on monocytes leading to
the production of multiple proinflammatory
cytokines, including IL-12, IL-8, and tumor
necrosis factor
• Hypersensitivity to P. acnes may also explain
why some individuals develop inflammatory
acne vulgaris while others do not
4- Inflammation
• Interleukin–1–alpha has been used in a
tissue model to induce follicular epidermal
hyperproliferation and comedone
formation
• Prior to duct rupture mediators of
inflammation diffuse though the follicular
duct into the dermis causing a type IV
(cellular) immune response
• Later, the duct ruptures causing a
macrophage giant cell foreign-body
reaction
• P.acnes is the source of antigen to which
the reaction is produced
• Toll receptors regulate the production of
cytokines which contribute to the
production of inflammation in acne
• Toll receptors look at P.acnes as abnormal
as it is not often present in follicles from
subjects without acne
Clinically
• Lesions are distributed over the areas rich
in sebaceous glands
• The face may be the only involved skin
surface, but the chest, the back, and the
upper arms are often involved
Types:
1- Comedonal acne :
-Blackheads(open comedones):result when a
pore is partially blocked, allowing some of
the trapped sebum , bacteria & dead
keratinocytes to
slowly drain to the
surface. The black
color is due to the
presence of melanin
- Whiteheads(closed comedones):result
when a pore is completely blocked.
Whiteheads are normally quicker in life
cycle than
blackheads
Sandpaper white comedones:
• Numerous(as many as 500)
• Very small
• Most often found on the forehead
• Feel rough to the touch
Macrocomedones:
• Greater than 1mm in diameter
• Black or white
2- Mild inflammatory acne is characterized
by painful inflammatory papules and
comedones
3- Moderate inflammatory acne has
comedones,inflammatory papules, and
pustules & greater numbers of lesions
4- Nodular acne is characterized by
comedones, inflammatory lesions, and
large nodules
(the term nodulocystic acne is
incorrect as acne cysts are
not true cysts as they are
NOT lined by epithelium).
Scarring is often evident
5-Acne conglobata:
• Characterized by large numbers of deep
nodules that frequently fuse to form
multiple draining sinuses
on the face and trunk
• It commonly heals
with scarring
• It may last up to the
age of 50 years
6- Acne fulminans:
• It is an uncommon, immunologically
induced, systemic disease in which the
offending antigen is P. acnes
• Patients are young males,
who quite suddenly
develop extensive
inflammatory lesions,
especially on the trunk
• Usually associated with fever,
leukocytosis, arthralgia, inflammatory bone
lesions, and transient glomerulonephritis
Scarring in acne
• Scarring occurs in up to 90% but socially
noticed scars occur in only 22% of cases
• Common scars are the ‘Ice picks’ scars
commonly found on the cheeks
• Hypertrophic scars and keloids can occur
less commonly
Classification of Acne Severity
I-Mild:
< 20 comedones, or < 15 inflammatory
lesions, or < 30 total lesions
II-Moderate
20 to 100 comedones, or 15 to 50
inflammatory lesions, or 30 to 125 total
lesions
III-Severe
> 5 cysts, or total comedo count > 100, or
total inflammatory count > 50, or > 125 total
lesions
Factors affecting acne
1-Diet
• A wealth of folklore has blamed acne on
certain foods, in particular chocolate and
pork fat, but scientific proof is lacking
2-Premenstrual flaring
• Flare occurs in up to70% of women 2-7
days before menstruation
• Possibly it is due to a change of hydration
of pilosebaceous epithelium
3-Sweating
• Excerbation occurs in up to 15% of cases
living in hot humid environment
• Ductal hydration may be responsible
4-UV
• There is no scientific evidence that sunlight
improves acne
• UV radiation may enhance the
comedogenicity of sebum
5-Other factors:
• Studies show conflicting results concerning
the effect of stress and smoking on acne
Histopathology
• Comedo development starts as an
expanding mass of lipid-impregnated
keratinous material, resulting in thinning
and ballooning-out of the follicular wall
• At the same time, the sebaceous glands
begin to atrophy and are replaced by
undifferentiated epithelial cells
•Open comedo has a
patulous orifice
&keratinous material
arranged in a lamellar
compact fashion
•Closed comedo has a
narrow distended orifice
&keratinous material is
not compact
• The initial event appears to be escape of lipid
through an edematous comedo wall, with the
development of a cellular reaction in the
adjacent dermis. Once complete
rupture has occurred, the entire contents of
the comedo are extruded into the dermis
• Inflammatory reaction is much greater, and
giant cells are common. Within
the inflammatory infiltrate, P. acnes may be
observed free and within polymorphs
• Depending upon the site and extent of
inflammation, these ruptured lesions may
appear as a pustule, a nodule, or
as a nodule surmounted by a pustule
Pustule following rupture of a sebaceous Nodule from a ruptured closed comedo.
