Download Dermatology

Dermatology
Assis. Prof. Adil A Noaimi
Acne
First we should learn some thing about……
* Sebum:In human sebum there are unique lipids, such as squalene and wax
esters not found anywhere else in the body nor among the epidermal
surface lipids.
A complex of lipid produced by holocrine cells disintegration where
by the whole cell casts will be excreted, this process is under control of
androgen which reaches its peak at age of 15-17 years in males and 1416 years in females.
Function of sebum:1. Keeps the skin in wet oily state and prevent loss of water.
2. Photoprotection.
3. Antimicrobial activity. Tenia is more common in children
before 10-12 years old because of lower amount of sebum
(Fungistatic).
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4. Delivery of fat-soluble anti-oxidants to the skin surface and proand anti-inflammatory activity exerted by specific lipids.
* Seborrhea:Is the production of excessive quantity of sebum, resulting in
greasy thick skin and greasy hair.
Causes of seborrhea:1. Multigenetic factor play a role and it has some family tendency.
2. Neurological condition (e.g. Parkinson or Cushion syndrome).
Treatment of seborrhea:By excessive washing using detergents.
Types of Acne:1- Acne Vulgaris: * Mild chronic self-limiting inflammation of pilosebaceous follicle,
usually presents in adolescence, but can affect any individual in the
course of his life after adolescence.
* Peak occurrence in females 14-16 years and in males 17-19 years and
continue to the 6th decade of life.
* It affects 5% of females & 1% of males.
* 85% of cases don't need consultation and treatment.
*During adolescence, acne vulgaris is more common in males than in
females. In adulthood, acne vulgaris is more common in women than
in men.
*By age 45 years, 5% of both men and women still have acne
Pathophysiology: - Androgen plays a major role in the pathogenesis of the disease.
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- 95% of androgen bound to plasma protein, while 5% is free which is
responsible for acne by stimulating the sebaceous glands to produce
sebum.
- Normal skin flora presents in the hair follicle secret lipase enzyme
which hydrolysis the triglyceride of the sebum into free fatty acids; the
later is irritant to the skin causing irritation to the infundibulum of the
hair follicle leading to squamation of the keratinocytes that leads to
obstruction of the hair follicle by (Comedone) (black head) causing more
sebum accumulation.
- This causes more inflammation and also causing attraction of the
neutrophils and lymphocytes by stimulation of the complement system;
these release inflammatory mediators (cytokines) causing more
inflammation and developing papule, nodule or pustule, that ruptures into
the dermis releasing its contents causing more inflammation; this whole
process causing scaring.
P acnes is an anaerobic organism present in acne lesions. The presence
of P acnes promotes inflammation through a variety of mechanisms. P
acnes stimulates inflammation by producing proinflammatory mediators
that diffuse through the follicle wall. Studies have shown that P
acnes activates
the
toll-like
receptor
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on
monocytes
and
neutrophils. Activation of the toll-like receptor 2 then leads to the
production of multiple proinflammatory cytokines, including interleukins
12 and 8 and tumor necrosis factor. Hypersensitivity to P acnes may also
explain why some individuals develop inflammatory acne vulgaris while
others do not.
- So the pathogenesis of acne vulgaris needs 3 elements:1- Androgen.
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2- Obstruction of Comedone.
3- Microflora.
- We can summarize the pathology as 2 steps:First: Lesion of acne results from obstruction of pilosebaceous follicles
due to hypersecretion of the sebum by the glands. Oxidation of follicle
contents at the skin surface produces comedones which impair the normal
flow of the sebum to the skin surface causing stagnation of the sebum
within pilosebaceous canal.
Second: Secondary infection may supervene. If there is seepage of
pilosebaceous contents into the surrounding dermis, a brisk and
prolonged inflammatory response ensues.
* Etiology:1. Genetic Factors:- Multiple gene play a role and it has some
familial tendency that makes it more severe.
2. Excessive production of Sebum in some people.
3. Endocrine Factor:- (Androgen & prolactine)
4. Microflora:- Mainly anaerobic P. acnes.
5. Diet:- Which can be triggering or exacerbating factor as spicy or
oil diet or sugar.
6. Mechanical Factor:- Post hair epilation acne.
7. Psychological & Emotional Factor.
8. Topical Drugs:- Steroids.
9. Premenstrual Exacerbation.
10.Immunological:-Through stimulation of complement system.
* Clinical Features:-
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1. Site:- Usually in the seborrheic areas; face, upper chest,
upper back and upper extremities. Also can affects scalp,
skin of penis and upper thigh.
