Pustular Psoriasis
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Pustular psoriasis is an uncommon form of psoriasis consisting of widespread pustules on an erythematous background, as shown in the image below.
See Psoriasis: Manifestations, Management Options, and Mimics, a Critical Images slideshow, to help recognize the major psoriasis subtypes and distinguish them from other skin lesions.
Pustular psoriasis may result in erythroderma. Cutaneous lesions characteristic of psoriasis vulgaris can be present before, during, or after an acute pustular episode.
The acute generalized type is also termed von Zumbusch variant. This form of pustular psoriasis is accompanied by fever and toxicity, and it may be fatal if proper supportive measures are not taken during the acute phase.
The annular (or circinate) type is also known as subacute generalized pustular psoriasis. It tends to run a subacute or chronic course with fewer systemic manifestations. A disproportionately high number of cases are found in the pediatric population. [1]
A juvenile or infantile type of pustular psoriasis has been described, but it is the least common form.
Additionally, several disease entities are considered, by some, to be variants of pustular psoriasis. These include the following:
Pregnancy-associated impetigo herpetiformis: Occurring predominately in the third trimester, this is a variant of acute pustular psoriasis that carries an increased risk of subsequent stillbirth or fetal abnormalities. [2]
Acrodermatitis continua of Hallopeau: Characterized by pustular eruptions of the tips of fingers and toes, cases are generally refractory to treatment. Subsets of these cases are considered variants of pustular psoriasis, particularly since they are indistinguishable histologically and in early clinical presentation. [3]
Sneddon-Wilkinson syndrome or subcorneal pustular dermatosis (SCPD): The disease follows a relapsing and remitting course that may develop into generalized pustular psoriasis. Occurring predominately in patients middle-aged or older, SCPD is associated with underlying malignancies (most commonly multiple myeloma and IgA monoclonal gammopathy) and pyoderma gangrenosum. [4]
Acute generalized exanthematous pustulosis (AGEP): Characterized by a widespread rash evolving into pustules, AGEP is associated with a prescribed drug in over 90% of cases. A minority of patients develop systemic involvement, most commonly hepatic, renal, and pulmonary systems. AGEP is associated with IL36RN mutations similar to those found in pustular psoriasis, palmoplantar pustulosis, and acrodermatitis continua of Hallopeau, which is not surprising given the similarities in clinical and immunologic features of these diseases. Taken together, some consider AGEP a drug-induced form of pustular psoriasis. [5]
For patient education information, see the Skin Conditions & Beauty Center, as well as Psoriasis, What Is Psoriasis?, Types of Psoriasis, Plaque Psoriasis, and Psoriasis Medications.
Enhanced polymorphonuclear leukocyte (PMNL) chemotaxis is much more pronounced in pustular psoriasis than in psoriasis vulgaris. [6] This observation has been attributed to either an intrinsic PMNL defect or to the presence of chemoattractants in the psoriatic epidermis. Although the principal stimulus that triggers the phenomenon of massive PMNL migration from the vasculature to the epidermis is unknown, several new pathways involved directly and indirectly with neutrophil chemotaxis have been the topic of recent investigations.
