One skin disease that is always hot for adolescents and
young adults is acne or acne in medical language. The disease is not fatal, but
it is troubling because it deals with the decline due to reduced confidence in
the beauty of the patient's face.
Acne is a common term for acne vulgaris, which is common in
adolescence when the hormonal changes that produce more oil. This condition
tends to run in his family and are completely harmless. But some people who
have severe cases may feel very depressed and lose confidence in yourself.
Unfortunately, until now there has been no way of healing is complete, although
there are some ways which are helpful. Fortunately, this condition will have
improved with age.
People who have never stepped on puberty usually experience
acne. In the medical world, the acne is known as acne vulgaris. Is a chronic
inflammation of the follicle pilocebaceous (one of the glands in the skin),
accompanied by a blockage and accumulation of keratin, characterized by
comedones, pustules, nodules, and cysts. The affected area is not only the face
but also the shoulders, chest, back, and upper arms.
Definition
Acne is an inflammatory reaction in the sebaceous follicles
in general and is usually accompanied by the formation of papules, pustules and
abscesses, especially in areas that contain many sebaceous glands, such as the
face, chest and upper back.
Acne vulgaris is a chronic inflammatory pilosebaceous
follicles characterized by comedones, papules, pustules, and cysts, on the area
- the area of predilection like face, shoulder upper part of the superior
extremity, chest, and back.
Acne vulgaris is an inflammation of the sebaceous follicles
characterized by comedones, papules, pustules, cysts and nodules in place
predileksinya, face, neck, upper trunk, and upper arms. Is primarily in
adolescents who usually involuting before the age of 25 years but may continue
into adulthood. He mainly produced in the skin that is oily aikbat excessive production
of excessive sebum glands sebaseanya place a lot.
Acne is a condition in which the skin pores clogged causing
beruntus-beruntus and abscesses (pockets of pus) are inflamed and infected.
Acne is a skin condition that commonly occurs in the form of
blockage in the pores of the skin, raised spots and inflamed, if infected into
absess (containing pus).
Acne is a skin condition that is experienced swelling
(abscesses) on the skin surface, where the oil-producing glands clogged and
contaminated with bacteria. And this acne usually begins at 12- 20 years old.
ETIOLOGY
A variety of factors. The cause of acne is very much
(multifactorial), among others: genetic, endocrine (androgen, pituitary
sebotropic factor, etc.), dietary factors, the activity of the sebaceous gland
itself, psychological factors, season, infectious bacteria (Propionibacterium
acnes), cosmetics, and chemicals more.
The exact cause is unknown, but many factors that influence:
1. sebum
sebum is the main factor causing acne. Acne is hard always
accompanied by spending a lot sebore
1. Bacteria
Microbes are involved in the formation of acne is
Corynebacterium acnes, Stafilococcus epidermidis and Pityrosporum ovale.
Of the three most important of these microbes that C. acnes
which works indirectly.
1. Hereditary
Hereditary factors are very influential on the size and
activity of pallid gland (sebaceous glands). If both parents have acne scars,
most likely children will suffer from acne.
1. hormone
The hormone androgen. This hormone plays an important role
because pallid gland is very sensitive to these hormones. Androgen hormones
derived from the testes and adrenal glands (adrenals). This hormone causes
great bertamabah pallid gland and increased sebum production.
On inquiry Pochi, Frorstrom et al. & Lim James found
that the plasma concentration of testosterone in male acne sufferers are no
different to not suffer akne.Berbeda with women, the plasma testosterone
greatly increased in patients with acne.
Estrogen. In physiological circumstances, estrogen does not
affect the production of sebum. Estrogen may reduce levels of gonadotropin from
the pituitary gland. Gonadotropin hormone has the effect of lowering the
production of sebum.
Progesterone. Progesterone, in a number of physiological not
have any effect on the effectiveness of the fat glands. Sebum production
remained during the menstrual cycle, but sometimes progesterone can cause
premenstrual acne.
The hormones from the pituitary gland. In mice, the hormone
thyrotropin, gonadotropin, and corticotropin from the pituitary gland is
required for the activity of pallid gland. On the failure of hiopofisis glands,
sebum secretion is lower than the normal person. The decrease sebum allegedly
caused by a hormone derived from baga sebotropik middle (intermediate lobe) of
the pituitary gland.