2. Morphology
of
the
lesion:-
The
primary
lesion
is
comedone, which has 2 types black heads (open type) with
compacted keratin in the infundibulum or closed (white
comedones) with non compacted keratin, which is more
dangerous and could rupture progress to papule, nodule or
cyst.
a. Papules:- Red and tender which develop after white
comedone.
b. Pustules:- The progression of papules.
c. The papule and pustule may develop to nodule, cyst (cystic
acne) that may lead to sinus tract (subcut. dissection).
d. Excoriating acne (acne excoriate):- Developed from simple
acne in those people who have the habit of excoriating lead
to more scarring.
e. Gram –ve. Folliculitis:- After topical or systemic antibiotics
abuse, the patient develops pustular lesion after 4 months of
good prognosis.
Differential diagnosis:
 Acne Conglobata
 Acne Fulminans
 Acne Keloidalis Nuchae
 Acneiform Eruptions
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 Folliculitis
 Perioral Dermatitis
 Rosacea
 Sebaceous Hyperplasia
 Syringoma
 Tuberous Sclerosis
Acne Vulgaris Workup
Laboratory Studies: The diagnosis of acne vulgaris is clinical. Note the
following:
 In a female patient with dysmenorrhea or hirsutism, a hormonal
evaluation should be considered. Patients with evidence of virilization
must have their total testosterone levels measured. Many authorities also
measure free testosterone, DHEA-S, luteinizing hormone, and folliclestimulating hormone levels.
 Skin lesion cultures to rule out gram-negative folliculitis are warranted if
the patient does not respond to treatment or improvement is not
maintained.
Histologic Findings: The microcomedo is characterized by a dilated
follicle with a plug of dense keratin with a surrounding mantle of
inflammatory cells. With progression of the disease, the follicular
opening becomes dilated, and an open comedo results. The follicular wall
thins, and it may rupture. Inflammation and bacteria may be evident, with
or without follicular rupture. Follicular rupture is accompanied by dense
inflammatory infiltrate throughout the dermis. Both polymorphonuclear
leucocytes and lymphoid cells are seen in this infiltrate. Foreign body
giant cell, granulation tissue, extensive fibrosis and scarring may develop.
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*Complications:It’s a self-limiting disease and aim of treatment is to prevent the
complications which are:1- Scarring:- which is of 2 types:a. Atrophic:- Depressed area (Chicken-pox like scar) may be
saucer-like (flat dish) or (ice-pick).
b. Hypertrophic (keloid scar):- elevated area of collagen
fibers occurs in those who have genetic susceptibility, in the
presternal area, upper chest and upper back.
2- Mental Scaring (Brain Scaring):- which may never clear up and
may cause neurosis-anxiety-depression and social isolation because
the face is passport of the body. Acne can be a very depressing
situation. It freezes personality development in the adolescent stage
and may create hostility, anger, and antisocial behavior. Associated
mood changes and depression have also been reported during
treatment.
2- Neonatal Acne:-
Developed during the 1st or 2nd years of life,
due to passage of androgen from the mother, presented as
comedones(black head), papules and may develop scar. If it was so
severe it may indicate a verilizing tumors.
3- Chemical Acne:* Due to exposure to certain chemicals or topical drugs that
may close
the opening of the hair follicles.
* Occur usually on thighs, forearms, hands and feet.
* The causes are:-
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- Cosmetics.
- Oil and greases (in case of car fixer).
- Topical corticosteroids.
- Coal tar distillate.
- Crude petroleum.
- Shaving soap.
4- Acne Estivale:- Duo to sun exposure for long time.
5- Epidemic Acne:- Duo to food contamination.
6- Steroid Acne.
7- Acne Medicamentosa:- Duo to drugs mainly; anti-TB drugs,
systemic steroids, Phenobarbitone, halogens (iodide), vitamin B12 and D
and actinomycin D.
8- Acne Fulminant:- with fever and joint pain.
9- Excoriating Acne:- In nervous patient.
10- Post Hair epilation Acne:- More in females on face, trunk
and legs, self limiting, exacerbates acne vulgaris, present as mono
morphous red papules.
11- Acne Conglobata:- Chronic suppurative form of acne
vulgaris characterized by cyst formation, burrowing abscess and irregular
scaring. It affects males more than females.
Treatment of Acne:1- Local Treatment:-
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A- Cleaning of no Value:- Because excessive wash dose
not remove the comedone and might trigger the
inflammation.
B- Peeling Agent:- Causes drying of the skin, it removes
the black head to prevent white comedones.
C- Drugs:1. Sulphur (if no comedone).
