Etiopathogenesis

Acne Vulgaris, experts confirm, is a disease whose etiology is universal and classically considered as a primary disorder of the pilosebaceous unit in which four factors A dermatologist has to spend much time on the first visit of a young man to get acne the patient feel comfortable and trust the professional. We must explain the concept which now has this condition, assuring him that modern medicine is well aware of this condition and there are many treatments to get the "control" of their injuries.

Acne vulgaris is a disease whose etiology is traditionally regarded as a primary disorder of the pilosebaceous unit, characterized clinically by recurrent episodes of inflammation, the presence of comedones, papules, pustules, nodules, abscesses, cysts and acne production cicatrices.En vulgar involving four factors namely:

1 - Obstruction of the pilosebaceous canal by hyperkeratosis of the excretory duct.

2 - Altered production of sebum (quantitative and / or qualitative).

3 - Biochemical changes in the surface lipids.

4 - Modification of the bacterial flora.

All these changes are directly or indirectly regulated by the levels of androgens produced at the gonadal, adrenal and peripheral tissues. The four factors are joined together resulting in acne inflammatory complications.

But what remains unclear is the first step of the process and why there are so conspicuous differences in the degree of injury between a patient and another. Probably the primary change is the alteration of the normal pattern of follicular keratinization, hyperkeratosis-keratosis determining follicular canal and consequently obstruct the pilosebaceous unit is the production of basic acne lesion: the comedo. As pathogenic variant of this traditional concept arises the theory of "primary deficiency of pantothenic acid.

We know the crucial role of this vitamin in many metabolic pathways and involved in the formation of coenzyme A and acyl carrier protein. The deficit in the AP cause, for example, impaired biosynthesis and oxidation of certain fatty acids. Well known skin changes due to this vitamin deficiency: hyperkeratosis, dermatitis, alopecia and graying prematuro.Cabe noted that the AP has a wide distribution in animal and plant tissues (hence the name is given as in Greek "pantos" means "everywhere"). Its deficiency is considered a rarity, due to the abundance of this vitamin in food.

Probably some patients with acne suffer a disruption in the absorption or metabolism of this substance.

Obstruction of the pilosebaceous canal: hyperkeratinization
Patients with acne have a Hypercornification manifested clinically by closed and open comedones. The cause is not clear to the classical hypothesis: the androgenic effect promote the irritant action of sebum lipids on the follicular canal. Early changes seen in the area infrainfundibular: there is increased epithelial proliferation and corneal cells are stuck together, unable to detach, the keratinous material becomes increasingly dense and disorganized and keratohyalin granules are increased. This leads to a hyperkeratosis of "retention" forming a true plug corneum. The walls of the dilating end infrainfundíbulo and thus constitutes the first lesion of acne: the closed comedo or whitehead. Hyperkeratosis is also seen at the mouth of the sebaceous gland. This results in the retention of sebum that the channel and gradually distends the gland. If the channel closed terms, the lesion is also evident as a closed comedo. The comedones normally contain tiny hairs and germs responsible for the inflammatory reaction. Note that the keratin is a powerful natural irritant.

Hydration
The hydration of keratin decreases follicular orifice and thus aggravating the acne: this accounts for the exacerbation of lesions in patients who work in laundries and kitchens. Perhaps this also justifies the increase in acne lesions in relation to the menstrual cycle: there has been a worsening of the same in the last week of the cycle, after the days when the canal is tighter because of the hydration keratin.

Bacterial Colonization
In acne there is an increase in sebum production compared with normal people. This not only depends on the sebaceous gland, but must be other hormone-like factors, bacterial or "metabolic" to play its role in the evolution of acne proceso.Probablemente begin at puberty as a result of a stimulation androgénica.Existen data that indicate that the fat plays an important role in this disease:

* You comedogenic: squalene, for example, has a great capacity to generate a microenvironment favorable for bacterial colonization and the production of comedones. It was found that saturated fatty acids of 10 a20C have the same capacity.

* It was found that the sebum of acne patients has decreased levels of linoleic acid. This expense would lead to ductal hyperkeratosis. It was also found an increase in the amount of squalene, a decrease of some free fatty acids and triglycerides increased in the surface lipids of acne patients.

* The controls acne by inhibiting sebaceous gland by different mechanisms of estrogen and androgen administration. Radiotherapy reduces sebum production.

* Free fatty acids are the most important fraction of tallow for the production of inflammation on todolos C8-C14 chain. For the reasons previously cited it appears that in periods of seborrhea is exacerbated acne, but it must be remembered that patients with seborrhea have no acne.