Presentation on theme: "Dermatology Cases December 7, 2013"— Presentation transcript:
1Dermatology Cases December 7, 2013 Frank Morocco D.O. FAOCD
2Case 151 y/o white male with 4 year history of silvery scaling thickened erythematous plaques on his knees, elbows and scalp. The patient has 25% BSA. Denies any joint pain.
3Psoriasis :A) Involves only the skin and should be managed exclusively by a dermatologistB) Is associated with multiple comorbidities including diabetes, hyperlipidemia, and arthritisC) Statins have been shown to worsen psoriasisD) Topical therapy should be continued as monotherapy for multiple years before switching to a different treatment modality
4PsoriasisPsoriasis is a hereditary, papulosquamous skin disorder that affects 3 to5 million people in the United States.Affects men and women equally.Psoriasis is a chronic and recurring disease that is best characterized by well-demarcated erythematous plaquesMost commonly plaques are seen on the elbows, knees, and the scalp
5Psoriasis Psoriasis is an immune mediated inflammatory skin disorder. TH1 driven with increase of IL-6, TNF-alpha and InterferonUnpredictableAge of onset bimodal 23 y/o and 55 y/oAggravated by emotional stressIn addition to its cutaneous manifestations, psoriasis has been associated with arthritis
6Psoriatic ArthritisPsoriatic arthritis affects an estimated 25% to 34% of patients with psoriasisMost commonly appears 10 years after the onset of psoriasisPsoriatic Arthritis: 5 patternsAsymmetric DIP with nail damage (16%)Arthritis mutilans with osteolysis of phalanges/metacarpals (5%)Symmetric polyarthritis-like RA with claw hands (15%)Oligoarthritis with swelling and tenosynovitis of one or a few hand joints (70%)Ankylosing spondylitis alone or with peripheral arthritis (5%)
8Psoriasis: Psoriatic Arthritis Psoriatic Arthritis (cont’d)X-rays resemble RA except:Erosion of terminal phalangeal tuftTapering or whittling of phalanges or metacarpalsCupping of proximal phalangesBony ankylosisOsteolysis of metatarsalsPrediliction for DIP and PIPSparing of MCP and MTPParavertebral ossificationAsymmetric sacroilitis; rarity of bamboo spine
9Burden of Psoriasis Quality of life A population-based survey looking at the association between quality of life and extent of disease.60% of patients report psoriasis affects their everyday life and 26% report a change or discontinuation of daily activities.This was higher than cancer and diabetes!!
10Burden of PsoriasisEconomicThe estimated total direct and indirect health care cost of psoriasis in the United States is billion dollars annuallyA two-year study by the National Psoriasis Foundation (NPF) found that having psoriasis is associated with decreased household incomes and reduced employment opportunities.Psoriasis patients have lower income and are less likely to work full-time.Psoriasis was reported as the primary reason for unemployment in 17% of patients with severe psoriasis.Psoriasis patients missed an average of 26 days of work each year due to complications of psoriasis
11CVD Risk Factors Associated with Psoriasis Psoriasis may predispose patients to increased risk of atherosclerotic disease.A chronic, proinflammatory state that fosters the development of the metabolic syndrome.40 % of psoriatic patients develop metabolic syndromeChronic inflammation to increased oxidative modifications of lipoproteins, which are more atherogenic than native lipoproteins
12CVD Risk Factors Associated with Psoriasis DiabetesThe studies suggest that psoriasis is associated with a 59% increased prevalence of diabetes and a 27% increased risk of developing diabetes among patients with psoriasisThe altered immune pathways may also predispose to impaired glucose tolerance and diabetesAggressive therapy ?
