Acne vulgaris and

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Acne vulgaris and acneiform eruptions :

Acne vulgaris and acneiform eruptions

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Acne is a chronic inflammatory disease of the pilosebaceous units,characterized by comedones , papules, pustules, nodules and often scar Occurrence - Very common, 85% of young people Age of Onset – Puberty 10 to 17 years ,may appear first at 25 years or older. Sex - More severe in male than female Genetic Aspects - Multifactorial genetic background Familial predisposition-majority of individuals with cystic acne have parent with history of severe acne Severe acne - XYY syndrome

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Etiology and Pathogenesis The pathogenesis of acne is multifaceted (4) basic steps have been identified (1) follicular epidermal hyperproliferation (2) excess sebum production (3) inflammation (4) presence and activity of Propioni bacterium acnes

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(1)Follicular epidermal hyperproliferation -Epithelium hair follicle hyperkeratotic with increased cohesion -Result plug in follicular ostium . causes downstream concretions of keratin, sebum and bacteria to accumulate in the follicle cause dilation of upper hair follicle producing a microcomedone -Stimulus for hyperproliferation and increased adhesion is unknown -Several proposed factors : androgen stimulation , linoleic /A , and IL-1 α activity

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Androgen stimulation - Dihydrotestosterone (DHT) is a potent androgen stimulate follicular keratinocyte proliferation -17β- hydroxysteroid dehydrogenase and 5a- reductase are enzymes responsible for converting DHEAS to DHT -Follicular keratinocytes show increased 17 β -HSD and 5a-reductase activities -Individuals with complete androgen insensitivity do not get acne Linoleic /A - essential fatty acid in skin ,decreased in pt e acne -Subnormal levels induce follicular keratinocyte hyperproliferation and produce pro-inflammatory cytokines IL-1 -contribute to keratinocyte hyperproliferation IL-1 R antagonists inhibit microcomedone formation

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(2)Excess sebum production -Pt with acne produce more sebum than without acne -One of the components of sebum-TG play a role in acne pathogenesis -TG are broken down into FFA by P acnes -FFA promote further bacterial clumping and colonization ,incite inflammation and comedogenic -Androgenic hormones increased sebocyte activity -Pt with acne have higher average serum androgen levels than unaffected control

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-Role of estrogen on sebum production not well defined -Dose of estrogen required to decrease sebum production greater than dose to inhibit ovulation (1) directly opposing effects of androgens (2) inhibit production of androgens via negative FB loop on pituitary gonadotrophin release (3) regulating genes that suppress sebaceous gland growth or lipid production

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(3)Inflammation Microcomedo continues to expand ,this distension causes follicular wall rupture Extrusion of keratin sebum and bacteria into dermis results in brisk inflammatory response Predominant cell type within 24 hours of comedo rupture is lymphocyte 1 to 2 days after , neutrophil predominant cell type

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(4) Propioni bacterium acnes Gram- positive, anaerobic, microaerobic bacterium found in the sebaceous follicle Adolescents with acne have higher concentrations compared to non-acne controls Cell wall of P acnes contains carbohydrate antigen stimulates antibody development Antipropionibacterium antibody enhances inflammatory response by activating complement Eliciting a delayed type hypersensitivity response and by producing lipases, proteases, hyaluronidases , and chemotactic factors Stimulate release of pro-inflammatory cytokines -IL-1, IL-8, IL-12, and tumor necrosis factor- α

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Clinical Findings History Classic acne vulgaris g radual onset of lesions around puberty Neonatal acne appears 2 weeks of age Infantile acne at 3 to 6 months of age Abrupt onset of acne should be consider underlying etiology Hyperandrogenism considered in female patient –acne severe, sudden onset, asso : with hirsutism or irregular menstrual periods Complete medication history important Drug-induced acne cause an abrupt onset, monomorphorous Can caused: anabolic steroids, corticosteroids, corticotrophin, phenytoin , lithium, isoniazid , vit B complexes, halogenated compounds & some chemotherapy Premenstrual flare about 70% of women flare Possibly, related to premenstrual change in hydration of pilosebaceous epithelium