1. Diet
Some authors exaggerate the influence of diet on acne, but
from the last investigation turns diet little or no effect on acne. In people
who eat a lot of carbohydrates and fatty substances, can not be ascertained
will terjkadi changes in expenditure composition of sebum or oil glands, not a
tool for spending the fats we eat.
1. Climate
In areas that have four seasons, acne usually intensified
during the winter, otherwise mostly improved in the summer.
Ultraviolet light (UV) has the effect of killing bacteria on
the skin surface. Moreover, these rays can also penetrate the lower epidermis
and upper dermis so the effect on bacteria that were inside the pallid gland.
UV rays can also hold exfoliation can help remove the blockage pilosebasea
channels.
According to Cunliffe, in the summer of acne obtained 60%
improvement, 20% no change, and 20% intensified. Great increases in the summer
acne is not caused by UV rays but by the amount of sweat on the circumstances
were very humid and the heat.
1. Psychic
In some patients, stress and emotional disturbances may
exacerbate acne. The exact mechanism is not yet known about it. Anxiety causes
sufferers aknenya mechanically manipulated, resulting in damage to the follicle
wall and raised beradang new lesions, another theory says that this
exacerbation caused by increased production of androgens from the adrenal
glands and sebum, even fatty acids in sebum increases.
1. cosmetics
The use of certain cosmetics ingredients, continuously for a
long time, can cause a mild form of acne which mainly consists of closed
comedones and papulopustular lesions on the cheeks and chin. Materials that
commonly cause acne is found in a variety of face cream powdery base
(faundation), moisturizer (moisturizer), retaining beige sun (sunscreen), and a
night cream. Which contain ingredients such as lanolin, pektrolatum, vegetable
oils and pure chemicals (butyl stearate, lauryl alcohol, and red dye D & C
and oleic acid).
Types of cosmetics that may cause acne does not depend on
the price, the brand, and the purity of the material. One can be more
comedogenic cosmetics without containing a special, but because these cosmetics
do contain a mixture of ingredients that are comedogenic or materials with
greater concentration. DiLeeds latest investigation failed to find a
relationship between duration of use and the number of cosmetic diapai with
great kane.
1. Chemical Substances
Some kinds of chemicals can cause erosion similar to acne
(akneform eruption), such as iodide, corticosteroids, INH, drug anticonvulsants
(difenilhidantoin, phenobarbital and trimetandion), tetracycline, vitaminB 12.
1. Reactivity
Besides the above factors still exist factor "X"
on the skin which is an important factor that determines the terrible acne.
EPIDEMIOLOGY
The incidence of acne vulgaris 80-100% in young adults, the
age group of 14-17 years in women and in men 16-19 years old. Nonetheless acne
vulgaris can also occur in younger or older than that age.
Although most acne occurs in adolescence or young adulthood,
but in reality acne also occur in various other age groups. Among others in
infants, children, even in the elderly. Acne is often associated with the
condition of the body, both in times of stress due to many problems, or can be
otherwise at the time was very happy.
At the time of puberty there is an increase of androgens
circulating in the blood which can lead to hyperplasia and hypertrophy of the
sebaceous glands.
CLASSIFICATION
The classification made by Plewig and Kligman in the book
Acne: Morphogenesis and Treament (1975):
acne:
A. Acne vulgaris and varieties:
acne tropicalis
acne fulminant
pyoderma fasiale
Acne and other mechanics
B. Acne venenata due to external kontaktan and varieties:
acne cosmetics
Pomeda acne
acne chlorine
Acne is caused by work
acne detergent
C. Acne komedonal due to physical agents and varieties:
Solar comedones
Acne radiation (x-rays, cobalt)
There are two types of acne: acne eruption true and
akneformis.
According grupper (1977) type of acne is as follows:
I.Acne True:
a. acne vulgaris
b. acne venenata
c. acne physics
a. Acne vulgaris:
1. acne troipika
2. acne mechanics
3. acne fulminant
4. pyoderma fasiale
5. acne neonatorum
6. acne because of hormones (testosterone, progesterone).
b. 1. Acne cosmetics
2. Ane chlorine
3. Acne office / work
c. 1. Acne Senile
2. Acne radiation
3 Acne estivalis
II. acneiform eruption
According to Frank (1979) akneformigs eruption was mixed:
1. Acne is not inflamed komedonal
2. Acne inflamed komedonal
3. mild acne papules
4. papulo-pustular acne
5. severe acne lesion rather a lot
6. Acne weight: nodes, cysts, many blackheads, papules,
pustules.
