Acne vulgaris, more commonly referred to simply acne, is a chronic inflammatory disorder of the pilocebaceous unit.
characterized by:
■ abnormalities in sebum production
■ follicular desquamation
■ bacterial proliferation
■ inflammation
Acne vulgaris is the most common cutaneous disorder.
It affects more than 17 million Americans.
Patients can experience significant psychological morbidity
and, rarely, mortality due to suicide.
Important that physicians are familiar with Acne Vulgaris and
its treatment.
affects all races and ethnicities with equal significance.
Darker skinned patients at increased risk for developing
post-inflammatory hyper-pigmentation and keloids.
Acne is polygenic and multi-factorial. Four main pathogenetic
factors contribute to the disease:
Propionibacterium acnes and Staphylococcus epidermidis
colonisation. :
bacteria found deep in follicles and stimulate the production
of pro-inflammatory mediators and lipases.
Inflammation and immune response. Inflammatory cells and
mediators efflux into the disrupted follicle, leading to the
development of papules, pustules, nodules, and cysts.
Sebaceous gland hyperplasia and excess sebum production.
Abnormal follicular differentiation.
Propionibacterium Acn
Propionibacterium acne is a gram-positive, non-motil rods relatively
slow growing typically aerotolerant anaerobic gram positive bacterium
S. epidermidis is a very hardy microorganism, consisting of
nonmotile, Gram-positive cocci, arranged in grape-like clust-
ers.is part of human skin flora and consequently part of human
flora. Although S. epidermidis is not usually pathogenic,
patients with compromised immune systems are often at risk
for developing acne.
The initial step in the development of acne is the formation of
the microcomedo.Follicular keratinocytes that exhibit increas-
ed cohesiveness do not shed normally, leading to retention
and accumulation.
Androgens stimulate enlargement of sebaceous glands and
increased sebum production, and the abnormal keratinaceo-
us material and sebum collect in the microcomedo.
This leads to a build-up of pressure, and whorled lamellar
concretions develop. At this stage, a non-inflammatory
comedo may be seen clinically.
This micro-environment allows the proliferation of bacterium,
which is part of the normal flora of follicles. This gram-positive
rod has low virulence but is capable of metabolising
triglycerides and releasing free fatty acids.This metabolism,
as well as its ability to activate complement, produces pro-
inflammatory mediators, including neutrophil chemo-
attractants.
With increased pressure and recruitment of inflammatory
mediators, the microcomedo may rupture and release
immunogenic keratin and sebum, thus stimulating an even
greater inflammatory response
Depending on the specific inflammatory cells present,suppur-
ative pustules or inflamed papules, nodules, or cysts may
develop. If a sufficient amount of inflammation and tissue
damage results, post-inflammatory hyperpigmentation and
scarring may result.
Closed comedone (whitehead) - a clogged follicle.
Whiteheads usually appear on the skin as small, round, white
bumps.
Open comedone (blackhead) - a plugged follicle that opens
and turns dark at the surface of the skin. Blackheads do not
indicate the presence of dirt.
Papules - inflamed lesions that appear as small, pink bumps
on the skin.
Pustules (pimples) - inflamed pus filled lesions that are red at
the base.
Cvsts and nodules - large, inflamed, pus filled lesions deep
under the skin that can cause pain and scarring.
Local symptoms :
include pain
tenderness.
Systemic symptoms:
most often absent
Severe acne with associated systemic signs and symptoms
such as Fever, Psychological impact on any patient
The goals of pharmacotherapy for acne vulgaris are to reduce
morbidity and to prevent complications.
Medication: Benzoyl Peroxide Antibiotics,Topical and Oral
retinoids
Benzoyl Peroxide :
Benzoyl peroxide is a first-line treatment for mild and
moderate acne vulgaris due to its effectiveness and mild side-
Topical and systemic antibiotics used in the treatment of
acne vulgaris are directed at Propionibacterium acnes.
They also have anti-inflammatory properties.
Minocycline
Doxycycline
Tetracycline
Retinoids
These agents decrease the cohesiveness of abnormal hyperproliferative
keratinocytes, and they may reduce the potential for malignant degene-
ration. They also modulate keratinocyte differentiation.
isotretinoin
Tretinoin topical
Adapalene
Tazarotene
Alternative treatments
Phototherapy with blue and red light emitted from special
fluorescent lights, LEDs, lasers, or dichroic bulbs.
Photodynamic therapy involving intense blue or violet light,
zinc, teat tree oil, heat therapy, salt water therapy are all
used for treating acne.
Prognosis
Acne of any severity usually remits spontaneously by the
early to mid-20s,but a substantial minority of patients,
usually women, may have acne into their 40s.
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