follicle. The original walls of the follicle In the upper portion of the lesion there is
can be seen at the follicular orifice. New lamellar keratinous material from the
strands of epithelial cells are migrating comedo. Below this, necrotic material is
from the epidermis to encapsulate the
being encapsulated by new epithelial
inflammatory mass, making the
cells. Multinucleated giant cells are
inflammatory material appear to be
present in the inflammatory infiltrate in
within the follicle
the dermis
Treatment
• Treatment should be directed toward the
known pathogenic factors involved in acne
i.e. follicular hyperproliferation, excess
sebum, P. acnes, and inflammation
• The grade and the severity of the acne
help in determining which of the following
treatments, alone or in combination, is
most appropriate
A-Topical treatments
1-Topical retinoids
They are
• Comedolytic
• Aanti-inflammatory
• They cause epidermal differentiation and, thus,
normalize follicular hyperproliferation and
hyperkeratinization
• They may be used alone or in combination with
other acne medications
• Because irritation, redness and peeling are
common, they are used once daily by night and
exposure time is increased gradually
• Four generations of topical retinoids are
available:
-1st generation:Tretinoin (Retin-A, Acnefree
0.025%, 0.05%, and 0.1% creams. Also
available as 0.01% and 0.025% gels )
-2nd generation:Isotretinoin (Isotrex 0.05%
gel )
-3rd generation:Adapalene gel, 0.1%
-4th generation:Tazarotene(Zarotex 0.05%
and 0.1% cream and gel )
• The use of mild, nondrying cleansers and
noncomedogenic moisturizers may help
reduce irritation
• Alternate-day dosing may be used if
irritation persists
• In general, the order of irritancy increases
as one progresses from the use of cream
preparations to gels to the solution
• Topical retinoids have been associated
with sun sensitivity. Instruct patients about
sun protection
2-Topical antibiotics
• Mainly used for their role against P. acnes
• They may also have anti-inflammatory
properties
• Topical antibiotics are not comedolytic
• Bacterial resistance (up to 58%)
developed to many of these agents. The
development of resistance is lessened if
topical antibiotics are used in combination
with benzoyl peroxide
•
•
•
•
•
Commonly prescribed topical antibiotics
include:
Erythromycin(acnebiotic,Acne zincomycin)
Clindamycin (dalacine T)
They are available in a variety of topical
agents
They may be applied once or twice a day
Gels and solutions may be more irritating
than creams or lotions
3- Benzoyl peroxide
(Panoxyl, Akneroxid cream and gel)
• Effective against P. acnes
• Bacterial resistance to benzoyl peroxide has
not been reported
• It is available in a variety of topical
forms(Akneroxide,Panoxyl lotions & creams)
• Used once or twice a day
• May cause a true allergic contact dermatitis.
More often, an irritant contact dermatitis
develops especially if used with tretinoin or
when accompanied by aggressive washing
4-Azelaic acid(Skinoren,Azaderm
20% cream)
• It is found naturally in wheat, and it is
produced by Malassezia furfur
• It is bactericidal, keratolytic and
antiinflammatory
• The cream is applied to the area affected once
daily, then if tolerated twice-daily after
thoroughly cleansing the skin
• Some improvement should be seen after
one month of using azelaic acid cream.
Further improvement should occur with
maximum results after six months'
continuous use
• It helps reduce pigmentation, so it's useful
for darker skinned patients whose acne
spots leave persistent brown marks
B- Systemic
Treatment
I-Systemic
Antibiotics
1-Tetracyclines
• They decrease the concentration of free
fatty acids in sebum. Their level is an
indication of the metabolic activity of the
organism and its secretion of other
proinflammatory products
• They may act through direct suppression of
the number of P. acnes, but part of its
action may also be due to its antiinflammatory activity
• Interactions:
-Bioavailability ↓ with antacids containing Al, Ca,
Mg, Fe, Bism
-Can decrease effects of oral contraceptives,
causing breakthrough bleeding and increased
risk of pregnancy
-Can increase effects of anticoagulants
• Their use during tooth development (last half of
pregnancy through age 8 y) can cause
permanent yellow-brown staining of teeth; also,
tetracyclines have been reported to inhibit
skeletal growth in the fetus
A-Tetracycline HCl(Tetracid 250
mg cap)
• It is usually given initially in a dose of 1000
mg/day(divided). The dose is often
decreased as improvement occurs and
may be continued at a level of 250 mg/day
for a minimum of 6 months
• Tetracycline should be taken on an empty
stomach to promote absorption
B- Doxymycine 100mg cap
(Vibramycine,
doxymycine,Tolexine)
• Aappears to be more effective than
tetracycline, and drug resistance is less
likely to occur
• Dose: 50 to 100 mg twice daily
• The major disadvantage of its use is that
it can produce photosensitivity reactions,
and patients should be switched to
another antibiotic, if possible, during the
summer months
C- Minocycline(minocine 50 mg
tab)
• Minocycline is given in divided dosages at
a level of 100 mg/day to 200 mg/day.