7. Acne conglobata.
Strauss in the book Dermatology in General Medicine (1993)
writes of acne consists of: 1. Acne vulgaris and 2. Miscellaneous types of acne
consisting of neonatal acne, acne excoriae des jeunes filles, drug acne,
occupational acne, acne tropikalis, acne stivalis , acne cosmetics, pomade
acne, acne detergent, mechanics acne, acne with facial edema, acne conglobata,
acne fulminant, and steatoma multiplex.
5. Pathogenesis
The pathogenesis of acne vulgaris is very complex,
influenced by many factors, and sometimes still controversial. Free fatty acids
are formed of triglycerides in the sebum causes the sebum viscosity increases
and cause obstruction and inflammation surrounding pilosebasea (comedogenic).
The formation of pus, nodes, and cysts occur afterwards.
There are four important things that is associated with
acne:
1. The increase in sebum secretion
2. The presence of follicular keratinization
3. bacteria
4. Inflammation (inflammatory).
1. The increase in the secretion of sebum
Acne usually starts during puberty when the sebaceous glands
enlarge and secrete more sebum. There is a great correlation between acne and
sebum production. Pallid gland growth and production of sebum under the
influence of androgens. In acne sufferers there is an increased conversion to
normal androgen hormones in the blood (testosterone) kebentuk more active metabolite
(5-alpha dihydrotestosterone). These hormones bind to the androgen receptor in
the cytoplasm and eventually led to the proliferation of sebum-producing cells.
Increased production of sebum in people with acne caused by
excessive end-organ response (end-organ hyperresponse) on a pallid gland to
normal levels of androgen in the blood. Proved that, in most patients, acne
lesions are found only in some places that are rich pallid gland.
Acne may also be related to the fat composition. Sebum is
comedogenic campuaran composed of squalene, wax (wax), esters of sterols,
cholesterol, polar lipids and triglycerides. In acne sufferers there is a
tendency to have levels of squalene and wax esters (wax) is high, whereas the
levels of fatty acids, especially acid leinoleik, low. Perhaps it is no
association with the occurrence of hiperkeratinisasi the sebaceous glands.
2. follicular keratinization
Pilosebasea keratinocytes in the channel caused by a buildup
korniosit in pilosebasea channel.
It can be caused by:
increasing eruption korniosis channel
pilosebasea
Release korniosit inadequate
The combination of the two
factors above.
There is an inverse relationship between secretion of sebum
and the concentration of linoleic acid in the sebum. According to Downing, a
result of increased sebum in acne sufferers, there is a decrease lenolik acid
concentration. It can cause acid deficiency lenoleik the follicular epithelium,
which will cause follicular hyperkeratosis and decrease barrier function of the
epithelium. Blackheads wall more permeable materials that cause inflammation.
Although lenoleik acid is an important element in seramaid-1, other fats may
also affect the pathogenesis of acne. Free sterol levels also decreased in comedones
causing an imbalance between free cholesterol with cholesterol sulfate so as
adhesion of corneocytes on akroinfundibulum increased, there follicular
hyperkeratosis.
3. bacteria
Three kinds of microbes involved in the pathogenesis of acne
is Acne corynebakterium, Stafylococcus epidermidis and Pityrosporum ovale
(malazzea furfur). Their sebore at puberty is usually accompanied by a rise in
the number of Corynebacterium acne, but there is no relation to the number of
bacteria on the skin surface or in the channel pilosebasea with great degrees
of acne. It seems that the three kinds of bacteria is not the primary cause of
the pathological process of acne. Some lesions may occur without any
microorganisms that live, while the other lesions that microorganisms may play
an important role. The bacteria may play a role in the length of each lesion.
Are the bacteria that dwell in the follicles (resident bacteria) held
exacerbations depending on the microenvironment within the follicle. According
to the hypothesis Saint-Leger squalene produced by pallid gland follicles and
glands are oxidized in these oxidation products can menyeebabkan occurrence of
blackheads. Reduced oxygen levels in the follicle and eventually became
C..Acnes colonization. These bacteria produce porphyrins, which when released
in the follicles will be a catalyst for the oxidation of squalene, so the
oxygen in the follicles plus reduced again. A decrease in oxygen pressure and
the high number of these bacteria can cause inflammation of the follicle. This
hypothesis can explain why acne can only occur in a few follicles, the
follicles while others remain normal
4. Inflammation
Factors that cause inflammation in acne is not known with
certainty. Originators chemotaxis is a cell wall and products produced by
C.Acnesseperti lipase, hyaluronidase, protease, lesitinase and nioranidase,
plays an important role in the inflammatory process.