13CVD Risk Factors Associated with Psoriasis Hyperlipidemia19 of 19 studies showed an association with hyperlipidemiaStudy subjects had higher levels of very low density lipoproteins, total cholesterol and LDL, and lower levels of cardioprotective high density lipoproteins (HDL)
14Anti-lipid lowering agents for psoriasis treatment. 63 pts32 pts on Atorvastatin 20mg/day31 pts on placebo80% reached PASI 75 in 6 months78% reach PASI 75 in 3 months with ustekinumabAlso showed significant reduction of CRP and TNF alpha after 3 weeks
15Psoriasis: TreatmentTopicals or localized tx (laser/pulsed light) for limited plaquesPhototherapyMTXCyclosporinBiologicsRotating therapies and combination therapies
16Psoriasis: Topical therapies Corticosteroids: Class I for 2 weeks, then weekend pulsesOcclusion for thick keratotic scaleLow-mid strength intertriginous and faceCan give ILK for refractory plaques and nail matrix and lateral nailfold monthlyTazarotene: modulates keratinocyte differentiation and hyperproliferation and suppresses inflammationCalcipotriene: keratinocyte differentiation
17Psoriasis: Light Therapy Burning can cause Koebner’s phenomenonArtificial UVB broad or narrow band254, 280, 290 are ineffective296, 300, 304, 313 give clearingNarrow band = 311 and is more effective than broad band
18PsoriasisPsoriasis is associated with comorbid conditions, including depression, arthritis, diabetes, hypertension, metabolic syndrome, and cardiovascular eventsA systemic inflammatory processes may underlie these disease processes.Treatment must involve a multidisciplinary approach between Dermatologists, PCP cardiologists and rheumatologists
19Case # 2-Patient S.S. is a 16 month old boy brought in to see you by his parents for an itchy rash.-“rashy skin” intermittently since birth. -worst during the winter months of the year.-Mom reports that he scratches in his sleep. The parents tell you that S.S. was hospitalized at age 6 months for reactive airway disease for which he required nebulizers.-His mom has strong allergies to pollens in the summer.-Dad has asthma. -S.S. uses Suave Berry Blast soap and shampoo in the bathtub.He takes one bath every other day.They have tried Vaseline intensive care lotion when his skin seems dry.
22Atopic Dermatitis Eptheilial barrier disruption 50% of atopic dermatitis caused by Filaggrin gene (FLG) disorderFLG encodes profilaggrin which is the major component of granular layer.Filaggrin makes up the the major scaffolding that forms the lipid cell envelope.
26FilaggrinFilaggrin is degraded and forms “natural moisturizing factor”Decreases pH which helps inhibit Staphylococcus aureus growthActivate enzymes in ceramide metabolismModulating the activity of serine proteasesEpidermal barrier repair is aimed at replacing ceramides, inhibition of elevated protease activity and decreasing skin pH
27Atopic DermatitisIn vitro studies have shown immunity still has major effect.IL-22 and IL-25 are involved in decreasing filaggrin expression.Decrease of active copies of fillagran by 5-10% can increase severity of atopic dermatitis.
28Atopic Dermatitis Other Factors Delayed introduction of solid foods, early life exposure to antibiotics, exposure to farm animals or ingestion of fish oils have no effect on development of ADBreast-feeding has been shown to have no effectPhysiologic and psychological benefits of breast feeding makes it preferred feeding modality even in children with risk of developing AD
29Highlights From NIAID Guidelines Children < 5 y/o with moderate to severe AD should be considered for food allegies to milk, egg, peanut wheat, and soy IF persistant atopic dermatitis with optimal treatment or if there is a history of immediate reaction after the ingestion of a specific food
30Highlights From NIAID Guidelines Fifty percent to 90% of presumed allergies are not allergic in natureSolid foods should not be delayed beyond 4 to 6 months, because this may paradoxically increase the incidence of food allergiesIndividuals without documented or proven food allergies should not avoid potential allergenic foods
31AD and ADHD Proposed Mechanisms Negative effect of inflammatory cytokines on central nervous systemIncreased stress and sleep disturbances due to pruritis.Lack of impulse control and use of stimulatory medication makes ADHD a risk factor for more severe AD