• Patients on minocycline should be
monitored carefully as the drug can cause
blue-black pigmentation, especially in the
acne scars, as well as the hard palate,
alveolar ridge, and anterior shins
2- Macrolides:
Erythromycine(erythrocine 500
tab), Azithromycin(Zithromax 250
tab,azrolid 500 tab)
• Erythromycine is the only safe antibiotic to
administer to pregnant women or children
• Dose 1000 mg/day orally (divided) on empty
stomach
• There is increasing evidence of the
development of erythromycin-resistant
strains of P. acnes Therefore, it is wise to
limit the use of oral erythromycin to those
cases where tetracyclines are
contraindicated (pregnancy&young
children)
• Azithromycin (500 mg 3 times weekly), can give
80% clearance in 12 weeks
3-Clindamycine
(Dalacine c,Clindacine,150 mg cap)
• Oral clindamycin has been used in the
past, but because of the potential of
pseudomembranous colitis, it is now rarely
used for acne
4-Trimethoprimsulfamethoxazole
(Sutrim,Septazole tab)
• Although effective in acne, the potential for
side effects is great. So, they should be
used only in patients with severe acne
who do not respond to other antibiotics
• If they are used, the patient must be
monitored for potential hematologic
suppression approximately monthly
II-Hormonal therapy
1-Contraceptive pills
• Two oral contraceptives are currently FDA
approved for the treatment of acne: Cilest
(norgestimate 250 µg + ethinyl estradiol 35
µg) and Estrostep (ethinyl estradiol 20 to 35
µg + norethindrone acetate1 mg )
• They increase SHBG, resulting in a decrease
in circulating free testosterone
• Estrogen supresses sebaceous gland leading
to decreasing sebum production by 25%
• Used in unresponsive cases in young women
after more conventional regimens have failed
• Improvement occurs after 2-4 months , but
relapses may occur if treatment is
discontinued
• Side effects include nausea, vomiting,
abnormal menses, weight gain, and breast
tenderness
• Rare but more serious complications
include thrombophlebitis, pulmonary
embolism, and hypertension
2-Spironolactone
(Aldactone,25,100 mg tab)
• Blocks the binding of androgens to
androgen receptors
• Good candidates for this drug are
individuals with a premenstrual flare-up of
their acne, acne onset after the age of 25,
oily skin, coexistent hirsutism, and acne
that has a predilection for the chin and
mandible
• Start patients on 50 to 100 mg/day taken
with meals. If no clinical response is seen
in 1 to 3 months, adjust the dose up to 200
mg/day if necessary. Once maintenance
has been achieved, try to lower the dose
to the lowest effective daily dose
• Menstrual irregularities and breast
tenderness are common side effects
• The drug should not be used during
pregnancy, because it may block the
normal development of male genitalia
• It alters potassium excretion (usually only
at higher doses and in only 10% of
patients). Serum electrolytes should be
monitored during initial institution of
therapy. Nausea, vomiting, and anorexia
are also common
3- Cyproterone acetate
(Diane:Cyproterone acetate 2mg and
Ethinylestradiol 35mcg tab)
• Blocks the androgen receptors
• Given as one tab/day starting from the first
day of menstruation for 21 days
• The drug is then stopped for 7 days during
which a small amount of menstrual blood
is seen
• Acne usually improves by 40-50% by the
third cycle and by 80-90% by the ninth
cycle
4- Prednisone (Hostacorten
5 mg tab)
• Useful in female patients, with severe
acne unresponsive to conventional
therapy, who suffer from adrenal gland
overproduction of androgens
• 2.5 to 7.5 mg, administered at night
• For individuals with an acute acne flare,
Prednisone can also be used in a dose of
20 mg/day for 1 week before an important
occasion such as a wedding
•
III- Isotretinoin
(Roaccutane;Netlook,
10,20,30 mg cap)
• The use of the oral retinoid, isotretinoin, has
revolutionized the management of severe
treatment-resistant acne
• The remarkable aspects of isotretinoin therapy
is that the response rate may be as high as
90% with one to two courses and the longevity
of the remission, which lasts for months to
years in the great majority of patients
• It causes normalization of epidermal
differentiation, depresses sebum excretion by
70%,it is anti-inflammatory, and even reduces
the presence of P acnes
Six months later
• Indications for treatment with isotretinoin
include:
1-Less than 50% improvement after 6
months of oral and topical therapy
2- scarring
3-Associated psychological distress
4-Acne that relapses quickly once
conventional therapy is discontinued
• The initial dose of isotretinoin is 0.5 to 1.0
mg/kg of the patient's body weight. Many of
the problems with this drug come from
starting at too high a dose
• For the first month, a patient may be started
at 20 mg daily. This allows for monitoring of
any adverse effects
• The daily dose may be increased each
month by an additional 20 mg (e.g., 20 mg
first month, 40 mg second month, 60 mg
third month, etc) to a dose of approx.1 mg/kg
• Because back and chest lesions respond
