Acne – Physiopathology

Sebum hyper secretion and hyper keratin channel follicular (due to growth and proliferation acceding corneocytes) lead to the formation pimple which then evolves towards microchist or open pimple.

Micro cysts are the starting points of the inflammatory lesions, papules, pustules of derma wounds their training with larger retention elements retention macro cysts. Comedogenesis explain the mechanisms that are not fully elucidated; it seems that major androgens have propionic bacterium acnes and determinism in the inflammatory response.

Sebum hyper secretion is essential for formation of acne lesions. Sebum glands are under the control of androgenic stimuli and are considered as sebum secretion is triggered and maintained by free testosterone and testicular origin dehydriepiandrosteron and delta 4 androstendion home suprarenal.

Since testosterone dosage in patients with acne may show levels of normal serum and urine, are considered to be a different responsiveness to androgen (a sebum glands) from one person to another. The persons with acnee  metabolized more androgens receptors in sebum – pilos (2 up to 20 times more than the healthy subjects).

Cells exist in sebum enzymatic equipment able to convert precursors androgenic metabolites in active sebaceous lipid biosynthesis Material: 17 beta hydroxy steroid dehydrogenase, 3 beta hydroxy steroid dehydrogenase and 5 alpha reductase. Biological endocelular efect produced by these enzymes is dihydrotestosterone which is a hormonal stimulus selective secretion of sebum. The fact that acne is represented equally in both sexes that you sebaceea secretion is under the control of androgenic supra renal and not under the control of testosterone.

Hyper sebum is assessed according to the secretions sebum. On top acne subjects this level is increased and proportionally with the severity of acne. Dosage should not be made only if hormonal forms of acne accompanied by hirsutism or acne resistant to treatment.