32Features Associated with Atopy Dennie-Morgan fold: linear transverse fold just below the lower eyelid“Normal” skin is subclinically inflamed, dry, scalyPityriasis alba:hypopigmentation with sclight scale on cheeks, upper arms, trunk in young children. Responsive to emollients and topical steroidsKeratosis pilaris:horny follicular lesions of outer aspects of upper arms, legs, cheeks, and buttocks; refractory to treatment
33Features Associated with Atopy Increased susceptibility of infection;Patients heavily colonized with Staph. Treatment of lesional skin reduces colonization even w/o ABXEczema herpeticum: generalized herpes simplex, sudden vesicular, pustular, crusted or eroded lesions. Become secondarily infected.Eczema vaccinatum: widespread vaccinia infxnExtensive flat wart or molluscum; poor tolerance to Tx
35Management of Atopy Infants and children: Avoid hot baths, alkaline soaps, vigorous rubbing and scrubbing.Short, once-a-day, tepid baths followed by a barrier cream using soak and smear; ointment bases are preferred.Immediate change of wet or soiled diapers.Nighttime sedating antihistamines for itchDietary restriction for a specific known antigen
36Management of Atopy Adults Avoid temperature extremes Hydrate dry skin especially in winterAvoid overbathing and hot waterAvoid woolBiofeedback techniques for emotional stress
37Topicals for Atopy Topical corticosteroids are the mainstay 1-2.5% hydrocortisone in infants. Monitor growth in infants and young children.Mid-potency (TAC) in older children and adults except on the face1-2x a day is enough to saturate receptors; more provides only emollient effectOcclusion increases penetration and receptor saturationMust be strong enough to control pruritus and remove inflammationRegular emollients: petrolatum, hydrophilic creams with ceremidesAnti-Staph therapy for acute flaresTopical calcineurin inhibitors
38Systemics for AtopyAntihistamines for sedation: hydroxyzine, diphenhydramine, or clopheniramine.The nonsedating antihistamines do not relieve pruritusShort courses of anti-Staph ABX, topical mupirocin for nasal carriageImmunosuppressives and antiproliferatives (Immuran, Cellcept, MTX) can be effective for unresponsive dzPhototherapy: PUVA, UVA, narrow-band UVB, or Goeckerman with tar may be helpful
39Atopic DermatitisIncreased risk of S. Aureus infection and colonization which leads to inflammationDecreased Human Beta-defensin-2 leads to increased MSSA.A recent study showed that diluted bleach baths plus intranasal mupirocin led to significant improvement in eczema severity scores.Typical recipe is ¼ cup of bleach for ½ tub of water and ½ cup of bleach for tub full of waterMupirocin was administered 5 consecutive days a month
40Atopic DermatitisWet dressing therapy was has been used in past for severe AD.Recent study from Mayo Clinic described their institution’s wet dressing therapy for inpatient hospitalizations.45% had 75%-100% clearance38% had 50%-75% clearance
41Atopic dermatitisTraditional AD management dogma consisted of application of anti-inflammatory medication to areas of “active”disease.Recent research shows a paradigm shift.After twice daily active treatment of AD flare, patients were given “proactive” twice weekly treatment with topical tacrolimus and had significant fewer AD flares
42Case 3An 18-year-old patient presents with a sore throat and signs of streptococcal pharyngitis. you start treatment with amoxicillin-clavulanate, and results of a rapid strep test are positive. The next day the patient calls regarding a new rash that has erupted all over his body. The palms and soles remain uninvolved
44Which one of the following is the most likely cause of this patient’s rash? a. Drug rashb. Pityriasis roseac. Streptococcal scalded skin syndromed. Mycoplasma pneumoniae. Psoriasis
45Guttate PsoriasisGuttate psoriasis classically presents after infection with streptococcus in children or young adults.Guttate psoriasis presents with scaly, “droplike” papules on the trunk and extremities.It is often mistaken for a drug rash because antibiotics may have been initiated for the streptococcal infection.Throat cultures for streptococcal pharyngitis should be obtained.Guttate psoriasis has a good prognosis and may disappear spontaneously or may benefit from phototherapy.
