| What is acne vulgaris? | • Inflammation of pilosebaceous units, which is very common
• Appears on the face, trunk, and rarely buttocks
• Occurs most frequently in adolescents
• Manifests as comedones, papulopustules, nodules, and cysts
• Results in pitted, depressed, or hypertrophic scars |
| How is epidemiology of acne vulgaris? | • OCCURRENCE: very common, affecting
approximately 85% of young people
• AGE OF ONSET: Puberty; may appear for the 1st
time around 25 years or older
• SEX: More severe in males than in females
• RACE: Lower incidence in Asians and Africans
• GENETIC ASPECTS: Multifactorial genetic background and familial predisposition. Most individuals with cystic acne have a parent(s) with history of severe acne. Severe acne may be associated with XYY syndrome (rare) |
| How is pathophysiology of acne vulgaris? | • Sebaceous gland (hyperseborrhea)
• Keratinocytes of the follicle (Follicular differentiation -> Keratinization)
• Bacteria: Cutibacterium acnes, Staphylococcus epidermidis
• Microbiome
• Innate immunity (1st line defense)
• Genetic predisposition
Cutibacterium is an inhabitant of normal human skin and sebaceous follicles, density of colonization increases at puberty and associates w/inflammatory lesions, they modulate expression of immune markers, there is diversity in types predominant ones are IA1, CC18, A1 |
| How is pathogenesis of acne? | • Key factors are follicular keratinization, androgens, and Cutibacterium acnes
• Follicular plugging (comedone) prevents drainage of sebum
• Androgens (quantitatively and qualitatively normal in serum) stimulate sebaceous glands to produce more sebum
• Bacterial (C. acnes) lipase converts lipids to fatty acids and produces proinflammatory mediators (ILI, TNFα), which lead to an inflammatory response
• Distended follicle walls break; sebum, lipids, fatty acids, keratin, and bacteria enter the dermis, provoking an inflammatory and foreign body response. Intense inflammation leads to scars |
| Picture of pathogenesis of acne? | . |
| What are contributing factors of acne vulgaris? | • Acnegenic mineral oils, rarely dioxin,
• Drugs: Lithium, hydantoin, isoniazid, glucocorticoids, oral contraceptives, iodides, bromides and androgens, and danazol
• Others Emotional stress can cause exacerbations
• Occlusion and pressure on the skin, such as leaning the face on the hands, is a very important and often unrecognized exacerbating factor (acne mechanica)
• Cow’s milk may be associated with acne |
| What are clinical manifestatiosn of acne vulgaris? | • DURATION OF LESIONS: weeks to months
• SEASON: often worse in fall and winter
• SYMPTOMS: Pain in lesions (especially the nodulocystic type)
• SKIN LESIONS:
- Comedones—open (blackheads) or closed (whiteheads); comedonal acne
- Papules and papulopustules—a papule topped by a pustule; papulopustular acne
- Nodules/cysts ; 1-4 cm from repeated follicle rupture and inflammation, abscess formation
- Sinuses : draining epitheliallined tracts, scars atrophic depressed or hypertrophic |
| What is comedonal acne? | • Acne vulgaris: comedones Comedones are keratin plugs that form within follicular ostia and are frequently associated with surrounding erythema and pustule formation
• Comedones associated with small ostia are referred to as closed comedones or “white heads”
• Those associated with large ostia are referred to as open comedones or “black heads”
Initial stage: Open Comedo: The black surface is oxidized melanin not oxidized fat or dirt
Closed Comedo: papule without a readily visible central
pore and without any clinical signs of inflammation |
| What is nodulocystic acne? | • Nodulocystic acne: it starts with comedones—both open and closed comedones which then transform into papulopustular lesions that enlarge and coalesce, eventually leading to nodulocystic acne
• The lesions are very painful, and it is understandable that nodulocystic acne also severely impacts the social life of these adolescents |
| What is acne conglobata? | • Acne conglobata In this severe nodulocys?c acne, there are large confluent nodules and cysts forming linear mounds that correspond to interconnec?ng channels
• Pustula?on, crus?ng, and scarring
• Lesions are very painful |
| What are special forms of acne? | • NEONATAL ACNE Occurs on the nose and cheeks in
newborns or infants, and is related to glandular development; transient and self healing