Chemotactic factor of low molecular weight (does not require
a complement to work on), when out of the follicle, can attract polimorfi
nucleus leukocytes (PMN) and lymphocytes. When you get into the follicles, PMN
can digest C. acnes and secrete hydrolytic enzyme which could lead to damage of
sebaceous follicles. Lymphocytes can be the originator of the formation of cytokines.
Soluble keratin material, contained in the horn cells and
fat from the pallid gland can cause non-specific reaction, which is accompanied
by macrophages and giant cells.
In the early stages of inflammation caused by C.Acnes, also
occurs activation of classical complement pathway and the alternative
(classical and alternative complement pathways). The response of the host
against the mediator is also very important. Moreover antibodies against
C.Acnes also increased in patients with severe acne.
There are four main mechanism of occurrence of acne.
• The oil glands become large (hypertrophy) with increased
sebum production (due to androgen hormone stimulation)
• hyperkeratosis (skin becomes thick) follicular epithelium
(cells growing fast and fill the space polisebaceous follicle and form a plug).
• The growth of bacteria, Propionibacterium acnes fast
(pilosebaceous follicles are clogged trap nutrients and sebum and promoting the
growth of germs.
• inflammation (inflammation) due to the byproducts of bacteria
Propionibacterium acnes.
The formation process begins with inflammation of the skin's
oil glands, and can cause blockage of the flow of sebum released by the
sebaceous glands in the skin's surface, causing the eruption to the surface of
the skin that starts with blackheads. Inflammatory process will then make
blackheads develop into papules, pustules, and cysts nodes. When inflammation
occurs downs scarring.
Oil gland duct blockage can occur because:
1. Changes in the amount and consistency of the oil glands
in the skin that occur due to various factors, among others: genetic, racial,
hormonal, weather, food, physical stress, etc. Occurs in acne vulgaris. Many
are on the face, neck, back, shoulders and upper arms.
2. Closing the outlet of the sebaceous glands by external
past, both from cosmetics, chemicals, detergents. This type of acne disebutakne
venenata. Only in exposed areas, usually on the face, arm and forearm, and the
calf.
3. The outlet of the sebaceous glands narrowed due to
ultraviolet radiation or radioactive rays, known as physical acne.
CLINICAL SYMPTOMS
Complaint that often arises is usually more for aesthetic
nuisance or beauty felt by the patient, not because of physical disorders in
general health. Indeed, sometimes acne causes annoying itching or even pain,
but generally no overall effect on the body caused.
Patients usually complain of skin eruption at the site of
predilection, namely in the face, shoulders, neck, chest, upper back, and upper
arms. Can be accompanied by intense itching. Skin eruptions such as blackheads,
papules, pustules, nodes, or cysts. Fill blackheads sebum is thick or dense.
The contents of the cyst is usually pus and blood.
Nomenclature diagnosis of acne vulgaris can be done by:
1. Severity of disease
Acne vulgaris is mild, severe, and moderate. Acne vulgaris
I, II, III, IIV.
1. Clinical Morphology
Acne vulgaris komedonal, Papulosa, Pustular, nodulo-cystic.
Acne vulgaris is also called Papulosa komedonal and without
inflammation. Nodulosa-cystic acne vulgaris referred to as existing
inflammation.
1. Combination 1 & 2
Acne vulgaris mild Papulosa
Pustular severe acne vulgaris.
Light weight determination of disease or the level I - II -
III - IV differ among investigators from one another.
Here is listed four gradation according SBURY PILL (1963)
I. Blackheads in the face
II. Comedones, papules, pustules, and more inflammation in
advance
III. Comedones, papules, pustules, and deeper inflammation
on the face, back and chest.
IV. Acne conglobata.
Forms lesions of acne vulgaris is a polymorph. Typical
lesions are blackheads. When there is inflammation will be formed papules,
pustules, nodules, and cysts. When cured, erythematous lesions can leave and
post-inflammatory hyperpigmentation, even sikatrik like mold can form ice
atrophic (Ice pick scars atropic lilac) and keloid. Lesions mainly arise in
areas that have a lot of pallid gland is like the face, back and chest.