2. Benzoyl Peroxide:- it has 3 effects:a- Powerful Keratolytic.
b- It is a powerful antimicrobial agent; rapidly destroy both surface
and ductal p.acne and yeast.
c- Anti-inflammatory effect: by decreasing the hydrolysis of
triglyceride to free fatty acids, so decrease its sensitivity to acne
vulgaris.
The lipophilic nature of benzoyl peroxide allows it to penetrate
the pilosebaceous duct. Once applied to the skin it decomposes to
release free oxygen radicals with potent bactericidal activity in the
sebaceous follicles and anti-inflammatory action.
3. Retinoic Acid:a. comedolytic agent.
b. Vitamin A derivative used systemically and topically.
c. Decrease seborrhea but causes photosensitivity.
d. The most commonly prescribed topical retinoids for acne
vulgaris include adapalene, tazarotene, and tretinoin.
Retinoid affect multiple pathogenic mechanisms contributing to the
development and recurrence of acne:
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 Effective in promoting normal desquamation of follicular
epithelium, they reduce comedons, inhibit the development of
new lesions, and facilitate extrusion of keratinous plugs.
 Have a marked anti-inflammatory effect, inhibiting the activity
of leucocytes, the release of proinflammatory cytokines and
other mediators, the expression of transcription factors and tolllike receptors (TLRs) involved in the immunomodulation.
 Help penetration of other active agents.
 Anti-seborrhea effect: a significant inhibition of sebocytes
proliferation, differentiation and lipid synthesis in vivo and vitro
was noticed after addition of retinoid.
 A secondary benefit of the unplugging process is that it render
the involved follicles less anaerobic, thus inhibiting the growth
of P.acne.
4. Azelaic acid:
This dicarboxylic acid is remarkably free from adverse actions
and has mild efficacy in both inflammatory and comedonal acne, it
is bactericidal for P.acne, it is also anti-inflammatory and inhibits
the formation of comedons by reducing the proliferation of
keratinocytes. It may help to lighter post inflammatory hyper
pigmentation. It is available as 20% cream and 20% gel, and can be
applied twice daily.
5. Topical Antibiotics:Topical antibiotics are mainly used for their role against P
acnes. They may also have anti-inflammatory properties. Topical
antibiotics are not comedolytic, and bacterial resistance may
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develop to any of these agents. The development of resistance is
lessened if topical antibiotics are used in combination with benzoyl
peroxide. (erythromycin, Clindamycin , ciprofloxacin lotion,
Nadifloxacin).
6. Alpha- and B-hydroxy acids:
Alpha hydroxyacids occur naturally in sugar cane, fruits, and milk
products.
Most commonly glycolic, lactic, citric and gluconic
acids are used. Alpha hydroxyacids cause stratum corneum
desquamation and have action as a comedolytic aiding the
treatment of comedonal acne
7. Others topical agents:
a. Tea lotion: Topical 2% tea lotion was used mainly as
antibacterial agent in the treatment of acne vulgaris. In addition
epigallcatechins gallate of tea was reported to modulate the
production and biological action of androgen and other
hormones.
b. Zinc acetate: prolong the residence time of topical antibiotic
on the skin.
c. Dapson, a synthetic sulfone that has been available for over
60 years, has known anti-inflammatory and antibacterial
properties. It is safe and effective in the treatment of acne
vulgaris.
d. Topical nicotinamide 4% has anti-inflammatory action and
does not induce P.acne resistance.
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e. Picolinic acid gel 10%: It is an intermediate metabolite of
the amino acid, tryptophan. It has antiviral, antibacterial, and
immunomodulatory properties.
D- Physical Therapy:1. Acne surgery:- Comedone removal, especially white comedone by
puncturing the cyst.
2. U/V:- is doubtful
3. X-ray therapy:- Only for severe refractory cases.
4. Cryotherapy:- By nitrous oxide probe used for cystic acne.
5. Intralesional corticosteroids:- Used for nodular and
cystic acne vulgaris and keloid.
Topical Steroids Are Contraindicated In Acne Treatment
2- Systemic Treatment:A- Antibiotics:Tetracycline, erythromycin, methoprime, amoxyl, ampicillin derivatives,
dapsone or azithromycine. Tetracycline is given by 250 mg capsule qid
for 3-6 months, this treatment may causes Gram –ve folliculitis.
