Acne Vulgaris by Alan R. Shalita, James Q. Del Rosso, Guy Webster

By Alan R. Shalita, James Q. Del Rosso, Guy Webster

The American zits and Rosacea Society is devoted to advancing the technological know-how on the topic of pimples and rosacea and to bettering communique among these attracted to those illnesses. this article isn't intended to be a complete treatise on all elements of zits, yet particularly to handle significant sights by way of stated idea leaders within the box within the wish that it'll bring about additional study, dialogue, and refinement of our innovations of either the pathogenesis and the therapy of acne.

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Thiboutot DM, Knaggs H, Gilliland K, et al. Activity of type 1 5 alpha reductase is greater in the follicular infrainfundibulum compared with the epidermis. Br J Dermatol 1997; 136:166 171. 46. Eady EA, Cove JH. Is acne an infection of blocked pilosebaceous follicles? Impli cations for antimicrobial treatment. Am J Clin Dermatol 2000; 1:201 209. 47. Guy R, Kealey T. Modeling the infundibulum in acne. Dermatology 1998; 196:32 37. 48. Webster GF. Inflammation in acne vulgaris. J Am Acad Dermatol 1995; 33: 247 253.

7th ed. New York: McGraw Hill, 2008. 24 INNATE IMMUNITY IN THE PATHOGENESIS OF ACNE VULGARIS 26. Williams IR, Rich BE, Kupper TS. Cytokines. , eds. Fitzpatrick’s Dermatology in General Medicine. 7th ed. New York: McGraw Hill, 2008. 27. Chu D. Development and structure of skin. , eds. Fitzpatrick’s Dermatology in General Medicine. 7th ed. New York: McGraw Hill, 2008. 28. McInturff JE, Kim J. The role of toll like receptors in the pathophysiology of acne. Semin Cutan Med Surg 2005; 24:73 78. 29. McInturff JE, Modlin RL, Kim J.

Patients with acne have a slightly higher level of this enzyme compared to patients without acne, indicating increased capacity for producing androgens (33). The role of androgens in comedo formation, and whether the increase in enzyme level is a consequence of acne or its cause, remains to be determined. However, it is known that androgenic stimulation leads to excessive ductal and infundibular hyperkeratinization. This effect is potentiated by synergistic growth factors, neuropeptides and IL-1a, and hyperproliferation and hypercornification of the follicular wall could be blocked by the addition of IL-1 receptor antagonist (19).

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