여드름.

01 —What it is

Acne vulgaris is a disease of the pilosebaceous unit — the structure containing a hair follicle and its associated oil gland. It affects up to 85% of people aged 12 to 24.^¹ It is by far the most common skin condition in adolescence. Despite this, it is also one of the most psychologically loaded — the Cardiff Acne Disability Index (CADI) consistently picks up impairment comparable to that seen in moderate asthma or epilepsy.^²

02 —The four-part biology

Four things go wrong together to make a spot:

• —Excess sebum. Androgens (the hormones that surge in puberty) cause oil glands to produce more sebum.
• —Follicular hyperkeratinisation. The lining of the hair follicle becomes sticky; dead skin cells do not shed properly. The pore clogs.
• —Bacteria. Cutibacterium acnes (formerly Propionibacterium acnes) thrives in the oily, blocked pore. It is not an 'infection' in the classical sense — these bacteria are part of normal skin flora; the problem is the change in their environment.
• —Inflammation. The immune system reacts to the bacterial activity and the trapped sebum. This is what produces the red, swollen, sometimes painful papules and cysts.

The four mechanisms map directly onto the four classes of acne medication, which is why combination treatment usually works better than single agents.

03 —The evidence-based treatment ladder

For mild–moderate acne (predominantly comedonal or inflammatory)

• —Topical retinoids (adapalene, tretinoin, trifarotene). These work on hyperkeratinisation — they normalise pore shedding. They are the single most important class of topical acne drug. Use nightly; expect 8–12 weeks for visible improvement; expect mild peeling and irritation at first. Adapalene 0.1% is available over-the-counter in some countries.
• —Benzoyl peroxide. Antibacterial and mildly comedolytic. Works on the bacteria and the inflammation. Bleaches towels and pillowcases — use a white pillowcase.
• —Topical antibiotics (clindamycin, erythromycin) — always combined with benzoyl peroxide to prevent resistance. Never used alone.
• —Azelaic acid. A gentler option; useful in skin of colour because it also helps post-inflammatory hyperpigmentation.

For moderate–severe acne (or failure of topical therapy)

• —Oral antibiotics — doxycycline or lymecycline, typically 3–6 months, always alongside a topical retinoid + benzoyl peroxide. Increasingly limited duration due to antimicrobial stewardship concerns.
• —Hormonal therapy — combined oral contraceptive pills with anti-androgen effects, or spironolactone. Effective in many people with acne flares around the menstrual cycle.
• —Isotretinoin (oral retinoid). The single most effective treatment for severe or scarring acne. Curative in many cases. Requires monitoring (liver function, lipids, pregnancy prevention in females of reproductive age) and is associated with mood-related side effects in a small minority. Prescribed by dermatologists.^³

For acne scarring

Prevent before it forms. Scarring is largely a function of duration and severity of inflammation. Effective early treatment is the best scar prevention. Established scarring is treated with combinations of laser, microneedling, chemical peels, and (for ice-pick scars) TCA CROSS or subcision — but these are second-line. Treat the active acne first.

The single biggest mistake in adolescent acne is waiting too long to escalate. Mild treatment for moderate disease produces moderate disease for years.

04 —What does not help (or helps less than advertised)

• —Excessive cleansing and scrubbing. Damages the barrier, often makes inflammation worse. Twice-daily gentle cleansing is the ceiling.
• —'Pore-minimising' toners. Pore size is largely genetic; products do not change it.
• —Dietary cure-alls. The evidence for a specific dietary trigger is mixed at best. High-glycaemic diets and skim dairy may worsen acne in some people; chocolate, fried food, and most other commonly-blamed foods do not have strong evidence.^⁴
• —'Detox' products. Skin does not detox; the liver and kidneys do.
• —Toothpaste, lemon juice, and other home remedies. Variable; usually irritating; occasionally cause chemical burns.

05 —Acne in skin of colour

Two specific considerations:

• —Post-inflammatory hyperpigmentation (PIH) is often more distressing than the acne itself. Aggressive treatment of inflammation upfront is the best PIH prevention. Azelaic acid, niacinamide, and (under dermatologist supervision) hydroquinone or tranexamic acid can help established PIH.
• —Keloid scarring risk is higher; avoid picking, and treat severe acne early to reduce risk.

06 —What to ask your doctor

• —Am I on the right combination of treatments for the type and severity of my acne?
• —How long should I expect to wait before judging if this is working?
• —Should I be considered for isotretinoin? (Especially if scarring or treatment-resistant.)
• —Is the acne affecting my mood, sleep, or school? How should we factor that in?
• —Do I have post-inflammatory hyperpigmentation or scarring that needs separate attention?

1. 01
   Lynn DD, Umari T, Dunnick CA, Dellavalle RP. The epidemiology of acne vulgaris in late adolescence. Adolesc Health Med Ther 2016;7:13-25. PMID 26955297
2. 02
   Mallon E, Newton JN, Klassen A, Stewart-Brown SL, Ryan TJ, Finlay AY. The quality of life in acne: a comparison with general medical conditions using generic questionnaires. Br J Dermatol 1999;140(4):672-676. PMID 10233319
3. 03
   Layton AM, Knaggs H, Taylor J, Cunliffe WJ. Isotretinoin for acne vulgaris — 10 years later: a safe and successful treatment. Br J Dermatol 1993;129(3):292-296. PMID 8286227
4. 04
   Bowe WP, Joshi SS, Shalita AR. Diet and acne. J Am Acad Dermatol 2010;63(1):124-141. PMID 20338665