B- Estrogen (Hormonal):Oral contraceptives increase sex hormone–binding globulin, resulting in
an overall decrease in circulating free testosterone. In females with
premenstrual exacerbation to decrease androgen production from the
ovaries, we can use cimetidine or spironolactone which is weak antiandrogenic drugs that can be used with caution for males. Pregnancy
must be avoided while taking spironolactone because of the risk of
feminization of the male fetus. Adverse effects of spironolactone include
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dizziness, breast tenderness, and dysmenorrhea. Ketoconazole may be
used
C- Oral Retinoid: - (Isotretinoid)
Used for nodulocystic acne to:- Prevent and minimize scarring.
- Decrease differentiation and rapid turn over.
- Decrease seborrhea.
- Change in media.
- And also act as immunonodulator.
Isotretinoin is a teratogen, and pregnancy must be avoided. Contraception
counseling is mandatory, and 2 negative pregnancy test results are
required prior to the initiation of therapy in women of childbearing
potential. The baseline laboratory examination should also include
cholesterol and triglyceride assessment, hepatic transaminase levels, and
a CBC count. Pregnancy tests and laboratory examinations should be
repeated monthly during treatment. Isotretinoin may heighten feelings of
depression and suicidal thoughts. Do not administer isotretinoin to a
depressed or suicidal teenager. Although a cause-and-effect relationship
has not been established, patients should be informed of this potential
effect and must sign a consent form acknowledging they are aware of this
potential risk.
D- Oral Corticosteroids: - (Short Course)
- For nodulocystic acne, but when we have recovery, we should decrease
the dose to (5mg/day) for 2 wks then stop.
- For acne Fulminant we should give steroids.
- Coadministration of isotretinoin with steroids at the onset of therapy
may be useful in severe cases to prevent initial worsening.
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3- Treatment of Complications:A- Scarring:- Dermobrasion (Mechanical or chemical peeling) to
remove the epidermis and to the upper part of dermis so a new skin will
be formed.
B- Keloid:- Intralesional steroid injection (don't excess
because it will become bigger).
C- Mental scarring:- Reassurance, psychotherapy and
antidepressant may be used.
D- Conglobata & Fulminant Acne:- Steroids and antibiotics.
Acne Rosacea
* Chronic disorder of the face, usually after 30 years old (middle
age
and older), characterized by vascular component (Erythema &
telengectasia) with or without acne form component (papules, pustules,
nodules) but there is neither comedones nor scarring and the rash is not
tender.
* Pathology:- Dilatation of the vessels in the papillary dermis & sebaceous
hyperplasia are hallmarks.
- Agranulomatous dermal inflammations infiltrate containing
giant cells, may be seen in chronic cases.
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* Clinical
Features:-
1. Erythema of the cheeks, forehead, chin and nose, start as
temporary then becomes persistent.
2. Telangectasia.
3. Papules and pustules, painless and not tender.
4. Swelling as result of the defect of the blood vessels, also
not tender.
5. Lymphoedema.
6. No scarring.
7. Site:- Middle of the face, nose (butterfly rash).
* DDx.:1- Acne Vulgaris. (See the comparison).
2- Light Sensitivity. (Rapid onset & Lack of pustules)
3- Contact Dermatitis. (Rapid onset & Lack of pustules)
4- Lupus Erythematosus. (Rapid onset & there is rash)
5- Peri-oral Dermatitis. (On chin & upper lip)
6- Dermatomycosis.
* Complications:-
1. Rhinophyma. (In severe chronic cases, particularly in
males; the sebaceous gland hypertrophy is concentrated on
the
nose and produce gross soft tissue overgrowth and
hypertrophy, the resulting appearance termed
{Rhinophyma}).
2. Rosacea Lymphoedema.
3. Ocular congestion may lead to blindness.
* Treatment:-
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1- Topical Rx:- Sulfur, flagyl, gamma benzedene,
hexachloride benzoyl peroxide.
(Topical Steroids Are Contraindicated)
2- Systemic Rx:- Broad spectrum antibiotics, tetracycline is the most powerful to
prevent keratitis and conjunctivitis, also azithromycine can be used.
- Retinoic Acid (Isotretinoid) in severe cases.
- Systemic Zink Sulfate.
3- Cosmetic therapy:- Severe Rhinophyma should be treated by
sharing and skin grafting to reshape the nose.
* Comparison
between Acne Vulgaris & Acne Rosacea:-
Acne Rosacea
Acne Vulgaris
Age
After 30 year
Any age (adolescent)
Sex
Female > male
Female = male
Site
Middle 1/3 of face
Face, chest, upper back, arms,
buttocks and male genitalia
C/F
Erythema,
Same lesions but they are tender
telangiectasia, papule,
with presence of comedones and
pustule, nodule,
scarring
swelling, no tender
Cause
Autoimmune.
Bacterial infection
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