Diagnosis, Classification and Treatment Mark T. Jansen MD

Name: Diagnosis, Classification and Treatment Mark T. Jansen MD
Uploaded: 2017-08-25T01:08:53+00:00
Duration: PTM22S35
Channel: Delilah Welch
Description: Diagnosis, Classification and Treatment Mark T. Jansen MD

Diagnosis, Classification and Treatment Mark T. Jansen MD
ACNE VULGARIS Diagnosis, Classification and Treatment Mark T. Jansen MD

Disclosures “I have nothing to disclose” Mark T. Jansen MD

Acne Incidence and Prevalence
Most common in 15 to 42 yo range Affecting up to 100% age 12 to 17 In US, 50 million experience acne each year Approximately 7.7 million acne-related visits in US each year

Cost Yearly, 2.2 billion spent on acne care in US
1.7 billion on prescriptions 320 million on OTC products Other costs related to office visits

Etiology Increased sebum production
Increased proliferation and decreased desquamation of keratinocytes Propionibacterium acnes in follicles (anaerobic diphtheroid, normal flora) Comedone formation / inflammation

Pathogenesis Adrenarche (prepubertal rise in DHEA-S)
Sebaceous gland hypertrophy Increased sebum production Sebum-growth medium P. acnes Proliferation of P. acnes surface proteins-inflammation by triggering humoral and cell-mediated immune response

Etiology Misconceptions
“Blackheads are caused by dirt and poor hygiene” “If you wash harder, you wouldn’t have acne” “You have acne because you eat too much chocolate”

Etiology Misconceptions?
Milk – Nurses Health Study (47,000) women. Insulin Growth Factor (IGF) - Acne Milk high in IGF > 3 portions of milk/week associated with ^ incidence Acne High glycemic foods ^ IGF

Etiology Misconceptions?
Family History - > 3 fold risk if 1st degree family member had acne Stress – No affect on sebum production but severity worse with ^ stress, especially males BMI – Positive association - ^ BMI with ^ risk of acne for females only

Types of Lesions Microcomedone – Precursor of the clinical lesions of acne (8 wks. to mature) Closed comedone Open comedone Inflammatory papule Inflammatory pustule Inflammatory nodule

Microcomedo

Closed Comedone

Open Comedone

Inflammatory Papules

Inflammatory Pustules

Inflammatory Nodules and Nodulocystic Acne (cystic acne conglobata)

Treatment Who is the “patient”? “Buy in” by patient
Simpler regimen better than complex Cost of therapy considerations

Treatment Pustules can be converted to nodules and papules quickly
Inflammation and Post-inflammatory hyperpigmentation (PIH) slower to improve Establish realistic timetable and treatment end-point Consider long term consequences of the disease – trivial/short term vs. significant long term (scarring)?

Psychosocial “Complications” of Acne

Psychosocial “Complications”
Acne correlated with higher rates of: Depression Anxiety Social withdrawal Poor self esteem Suicide ideation Overall quality of life

General Guidelines Negotiate patient “buy in”
Establish realistic goals of treatment Simplify regimens Consider cost of therapy Inquire about OTC products that may ^ side effects or sabotage therapy Encourage water-based lotions, cosmetics and hair products (less comedogenic) over oil-based products

Treatment Most effective treatment addresses core factors promoting disease: Follicular hyperproliferation and abnormal desquamation Increased sebum production Propionibacterium acnes (P. acnes) proliferation Inflammation

Pathogenesis Specific Agents
Follicular hyperproliferation and abnormal desquamation Topical Retinoids (Tretinoin, Adapalene and Tazarotene) normalize follicular hyperkeratosis and normalize desquamation which prevents formation of micorcomedo

Topical Retinoids Vitamin A derivatives bind to receptors in keratinocytes Normalize follicular keratinization Decrease cohesiveness of keratinocytes reducing follicular occlusion and microcomedo formation

Topical Retinoids Anti-inflammatory effects Bind specifically to receptors that down regulate formation of pro-inflammatory protein AP-1 and expression of toll-like receptor (TLR)-2

Topical Retinoids Accelerate resolution of acne-induced post-inflammatory hyperpigmentation (PIH) PIH more common in patients with darker complexions

Topical Retinoids Tretinoin (Retin-A, Retin- Micro and generics) Adapalene (Differin and generics) Tazarotene (Tazorac – no generic psoriasis – pregnancy X)

Topical Retinoids Pearls of application Tretinoin (Retin-A) photo labile so night-time application preferred Only 19% stable 2 hours after UV sunlight exposure

Topical Retinoids Pearls of application Avoid tretinoin with benzoyl peroxide Oxidizes tretinoin especially with light exposure, inactivating drug

Topical Retinoids Pearls of Application Adapalene (Differin) and tretinoin gel microsphere (Retin-A Micro) more light stable Adapalene more stable in presence of benzoyl peroxide (combo Epiduo)