46Case 4A 28-year-old man presents with a rash and pruritus that has been present for 3 weeks. He has no history of skin or other health problems and is not receiving any medications. He has used no new products on the skin and has not frequented wooded areas. On examination, he has red papules and excoriations on the wrists, groin, and axillae and nodular areas on his scrotum
48A) Mineral oil preparation of a skin scraping To identify the cause of this patient’s rash and pruritus, which one of the following is the best laboratory test?A) Mineral oil preparation of a skin scrapingB). Tissue transglutaminase measurementC). Skin biopsyD). Lyme disease serologyE). Skin biopsy for tissue culture
49ScabiesScabies is caused by infestation of the epidermis with the mite.Infestation occurs as a result of direct skin-to-skin contact; fomite transmission is uncommon.Scabies causes epidemics in schools, nursing homes, and hospitals.Pruritus is the major complaint, prominently at night, and there is often a history of itching or rash in family membersThe rash is due to hypersensitivity reaction to the mite protein.It can take 4 to 6 weeks after initial mite exposure to develop signs or symptoms of scabies infestation
50ScabiesClinical features include inflammatory, excoriated papules in the web spaces of the hands and feet, the axillae, groin, wrists, and areolae, and submammary sites in women.Facial or scalp involvement is uncommon, except in children and elderly persons.Nodules or thickened areas in the scrotum are also a helpful clue
51ScabiesThe pathognomonic finding is a burrow, commonly located on the hands.Identification of mites, eggs, or fecal material on a scabies preparation is diagnostic.Treatment of classic scabies includes the topicalapplication of permethrin, and/or oral ivermectin
52Scabies treatment Permethrin is the gold standard therapy Ivermectin is an effective oral alternative that is especially useful in crusted scabies, patients who are bedridden, and in institutional outbreaks.Treatment failures still occur, mostly secondary to application error (ie, failure to treat the face and scalp or close contacts, failure to reapply medication) or failure to decontaminate fomites.
53ScabiesThere has been a recent shift in standard of care for scabies treatment.Routine treatment of the scalp and face and re-treating patients between day 4 and 7 based on the scabies life cycle to ensure more efficient mite eradication.Practitioners should attempt to treat all close contacts simultaneously with the source patient.
54Scabies 300 volunteers who lay nude in warm beds recently vacated by scabetic hosts infected with <20mites, 4 (1.3%) became infested.The number rose to 15% when hosts had >50 mitesMay live on fomites hrs in warm humid environmentMay live on fomites 19 DAYS in cool environment!!!To eradicate mites, all fomites should be placed in a dryer for 10 minutes on a high setting, furniture and carpets vacuumed, and nonlaunderables isolated for a minimum of 2 days
55Case 5An 18-year-old man originally presented to your urgent care clinic 4 weeks ago with a small abscess on his knee. He was otherwise healthy and taking no medications. The abscess was incised and drained at the clinic, and the culture and susceptibility studies showed this lesion to be a methicillin-resistant Staphylococcus aureus infection. He now presents with a new abscess.On physical examination, his temperature is 37°C, blood pressure is 118/76 mm Hg, and heart rate is 80 beats/min. Skin examination shows a 2x2-cm erythematous plaque on the forearm with a central fluctuant area. There are areas of healing skin on the knee.
57A). Education on wound care and personal hygiene B). Oral rifampin After incision and drainage of the current abscess, which one of the following is the most important intervention to prevent recurrence of infections in this patient?A). Education on wound care and personal hygieneB). Oral rifampinC). Intravenous vancomycinD). Oral clindamycinE). Combination treatment with oraltrimethoprim-sulfamethoxazole and minocycline
58MRSAThis patient presents with the typical history and physical findings of a skin and soft tissue infection (SSTI) with community-associated methicillin-resistant S aureus (CA-MRSA).Infections caused by CA-MRSA usually present as a solitary abscess, cellulitis, or soft tissue infection, often with central necrosis.Recurrence in an individual is commonThis strain of MRSA has a distinct genetic resistance element (SCCmec IV) and toxin (Panton-Valentine leukocidin toxin) and develops in populations with close physical contact.While resistant to beta-lactam antibiotics, CA-MRSA isolates often remain sensitive to other antibiotics such as clindamycin,trimethoprim-sulfamethoxazole, and minocycline