Acne excoriée
• Usually occurs in young women, and is associated
with extensive excoriations and scarring resulting from emotional and psychological problems (obsessive compulsive disorder)
• The condition is more common in young women |
| What is SAHA? | • Testosterone,
• Androstene dione
• DHEA, DHEAS,
• In women of childbearing age, LH and FSH may be measured
• Pelvic ultrasound should be performed to look for PCO syndrome if there is a suspicion of hyperandrogenism (e.g. hirsutism, clitoromegaly, very early development of pubic or axillary hair) |
| What is acne fulminans? | Painful, haemorrhagic pustules, friable plaques and large, necrotic, ulcerating nodules mainly on the back but may involve the chest, face, neck and shoulders
• Association with systemic manifestations malaise, fever, chill, weight loss, diffuse myalgia, polyarthralgia, EN, hepatosplenomegaly, bone lesions, increased inflammatory markers (e.g. leukocytosis, neutrophilia, elevated ESR or CRP) and elevated LFT’s
• Comedones are uncommon and polyporous comedones are absent
• The condition typically occurs in individuals aged
13–16 years with a male to female ratio of 3:1 |
| How is dx and differential of acne? | • Comedones are required for diagnosis of any type of acne
• Comedones are not a feature of acnelike conditions
• Face: S. aureus folliculitis, pseudofolliculitis barbae, rosacea, and perioral dermatitis
• Trunk: Malassezia folliculitis, Pseudomonas folliculitis, S. aureus folliculitis |
| What are labs for acne? | • No laboratory examinations required
• In the overwhelming majority of acne patients, hormone levels are normal. If an endocrine disorder is suspected, determine free testosterone, folliclestimulating hormone, luteinizing hormone, and dehydroepiandrosterone sulfate (DHEAS) to exclude hyperandrogenism and PCOS
• Recalcitrant acne can also be related to congenital adrenal hyperplasia (11β or 21β hydroxylase deficiency)
• If systemic isotretinoin treatment is planned, determine transaminase (ALT, AST), triglyceride, and cholesterol levels |
| How is management of mild acne? | • The goal of therapy is to remove any plugging of the pilar drainage, reduce sebum production, and treat bacterial colonization. The longterm goal is prevention of scarring
• I. Mild Acne:
• Topical antibiotics (clindamycin and erythromycin) and benzoyl peroxide gels (2%, 5%, or 10%). Topical
retinoids (retinoic acid, adapalene, or tazarotene) require detailed instructions regarding gradual increases in concentration from 0.025% to 0.1% cream or gel. Best combined with benzoyl peroxide–mycin gels.
• Acne surgery (extractions of comedones) is helpful only when properly done and after pretreatment with topical retinoids. |
| How is management of moderate acne? | II. MODERATE ACNE Add oral antibiotics to the above regimen. Doxycycline is most effective, starting at 100 mg twice daily and tapering to 50 mg daily as acne lessens. Use of oral isotretinoin in moderate acne to prevent scarring has become much more common and is very effective |
| How is management of severe acne? | • In addiWon to topical treatment, systemic treatment with isotretinoin is indicated for cystic or conglobate
acne, or any other acne refractory to treatment
• This retinoid inhibits sebaceous gland function and keratinization, which is very effective. Oral isotreWnoin
leads to complete remission in almost all cases, lasting for months to years in the majority of patents
• Indications for Oral Isotretinoin: Moderate, recalcitrant, and nodular acne
• Contraindications: Isotretinoin is teratogenic and effective contraception is imperative. Concurrent tetracycline and isotretinoin may cause pseudotumor cerebri (benign intracranial swelling). Therefore, the two medicaWons should never be used together
Isotretinoin, 0.5 to 1 mg/kg daily given in divided doses with food to a total goal dose of 120 to 150 m |
| What are other systemic tx for acne? | • Adjunctive systemic glucocorticoids may be required in severe acne conglobata, acne fulminans, and SAPHO syndrome
• The TNFα inhibitor infliximab and anakinra are investigational drugs in these severe forms and show
promising effects
• For inflammatory cysts and nodules, intralesional triamcinolone is helpful (0.05 mL of a 3 to 5 mg/mL solution)
• Spironolactone for acne and hisrsutism |