Blackheads commonly known senagai black heads (open
comedones) and a white head (closed comedones). Blackheads DAPT be basic in
acne lesions. He is due to the function of the sebaceous follicular wrong hole
or by process hiperkeratinisasi wrong with follicular lubah. Stoppers produced
follicle mouth blackheads and papules dilate formed by inflammation around the
blackheads. Small cysts, pustules, papules that have been infected or may form
around blackheads. Besides it can be seen nodules, granulomatous infiltration
in inflammation because of the fatty acid or piokokus, scarring and keloids.
II.7 DIAGNOSIS
Although one of lesions are more dominant than the other
lesions, the diagnosis is generally based on a mixture of acne vulgaris lesions
formed comedones, papules, nodules on the face, back and chest.
The diagnosis of acne vulgaris is established on the basis
of clinical and ekskokleasi sebum, clogging sebum expenditures with blackheads
extractor (spoon Unna). Sebum that clogs the follicle appears as a solid mass
such as a candle or a softer mass like rice which ends sometimes black.
Histopathologic examination showed a picture that is not
specific form of chronic inflammatory cell infiltration around the sebaceous
follicles with masses of sebum in the follicle. Cysts, inflammation is gone
replaced with connective tissue barrier liquid mass sebum mixed with blood,
dead tissue, and keratin loose.
Microbiological examination of the microorganisms which have
a role in the etiology and pathogenesis of the disease can be done full
microbiology lab for research purposes, but the results are often
unsatisfactory.
Examination and lipid composition of the skin surface (skin
surface lipids) can also be done for similar purposes. In acne vulgaris free
fatty acid content (free fatty acid) increases and therefore the prevention and
treatment of used ways to lower it.
Definite diagnosis according Orkins (1991)
Disease pleomorphic with a mix of open
comedones ( "blackheads"), closed comedones ( "white
heads"), papules, pustules, nodules, and may scar (scar)
Most of attacking teen
Generally, most in advance, also in the
back and chest, more in the middle (center)
According Andrianto and Sukardi (1988)
The diagnosis of acne is as follows:
Must be searched factors that cause or
originators including patient age
Clinical blackheads and found their
typical localization.
II.8. DIFFERENTIAL DIAGNOSIS
1. acneiform eruptions caused by drugs such as
corticosteroids, INH, barbiturates, iodide, bromide, difenilhidantoin,
trimetadion, ACTH, and other-other. Clinical form of eruption of
papules-papules that arise in various places on the skin without blackheads,
sudden onset, and sometimes fever. Can occur at any age.
2. True acne, such acne and acne venenata komedonal by
physical stimulation. Generally monomorfi lesions, no itching, can be comedones
or papules, with a predilection for on-site chemical contact or stimulation
fisisnya.
3. Rosacea (formerly: acne rosacea). Is a chronic
inflammatory disease in aerah advance with the symptoms of erythema, pustules,
teleangiektasis and sometimes with hypertrophy of the sebaceous glands in the
nose, cheeks, chin, and forehead. Can be accompanied by papules, pustules, and
nodules or cysts. Blackheads are not there, cause is food or hot drinks.
4. Perioral dermatitis that occurs primarily in women.
Polimorfi clinical form of erythema, papules, and pustules around the mouth
itch.
II.9. MANAGEMENT
The management of acne vulgaris include efforts to prevent
the eruption (preventive) and attempt to get rid of acne that occurs
(curative). Both of these efforts must be made simultaneously considering that
the disorder is due to many factors (multifactorial), both internal factors of
his own body (race, familial, hormonal), as well as external factors (food,
season, stress) that sometimes can not be avoided by people.
Treatment of acne
The goal of treatment is to prevent sikatrik acne and reduce
the frequency and severity of exacerbations acne, for that, in addition to the
necessary drugs are also required good cooperation between the patient with the
doctor who treated him.
General and Encouragement Mental A.Nasehat
1. Information
a. the patient must be explained that acne is caused by a
type of skin and hormonal changes during puberty, causing sebore and increased
production of horns in the canal pallid gland because pallid gland excessive
reaction against sex hormone levels are normal.
b. Nature is a recurrent acne-kumatan and we can only reduce
and control aknenya and not a cure.
c. Treatment of acne shares based on the type, severity,
localization, and of lesions. Treatment takes a long time and the possibility
of side effects diseratai.
d. 92% of acne patients will respond to treatment.
2. Treatment
1) Treatment in advance
The use of bacteriostatic soaps and detergents are not
recommended, even excessive use of soap is aknegenik and can cause acne
intensified (acne venenata).