59MRSAThe primary treatment for a small, simple cutaneous abscess is incision and drainage of the abscess.Management of recurrent MRSA infections should focus on education about appropriate wound care and personal hygiene.Instruction should include keeping draining wounds covered with clean, dry bandages, maintaining good personal hygiene with regular bathing , cleaning of hands, and avoiding reusing or sharing personal items.Clinicians should consider attempting decolonization if a patient experiences a recurrent SSTI despite optimal wound care and hygiene measures.Decolonization strategies may include nasal decolonization with mupirocin twice a day for 5 to 10 days and body decolonization with a skin antiseptic solution (chlorhexidine) for 5 to 14 Days or dilute bleach baths.`
61Infantile Hemangiomas Infantile hemangiomas are the most common tumor of infancy and arise in 5% to 10% of infantsGlucose 1 transporter (GLUT-1) has be shown to be specific for infantile hemangiomas
62Infantile Hemangiomas The expected proliferation phase of hemangiomas is during the first year of life with rapid growth until 6-9 months of age.A recent found most rapid growth between age weeksBest age for referral 4 weeks oldHemangioma precursors were present at birth in 65% of patients
63Infantile hemangiomas Early white discoloration heralds impending ulcerationUsually seen before 3months of ageIn contrast to the whitish gray color of involution seen several moths later
64Infantile hemangiomas One of the greatest breakthroughs in pediatric dermatology has revolved around IH and propranolol.Mechanism of action is unknownVasocostrictionBlocking proangiogenic signalsApoptosis of endothelial cells
65Infantile Hemangioma2008- The discovery was made after 2 children with cardiac issues were treated with oral beta blockers with great effectivenesschildren treated with oral propranolol all had good response
66Infantile Hemangioma2011 – 40 pts given 2 mg/kg per day divided 3 times daily for 6 months.Baseline electrocardiogram, echocardiogram, and laboratory evaluations were performed. Monitoring of heart rate, blood pressure, and blood glucose was performed at each visit.No signiﬁcant hypoglycemia, hypotension, or bradycardia occurred.Growth stopped at 4 weeks
67Infantile hemangiomas 2011- Propranolol vs corticosteroidsmulticenter retrospective analysis139 patients82% achieved clearance of 75% or more on propranolol compared to 29% who were receiving oral corticosteroidsThis study helped show superior efficacy with fewer side effects.
68Ulcerated IHInfantile Hemangiomas that ulcerate are prone to considerable morbidity with pain, infection, and scarringChallenging to treatWhen compared to traditional modalities for treatment (PDL, wound care, oral antibiotics and oral corticosteroids) propranolol was found to shorten time to healing after the onset of ulcerationAverage time to heal from onset of ulceration with propranolol 8.7 weeks compared to 22.4 weeks with wound careHead and neck hemangiomas 4.3 weeks to heal and 14.5 days to achieve pain control
69IHPropranolol is now considered standard of care for severe IH but it is being used more in less aggressive IH.Most patients are started on a low dose and titrated up to 2 mg/kg/day in divided dosesRare side effects include hypoglycemia, hypotension, and exacerbation of asthmaMore common side effects are cold extremities and night terrors
70IH Other systemic beta blocker are being examined. Atenolol is a hydrophilic beta-1 antagonist that may decrease pulmonary side effects and sleep disturbances.Nadolol has been compared to propranolol in a small case study which showed superior efficacy decreased side effects and easier dosing schedules due to a longer half life.Topical beta-blocker in the form of timolol has been tried with success for superficial small hemangiomas not requiring systemic treatment
72Tinea CapitisTinea capitis occurs mainly in children, although it may be seen at all ages.Boys have tinea capitis more frequently than girlsTinea Capitis is more prominent in African Americans
73Tinea CapitisTinea capitis must be differentiated clinically from chronic staphylococcal folliculitis, psoriasis, seborrheic dermatitis, various inflammatory follicular conditions.The distinctive clinical features of tinea capitis are broken-off stumps of hairs, often in rounded patches in which there are crusts or pustules and few hairs.The broken-off hairs are loose and when examined are found to be surrounded by, or to contain, the fungus.Diffuse seborrheic scaling with hair loss is a common presentation of T. tonsurans infections.
74Tinea CapitisIn seborrheic dermatitis the involved areas are covered by fine, dry, or greasy scales. Hair may be lost, but the hairs are not broken.Atopic dermatitis is rarely associated with localized scalp involvement, and clinical examination frequently reveals more typical generalized findings.In psoriasis, well-demarcated, sometimes diffuse,areas of erythema and white or silver scaling are noted.Lichen simplex chronicus is frequently localized to the inferior margin of the occipital scalp.