less than facial lesions, dosages as high as 2
mg/kg per day may be necessary
• There appears to be no advantage to single
versus divided dose, but isotretinoin
absorption is enhanced by taking it with
meals
• Patients with severe acne, particularly those
with granulomatous lesions, will often
develop marked flares of their disease when
isotretinoin is started. Therefore, the initial
dosing should be low, even below 0.5 mg/kg
per day. These patients often need pretreatment for 1 to 2 weeks with prednisone
(40 to 60 mg per day), which may have to be
continued for the first 2 weeks of therapy
• Clinical results can be obtained with dosages
as low as 0.1 mg/kg per day. However, with
such dosages, the incidence of relapses after
therapy is greater
• Isotretinoin is usually given for 20 weeks, but
the length of the course of treatment is not
absolute; in patients who have not shown an
adequate response, therapy can be
extended, if necessary
• Some improvement is usually seen for 1 to 2
months after isotretinoin is discontinued, so
that total clearing is not a necessary endpoint
for determining when to discontinue therapy
• Because the skin will often continue to
clear after drug administration has been
stopped, at least a 2-month waiting period
and preferably a 6-month period is advised
before one commits a patient to a second
course of therapy
• In a 10-year follow-up study, 61% of
patients were free from acne
• Of those who relapsed, 23% required a
second course
• Ninety-six percent had relapsed within 3
years of therapy
• Truncal acne had a higher relapse rate
• Patients given a cumulative dose of 120
mg/kg overall were less likely to relapse
• Using isotretinoin during pregnancy resulted
in spontaneous abortion or birth defects in
83% of cases, so it should be given only to
cases not responding to other therapy
• Furthermore, women who are of childbearing
age must be fully informed of the risk of
pregnancy. The patient must either avoid
sexual exposure totally or should employ two
highly effective contraception techniques
such as the use of an oral contraceptive and
condoms with a spermicidal jelly
• Contraception must be started at least 1
month before isotretinoin therapy
• The patient must have a negative serum
pregnancy test at the time when therapy is
decided upon and on the second or third
day of the next menstrual period or 11
days after the last unprotected intercourse
in a woman who is amenorrheic
• Contraception should continue throughout
the course of isotretinoin and for 1 month
after stopping treatment
• The pregnancy test should be repeated
monthly to maintain patient awareness
• Because the drug is not mutagenic, there
is no risk to a fetus conceived by a male
who is taking isotretinoin
• Cheilitis of varying degrees is found in
almost all cases
• Other side effects that are likely to be seen
in over 50 % of patients are dryness of the
mucous membranes, xerosis,
conjunctivitis, and pruritus
• Less frequent side effects include bone
and joint pain; thinning of hair; headache;
palmoplantar desquamation; and nausea
and vomiting
• Laboratory abnormalities include elevations
in triglycerides, ESR, platelet count, liver
function tests, and white blood cells in the
urine and decreases in red blood cell
parameters, white cell counts, and highdensity lipoprotein levels
• The elevation of triglycerides, which is doserelated, is of particular concern because it is
often accompanied by a decrease in the
high-density lipoprotein levels, which may
increase the risk of coronary artery disease
• Associated mood changes and depression
have been reported during treatment.
Although the cause is not clear, patients
should be informed of this potential effect
• The patient is considered at high risk for
abnormal healing and development of
excessive granulation tissue following
procedures. Many dermatologists delay
elective procedures, such as dermabrasion
or laser resurfacing, for up to a year after
completion of therapy. Other procedures to
be avoided during therapy include tattoos,
piercings, leg waxing, and other epilation
procedures
Therapeutic decisions
• Comedonal Acne: Topical tretinoin or
adapalene(less irritant) is the treatment of
choice. Starting with a lower concentration of the
cream (available as 0.025, 0.05, and 0.1%) or
gel (available as 0.01 and 0.025%) and
increasing the concentration if local irritation
does not occur. Topical azelaic acid has some
comedolytic activity. It is less potent than
tretinoin but may be useful in patients who
cannot tolerate topical tretinoin or other retinoids
• Mild Inflammatory Acne :Most patients
have a response after two to four weeks of
twice-daily application of a topical
antibiotic, topical benzoyl peroxide, or the
combination of benzoyl peroxide and
erythromycin. Treatment should be
continued until no new lesions develop
and then should be slowly discontinued
•Moderate inflammatory acne:
-The combination of a topical retinoid
applied once daily and either a topical or a
systemic antibiotic is the best approach.