According Plewig Kligman not proven that washing the face
will grow less in great or too seing face wash pointless. Washing your face
removes only fat that is on the surface of the skin, but does not affect the
existing fat in the follicle.
2) treatment of scalp and hair
As well as cleaning the face, scalp treatment also had no
effect on acne. Although according to many authors dandruff and seborrheic
dermatitis is more prevalent in people with acne, Plewig and Kligman investigation
failed to prove it. The use of shampoo containing a drug for acne sufferers
with dandruff, should be banned because it can aggravate acne and can
ketombenya recurrent back in a few weeks.
3) Cosmetics and other materials
Material-bahn which is aknegenik more influence on acne
sufferers. This material can form blackheads faster and more skin acne
sufferers. The patient should be advised to discontinue use of cosmetics thick
and just wear cosmetics lightweight, non-greasy and contains no drugs (non-medicated).
4) Diet
According to the new theory of food's effect on acne is
doubted by many investigators, the special diet is not recommended in patients
with acne.
5) Emotional and psychosomatic factors
In people who have a predisposition acne and emotional
stress can cause exacerbation or aknenya intensified. It should also be advised
to not fingering, massaging and rubbing acne, because it can cause a condition
called "acne mechanics".
B. Medicine
There are three things that are important in the treatment
of acne:
a. Prevents blackheads: commonly used materials exfoliation
b. Prevent or alleviate the outbreak mikrokomedo
reaksikeradangan.dalam this case, antibiotics have an effect.
c. Speeding beradang resolution.
Each chemical or physical irritants can increase blood flow,
may accelerate the regression of lesions beradang, because it can accelerate
the loss of mediator perradangan and toxic materials:
Physical irritants:
• UV Sinar
• Slush Cryo: CO2 solid,
liquid nitrogen, and freon.
Chemical irritants:
Resorcinol, sulfur, phenol, salicylic acid and others.
Acne treatment requires a long time until many months or
even years. To control the disease and prevent sikatrik. Mild acne requires
only a topical therapy, while patients with moderate and severe acne requires
oral and topical therapy. Patients may require periodic oral antibiotics for 6
months, ssedangkan topical therapy is required during the course of the
disease.
I. Topical treatments
Topical treatment that most of the benzoyl peroxide, vitamin
A acid and topical antibiotics.
Sulfur and resorcinol has been used for many years as the
material is held exfoliation (peeling) or dry up pimples. Sulfur still used
today. Substances may be comedogenic and comedolytic. This substance is a
"counter irritant" effective. Salicylic acid in propelen - glycol and
ethyl lactate may also be useful.
1. Tretinoin (vitamin A acid)
Kerass Tretinoin is a drug that can cause severe erythema
with pengelupaan skin, usually accompanied by a feeling like stinging or
burning, at the beginning, patients are encouraged to use the drug once a day
at night. In the event of erythema and diskuamasi after five days dpat drugs
used twice a day. The effect depends on the concentration, the basic material
used, the treated skin type and age of the patient. In general, the results of
new therapies looked after 8 weeks of treatment.
How it works tretinoin:
• comedolytic: preventing the cells horn attached to one
another by inhibiting the formation tonofilamen and reduce the bond between the
cells of keratin
• Accelerate the follicular epithelial cell turnover
• follicular epithelium that forms mikrokomedo become more
permeable, so that the toxic materials can be easier to get out and blackheads
will break.
• As a "counter-irritants", as it causes increased
vascularity and helps resorption papules and nodules which are difficult to
disappear.
On the use of tretinoin is recommended:
a. Avoiding the sun
b. Do not wash your face too often
c. Do not wear too many drugs
d. Careful use of the corner of the mouth, nose, and mucous.
Iso tretinoin. Disbanding premises tretinoin, nature
komedogeniknya 80% of tretinoin, anti-inflammatory and less likely ritatif.
2. Benzoyl peroxide
These substances not only kill bacteria but also causes desquamation
and also the incidence of clots in ddalm follicles. At the beginning of
treatment, the patients feel like a burn. These symptoms will be reduced in a
few weeks. Should be started on a low dose first, then gradually replaced with
high doses. The side effects of chronic use is sensitization in contact (2.5%
of cases).
