Type Cause or Pathogenesis Histology * Clinical Features
Contact dermatitis Topically applied antigens Spongiotic dermatitis Marked itching, burning, or both; requires antecedent
Atopic dermatitis Unknown; may be heritable Spongiotic dermatitis Erythematous plaques in flexural areas; family history
of eczema, hay fever, or asthma
Drug-related eczematous dermatitis Systemically administered antigens or
haptens (e.g. penicillin)
Spongiotic dermatitis; infiltrate often
deeper with abundant eosinophils
Temporal relationship to drug administration; remits
with cessation of drug
Eczematous insect bite reaction Locally injected antigen or toxin Spongiotic dermatitis; wedge-shaped
infiltrate; many eosinophils
Papules, nodules, and plaques with vesicles; may be
linear when multiple
Photoeczematous eruption Ultraviolet light Spongiotic dermatitis; infiltrate that
diminishes gradually with depth
Occurs at sites of sun exposure; may require associated
exposure to systemic or topical antigen; photopatch
testing may help in diagnosis
Primary irritant dermatitis Repeated trauma or chemical irritants (as
Spongiotic dermatitis in early stages;
acanthosis predominates in later stages
Localized mechanical or chemical irritants
*All types, with time, may develop chronic changes, with prominent acanthosis of the epidermal layer.
The most obvious example is an acute contact reaction to topical antigens such as poison ivy, characterized by pruritic, edematous, oozing plaques, often containing small and large
blisters (vesicles and bullae) ( Fig. 25-25A ). Such lesions are prone to bacterial superinfection, which produces a yellow crust (impetiginization). With time, persistent lesions become
less "wet" (fail to ooze or form vesicles) and become progressively scaly (hyperkeratotic) as the epidermis thickens (acanthosis).
This has been well studied in dermatitis due to contact hypersensitivity (e.g., poison ivy dermatitis). Initially, antigens at the epidermal surface are taken up by dendritic Langerhans
cells, which then migrate by way of dermal lymphatics to draining lymph nodes ( Fig. 25-26 ). Here, antigens, now processed by the Langerhans cell, are presented to naive CD4 T cells,
which are activated and develop into effector and memory cells ( Chapter 6 ). On antigen re-exposure,
Figure 25-25Eczematous dermatitis. A, In an acute allergic contact dermatitis, numerous vesicles appear at the site of antigen exposure (in this case, laundry detergent that persisted in
clothing). B, Histologically, intercellular edema produces widened intercellular spaces within the epidermis, eventually resulting in small, fluid-filled intraepidermal vesicles.
Figure 25-26Schematic diagram of mechanisms of allergic contact dermatitis. D, antigen; Ln, naive T lymphocyte; Lm, memory T lymphocyte.
Figure 25-27Erythema multiforme. A, The target-like clinical lesions consist of a central blister or zone of epidermal necrosis surrounded by macular erythema. B, Early lesions show
lymphocytes collecting along the dermal epidermal junction where basal keratinocytes have begun to become vacuolated.
Figure 25-28Clinical evolution of psoriasis. Early and eruptive lesions may be dominated by signs of inflammation and erythema (left). Established, chronic lesions demonstrate
erythema surmounted by characteristic silver-white scale (right). Rarely, the early inflammatory phase predominates throughout the course of the disease (pustular psoriasis).
Figure 25-29Psoriasis. Histologically, established lesions demonstrate marked epidermal hyperplasia, parakeratotic scale, and, importantly, minute microabscesses of neutrophils within
the superficial epidermal layers.
Figure 25-30Lichen planus. A, A solitary lesion of lichen planus (glistening surface is due to application of mineral oil, rendering the scale transparent). This flat-topped pink-purple,
polygonal papule shows prominent Wickham striae that are more easily appreciated through the transparent scale. B, Biopsy of one of the lesions demonstrates the bandlike infiltrate of
lymphocytes at the dermoepidermal junction and pointed rete ridges (saw-toothing; compare with Fig. 25-1 ).
Figure 25-31Lupus erythematosus. A, These chronic plaques show a thinned and glistening (atrophic) epidermis, areas where dilated and tortuous dermal vessels are apparent, and
central hypopigmentation surrounded by peripheral hyperpigmentation. Note areas of early hair loss due to follicular involvement. B, There is an infiltrate of lymphocytes within the
superficial and deep dermis, marked thinning of the epidermis with loss of normal rete ridges, and hyperkeratosis.
Figure 25-32Granular deposits of immunoglobulin (here IgG) and complement at the dermoepidermal junction constitute a positive "band test" in lupus erythematosus.