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Cutaneous lesions Primary site is face (99%)and back(60%), chest(15%), and shoulders. trunk, lesions concentrated near midline Seborrhoea is frequent and distressing feature Lesions may be either noninflammatory or inflammatory Noninflammatory lesions are comedos , which may be either open (blackheads )or closed (whiteheads) Open comedone -flat or slightly raised lesion with central dark-colored follicular impaction of keratin and lipid Closed comedone -pale, slightly elevated, small papules and do not have clinically visible orifice ,stretching skin is aid in detection Inflammatory lesions vary from small papules with a red border to pustules to large, tender, fluctuant nodules

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closed comedones which are only seen clearly on stretching the skin

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Mild acne Moderate acne Severe acne

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Scarring complication of both noninflammatory and inflammatory acne 4 general types of acne scars: ice pick, rolling, boxcar, and hypertrophic Ice pick-narrow deep scars widest at surface of skin and taper to a point in dermis Rolling scars -shallow wide scars have undulating appearance Boxcar scars -wide, sharply demarcated , width is similar at surface and base Especially on trunk, scars may be hypertrophic.

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Differential diagnosis Acne is rarely misdiagnosed Rosacea -occurs in older patients and lacks comedones , nodules, cysts or scarring -presence of facial flushing and specific triggers, including heat, spicy food or alcohol Perioral dermatitis -females, lesions itch, skin is dry and no comedones Milia -Whiteheads (closed comedones ) may be confused with milia.Milia represent subepidermal keratin cysts predominantly infraorbital in distribution Gram negative folliculitis and rarely Candida or S. epidermidis folliculitis may present as multiple pustules

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Treatment of Acne The mechanism of action of the most common treatments for acne can be categorized in the following categories Correct the altered pattern of follicular keratinization Decrease sebaceous gland activity Decrease the follicular bacterial population, particularly P acnes Exert an anti-inflammatory effect General principle Avoidance of specific foods is not necessary Scrubbing of face will not only increase irritation but may worsen acne due to friction Utilization of only prescribed medications and avoidance of potential drying over-the-counter products, such as astringent, harsh cleansers or antibacterial soaps, should be emphasized Twice daily washing with a gentle cleanser followed by application of acne treatments may encourage

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TopicalAgents AZELAIC ACID- available in 20% cream or 15% gel - dicarboxylic acid has both antimicrobial and comedolytic properties -competitive inhibitor of tyrosinase , decreasing pigmentation -can be used in post-inflammatory hyperpigmentation -transient burning can occur and safe in pregnancy BENZOYL PEROXIDE - powerful antimicrobial agent -decrease hydrolysis of triglycerides -preparations available in creams, lotion, gels, washes -significant dryness and irritation -bacteria are unable to develop resistance making it ideal agent for combination therapy

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TOPICAL ANTIBIOTICS – -Erythromycin and clindamycin are most commonly used -Increased levels of P acnes resistance have been reported – -Development of resistance is less likely treated with a cobination of benzoyl peroxide Sulfur/sodium sulfacetamide and salicylic acid -Still found in several over-the-counter preparation - Sulfacetamide preparation mildy effactive in both acne and rasacea

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RETINOIDS bind to and activate retinoic acid receptors (RARs) and in turn activate specific gene transcription Tretinoin (all-trans retinoic acid) (0.025%,0.05%,0.1%)-potent comedolytic and anti- inflammatory properties -all retinoids can contact irritants with alcohol-based gels and solutions -advising patients to apply on alternate nights during first few weeks of treatment ensure greater tolerability -regular use of sunscreen due to thinning of stratum corneum -ideal for maintenance therapy of acne - Tretinoin is inactivated by concomitant use of benzoyl peroxide -should apply tretinoin at bedtime Adapalene -synthetic retinoid - Photostable and can be used in conjunction with benzoyl peroxide without degradation - Adapalene 0.1 % gel have greater or equal efficacy to tretinoin 0.025 % gel with greater tolerability Tazarotene -synthetic retinoid potent comedolytic agent -Irritant properties of tazarotene can be minimized by use of short-term contact therapy -medication is applied for 5 minutes then washed off with a gentle cleanser -Should not use in preganancy