The choice between topical and systemic
antibiotic therapy usually depends on the
extent of skin involvement and the severity
of the inflammation
- Benzoyl peroxide plus erythromycin are
the most effective topical antimicrobial
therapies
- Usually four to six weeks are needed to
reduce P. acnes and to curtail the
formation of new inflammatory lesions
- Patients treated with an oral antibiotic may
also be given topical antibiotics,
particularly when the dose of the oral drug
is reduced. In general, the dose of an
antibiotic should not be reduced before
two to four months. Long-term control
requires the suppression of P. acnes for
prolonged periods
• Nodular acne:
-Systemic isotretinoin is the treatment of choice,
particularly those who have scarring
-An alternative to systemic isotretinoin in women
with persistent acne that is unresponsive to
therapy with antibiotics and topical tretinoin is
therapy with estrogen or an antiandrogen
- For patients with larger inflammatory lesions,
local injection of a corticosteroid is effective
• Acne conglobata:
Oral isotretinoin is the treatment of choice in
patients with this type of acne; in some, systemic
corticosteroid therapy may be given before or
concomitantly with isotretinoin
• Acne fulminans:
Oral corticosteroids are the therapy of choice
C-Physical modalities
1-Chemical Peels
Light chemical peels of glycolic acid and
other chemical agents are used to loosen
blackheads and decrease acne papules
2-Comedo Extraction
• Used primarily in patients who do not
respond to comedolytic agents
• Patient is treated first with a topical
retinoid for 3 to 4 weeks
• This procedure is done using the comedo
extractor and should only be performed by
a dermatologist as inaccurate placement
of the comedo extractor
may serve only
to push the inflammatory
material further into
the skin
• The removal of open comedones does not
materially influence the course of the
disease because these lesions do not
become inflammatory,but they are
removed for cosmetic purposes
• In contrast, closed comedones should be
removed to prevent their rupture. The
material contained within the comedo can
be removed only after the orifice is gently
enlarged with a no. 25 needle or other
suitable sharply pointed instrument
3-Laser:.Nd:YAG, diode, and Er:glass
lasers show promise in the treatment of
inflammatory acne and clinical
improvement in acne scars. Treatments
are typically performed monthly for 4 to 6
months. Pulsed dye lasers can be used to
minimize erythema of active acne lesions
and acne scars
4-Photodynamic therapy: Significant
clearence for at least 20 weeks was
reported
5-Ultraviolet light : Exposure to sunlight
or UVB sunlamps may be moderately
effective in some patients
6-Cryosurgery:Freezing with liquid
nitrogen will hasten resolution of old
nodules(>7 days)
6-Intralesional Steroids Injection
• Intralesional steroid injection either by the
use of an insulin syringe or by the
Dermojet, usually dramatically decreases
the size of deep nodular lesions
• The injection of 0.05 to 0.25 mL per lesion
of a triamcinolone acetonide suspension
(2.5 to 10 mg/mL) is recommended as the
anti-inflammatory agent. It is often has to
be repeated every 2 to 3 weeks
• Most lesions, particularly early ones, will
flatten and disappear within 48 hours of
injection
D-Treatment of scars
1-Laser skin resurfacing: Ablative
CO2/Er:YAG laser skin resurfacing can
improve the appearance of acne scars of
all types but requires significant postoperative wound care and recovery time
2-Dermabrasion using high-speed
diamond buffing drills can remove small
and superficial scars and sometimes deep
scars
3-Fat transfer and injection of filler
substances can be used to elevate acne
scars
General points
• Soaps, detergents, and astringents can
remove sebum from the surface of the skin
but do not alter sebum production and are of
no therapeutic value. In fact, vigorous
scrubbing can aggravate acne by promoting
the development of inflammatory lesions
• Dietary restrictions have no role in therapy
• The patient should be advised against
picking, pinching or squeezing
noninflammatory or inflamed lesions, which
can aggravate the acne and cause scarring
Acne variants
1-Acne excoriée
• Occurs predominantly in females
• Some primary inflammatory acne lesions
may be present, and in other patients no
lesions can be found
• Patients play with the skin to exacerbate
even the smallest lesions. There is often
some personality or psychological problem
• There are no active acne lesions, only
scratch marks, sores and scars.
All the inflammatory
lesions and
comedones
have been
removed by
picking or
squeezing
• Treatment is with 1g/day of tetracycline for
months and advice not to pick the spots
• Topical treatment tends to irritate the skin
and aggravate the problem
• In the group with virtually no acne spots,
pimozide (2mg twice a day) and
appropriate psychotherapeutic procedures
may help
2-Drug-induced acne/acneiform
eruptions
• Folliculitis may appear following
administration of glucocorticoids or
corticotropin or prolonged use of topical
steroids. A similar eruption can occur due
to iodides and bromides(e.g. sedatives,
expectorants) and INH. Androgens
including anabolic steroids and
gonadotrophins, may precipitate acne,
especially in athletes who take illegal
performance-enhancing drugs
• It differs from acne vulgaris in the type of
lesions observed and its distribution:
1-The lesions are usually all in the same stage
of development, consisting of small pustules
and red papules. Postinflammatory hyperpigmentation may occur,
but comedones, cysts,
and scarring are unusual
2-In contrast to acne
vulgaris, they appear
mainly on the trunk,
shoulders, and upper
arms,with lesser
involvement of the face
3-Externally induced acne
• A-Cosmetic acne:
• Cosmetic companies are testing their
compounds adequately for
comedogenicity before marketing.