Figure 25-33Schematic representation of sites of blister formation. A, In a subcorneal blister, the stratum corneum forms the roof of the bulla (as in impetigo or pemphigus foliaceus). B,
In a suprabasal blister, a portion of the epidermis including the stratum corneum forms the roof (as in pemphigus vulgaris). C, In a subepidermal blister, the entire epidermis separates
from the dermis (as in bullous pemphigoid and dermatitis herpetiformis).
Figure 25-34Pemphigus vulgaris. A, Eroded plaques are formed on rupture of confluent, thin-roofed bullae, here affecting axillary skin. B, Suprabasal acantholysis results in an
intraepidermal blister in which rounded (acantholytic) epidermal cells are identified (inset).
Figure 25-35Direct immunofluorescence of pemphigus vulgaris. There is deposition of immunoglobulin along the plasma membranes of epidermal keratinocytes in a fishnet-like
pattern. Also note the early suprabasal separation due to loss of cell-to-cell adhesion (acantholysis).
Figure 25-36Bullous pemphigoid. Clinical bullae (A) result from basal cell layer vacuolization, producing a subepidermal blister (B). Histopathology of the edge of an early lesion
showing the onset of epidermal separation from the underlying dermis. Eosinophils, as well as lymphocytes and occasional neutrophils, may be intimately associated with basal cell layer
destruction, creating the subepidermal cleft.
Figure 25-37 A, Linear deposition of complement along the dermoepidermal junction in bullous pemphigoid; the pattern has been likened to ribbon candy. B, Bullous pemphigoid
antigen is located in the lowermost portion of the basal cell cytoplasm in association with hemidesmosomes (HD), with blister formation affecting the lamina lucida (LL) of the basement
membrane zone. LD, lamina densa; AF, anchoring fibrils.
Figure 25-38Dermatitis herpetiformis. A, Clinical lesions consist of intact and eroded erythematous blisters that are often grouped together. B, Histologically, neutrophilic
microabscesses selectively involve the dermal papilla.
Figure 25-39Dermatitis herpetiformis. A, Papillary dermal microabscesses are associated with zones of dermoepidermal cleavage that eventually coalesce to form a clinical blister. B,
By direct immunofluorescence, these abscesses are rich in IgA and fibrin deposits.
Figure 25-40Epidermolysis bullosa. A, Junctional epidermolysis bullosa showing typical erosions in flexural creases. B, A noninflammatory subepidermal blister in this case has formed
at the level of the lamina lucida (Giemsa-stained section).
Figure 25-41Porphyria. A noninflammatory blister is forming at the dermoepidermal junction; note the seemingly rigid dermal papillae at the base that contain the altered superficial
Figure 25-42Acne. A, Inflammatory acne is characterized clinically by erythematous papules and pustules, with the possibility of eventual scarring. B, A portion of a hair shaft piercing
the follicular epithelium and eliciting an inflammatory response and fibrosis.
Figure 25-43Verruca vulgaris. A, Multiple papules with rough pebble-like surfaces. B (low power) and C (high power), histology of the lesions show papillomatous epidermal
hyperplasia and cytopathic alterations that include nuclear pallor and prominent keratohyaline granules. D, In situ hybridization showing viral DNA within epidermal cells.
Figure 25-44Molluscum contagiosum. A focus of verrucous epidermal hyperplasia contains numerous cells with ellipsoid cytoplasmic inclusions (molluscum bodies) within the stratum
granulosum and stratum corneum.
Figure 25-45Tinea. A, Characteristic plaque of tinea corporis. Routine histology (B) shows the picture of mild eczematous (spongiotic) dermatitis, and periodic acid-Schiff stain reveals
deep red hyphae and yeast forms (C) within the stratum corneum.
Figure 25-46 A, Pediculosis. Egg case (nit) of head louse attached to hair shaft. B, Portions of a scabies mite within a burrow involving the stratum corneum.
1. Virchow R: Cellular Pathology. London, John Churchill, 1860, p 33.
2. Williams IR, Kupper TS: Immunity at the surface: homeostatic mechanisms of the skin immune system. Life Sci 58:1485, 1996.
3. Murphy GF: The secret of "NIN," a novel neural immunological network potentially integral to immunologic function in human skin. In Nickoloff BJ (ed): Mast Cells, Macrophages
and Dendritic Cells in Skin Disease. Boca Raton, FL, CRC Press, 1993, pp 227–244.