The interleukin (IL)‒36 receptors are expressed constitutively on dermal dendrocytes, CD4+ T cells, and macrophages and, when activated, promote maturation of monocyte-derived dermal dendrocytes and inductions of cytokines, including IL-1, IL-6, IL-23, tumor necrosis factor-alpha (TNF-a) , and interferon-gamma (INF-g), which promote neutrophil migration. [7]
A subset of IL-23‒responsive CD4+ T-cells, identified as Th17 cells, induce IL-17 and IL-22, which, in turn, induce production of IL-6, IL-8, and CXCL5, which promote differentiation, activation, and migration of neutrophils and provide a positive feedback loop for Th17 cell differentiation. Significantly increased levels of IL-17 have been identified in lesional skin of pustular psoriasis versus nonlesional skin of the same patients. [7]
IL-6 signaling has gained recent attention for its role in the pathogenicity of pustular psoriasis. The IL-6-receptor subunit functions as both a membrane-bound receptor and a soluble receptor. This dual functionality separates it from all other known cytokine receptors that function only as membrane-bound forms. The IL-6/IL-6R complex, together with the ubiquitously expressed gp130, activate the JAK/STAT kinase and the RAS/MEK/ERK/MAPK kinase pathways, which ultimately augment nuclear gene expression. The downstream effects of IL-6 include synthesis of acute phase reactants, B-cell maturation, T-cell differentiation, positive influence on Th17 cell development, maturation neutrophils from myeloid progenitors, increased expression of ICAM-1 and other endothelial adhesion molecules that enhance neutrophil migration, and release of proinflammatory cytokines, such as IL-23 and IL-17, to further promote the Th17 positive feedback loop. [7]
Electron microscopic studies have shown the presence of basal keratinocyte herniations in lesions of pustular psoriasis. These are cytoplasmic processes from basal keratinocytes that protrude into the dermis through gaps in the basal lamina. These herniations are mostly clustered over collections of neutrophils in the dermis. This finding suggests an increased production of neutrophilic proteolytic enzymes in the dermis of pustular psoriasis patients.
Immunohistochemical methods have determined the involvement of some of these proteases and their inhibitors in the development of pustules.
Elastase is a proteolytic enzyme released by PMNLs during the process of extravasation and migration through the dermoepidermal junction. One study found an epidermal elastase inhibitor (skin-derived antileukoproteinase) expressed in psoriatic skin prior to the influx of PMNLs, which disappeared when the composition of the infiltrate changed. This finding was not confirmed by other studies.
Additional studies investigating other potential mechanisms have shown decreased natural killer cell activity in generalized pustular psoriasis. An increased incidence of HLA-B27 also has been found among patients with pustular psoriasis. This haplotype is seen in psoriasis patients with peripheral arthritis, as well as in patients with ankylosing spondylitis and reactive arthritis.
Homozygous, compound heterozygous, and single heterozygous missense mutations in a gene (IL36RN) that encodes a soluble anti-inflammatory cytokine, an IL-36‒receptor antagonist, have been associated with autosomal recessive inherited and sporadic generalized pustular psoriasis, AGEP, acrodermatitis continua of Hallopeau, and palmoplantar pustulosis. [5, 8, 9] The presence of these mutations is associated with unopposed release of inflammatory cytokines, including IL-6, IL-8, IL-1a, IL-1b, TNF-a, and INF-g, which promote neutrophil activation and migration. [7]
The following factors can reportedly trigger an eruption of pustular psoriasis:
Withdrawal of systemic steroids, [10] potent topical steroids, [11] or cyclosporine [12]
Drugs, including salicylates, iodine, lithium, phenylbutazone, oxyphenbutazone, trazodone, penicillin, hydroxychloroquine, calcipotriol, interferon-alpha, recombinant interferon-beta injection, [13] terbinafine, [14] and bCG vaccination [15]
Strong, irritating topical medications, including tar, anthralin, steroids under occlusion, and zinc pyrithione in shampoo
Cutaneous infections (eg, Staphylococcus aureus, Streptococcus epidermidis) [16]
Sunlight or phototherapy
Cholestatic jaundice
Hypocalcemia
Idiopathic in many patients
Pustular psoriasis is uncommon in the United States. The prevalence of pustular psoriasis in Japan is 7.46 cases per 1 million people.
Pustular psoriasis affects all races.
The male-to-female ratio for pustular psoriasis is 1:1 in the United States. Globally, a female predominance has been reported. [17, 18] The female-to-male ratio is 3:2 in children.