Pathogenesis Specific Agent
Agent Pro Con Tretinoin Generic available, multiple Degraded by light and strengths 0.01% gel, 0.025% benzoyl peroxide. cream/gel, 0.05% cream, Avoid in pregnancy. 0.1% cream gels more irritating than creams Adapalene Generic available in 0.1% Some formulations trade cream/gel. Trade name name only. Avoid in only in 0.1% lotion, 0.3%gel pregnancy Light stable. Less irritating. Can be used with BP Tazarotene Psoriasis and acne. Best No generic currently. Most for PIH. Most effective irritating. Pregnancy Available in 0.05% and 0.1% category X cream or gel

Retinoid Intolerance Irritation, dryness and flaking, worse in 1st month Avoid concomitant harsh soaps, toners, astringents, alpha hydroxy acids and salicylic acids

Retinoid Intolerance Consider application every 2nd or 3rd night Avoid “typical” soaps which have a pH of 9 to 10. Use synthetic detergent cleansers with a pH of 5.5 to 7 (Cetaphil, Dove Sensitive Skin Bar)

Retinoid Intolerance For true retinoid intolerance, consider alternatives: Azelaic acid – 15% gel (Finacea) and 20% cream (Azelex). Antimicrobial, comedolytic and anti-inflammatory comparable efficacy to tretinoin 0.05% cream

Retinoid Intolerance Alternatives continued: Salicylic acid. Induces keratolysis. Available in gel and pads with 0.5% and 2% as well as multiple products (cream, cloths, foam, cleansers, patches, pads, soaps, shower gels) of 2% concentration

Sebum production and the role of Androgens DHEA-S – Testosterone – DHT (all in the sebaceous gland) DHT attaches to receptors in the sebaceous gland that upregulate sebum production

Anti-androgenic agents OCAs – Low dose combination products estrogen dominant which makes them “anti-androgenic” Drospirenone containing pills (Yazmin and Yaz) may be superior in anti-androgenic effect (potassium sparing – monitor potassium during 1st cycle)

Third generation progestins Norgestimate Desogestrel (Less androgenic) Gestodene Second generation progestins Levonorgestrel Norethindrone (More androgenic)

Progestin-only Contraceptives Androgenic Low dose (mini-pill) Medroxyprogesterone injections Levonorgestrel IUD (Mirena) Etonogestrel implant (Implanon)

Androgen Receptor Blockers Spironolactone – Blocks androgen receptors and inhibits androgen biosynthesis (off-label use) 50 to 100mg/day in two divided doses

Spironolactone (continued) Monitor for hyperkalemia and hypotension at 4 and 6 wks. Black box warning (tumorigenic in chronic toxicity animal studies) Pregnancy category C – feminization of male fetus. Strongly consider OCAs

Antimicrobials Reduce Colonization of P. acnes Topical antimicrobials Oral antimicrobials (antibiotics)

Topical Antimicrobials Benzoyl peroxide (antimicrobial and comedolytic) Clindamycin Erythromycin Sulfacetamide Dapsone

Benzoyl peroxide Available in US in both Rx and OTC in 2.5% up to 10% gels, lotions, bars, pads, masks and liquid cleansers Applied BID Higher concentration not necessarily better. Higher concentrations more irritating and all may bleach hair/clothing

Clindamycin 1% concentrations in gel, solution, lotion, foam and pledgets Not effective as monotherapy. Use in combination with either retinoids or benzoyl peroxide to increase efficacy and reduce bacterial resistance.

Clindamycin Generic widely available in all forms Topical may be irritating. Prolonged use may predispose to fungal or bacterial superinfections including C. difficile. Warn to notify if patient develops diarrhea or bloody stool. Less likely than with oral form Pregnancy risk B

Erythromycin 2% concentrations in gel and solution formulations Avoid monotherapy. Consider combination with retinoid or benzoyl peroxide to increase efficacy and decrease bacterial resistance

Erythromycin Generic widely available in all forms May be irritating. Minimal systemic absorption. Potential for GI side effect minimal. Pregnancy risk B

Sulfacetamide Typically combined with 5% sulfur Not usually 1st line therapy Avoid in patients with allergy to sulfa or sulfonamide

Sulfacetamide Widely available as 10% gel, liquid, suspension, cream, lotion and pads Pregnancy risk C. Consider avoiding in potentially fertile females

Dapsone Topical 5% dapsone gel is newest topical antimicrobial that also has anti-inflammatory activity Unlike oral dapsone, no practical concern for use in individuals with G6PD deficiency. No associated hemolytic anemia or met- hemoglobinemia issues

Dapsone Not a sulfa. Not contraindicated in sulfa allergic patients Applied BID. No generic. May discolor skin/hair yellow-orange when used with benzoyl peroxide