75Tinea CapitisNumerous clinical trials exist that demonstrate the effectiveness of itraconazole, terbinafine, and fluconazole.Despite these studies, griseofulvin remains the most commonly used antifungal agent in children.A meta-analysis of published studies shows mean efficacy for griseofulvin treatment of about 68% for Trichophyton sppFor the ultramicronized form, doses start at 10 mg/kg/day. The tablets can be crushed and given with ice cream.Grifulvin V oral suspension is less readily absorbed. The dose is 20 mg/kg/day.Treatment should continue for 2–4 months, or for at least 2 weeks after negative laboratory examinations are obtained.Doses much higher than those reflected in drug labeling are commonly needed.
76Tinea CapitisFor Trichophyton infections, terbinafine is commonly effective in doses of 3–6 mg/kg/day for 1–4 weeks.Alternate dosing schedules for terbinafine include one 250 mg tablet for patients over 40 kg, 125 mg (half of a 250 mg tablet) for those 20–40 kg, and 62.5 mg (one-quarter of a 250 mg tablet) for those under 20 kg.Selenium sulfide shampoo or ketoconazole shampoo left on the scalp for 5 min three times a week can be used as adjunctive therapy to oral antifungal agents to reduce the shedding of fungal spores.Combs, brushes, and hats should be cleaned carefully and natural bristle brushes
79Pityriasis RoseaMild inflammatory exanthem: salmon-colored oval/circinate papules/macules with collarette scaleHanging curtain sign: scales fold across lines of stretched skinLong axis parallels lines of cleavageHerald patchAge in spring and autumnMay have mild pruritusSpontaneous resolution after 3-8 weeksInverse and papular variants
80Pityriasis RoseaEtiology: may be associated with HHV-6 and 7 reactivationA similar eruption may occur as reaction to drugsHistology: mild acanthosis, focal parakeratosis, erythrocyte extravasion, spongiosis, mild dermal perivascular infiltrateDDX: seb derm, tinea corporis, macular syphilid, drug eruption, viral exanthem, PSOTreatment: most require noneUVB may expedite the involutionCorticosteroid lotions or creams, oral antihistamines, erythromycinemollients
81Case 9 15-year-old male Non-inflammatory & inflammatory papules Face onlyOpen/closed comedonesPapulesDiagnosis ?Treatment Plan?
82Treatment Approach Non-inflammatory Acne Mild Inflammatory Acne Moderate-Severe InflammatoryAcnePregnantAzelaic Acid (Cat B)Clindamycin Lotion (Cat B)Topical TherapiesRetinoidsAntibioticsSalacylic AcidBPO+/- WashesOral antibioticsTetracyclinesAdjunctive TherapiesSevere or ScarringIsotretinoinAdjunctive TherapiesOCPs, chemical peels,anti-androgensFailure of oralantibiotics
83Treatment ApproachEarly, appropriate treatment is best to minimize potential for acne scarsApproach should be multi-therapy, not monotherapyCombination of a topical retinoid and antimicrobial agent remains the preferred approach for almost all patients with acneThiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group. J Am Acad Dermatol 2009;60:S1-50.
84Treatment ApproachTopical retinoids should be first-line agents in acne maintenance therapyAvoid contributing to antibiotic resistanceThiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group. J Am Acad Dermatol 2009;60:S1-50.
85Benzoyl Peroxide Mechanism of action1 Advantages Formulations Bactericidal for P. acnesInhibits triglyceride hydrolysisDecreases inflammation of acne lesionsAdvantagesNo resistance demonstrated to date1When used in combination with a topical antibiotic can help to prevent resistance2Activity is enhanced when combined with other topicals (i.e. clindamycin)1,2FormulationsOTC & prescriptionWashes, gels, lotion, solution1. Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.2. Thiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group. J AmAcad Dermatol 2009;60:S1-50.