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SYSTEMIC THERAPY Broad-spectrum antibiotics are widely used in Tx inflammatory acne Tetracyclines -most commonly used -Oral administration of tetracycline does not alter sebum production -Decreases in free fatty acid formation also have been reported with erythromycin, clindamycin and minocycline -several weeks Tx often required for maximal clinical benefit -Tetracycline direct suppression of the number of P acnes -should be taken on an empty stomach to promote absorption Doxycycline is administered in dosages of 50 to 100 mg twice daily -major disadvantage photosensitivity reactions, including photo- onycholysis , Minocycline -100 mg/day to 200 mg/day -can cause blue-black pigmentation, in acne scars,hard palate, alveolar ridge, and anterior shins -autoimmune hepatitis and systemic lupus erythematosus —like syndrome

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Minocycline pigmentation in acne scars Minocycline pigmentation in the sclera

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M ACROLIDES Erythromycin - Prevalence of erythromycin-resistant strains of P acnes its use generally limited to pregnant women or children Azithromycin in the treatment 250 mg to 500 mg orally three times a week TRIMETHOPRIM-SULFAMETHOXAZOLE - Trimethoprim-sulfamethoxazole combinations should be used only in patients with severe acne who do not respond to other antibiotics CLINDAMYCIN AND DAPSONE - Less commonly used antibiotics Oral clindamycin can cause pseudomembranous colitis, it is now rarely used for acne - Dapsone sulfone often used for cutaneous neutrophilic disorders useful for severe markedly inflammatory acne -50 to 100 mg daily for 3 months -Glucose-6-phosphate dehydrogenase levels should be examined before initiation of therapy Antibiotics and Bacterial Resistance- Overall resistance is highest with erythromycin and least resistance is with minocycline

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HORMONAL THERAPY OF ACNE -To counteract the effects of androgens on the sebaceous gland -Anti-androgens or agents designed to decrease the endogenous production of androgens -including oral contraceptives, glucocorticoids , or gonadotropin -releasing hormone ( GnRH ) agonists Oral Contraceptives Glucocorticoids - high-dose systemic glucocorticoids may benefit in treatment of acne -use usually restricted to overlapping with isotretinoin to limit any potential flaring at start of treatment

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Gonadotropin -Releasing Hormone Agonists - GnRH agonists such as leuprolide , act on pituitary gland to disrupt its cyclic release of gonadotropins -net effect is suppression of ovarian steroidogenesis in women -used in treatment of ovarian hyperandrogenism - side-effect- menopausal symptoms and bone loss Antiandrogens Spironolactone -functions androgen receptor blocker and inhibitor of 5α-reductase -reduce sebum production - Side effects- hyperkalemia , irregular menstrual periods, breast tenderness, headache, and fatigue -risk of feminization of a male fetus if a pregnant female take medication

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Cyproterone acetate- progestational anti-androgen -blocks androgen receptor -combined with ethinyl estradiol in an oral contraceptive formulation used in Tx of acne Flutamide - androgen receptor blocker -in combination with oral contraceptives for treatment of acne or hirsutism in females

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Isotretinoin -management of severe treatment-resistant acne -also effective in gram-negative folliculitis , pyoderma faciale , and acne fulminans -get remission in almost all cases and longevity of remission lasts for months to years -mechanism of action not completely known -produces profound inhibition of sebaceous gland activity -side effects-mimicking those seen in chronic hypervitaminosis A syndrome -side effects tends to be dose dependent