Consequently, with the exception of very
greasy, occlusive products, cosmetics are
infrequent etiologic agents for acne
• Occurs as folliculitis in the perioral area of
mature females, especially those who had
acne as adolescents and have used
cosmetics for a long time
• The area to which the cosmetic was
applied is studded with closed and open
comedones and some papules& pustules
• Treatment with
topical retinoids or
benzoyl peroxide is
usually successful
B-Pomade acne:
• Pomades are greasy preparations used to
'defrizz' curly Negroid hair. The rash is
similar to cosmetic acne but consists of
non-inflamed lesions around the forehead
and other areas where
greasy pomades may
extend onto the hairless
skin
• Treatment is with topical
retinoids
C-Oil and Tar acne:
• Acne from these agents tends to be quite
inflammatory with large comedones, papules,
pustules, large nodules, and true cysts. Tar
acne is often accompanied by
hyperpigmentation
• The lesions are not restricted to the face and,
in fact, are more common on covered areas
where intimate contact with clothing
saturated with the offending compound is
maintained
D-Chloracne
• It is caused by exposure to halogenated
aromatic hydrocarbons, which are most often
found in fungicides, insecticides, herbicides and
wood preservatives
• It is the most common skin sign of dioxin
poisoning (formed as a by-product of the
manufacture, molding, or burning of organic
chemicals and plastics that contain chlorine)
• There are open and
closed comedones with
uninflamed nodules and
cysts
• Lesions are most often
seen on the cheeks,
behind the ears, in the
axilla and in the groins
• Topical therapy with retinoids worth a trial
• Long-term oral antibiotic therapy may be
needed for the inflammatory lesions
• Gentle cautery under local anaesthetic
cream (EMLA applied for 90min under
polythene occlusion) produces excellent
results
E-Mechanical acne:
• Acne occurs at the site
of physical trauma, e.g.
by occluding the skin
with adhesive tape or
continuous friction
with a belt or a violin
in violin players
• Treatment is the same
as for other forms of
acne, plus removal
of the cause
•
•
•
•
4- Infantile and juvenile acne
Presents as facial acne at around 3-24
months, and may last up to 5 years of age
Mainly affects males
The lesions are more
localized than in adults
and particularly affect
the cheeks. All acne
lesions can be found
Patients may develop
significant acne as
teenagers
• May result from excess androgen due to
transplacental stimulation of the adrenal
gland, as most sufferers have elevated
plasma adrenal androgen
• Treatment consists of oral erythromycin
(125mg three times a day) for 6 months,
and topical therapy (preferably benzoyl
peroxide, erythromycin or retinoids) is
essential until lesions have totally
disappeared
ROSACEA
Etiology
• The etiology of rosacea is unknown
• Several factors may play a role in its
development
1-Vasculature
• Increased blood flow and increased
numbers of blood vessels that are closer
to the surface of the face skin are thought
to be responsible for the redness and
flushing associated with rosacea
• Furthermore, vasodilatation, the normal
response to hyperthermia, is thought to be
exaggerated in rosacea patients
2-Climatic exposures
• Exposure to solar irradiation damages
cutaneous blood vessels and dermal
connective tissue. This may explain why
rosacea predominately affects the facial
convexities and has a tendency to flare in
the spring and summer
• However, other studies suggest the
contrary, i.e. most patients' symptoms do
not worsen in the sunlight and do not flare
with an acute exposure to ultraviolet light
3-Dermal matrix degeneration
• There is:
- damage to the blood vessels endothelium
leading to leaking of serum proteins,
inflammatory mediators, and metabolic waste
- degeneration of the dermal matrix leading to
poor tissue support of cutaneous vessels
• However, it is not known which process starts
first leading to subsequent occurrence of the
other
4-Chemicals and ingested agents
• Most evidence does not support that dietary
factors (e.g. spicy foods and hot drinks) play
a main role in the pathogenesis
• Certain medications such as the
antiarrhythmic amiodarone (Cordarone) ,
topical steroids, nasal steroids, and high
doses of vitamins B-6 and B-12 may cause
flares
5-Microbial organisms
• Demodex species (mites that normally
inhabit human hair follicles) may play a
role in the pathogenesis of rosacea
• Demodex prefers skin regions
that are affected in rosacea,
such as the nose and cheeks
• Conflicting evidence exists regarding the
role of demodex in rosacea:
-Some studies showed an immune
response of helper-inducer T cell infiltrates
surrounding the Demodex antigens
-Others showed that Demodex is found in
large numbers of healthy individuals
without rosacea
• All ages can be affected, including
pediatric patients. Peak incidence occurs
in the fourth to seventh decades
• More than 10% of the general population
in USA exhibits dermatologic
characteristics of rosacea; of these, up to
60% experience ocular complications
• Rosacea occurs much more commonly in
fair-skinned white patients
• In races with increased skin pigmentation it
may be underreported, rather than less
prevalent
• Females are affected with rosacea twice as
often as males
• However, disease manifestations, especially
rhinophyma, are frequently more severe in
males than in females
Clinically
• Four clinical types of rosacea exist:
1-Erythematotelangiectatic type
• Central facial flushing,
often accompanied by
burning or stinging
• The redness usually
spares the periocular
skin
• These patients usually have skin with a
fine texture
•The erythematous areas of the face
at times appear
rough with scale
likely due to
chronic,
low-grade
dermatitis
• Frequent triggers to flushing include
acutely felt emotional stress, hot drinks,
alcohol, spicy foods, exercise, cold or hot
weather, and hot baths and showers.