4. Johnson KO: The roles and functions of cutaneous mechanoreptors. Curr Opin Neurobiol 11:455, 2001.
5. Lavker RM, et al: Hair follicle stem cells. J Investig Dermatol Symp Proc 8:28, 2003.
6. Deguchi M, et al: 12E2: a cloned murine dermal cell with features of dermal dendrocytes and capacity to produce pathologic changes resembling early Kaposi's sarcoma Am J Pathol
7. Fishman P, et al: Autoantibodies to tyrosinase: the bridge between melanoma and vitiligo. Cancer 79:1461, 1997.
8. Le Poole IC, et al: Presence of T cells and macrophages in inflammatory vitiligo skin parallels melanocyte disappearance. Am J Pathol 148:1219, 1996.
9. Mandelcorn-Monson RL, et al: Cytotoxic T lymphocyte reactivity to gp 100, MelanA/MART-1, and tyrosinase, in HLA-A2-positive vitiligo patients. J Invest Dermatol 121:550,
10. Norris W: A case of fungoid disease. Edinburgh Med Surg J 16:562, 1820.
11. Clark WH Jr, et al: Origin of familial malignant melanomas from heritable melanotic lesions: the BK mole syndrome. Arch Dermatol 114:732, 1978.
12. Kamb A, Herlyn M: Malignant melanoma. In Vogelstein B, Kinzler K (eds.): The Genetic Basis of Human Cancer, New York, McGraw-Hill, 2002, pp 515–525.
13. Greene MH: Genetics of cutaneous melanoma and nevi [review]. Mayo Clin Proc 72:467, 1997.
14. Monzon J, et al: CDKN2A mutations in multiple primary melanomas. N Engl J Med 338:879, 1998.
15. Greene MH, et al: The high risk of melanoma in melanoma prone families with dysplastic nevi. Ann Intern Med 102:458, 1985.
16. van Duinen CM, et al: The distribution of cellular adhesion molecules in pigmented skin lesions. Cancer 73:2131, 1994.
17. Hussein MR, Wood GS: Molecular aspects of melanocytic dysplastic nevi. J Mol Diagn 4:71, 2002.
18. Shannon JA, Kefford RF, Mann GJ: Responses to ultraviolet-B in cell lines from hereditary melanoma kindreds. Melanoma Res 11:1, 2001.
19. Clark WH, et al: A study of tumor progression: the precursor lesions of superficial spreading and nodular melanoma. Hum Pathol 15:1147, 1985.
20. Crowson AN, et al: The precursors of malignant melanoma. Recent Results Cancer Res 160:75, 2002.
21. Weedon D: Lentigines, nevi, and melanomas. In Weedon D: Skin Pathology, 2nd ed. Edinburgh, Churchill Livingstone, 2002, pp 803–858.
22. Breslow A: Prognosis in cutaneous melanoma: tumor thickness as a guide to treatment. Pathol Annu 15:1, 1980.
23. Kim JC, Murphy GF: Dysplastic melanocytic nevi and prognostically indeterminate nevomelanocytic proliferations ("PINM Tumors"), In Clinics in Laboratory Medicine,
Philadelphia, WB Saunders, 2000, pp 691–712.
24. Elder DE, Murphy GF: Melanocytic tumors of the skin. In Rosai J, Sobin LH (eds.): Atlas of Tumor Pathology, Third Series, Fascicle 1. Washington, DC, Armed Forces Institute of
Pathology, 1991, pp. 183–185.
25. Clark WH Jr, et al: Model predicting survival in stage I melanoma based on tumor progression. J Natl Cancer Inst 81:1893, 1989.
26. Balch CM, et al: Final version of the American Joint Committee on Cancer staging system for cutaneous melanoma. Clin Oncol 15:3635, 2001.
27. Chen M, et al: Acantholytic variant of seborrheic keratosis. J Cutan Pathol 17:27, 1990.
28. Ellis DL, et al: Melanoma, growth factors, acanthosis nigricans, the sign of Leser-Trélat, and multiple acrochordons. A possible role for alpha-transforming growth factor in
cutaneous paraneoplastic syndromes. N Engl J Med 317:1582, 1987.
29. Torley D, Bellus GA, Munro CS: Genes, growth factors and acanthosis nigricans. Br J Dermatol 147:1096, 2002.
30. Murphy GF, Elder D: Non-melanocytic tumors of the skin. In Rosai J, Sobin LH (eds.): Atlas of Tumor Pathology, Third Series, Fascicle 1. Washington, DC, Armed Forces Institute
of Pathology, 1991, pp 61–154.