Combination Topical Therapy Combination topical therapy shown to be more effective than monotherapy Evidence-based confirmation of superior efficacy of topical retinoids in combination with topical clindamycin, erythromycin or benzoyl peroxide

Combination Topical Therapy Two fixed antimicrobial / retinoid combinations available in US Clindamycin 1.2% / tretinoin 0.025% gel (Ziana, Veltin) Benzoyl peroxide 2.5% / adapalene 0.1% (Epiduo)

Combination Topical Therapy Resistance to topical antibiotics now widespread No resistance of P. acnes to benzoyl peroxide yet Combining topical antibiotics with benzoyl peroxide decreases development of resistance and improves treatment efficacy

Combination Topical Therapy Topical benzoyl peroxide / antibiotic combinations in US: BP 5% / clindamycin 1% gel (Benzaclin, Duac) BP 5% / erythromycin 3% gel (Benzamycin) BP 2.5% / clindamycin 1.2% gel (Acanya)

Topical Therapy Azelic acid – antimicrobial, comedolytic and anti-inflammatory properties 20% cream (Azelex), 15% gel (Finacea - approved in US for rosacea only) applied BID Equally efficacious to tretinoin 0.05% cream, BP 5% gel or 2% erythromycin

Oral Antibiotics Indicated for moderate to severe inflammatory acne May be used for patients with milder acne of the trunk where application of topicals are more problematic

Oral Antibiotics Inhibit growth of P. acnes in pilosebaceous unit Tetracycline class have anti-inflammatory properties too Systemic antibiotics tend more rapid clinical improvement than topicals but carry risk of more side effects (candidiasis, GI distress, significant allergic or toxic reaction)

Oral Antibiotics Prescribe for a limited course of 3 to 6 months to reduce risk of antibiotic resistance Consider discontinuation as acne improves No consensus as stopping systemic drug abruptly or in tapering fashion

Oral Antibiotics Tetracyclines (doxycycline, minocycline) Macrolides (erythromycin, azithromycin) Trimethoprim-sulfamethoxazole Clindamycin

Oral Antibiotics Emerging resistance of P. acnes 20% in % in 1996 Most common with erythromycin Least common with minocycline

Oral Antibiotics Reducing emergence of resistance: Use only when necessary. Limit treatment to < 6 mos. Stop if no additional improvement noted Give choice a minimum of 6 to 8 weeks (length of time-microcomedone to mature clinical lesion)

Oral antibiotics Reducing resistance continued: Change after 6 to 8 weeks if no response Partial response – continue 1st choice and reassess in 6 to 8 more weeks

Oral Antibiotics Reducing resistance continued: If stopped antibiotic needs to be restarted and was effective, resume same drug as long as works Avoid combination therapy with oral and topical antibiotics that have different mechanism of action Prescribe topical BP at start of oral antibiotic therapy

Oral Antibiotics Reducing resistance continued: Consider topical retinoid at initiation of oral antibiotic. Decreases resistance and more efficacious Consider topical retinoids for long term maintenance to decrease oral antibiotic use and sustain improvement

Oral Antibiotics Macrolides – Erythromycin, azithromycin Resistance now common GI side effects Consider only in patients where tetracyclines are contraindicated

Oral Antibiotics Tetracyclines – Hard to get tetracycline. Inactivated by food Doxycycline / minocycline not affected by food. Have anti-inflammatory effects. Minocycline has less resistance than doxycycline but generally higher cost

Oral Antibiotics Tetracyclines continued: Avoid < 9 yo and women who are or may become pregnant – teeth GI distress Esophagitis Pseudotumor cerebri, vertigo (minocycline) Photosensitivity, skin or liver discoloration

Oral Antibiotics Subantimicrobial doxycycline Maintains anti-inflammatory activity without antibacterial effect Maintains improvement in inflammatory acne without inducing resistance. 20mg BID

Oral Antibiotics Alternative oral antibiotics Trimethoprim – sulfamethoxazole Effective in more severe, recalcitrant acne but with associated risk of photosensitivity, bone marrow suppression and Stevens-Johnson syndrome

Oral Antibiotics Clindamycin – Risk of pseudomembranous colitis (C. diff ) Cephalexin – Little evidence. Hydrophilic so doesn’t penetrate pilosebaceous unit well. May promote MRSA

Isotretinoin Reserved for severe, recalcitrant nodulo-cystic acne Restricted prescribing (iPLEDGE) Severe teratogenic effects

Summary Negotiate patient “buy in” Simplify treatment regimens
Cost conscious Evidence based Remember pregnancy potentials Good “stewardship” of oral antibiotics Psychological considerations

Summary Target areas of pathophysiology Follicular hyperproliferation, abnormal desquamation Increased sebum production P. acnes proliferation Inflammation

Diagnosis, Classification and Treatment Mark T. Jansen MD

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