2. Some facts abut acne 1. peak age 12 to 18 yo 2. more severe
in males 3. most common affected sites face truncal 3. CPG to
provide an evidencebased guidance for primary care physicians and
other healthcare providers to identify the appropriate management
of acne. CPG 4. Pathogenesis **** multifactorial. Acne vulgaris can
be divided into noninflammatory (open and closed comedones) and
inflammatory (papules, pustules and nodules) lesions. The most
important factors involved are: a. Increased sebum production b.
Propionibacterium acnes proliferation c. Altered follicular
keratinisation d. Inflammation 5. 1) INCREASED SEBUM PRODUCTION
Androgen Mediated Sebum Production - overstimulation of the gland
by high levels androgens or by hypersensitivity of normal levels
androgens - regulate genes responsible for sebaceous gland growth
and sebum production. -The pilosebaceous unit possesses the steroid
metabolising enzymes that convert DHEAS to testosterone and DHT. -
Testosterone is also converted to the more potent androgen i.e. DHT
by the enzyme 5-reductase. 6. B)Propionibacterium (P) acnes
Proliferation normal anaerobic resident of pilosebaceous unit that
colonises acne prone areas of the skin (in sebaceous hair follicle)
7. proliferation of these bacteria is responsible for the
initiation of inflammation. inflammatory response to the bacterium
and these metabolic by products leads to the formation of papules,
pustules, and nodules 8. c) Altered Follicular Keratinisation - In
patients with acne, the rate of keratinocyte desquamation at the
follicular infundibulum is altered. - The keratinocytes accumulate
and become interwoven with monofilaments and lipid droplets - This
accumulation of cells and sebum results in the formation of
microcomedones (the microscopic precursor to all acne lesions) -
There is also the presence of 5-reductase activity in the
infrainfundibular segments of sebaceous follicles which increases
androgen production and subsequent follicular hyperkeratosis 9. D)
Inflammation - Cellular products from P. acnes stimulate the
recruitment of CD4 ,lymphocytes and subsequently neutrophils -
These inflammatory cells penetrate the follicular wall, causing
disruption of the follicular barrier. - This leads to the release
of lipids, shed keratinocytes and P. acnes into the surrounding
dermis, inciting further recruitment of inflammatory cytokines and
neuropeptides including substance **Linoleic acid has also been
found to regulate IL-8 secretion and reduce the inflammatory
reaction **Hence, deficiency of linoleic acid may increase
hyperkeratinisation of the epidermis. 10. Risk and aggravating
factors Risk factors Aggravating factors A significant positive
family history of acne has been demonstrated especially when acne
is found in: twins (p