Ways of working:
• Anti-bacterial strong
• comedolytic
• "counter-irritant"
Compared with vitamin A acid benzoyl peroxide
a. less irritating and unpleasant taste for people.
b. No cause great increase (flare-ups) acne in the first
month of treatment.
c. Drying the pustules are more precise than tretinoin.
d. In the form of blackheads, less effective than tretinoin.
The combination of vitamin A acid with benzoyl peroxide.
When vitamin A acid and benzoyl peroxide are used together, the synergistic
effect is obtained, but unfortunately they can not be used together in a single
base material. Vitamin A acid can cause the skin more permeable thereby
increasing the concentration of benzoyl peroxide in the network.
1. Topical Antibiotics
The use of antimicrobial agents can be justified, when
reducing the population of C. acnes or metabolites such as lipase or
porphyrins. But none bahanyang materials such effect is present in the form of
creams, solutions, gels, and soaps.
Antibiotics are often used:
Clindamisin 1%: relatively stable, except in some cases of
pseudomembranous colitis occur.
Erythromycin 2%: do not hold an irritant and can cause
contact dermatitis.
Tetracycline 0.5% -5%: it is now rarely used because it
causes the skin yellow.
1. Acid aseleik
A dikarbosilisik which can reduce the number of C. acnes.
The effect:
Same with benzoyl peroxide, vitamin A acid, eritromisi
topical, oral tetracycline.
Reducing granules keratohialin channel pilosebasea
Iritasinya nature is smaller and well tolerated DAPT
Have anti-inflammatory effects
1. alpha hydroxy acids (AAAH)
Work mechanism
Low concentrations: reduce cohesion korniosit useful for
lesions that are not beradang.
High concentrations:
Epidermolysis subkorneal roof pustule rupture.
Dermis: synthesize new collagen.
Effects of alpha acid hodroksi depending on the kind,
concentration, vehikulum, time of exposure and other conditions.
1.
Physical Irritants
II. Oral treatment
1. Oral Antibiotics
Because these drugs are used in
the long term, toxicity should be low. In this case, the antibiotic
tetracycline is primary, because it was known to the activity and toxicity. It
seems erythromycin also have the same therapeutic effect and is quite safe.
Oral antibiotics are the primary
indication papulopustular moderate to severe forms of acne conglobata.
Antibiotics are never used alone,
but together with drugs that hold exfoliation.
a. tetracycline
The most well known is the HCL
tetracycline, doxycycline, minocycline.
Effective against acnes
Corynebakterium invitro
Can inhibit the lipase extra
cellular issued by the bacteria.
Concentrated at the site of
inflammation.
Conventional Dosage: 1 gram per
day of tetracycline given half an hour before meals.
Minocycline: better absorbed and
is not affected by food, but expensive. A dose of 50-100 mg per day.
Dimiklosiklin 600 mg per day
b. erythromycin
Erythromycin is the drug of
choice for patients who are sensitive to tetracyclines or pregnant women.
Erythromycin and erythromycin
stearate is an acceptable form.
Have a bactericidal effect
against C. acnes.
Not inhibit lipase C. acnes.
Dosage: 1 gr / day
c. Lincomycin and clindamycin
Both the new and the drug most
equal effectiveness. Often menyebabka pseudomembranous colitis.
clindamycin:
Effective for cystic acne is
formed
Absorbsinya not affect food
Can inhibit the lipase C. acnes.
d. trimethoprim
This drug is as effective as
tetracycline, can be administered in patients who did not respond / intolerant
to tetracycline and erythromycin. Useful for gram-negative folliculitis.
1. DDS (Diamino Diphenyl sulfone)
Such as sulfonamides, DDS can
inhibit the use of PABA (Para Amino Acid benzoid) by bacteria. This medicine is
only digunaka for inflammatory acne terrific, such as acne conglobata and
papulo pustules are intractable.
DDS is never used alone, usually
together with antibiotics and drugs that can hold exfoliation.
How it works DDS:
-Anti-Inflammatory such as
corticosteroids
-Mustabilir Lysosomes.
-Side effects ; leukopenia,
agranulocytosis, nausea, vomiting, headache and skin reactions.
1. hormone
a. corticosteroids
Corticosteroids are useful for
intra lesions and sinus nodulocystic lesions in acne conglobata. Rapidly reduce
inflammation and prevent sikatrik. Used solution with a concentration of 2.5 mg
/ ml and injected can be repeated every 1 to 2 weeks.