These patients also report that the burning
or stinging is exacerbated when topical
agents are applied.
2-Papulopustular rosacea
• It is the classic presentation of rosacea
• Patients are middle aged &predominately
present with a red central
portion of their face containing
small erythematous papules
surmounted by pinpoint
pustules
• Telangiectasias may be
present but may be difficult to
distinguish from the
erythematous background
3-Phymatous rosacea
• There are marked skin thickenings and
irregular surface nodularities of
the nose, chin, forehead,
one or both ears,
and/or the eyelids
4-Ocular rosacea
• Ocular manifestations may precede the
cutaneous signs by years. Yet, frequently
they develop concurrently with dermatologic
manifestations
• They include blepharitis,
conjunctivitis, inflammation
of the meibomian glands, and conjunctival
telangiectasias. Patients may describe eye
stinging or burning, dryness, irritation with
light, or foreign body sensation
Histopathology
• Dilatation of upper and mid-dermal vessels
and lymphatics with perivascular and
perifollicular
lymphohistiocytic infiltrate
is generally
present in all
cases
• Reflecting the clinical presentation, various
other pathologic changes can be seen
from case to case,
including neutrophils
accumulation,
resulting in a
superficial pustule
• Granulomatous infiltrates, with epithelioid
histiocytes forming a tuberculoid pattern
are reported to occur
in about 10% of all
cases, and caseation
necrosis has been
identified in about
10% of these patients
Treatment
I-General measures
• Where possible, reduce factors causing
facial flushing
• Avoid oil-based facial creams
• Never apply a topical steroid
• Use light oil-free facial sunscreens
• Keep your face cool: minimize your exposure
to hot or spicy foods, alcohol, hot showers
and baths and warm rooms.
II-Oral antibiotics
• Several courses are often needed from
time to time as the antibiotics do not cure
the disorder
1-Tetracyclines
• Tetracycline 250 mg PO qd to 500 mg PO
tid or Doxymycine
• Prescribed for 6 to 12 weeks, the duration
and dose depending on the severity
2-Metronidazole
(Flagyl,Flagycure 250 mg)
• Aactive against various anaerobic bacteria
and protozoa
• Beneficial against papules and pustules of
rosacea
• Topical applications are helpful for mild
disease and as an adjuvant to systemic
therapy
• Dose: 200 mg PO bid
Topical: Wash affected area and apply a
thin film to affected area bid
• May increase toxicity of anticoagulants,
lithium, and phenytoin; cimetidine
• Usually safe in pregnancy but benefits
must outweigh the risks
• Adjust dose in hepatic disease; monitor for
seizures and development of peripheral
neuropathy
3-Erythromycin (Erythrocine)
• Can be used when tetracyclines are not
tolerated or are contraindicated
• Dose: 500 mg PO bid
4-Clindamycin (DalacineT 10
mg/ml sol)
• Effective against mild-to-moderate
papulopustular rosacea
• Dose : Apply to affected area qd
5-Azithromycin (Zithromax)
• Dose 500 mg PO on day 1, followed by
250 mg PO qd for next 4 days
• Interactions : Toxicity increases with
coadministration of fluconazole and
pimozide
• May increase toxicity of anticoagulants,
cyclosporine, tacrolimus, digoxin
• Usually safe in pregnancy but benefits
must outweigh the risks
III-Isotretinoin
(Ro-ccutane,Netlook,10,20,30 mg cap)
• Recent research showed a role of vascular
endothelial growth factors (VEGF) in
rosacea
• Retinoids appear to modulate the
expression of VEGFs in the skin; this may
explain the therapeutic benefit of
isotretinoin in the treatment of rosacea
• May be helpful for recalcitrant disease, but
recurrence is common
• Dose: 0.5-1 mg/kg/d PO divided bid for 4
months
• InteractionsToxicity may occur with
vitamin A coadministration; pseudotumor
cerebri or papilledema may occur when
coadministered with tetracyclines;
isotretinoin may reduce plasma levels of
carbamazepine and contraceptive efficacy
• PregnancyX - Contraindicated in
pregnancy
1 month after
oral isotretinoin
Treatment of erythema
• Oral and topical antibiotics are often
ineffective in the treatment of erythema
and flushing. Low-dose clonidine
(Catapres; 0.05 mg twice daily) may be
effective in controlling flushing, especially
in women who are postmenopausal
• A nonselective beta blocker (such as longacting propranolol [Inderal], 80 to 240 mg
daily, and nadolol [Corgard], 40 to 80 mg
daily) may also be used
Treatment of telangectasia
• Treatment with a pulsed dye laser may be
effective in advanced cases and if
performed by an experienced physician,
laser therapy usually has no complications
• Temporary hyperpigmentation of treated
areas may occur in 5 to 20 percent of
patients.