The average age among adult patients with pustular psoriasis is reported between 48 and 50 years. [17] The average age of onset of acute generalized pustular psoriasis is 41 years. [17]
Children aged 6 weeks to 10 years can be affected, though rarely. One case described generalized pustular psoriasis in a 6-week-old infant. [19] The mean age of onset for annular pustular psoriasis in pediatric populations is 6 years. [1]
In generalized pustular psoriasis, the skin initially becomes fiery red and tender. Patients may have a preceding history of psoriasis, although this is not a requirement. [11] Constitutional signs and symptoms include headache, fever, chills, arthralgia, malaise, anorexia, and nausea. Within hours, clusters of nonfollicular, superficial, 2- to 3-mm pustules may appear in a diffuse pattern.
Flexural and anogenital areas are most commonly involved in pustular psoriasis. Less often, facial lesions occur. Pustules can appear on the tongue and develop subungually, resulting in dysphagia and nail shedding, respectively. [20] Pustules coalesce within 1 day to form lakes of pus that dry and desquamate in sheets, leaving behind a smooth, erythematous surface on which new crops of pustules may recur.
Episodes of pustulation occur for days to weeks, causing the patient severe discomfort and exhaustion. A telogen effluvium type of hair loss may develop in 2-3 months.
Upon remission of pustules, most systemic symptoms disappear. However, patients can experience an erythrodermic state or residual lesions of psoriasis vulgaris.
Circinate or annular-type pustular psoriasis predominates in childhood and runs a more subacute course with less severe manifestations. Often, recurrent episodes of annular or circinate erythematous plaques are seen, with pustules and scaling along the periphery. [1] These lesions appear primarily on the trunk and undergo peripheral expansion with central healing over hours to days. Other systemic signs and symptoms are either mild or absent.
The juvenile/infantile type of pustular psoriasis typically has a benign course. Systemic involvement is not common, and spontaneous remissions frequently occur.
Patients appear distressed, often tachypneic, tachycardic, and febrile. The oropharyngeal mucosa may be hyperemic, and a geographic tongue or fissured tongue may be appreciated. Skin findings include a generalized or patchy erythema studded with interfollicular pustules that may have an annular or generalized/nonspecific configuration.
Lesions appear on the trunk, extremities, and, rarely, on the face. Flexural and anogenital accentuation may be present. Pustulation may also involve the nail beds, resulting in onychodystrophy, onycholysis, and defluvium unguium.
Peripheral scaling may be observed, especially in areas that have undergone pustulation. The rest of the physical examination depends on systemic complications.
The following conditions can mimic signs and symptoms of pustular psoriasis:
Findings include the following:
Complete blood cell (CBC) count with absolute lymphopenia coinciding with polymorphonuclear leukocytosis up to 40,000/µL
Elevated erythrocyte sedimentation rate (ESR)
Serum chemistries – Increased plasma globulins; decreased albumin, calcium, and zinc; elevated BUN and creatinine if the patient is oligemic; elevated liver enzymes (aspartate transaminase [AST], alanine transaminase [ALT]) if liver damage has occurred
Urinalysis – Positive albumin; positive casts
Bacterial cultures and sensitivities of pustules – Negative in the absence of secondary infection, as are Tzanck preparations and viral cultures; loss of the cutaneous barrier may result in bacteremia
The overall architecture of the epidermis is similar to patients with psoriasis vulgaris, exhibiting parakeratosis, elongation of rete ridges, and thinning of the suprapapillary epidermis. The superficial dermis shows a mononuclear infiltrate and numerous neutrophils migrating from papillary capillaries to the epidermis. Neutrophils in the epidermis can aggregate between keratinocytes, where there is also spongiosis, forming pustules known as spongiform pustules of Kogoj, a characteristic histologic feature. [21]
Patients with generalized pustular psoriasis eruptions may require hospitalization to ensure adequate hydration, bed rest, and avoidance of excessive heat loss. Supportive therapy with bland topical compresses and saline or oatmeal baths helps sooth and debride affected areas.