1.
a. Estrogen and birth control
pills
Required relatively large doses
of estrogen that can cause feminization effects in men and menstrual disorders
in women. This hormone is better administered in pill form antihormon
containing estrogen and progesterone, especially for premenstrual acne.
Sometimes it seems paradoxical effect and visible pustules grow in the first
few months until the second month.
1.
a. anti-androgens
This hormone can prevent pallid
gland held a reaction to the [testosterone, cyproterone acetate together
esrogen only be used in women with acne and sebore great. Papulopustula
resistant acne and acne conglobata refractory.
Lately already produced a birth
control pills with low estrogen levels containing 2 mg of cyproterone acetate
and 35 mg ethinylestradiol.
Side effects such as decreased
libido, lethargy, nausea, weight gain and irregular bleeding.
1. Vitamin A
Can be administered orally
together with oral and topical antibiotics, vitamin A acid is highly effective
for acne nodules and cystic forms were terrific.
Allegedly this vitamin affects
the production or androgen metabolism.
Dosage: 50000-100000 Iu / day
1. Isoretinoit
A form of 13-cis / retinoic acid
is used for the treatment of cystic acne forms and konglobata.
In most cases, these drugs
provide complete remission for months - months to years.
Dose: 1 mg / kg / day.
Side effects: skin disorders and
mucous selapu such as cheilitis, serosis and bleeding nose. Isoretinoit is
keratogenik.
1. Zinc (Zink)
The effect is not known with
certainty, but it is suspected to have an inflammatory effect. These elements
affect the epithelialization, aktiitas enzyme in the metabolism of vitamin A,
and repair impaired leukocyte chemotaxis.
Dosage: 3 200 mg /
day.
1. Diuretics
Often exacerbation of acne 7-10
days before menstruation. This may be due to fluid retention before
menstruation, accompanied by hydration of the dermis and also edema in keratin.
Most investigators give diuretics one week prior to menstruation. Cuncliff and
William advocated kuarng than one week prior to menstruation, but Kligman did
not recommend granting the diuretics.
C. Special Measures
1. The extraction of blackheads
2. Incision and drainage
3. excision
4. Cryotherapy
5. Injection of collagen
6. and intralesional
corticosteroid injections
7. Laser CO2
8. Repair scarring
a. dermabrasion
b. chemical surgery
- tretinoin
- Alpha Hydroxy Acids useful for
smoothing sukatrik shallow.
According to Adhi Juanda (1999)
treatment of acne as follows:
1. Topical:
A. Materials - irritant
ingredients for example:
- Resorcinol 3%
- Salicylic acid 3-5%
- Acid vitamin A 0.05%
A. Anti-bacterial:
- Tetracycline 1%
- Eritromoisin 1%
- Clindamycin 1%
- Benzoyl Peroxide 2.5%
A. Other:
- Sulfur 4-20%
- Corticosteroids
- Ethyl lactate 10% in glycerin
5-10% and 80-85% ethanol.
II. systemic
A. Antibacterial:
-tetrasiklin 3-4 250 mg daily (the drug of choice)
-Minosiklin: 2 50 mg daily
-Kotrimoksasol: 2 grams a day, if
it has improved lowered 1 gram a day
-Linkomisin: 3 500 mg a day
-Klindamisin: 4 150 mg a day
A. Hormonal:
- Estrogen
- Anti-androgens
- Corticosteroids intra-lesion
A. Retinoids and vitamin A:
- Vitamin A 3 150,000 IU a day
- Retinoit 1-2 mg / kg daily
A. Other:
- Non-steroidal anti-inflammatory
(ibuprofen)
- Dapsone 2 100 mg
Dapsone (DDS) = diamino diphenyl
sulfone has anti-inflammatory properties that may be useful for the treatment
of acne nodulocystic / konglobata. DDS combination with antibiotics can
accelerate the repair of the lesion. Dose, orally 2 100 mg /
day of 4-week immersion.
III. other treatments
Such actions as sebum expenditure
by means of blackhead extractor or electric surgical, surgical frozen, and
intralesional injection.
IV. Skin hygiene and care for
those who need a diet can be recommended.
II.10. PROGNOSIS
Generally the prognosis is good,
but most sufferers are often recurrent. Acne vulgaris is generally cured before
reaching the age of 30-40's. Rarely acne vulgaris settled until a parent or
achieve gradations so severe need hospitalization in the hospital. However
there are intractable, there may be a genetic factor. When many sikatrik
dermabrasion can be done by an expert.