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- Cheilitis ,50% dryness of the mucous membranes, xerosis , and pruritus -Thinning of hair -Ophthalmologic - xerophthalmia , night blindness, conjunctivitis, keratitis , and optic neuritis - Pseudotumor cerebri ( benign intracranial hypertension) risk is increased with concomitant use of tetracyclines -Depression, suicide, psychosis, and aggressive and/or violent behavior -Elevation in liver enzymes 15 %,Elevated levels of serum triglycerides 25%

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- Myalgias creatine phosphokinase levels should be evaluated for possible rhabdomyolysis . - Teratogenic effects in fetus -Women of childbearing age must use two highly effective contraception -Contraception must be started at least 1 month before isotretinoin therapy 1 month after stopping treatment - Tecommended daily dosage 0.5 to 1.0 mg/kg/day -Typical course of isotretinoin 20 weeks -Laboratory monitoring -baseline complete blood count and liver function tests, serum triglyceride levels INTRALESIONAL GLUCOCORTICOIDS - D ramatically decrease size of deep nodular lesions -Injection of 0.05 to 0.25 mL per lesion of triamcinolone acetate suspension (2.5 to 10 mg/ mL ) -Repeated every 2 to 3 weeks - Hypopigmentation and atrophy

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ACNE VARIANTS Neonatal Acne -Occur in up to 20 percent of healthy newborns -Lesions usually appear around 2 weeks of age and resolve spontaneously within 3 months -Small, inflammed papules across nasal bridge and cheeks - Comedone absent -Sebum excretion rates in newborns transiently elevated in perinatal period - Malassezia sympodialis, normal commensal on human skin, may also play a role -Improvement with ketoconazole cream

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Infantile Acne -Presents at 3 to 6 months of age and usually marked by the presence of comedones -Papules, pustules, and nodules present on face and scarring occur -Infantile acne is caused in part by transient elevation of DHEA produced by immature adrenal gland -Around 1 year of age, hormone levels begin to stabilize -Usually resolves around 1 to 2 years of age -Treatment-topical retinoids and benzoyl peroxide -Oral therapy with erythromycm , trimethoprim , or isotretinoin

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Acne Conglobata -Severe form of nodular acne -Most common in teenage males ( conglobate means shaped in a rounded mass or ball) -Back, buttocks, chest, lesser extent, on abdomen, shoulders, neck, face, upper arms, and thighs - Comedones have multiple openings draining lesions discharge foul- smelling serous, purulent, or mucoid material -Subcutaneous dissection with formation of multichanneled sinus tracts -Healing depressed and keloidal scars -Management is very difficult and effect of treatment often temporary -Including intensive high-dose therapy with antibiotics, intralesional glucocorticoids , systemic glucocorticoids , surgical débridement -Use of isotretinoin has produced dramatic results Sinus formation in acne conglobata

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Acne Fulminans -Known as acute febrile ulcerative acne) is the most severe form of nodular acne accompanied by systemic symptoms -Sudden appearance of massive, inflammatory, tender, oozing, friable plaques with hemorrhagic crusts characterize acne fulminans -Lesions predominate on back and chest, rapidly become ulcerative, and heal with scarring -Occur primarily in teenage boys -Patients febrile, leukocytosis , polyarthralgia , myalgia , hepatosplenomegaly -Radiologic examination lytic bone lesions -Accompanying erythema nodosum -Systemic glucocorticoid therapy, along with oral antibiotics and intralesional glucocorticoids - Isotretinoin benefit in these patients,to prevent explosive flares, systemic glucocorticoids must be started before isotretinoin - Dapsone in conjunction with isotretinoin associated with erythema nodosum A patient with severe truncal acne who had acne fulminans. A patient with severe truncal acne who had acne fulminans.