There is no criterion standard therapy for pustular psoriasis. Disease severity and extent of skin involvement help guide treatment.
Current recommendations include initiation of systemic medications together with the proper supportive measures. Oral retinoids (acitretin, isotretinoin), methotrexate, cyclosporine, and infliximab are considered first-line therapies by the National Psoriasis Foundation Medical Board. [22] Hydroxyurea and 6-thioguanine have also been used with success. [23, 24]
In children, acitretin, cyclosporine, methotrexate, and etanercept are options for first-line therapy; however, no randomized controlled trials exist to confirm efficacy. [22]
Second-line therapies include biologic agents (etanercept and adalimumab) or topical treatments (corticosteroids, calcipotriene, tacrolimus) for more localized disease on the palms and soles. [22] An example of the palmoplantar condition is seen in the image below. [25] Guidelines regarding these second-line therapies are needed, as anecdotal reports describe paradoxical induction of pustular psoriasis with some biologics. [26, 27]
Combination therapy with use of a first- and second-line agent can also be considered. [22]
The study of IL35RN gene mutations in the pathogenesis of generalized pustular psoriasis has led to new advances in treatment. Case reports have documented success with IL-1 receptor antagonists (eg, anakinra), and clinical trials are currently underway. [28, 29]
Case reports describe the efficacy of the drug tocilizumab in the treatment of biologic-induced plantar pustular psoriasis. [30] Tocilizumab is a monoclonal antibody that blocks IL-6 activity at both soluble and membrane-bound complexes, thus inhibiting IL-6‒dependant STAT1/STAT3 activation. However, reports describe rheumatoid arthritis patients treated with tocilizumab who develop paradoxical biologic-induced psoriasiform dermatitis. [31] Tofacitinib, a Janus kinase inhibitor, has also been tested as a potential therapy for psoriasis, but efficacy in pustular psoriasis is still undetermined. [32]
Several case reports discuss treatment of pustular psoriasis in pregnancy. Cyclosporine has been used with success in such cases, as well as infliximab (5 mg/kg). [33] The woman on infliximab delivered a healthy female baby via cesarean delivery. The neonate breastfed for 1 month and developed normally. No detectable adverse effects were noted, despite potential exposure to infliximab throughout gestation and breastfeeding. [34]
Patients usually have too much systemic toxicity and erythema during a flare to tolerate oral psoralen plus ultraviolet-A (PUVA). Treatment also requires frequent clinic visits (up to 4 d/wk), which is logistically difficult.
However, several studies have reported that PUVA is safe and effective in controlling flares of pustular psoriasis. Typically, PUVA is started once the patient has been stabilized on acitretin. PUVA has also successfully been used in combination with oral cyclosporine. [22]
While little is written regarding the use of phototherapy for pustular psoriasis, [35] narrow-band UV-B may be a reasonable choice since it has achieved therapeutic effects similar to those of PUVA in other forms of psoriasis.
Acitretin is administered first at 0.2-0.5 mg/kg for 7 days, and then PUVA is added 3 times per week. As lesions resolve, acitretin can be withdrawn, and maintenance phototherapy with PUVA or narrowband UV-B can be continued as needed.
Request consultations with medical subspecialists according to the degree of systemic involvement.
Older patients with von Zumbusch type have a poor prognosis. Death can result from sepsis, renal, hepatic, or cardiorespiratory failure during the acute erythrodermic stage.
Patients with a history of chronic psoriasis vulgaris prior to generalized pustular eruption tend to have a better prognosis than patients with more atypical forms of psoriasis.
In children, as long as serious secondary infections are avoided, episodes of pustular psoriasis have a good prognosis.
There is no cure for pustular psoriasis. Recurrent flares are common, even years after diagnosis. Patients often require continued therapy and avoidance of precipitating factors. [17]
Occasionally, acute respiratory distress syndrome may complicate generalized pustular psoriasis.