31. Hanssen AM, Fryns JP: Cowden syndrome. J Med Genet 32:117, 1995.
32. LeBoit PE: Can we understand keratoacanthoma? Am J Dermatopathol 24:116, 2002.
33. Perez MI, et al: P53 oncoprotein expression and gene mutations in some keratoacanthomas. Arch Dermatol 133:189, 1997.
34. Matsumura Y, Ananthaswamy HN: Short-term and long-term cellular and molecular events following UV irradiation of skin: implications for molecular medicine. Expert Rev Mol
Med 4:1, 2002.
35. Penn I: Neoplastic consequences of transplantation and chemotherapy. Cancer Detect Prev 1 (suppl):149, 1987.
36. Duthie MS, Kimber I, Norval M: The effects of ultraviolet radiation on the human immune system. Br J Dermatol 140:995, 1999.
37. Beissert S, Schwarz T: Mechanisms involved in ultraviolet light-induced immunosuppression. J Investig Dermatol Symp Proc 4:61, 1999.
38. Lu S, et al: No evidence of human papillomavirus DNA in actinic keratosis. Arch Dermatol Res 287:649, 1995.
39. Green CL, Khavari PA: Targets for molecular therapy of skin cancer. Semin Cancer Biol 14:63, 2004.
40. Bale AE: The nevoid basal cell carcinoma syndrome: genetics and mechanism of carcinogenesis. Cancer Invest 15:180, 1997.
41. Al-Ghazal SK, et al: Merkel cell carcinoma of the skin. Br J Plast Surg 49:491, 1996.
42. Miller DL, Weinstock MA: Nonmelanoma skin cancer in the United States: incidence. J Am Acad Dermatol 30:774, 1994.
43. Ries LAG, et al: SEER Cancer Statistics Review, 1993–1997. Bethesda, MD, National Cancer Institute, 2000.
44. Tsao H: Update on familial cancer syndromes and the skin. J Am Acad Dermatol 42:939, 2000.
45. Gorlin RJ, Goltz RW: Multiple nevoid basal-cell epithelioma, jaw cysts and bifid rib: a syndrome. N Engl J Med 262:908, 1962.
46. Mirowski GW, et al: Nevoid basal cell carcinoma syndrome. J Am Acad Dermatol 43:1092, 2000.
47. Rees J: Skin cancer. In B Vogelstein, KW Kinzler: The Genetic Basis of Human Cancer, New York, McGraw-Hill, 2002, pp 539–548.
48. Hahn H, et al: Mutations of the human homologue of Drosophila patched in the nevoid basal cell carcinoma syndrome. Cell 85:841, 1996.
49. Bonifas JM, et al: Activation of expression of hedgehog target genes in basal cell carcinoma. J Invest Dermatol 116:739, 2001.
50. Cohen MM, Jr: The hedgehog signaling network. Am J Med Genet 123A:5, 2003.
51. Nilsson M, et al: Induction of basal cell carcinomas and trichoepitheliomas in mice overexpressing GLI1. Proc Natl Acad Sci U S A 97:3438, 2000.
52. Bale AE, Yu K-P: The hedgehog pathway and basal cell carcinomas. Hum Mol Genet 10:757, 2001.
53. Kim MY, et al: Mutations of the p53 and PTCH gene in basal cell carcinomas: UV mutation signature and strand bias. J Dermatol Sci 29:1, 2002.
54. Lacour JP: Carcinogenesis of basal cell carcinomas: genetics and molecular mechanisms. Br J Dermatol 146 (Suppl) 61:17, 2002.
55. D'Errico M, et al: UV mutation signature in tumor suppressor genes involved in skin carcinogenesis in xeroderma pigmentosum patients. Oncogene 19:463, 2000.
56. Einspahr JG, Bowden GT, Alberts DS: Skin cancer chemoprevention: strategies to save our skin. Recent Results Cancer Res 163:151, 2003.
57. Ortonne JP: From actinic keratosis to squamous cell carcinoma. Br J Dermatol 146 (Suppl) 61:20, 2002.
58. Soenge H, Ananthaswamy HN: Mechanisms of induction of skin cancer by UV radiation. Frontiers Biosci 2:538, 1997.
59. Majewski S, et al: Epidermodysplasia verruciformis. Immunological and nonimmunological surveillance mechanisms: role in tumor progression. Clin Dermatol 15:321, 1997.
60. Chin L: The genetics of malignant melanoma: lessons from mouse and man. Nat Rev Cancer 3:559, 2003.
61. Hayward NK: Genetics of melanoma predisposition. Oncogene 22:3053, 2003.
62. Piepkorn M: Melanoma genetics: an update with focus on the CDKN2A(p16)/ARF tumor suppressors. J Am Acad Dermatol 42:705, 2000.