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SAPHO Syndrome -Manifested by synovitis , acne, pustulosis , hyperostosis, and osteitis -Predominantly associated with hyperostosis of the anterior chest, palmoplantar pustulosis , hidradenitis suppurativa , and acne fulminans PAPA Syndrome -Acne variant with systemic symptoms, is marked by sterile pyogenic arthritis, pyoderma gangrenosum , and acne -Patients may give history of sterile cutaneous abscesses, inflammatory bowel disease, and pancytopenia after administration of sulfa-containing medications - Autoinflammatory disorder inherited in autosomal dominant manner Acne Excoriee -Occurs primarily in young women who picking at their skin -Mild acne may be present and accompanied by extensive excoriations -Underlying depression, anxiety, obsessive-compulsive disorder, or a personality disorder -Antidepressants and psychotherapy can be helpful

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Acne Mechanica - Acneiform eruptions have observed after repetitive physical trauma to skin such as rubbing -Can occur from clothing (belts and straps) or sports equipment (football helmets and shoulder pads) -Obstruction of pilosebaceous gland results in comedo formation -Well-defined, lichenified , hyperpigmented papule or plaque interspersed with comedones -A classic example -fiddler’s neck Acne with Solid Facial Edema -A rare and disfiguring variant of acne vulgaris also known as Morbihan disease -Woody edema of mid-third face with erythema and acne -Spontaneous resolution does not occur -Treatment with low dose isotretinoin (0.2 to 0.5 mg/kg/ day) alone or in combination with oral glucocorticoids , ketotifen (1 to 2 mg/ day), or clofazimine for 4 to 5 months

acneiform eruptions :

Steroid Folliculitis -After administration of systemic glucocorticoids or corticotropin -2 weeks after steroids started -after prolonged application of topical glucocorticoids to face -Lesions all in same stage , small pustules/ red papules - mainly on trunk, shoulders, and upper arms, lesser on face -Post-inflammatory hyperpigmentation - Comedones , cysts, and scarring are unusual -Treatment consists primarily of stopping any corticosteroid use -Topical retinoids and antibiotics Drug-Induced Acne - Monomorphic , diffuse papular eruption mimics steroid folliculitis -Halogenated compounds containing either bromides or iodides are found in cold and asthma remedies, sedatives, radio-opaque contrast material acneiform eruptions

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Epidermal Growth Factor Receptor Inhibitor—Associated Eruption Are used non-small cell lung cancer, colorectal cancer and breast cancer Perifollicular papulopustular eruption on face & upper torso Eruption occurs in up to 86% Presence and severity of eruption correlate with positive treatment response If eruption is absent, dosing may be inadequate, or tumor unresponsive to therapy Occupational Acne and Chloracne Coal tar derivatives, insoluble cutting oils, and chlorinated hydrocarbons Chloracne caused from chlorinated hydrocarbons found in fungicides, insecticides, and wood preservatives Quite inflammatory and large comedones , papules, pustules, large nodules, and true cysts Tar acne accompanied by hyperpigmentation Lesions are more common on covered areas with intimate contact to clothing saturated with offending compound Treatment with topical or oral retinoids and oral

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Gram-Negative Folliculitis -Occur in patients with pre-existing acne vulgaris treated with long-term oral antibiotics, especially tetracyclines -Usually give history of initial success with oral tetracyclines followed by worsening of acne - Papulopustules concentrated around nose or as deep-seated nodules -Culture of lesions reveal Enterobacter , Kiebsiella , or Escherichia papulopustules or Proteus in nodules -Improves with oral isotretinoin for 4 to 5mnths A patient with the typical multiple pustules of Gram-negative folliculitis .

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Acne Aestivalis - Monomorphous eruption, consists of multiple, uniform, red, papular lesions seen after sun exposure -Occurred in women, mainly 20 to 30 years old -Lesions are common on shoulders, arms, neck Apert Syndrome ( acrocephalosyndactyly ) - Autosomal dominant disorder marked by synostoses of the cranium, vertebral bodies and hands and feet -Diffuse acneiform eruption that often involves the arms, buttocks, and thighs -Typically very resistant to treatment but excellent responses to isotretinoin -Severe seborrhea, nail dystrophy, and cutaneous and ocular hypopigmentation .

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