Other possible complications in pustular psoriasis include the following:
Secondary bacterial skin infections, hair loss (telogen effluvium), and nail loss
Hypoalbuminemia secondary to loss of plasma protein into tissues
Hypocalcemia
Renal tubular necrosis as a result of oligemia
Liver damage as a result of oligemia, neutrophilic cholangitis, [36] and general toxicity
Malabsorption and malnutrition
Death in pustular psoriasis may occur secondary to cardiorespiratory failure. This usually occurs in untreated patients.
Liao PB, Rubinson R, Howard R, Sanchez G, Frieden IJ. Annular pustular psoriasis–most common form of pustular psoriasis in children: report of three cases and review of the literature. Pediatr Dermatol. 2002 Jan-Feb. 19(1):19-25. [Medline].
Oumeish OY, Parish JL. Impetigo herpetiformis. Clin Dermatol. 2006 Mar-Apr. 24(2):101. [Medline].
Sehgal VN, Verma P, Sharma S, et al. Acrodermatitis continua of Hallopeau: evolution of treatment options. Int J Dermatol. 2011 October. 50(10):1195-211. [Medline].
Cheng S, Edmonds E, Ben-Gashir M, Yu RC. Subcorneal pustular dermatosis: 50 years on. Clin Exper Dermatol. 2008 May. 33:229-33. [Medline].
Szatkowski J, Schwartz RA. Acute generalized exanthematous pustulosis (AGEP): A review and update. J Am Acad Dermatol. 2015 November. 73(5):843-8. [Medline].
Zelickson BD, Pittelkow MR, Muller SA, Johnson CM. Polymorphonuclear leukocyte chemotaxis in generalized pustular psoriasis. Acta Derm Venereol. 1987. 67(4):326-30. [Medline].
Saggini A, Chimenti S, Chiricozzi A. IL-6 as a druggable target in psoriasis: focus on pustular variants. J Immunol Res. 2014 July 13. 2014 July 13:1-10. [Medline].
Setta-Kaffetzi N, Navarini AA, Patel VM, et al. Rare pathogenic variants in IL36RN underlie a spectrum of psoriasis-associated pustular phenotypes. J Invest Dermatol. 2013 May. 133(5):1366-9. [Medline].
Onoufriadis A, Simpson MA, Pink AE, et al. Mutations in IL36RN/IL1F5 are associated with the severe episodic inflammatory skin disease known as generalized pustular psoriasis. Am J Hum Genet. 2011 September 09. 89(3):432-7. [Medline].
Brenner M, Molin S, Ruebsam K, Weisenseel P, Ruzicka T, Prinz JC. Generalized pustular psoriasis induced by systemic glucocorticosteroids: four cases and recommendations for treatment. Br J Dermatol. 2009 Oct. 161(4):964-6. [Medline].
Borges-Costa J, Silva R, Gonçalves L, Filipe P, Soares de Almeida L, Marques Gomes M. Clinical and laboratory features in acute generalized pustular psoriasis: a retrospective study of 34 patients. Am J Clin Dermatol. 2011 Aug 1. 12(4):271-6. [Medline].
Hong SB, Kim NI. Generalized pustular psoriasis following withdrawal of short-term cyclosporin therapy for psoriatic arthritis. J Eur Acad Dermatol Venereol. 2005 July. 19(4):522-3. [Medline].
Tobin AM, Langan SM, Collins P, Kirby B. Generalized pustular psoriasis (von Zumbusch) following the use of calcipotriol and betamethasone dipropionate ointment: a report of two cases. Clin Exp Dermatol. 2009 Jul. 34(5):629-30. [Medline].
Duckworth L, Maheshwari MB, Thomson MA. A diagnostic challenge: acute generalized exanthematous pustulosis or pustular psoriasis due to terbinafine. Clin Exp Dermatol. 2012 January. 37(1):24-7. [Medline].