86Retinoids Most important class of drugs used to treat acne Topical form of vitamin AMechanism of Action1Normalize follicular keratinizationAct on the microcomedoneProper instruction on application is essential to complianceGradual application with small amount of drug“Training for a marathon”1. Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
87Retinoids “Least Irritating” (most tolerable) “Moderately Irritating” Adapalene gel (Differin® 0.1%, 0.3%)May be appropriate starting point for ethnic and/or sensitive skin“Moderately Irritating”Tretinoin (cream, gel)Tretinoin 0.01%, 0.05%, 0.025%Retin-A Micro® 0.1%, 0.04%Atralin™ Gel 0.05%Renova® 0.02%, 0.05%“Most Irritating” (least tolerable)Tazarotene (Tazorac®/Avage® 0.05%, 0.01%)Wolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
88Topical Antibiotics Erythromycin Clindamycin phosphate 1% Azelaic acid Akne-mycin® 2% gel, Erygel ® 2% gel,Resistance of some P. acnes strainsUsage fallen out of favorClindamycin phosphate 1%Generic, Cleocin T® (lotion, gel, solution), Evoclin® foamAntibiotic-associated colitis very unlikelyWork best in combination with BPOGood choice for pregnant women (Pregnancy Category B)Azelaic acidFinacea™Bacteristatic/bactericidal against P. acnesWolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
89Combination Therapies Clindamycin/Benzoyl peroxideClindamycin phosphate 1%/benzoyl peroxide 5% (Benzaclin®Gel)Clindamycin phosphate 1%/benzoyl peroxide 5% (Duac®Gel)Clindamycin phosphate 1.2% /benzoyl peroxide 2.5% (Acanya™ Gel)Erythromycin/Benzoyl peroxideErythromycin 3%/benzoyl peroxide 5% (Benzamycin®)Retinoid/Benzoyl peroxideAdapalene 0.1%/benzoyl peroxide 2.5% (Epiduo™ Gel)Retinoid/ClindamycinTretinoin 0.025%/Clindamycin phosphate 1.2% (Ziana® Gel)Thiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group. J Am Acad Dermatol 2009;60:S1-50.
91Treatment Approach Non-inflammatory Acne Mild Inflammatory Acne Moderate-Severe InflammatoryAcnePregnantAzelaic Acid (Cat B)Clindamycin Lotion (Cat B)Topical TherapiesRetinoidsAntibioticsSalacylic AcidBPO+/- WashesOral antibioticsTetracyclinesAdjunctive TherapiesSevere or ScarringIsotretinoinAdjunctive TherapiesOCPs, chemical peels,anti-androgensFailure of oralantibiotics
92Oral Antibiotics Therapeutic role in acne Dosing Reduction of P. acnes Anti-inflammatory activityDosingStart high then taper down after control is achievedUse PRN during flaresDo not use as monotherapyWolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
94How to Prevent Resistance Combine a topical retinoid plus an antimicrobialLimit the use of antibiotics to short periods and discontinue when there is no further improvement or the improvement is only slightCo-prescribe a BPO-containing product or use as washoutOral and topical antibiotics should not be used as monotherapyThiboutot D, et al. New insights into the management of acne: An update from the Global Alliance to Improve Outcomes in Acne Group. J Am Acad Dermatol 2009;60:S1-50.
95Case 11 19-year-old female moderate to severe inflammatory acne Regular menstrualcycles (+ flares)Face involved scarringChest, back sparedNodular lesions alongjawlineComedonesScarringTreatment plan?
96Treatment Approach Non-inflammatory Acne Mild Inflammatory Acne Moderate-Severe InflammatoryAcnePregnantAzelaic Acid (Cat B)Clindamycin Lotion (Cat B)Topical TherapiesRetinoidsAntibioticsSalacylic AcidBPO+/- WashesOral antibioticsTetracyclinesAdjunctive TherapiesSevere or ScarringIsotretinoinAdjunctive TherapiesOCPs, chemical peels,anti-androgensFailure of oralantibiotics
97IsotretinoinApproved for the treatment of severe recalcitrant nodular acne in 1982Member of the Vitamin A familyEffects on acneNormalizes the keratinization processReduces sebocytes and secretionsReduces inflammationReduction in numbers of P. acnesWolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
98Isotretinoin Pre-medication counseling Dosing 1-2 mg/kg/day Side EffectsContraceptionCompliance/duration of treatmentLaboratory monitoringiPledge registrationDosing 1-2 mg/kg/dayGoal mg/kg over course of treatmentWolverton SE. editor Comprehensive Dermatologic Drug Therapy 2nd Ed. Philadelphia: Saunders Elsevier; 2007.
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