Treatment of rhinophyma
• The initial stages of rhinophyma may
respond to antibiotic treatment, but more
advanced cases must be treated with
surgery
• A number of techniques have been
advocated, including dermabrasion,
cryosurgery, and excision of hypertrophic
tissue by electrosurgery or with a laser
PERIORAL DERMATITIS
Etiology
• An underlying cause cannot be detected in
all patients
• Topical steroids:Many patients abuse
topical steroid preparations. No clear
correlation exists between the risk of POD
and strength of the steroid or the duration
of the abuse
• Cosmetics: Fluorinated toothpaste; skin
care ointments and creams, especially
those with a petrolatum or paraffin base
are suggested to be causative factors
• Physical factors: UV light, heat, and wind
worsen POD
• Microbiologic factors: Fusiform spirilla
bacteria, Candida species, and other fungi
have been cultured from lesions. Their
presence has no clear clinical relevance
• Miscellaneous factors: Hormonal factors are
suspected because of an observed
premenstrual deterioration. Oral contraceptives may be a factor
• The incidence is estimated to be 0.5-1% in
industrialized countries
• The incidence seems to be lower in less
developed countries, but no statistics are
available
• Women account for an estimated 90% of
the cases
• Perioral dermatitis can occur in children,
but the vast majority of patients are aged
20-45 years
Clinically
• Skin lesions occur as grouped follicular
reddish papules, papulovesicles, and
papulopustules on an erythematous base
• They are located in the perioral area,
nasolabial fold, and lateral portions of the
lower eyelids
• Symptoms consist
of a sensation of
burning and
tension but itching
is rare
• Histologic findings are similar to those of
rosacea
Treatment
• The patient should be advised that
remission might not occur for weeks,
despite correct treatment
• In every case, an initial worsening of the
symptoms may occur with treatment,
especially if topical steroids are withdrawn.
The patient should be made aware of this
complication. In cases of preceding longterm abuse of topical steroids, steroid
weaning with low-dose 0.1-0.5%
hydrocortisone cream can be tried initially
• Zero-therapy is based on the idea that by
ceasing use of all topical medications and
cosmetics, the underlying causative factor
for POD is eliminated. This form of therapy
is appropriate in very compliant patients.
This therapeutic option is often limited
because of the patient's tendency to
overtreat his or her condition
• In severe forms of POD, systemic
treatment with antiacne drugs is required
• In unresponsive and granulomatous forms,
oral isotretinoin may be considered
• In cases with minor presentations, as well
as in children and pregnant women,
individualized topical therapy is generally
recommended
• Pimecrolimus cream significantly reduced
the Severity Index compared with
vehicle in a randomized, double-blind
study
STEATOCYSTOMA MULTIPLEX
Etiology
• It is a rare familial disorder of the
pilosebaceous unit that has an autosomal
dominant transmission
• Both sexes are equally affected
• Cysts present during adolescence and
early adulthood. SM is a lifelong condition
Clinically
• Cysts are concentrated
in areas with high No.
of sebaceous glands
(upper torso, proximal
extremities) but can
present anywhere on
the skin (ie, face,groin)
• The involved area becomes studded with deep,
flesh-to-yellow colored, superficial, dermal
papules
• Some lesions may become inflamed, and
erythema may surround them
• When a cyst spontaneously ruptures to the
skin surface or is incised and drained
intentionally, the contents appear as an
odorless creamy or oily fluid
Histopathology
• Cysts are located in the mid dermis
• The cyst wall is lined by squamous
epithelium with a toothed surface
• Walls contain flattened lobules of sebaceous
glands among the epithelial cells
• Each cyst is attached to
overlying normal epidermis
by thin strands of undifferentiated epithelial cells
• The cystic space contains
keratin, vellous hair, sebum etc
Treatment
• The patient may desire intervention for
cosmetic reasons
• Unfortunately, isotretinoin (despite known
effects of decreasing sebaceous gland
activity) has shown inconsistent results,
according to the literature. In at least 1
patient, isotretinoin appeared to worsen
the condition, which necessitated
cessation of the drug
Surgical Care
• Aspiration: Individual cyst contents can
be aspirated through an 18-gauge needle,
but the effect is only temporary
• This technique is thought to be the
treatment of choice for facial lesions
because the scarring associated with
excisional approaches is avoided
• Surgical excision: Excision of all cysts on
a patient is not feasible because of the
large numbers of cysts usually present
• However, excision of some of
the larger lesions can be performed using a small surgical
punch or a sharp-tipped cautery
point to puncture the cyst wall.
The cyst's contents then can be
expressed prior to everting the
cyst lining with forceps to destroy it by electrodesiccation The
wound heals by 2ry intension
• Carbon dioxide laser: At least 1
published report exists of the successful
treatment of SM using a carbon dioxide
laser