Wee JS, Natkunarajah J, Moosa Y, Marsden RA. Erythrodermic pustular psoriasis triggered by intravesical bacillus Calmette-Guérin immunotherapy. Clin Exp Dermatol. 2012 June. 37(4):455-7. [Medline].
Cassandra M, Conte E, Cortez B. Childhood pustular psoriasis elicited by the streptococcal antigen: a case report and review of the literature. Pediatr Dermatol. 2003 Nov-Dec. 20(6):506-10. [Medline].
Choon SE, Lai NM, Mohammad NA, Nanu NM, Tey KE, Chew SF. Clinical profile, morbidity, and outcome of adult-onset generalized pustular psoriasis: analysis of 102 cases seen in a tertiary hospital in Johor, Malaysia. Int J Dermatol. 2014 June. 53(6):676-84. [Medline].
Brunasso AM, Puntoni M, Aberer W, Delfino C, Fancelli L, Massone C. Clinical and epidemiological comparison of patients affected by palmoplantar plaque psoriasis and palmoplantar pustulosis: a case series study. Br J Dermatol. 2013 June. 168(6):1243-51. [Medline].
Chao PH, Cheng YW, Chung MY. Generalized pustular psoriasis in a 6-week-old infant. Pediatr Dermatol. 2009 May-Jun. 26 (3):352-4. [Medline].
Hubler WR Jr. Lingual lesions of generalized pustular psoriasis. Report of five cases and a review of the literature. J Am Acad Dermatol. 1984 Dec. 11(6):1069-76. [Medline].
Heng MC, Heng JA, Allen SG. Electron microscopic features in generalized pustular psoriasis. J Invest Dermatol. 1987 Aug. 89(2):187-91. [Medline].
Robinson A, Van Voorhees AS, Hsu S, et al. Treatment of pustular psoriasis: from the Medical Board of the National Psoriasis Foundation. J Am Acad Dermatol. 2012 Aug. 67(2):279-88. [Medline].
Rosenbaum MM, Roenigk HH Jr. Treatment of generalized pustular psoriasis with etretinate (Ro 10-9359) and methotrexate. J Am Acad Dermatol. 1984 Feb. 10(2 Pt 2):357-61. [Medline].
Wolska H, Jablonska S, Bounameaux Y. Etretinate in severe psoriasis. Results of double-blind study and maintenance therapy in pustular psoriasis. J Am Acad Dermatol. 1983 Dec. 9(6):883-9. [Medline].
Ghate JV, Alspaugh CD. Adalimumab in the management of palmoplantar psoriasis. Dermatol Online J. 2009 Jul 15. 15(7):15. [Medline].
Manni E, Barachini P. Psoriasis induced by infliximab in a patient suffering from Crohn’s disease. Int J Immunopathol Pharmacol. 2009 Jul-Sep. 22(3):841-4. [Medline].
Ibis N, Hocaoglu S, Cebicci MA, Sutbeyaz ST, Calis HT. Palmoplantar pustular psoriasis induced by adalimumab: a case report and literature review. Immunotherapy. 7(7). 2015 July:717-20. [Medline].
Hüffmeier U, Wätzold M, Mohr J, Schön MP, Mössner R. Successful therapy with anakinra in a patient with generalized pustular psoriasis carrying IL36RN mutations. Br J Dermatol. 2014 January. 170(1):202-4. [Medline].
Rossi-Semerano L, Piram M, Chiaverini C, De Ricaud D, Smahi A, Koné-Paut I. First clinical description of an infant with interleukin-36-receptor antagonist deficiency successfully treated with anakinra. Pediatrics. 2013 October. 132(4):1043-7. [Medline].
Jayasekera P, Parslew R, Al-Sharqi A. A case of tumour necrosis factor-α inhibitor- and rituximab-induced plantar pustular psoriasis that completely resolved with tocilizumab. Br J Dermatol. 2014 December. 171(6):1546-9. [Medline].
Palmou-Fontana N, Sánchez Gaviño JA, McGonagle D, García-Martinez E, Iñiguez de Onzoño Martín L. Tocilizumab-induced psoriasiform rash in rheumatoid arthritis. Dermatology. 2014 July. 228(4):311-3. [Medline].
Hsu L, Armstrong AW. JAK inhibitors: treatment efficacy and safety profile in patients with psoriasis. J Immunol Res. 2014 May 05. 2014:283617.:1-7. [Medline].
Hazarika D. Generalized pustular psoriasis of pregnancy successfully treated with cyclosporine. Indian J Dermatol Venereol Leprol. 2009 Nov-Dec. 75(6):638. [Medline].
Puig L, Barco D, Alomar A. Treatment of psoriasis with anti-TNF drugs during pregnancy: case report and review of the literature. Dermatology. 2010. 220(1):71-6. [Medline].
Honigsmann H, Gschnait F, Konrad K, Wolff K. Photochemotherapy for pustular psoriasis (von Zumbusch). Br J Dermatol. 1977 Aug. 97(2):119-26. [Medline].
Viguier M, Allez M, Zagdanski AM, et al. High frequency of cholestasis in generalized pustular psoriasis: Evidence for neutrophilic involvement of the biliary tract. Hepatology. 2004 August. 40(2):452-8. [Medline].
Annie O Morrison, MD Fellow in Dermatopathology, Cockerell Dermatopathology
Annie O Morrison, MD is a member of the following medical societies: Academy of Clinical Laboratory Physicians and Scientists, American Society for Clinical Pathology, American Society of Dermatopathology, College of American Pathologists, Digital Pathology Association, International Society of Dermatopathology, Phi Beta Kappa, United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.
Christie A Riemer, MD, (NRM) Resident Physician, Department of Dermatology, Mayo Clinic School of Graduate Medical Education
Christie A Riemer, MD, (NRM) is a member of the following medical societies: American Academy of Dermatology, American Medical Student Association/Foundation
Disclosure: Nothing to disclose.
Clay J Cockerell, MD Director, Clinical Professor, Department of Dermatology, Division of Dermatopathology, University of Texas Southwestern Medical Center
Clay J Cockerell, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, International AIDS Society, International Academy of Pathology, International Society for Dermatologic Surgery, North American Clinical Dermatologic Society, Society for Investigative Dermatology, Southern Medical Association
Disclosure: Nothing to disclose.
David F Butler, MD Former Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for MOHS Surgery, Association of Military Dermatologists, Phi Beta Kappa
Disclosure: Nothing to disclose.
Christen M Mowad, MD Professor, Department of Dermatology, Geisinger Medical Center
Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, American Academy of Dermatology, Phi Beta Kappa
Disclosure: Nothing to disclose.
Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
Mark G Lebwohl, MD Chairman, Department of Dermatology, Mount Sinai School of Medicine
Mark G Lebwohl, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Received none from Amgen for consultant & investigator; Received none from Novartis for consultant & investigator; Received none from Pfizer for consultant & investigator; Received none from Celgene Corporation for consultant & investigator; Received none from Clinuvel for consultant & investigator; Received none from Eli Lilly & Co. for consultant & investigator; Received none from Janssen Ortho Biotech for consultant & investigator; Received none from LEO Pharmaceuticals for consultant & inves.
Carlos Ricotti, MD Fellow, Department of Dermatology, Division of Dermatopathology, University of Texas Southwestern School of Medicine
Carlos Ricotti, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society of Dermatopathology, International Society of Dermatopathology
Disclosure: Nothing to disclose.
The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous authors Elma Baron, MD; Charles R Taylor, MD; John D Wilkinson, MD, MBBS, MRCS, FRCP; John Reed, MBBS, MRCP; Sarah E Dick, MD; and Abby S Van Voorhees, MD, to the development and writing of the source articles.
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