63. Chin L, et al: Malignant melanoma: modern black plague and genetic black box. GenesDevelop 12:3467, 1998.
64. Cannon-Albright LA, et al: Assignment of a locus for familial melanoma, MLM, to chromosome 9p13-p22. Science 258:1148, 1992.
65. Kannengiesser C, et al: CDKN2A as a uveal and cutaneous melanoma susceptibility gene. Genes Chromosomes Cancer 38:265, 2003.
66. Sharpless NE, Chin L: The INK4/ARF locus and melanoma. Oncogene 22:3092, 2003.
67. Hussussian CJ, et al: Germline p16 mutations in familial melanoma. Nature Genet 8:15, 1994.
68. Houghton AN, Polsky D: Focus on melanoma. Cancer Cell 2:275, 2002.
69. Pavey SJ, et al: Loss of p16 expression is associated with histological features of melanoma invasion. Melanoma Res 12:539, 2002.
70. Pomerantz J, et al: The INK4a tumor suppressor gene product, p19ARF, interacts with MDM2 and neutralizes MDM2's inhibition of p53. Cell 92:713, 1998.
71. Rizos H, et al: A melanoma-associated germline mutation in exon 1 b inactivates p14ARF. Oncogene 20:5543, 2001.
72. Randerson-Moor JA, et al: A germline deletion of p14ARF but not CDKN2A in a melanoma-neural system tumour syndrome family. Hum Mol Genet 10:55, 2001.
73. Soufir N, et al: Prevalence of p16 and CDK4 germline mutations in 48 melanoma-prone families in France. The French Familial Melanoma Study Group. Hum Mol Genet 7:209,
74. Davies H, et al: Mutations of the BRAF gene in human cancer. Nature 417:949, 2002.
75. Pollock PM, et al: High frequency of BRAF mutations in nevi. Nat Genet 33:19, 2002.
76. Dong J, et al: BRAF oncogenic mutations correlate with progression rather than initiation of human melanoma. Cancer Res 63:3883, 2003.
77. Calonje E: Is cutaneous benign fibrous histiocytoma dermatofibroma a reactive inflammatory process or a neoplasm? Histopathology 37:278, 2000.
78. Zegler BG, et al: Dermatofibroma (fibrous histiocytoma): an inflammatory or neoplastic disorder? Histopathology 38:379, 2001.
79. Lever WF, Schaumburg-Lever G: Histopathology of the Skin. Philadelphia, JB Lippincott, 1997, p 593.
80. Laman JD, et al: Langerhans-cell histiocytosis 'insight into DC biology'. Trends Immunol 24:190, 2003.
81. Berger CL, Edelson RL: Current concepts of the immunobiology and immunotherapy of cutaneous T cell lymphoma: insights gained through cross-talk between the clinic and the
bench. Leuk Lymphoma 44:1697, 2003.
82. Uchiyama T: Human T cell leukemia virus type I (HTLV-1) and human disease. Ann Rev Immunol 15:15, 1997.
83. Bakels V, et al: Immunophenotyping and gene rearrangement analysis provide additional criteria to differentiate between cutaneous T-cell lymphomas and pseudo-T-cell
lymphomas. Am J Pathol 150:1941, 1997.
84. Longley BJ, et al: Somatic c-KIT activating mutation in urticaria pigmentosa and aggressive mastocytosis: establishment of clonality in a human mast cell neoplasm. Nat Genet
85. Longley BJ, et al: Chronically KIT-stimulated clonally derived human mast cells show heterogeneity in different tissue microenvironments. J Invest Dermatol 108:792, 1997.
86. Nettis E, et al: Clinical and aetiological aspects in urticaria and angio-oedema. Br J Dermatol 148:501, 2003.
87. Schon MP, Zollner TM, Boehncke WH: The molecular basis of lymphocyte recruitment to the skin: clues for pathogenesis and selective therapies of inflammatory disorders. J Invest
Dermatol 121:951, 2003.
88. Haas N, Hermes B, Henz BM: Adhesion molecules and cellular infiltrate: histology of urticaria. J Investig Dermatol Symp Proc 6:137, 2001.
89. Murphy GF, et al: Topical tretinoin replenishes CD1a-positive epidermal Langerhans cells in chronically photodamaged human skin. J Cutan Pathol 25:30, 1998.
90. Steinhoff M, et al: Modern aspects of cutaneous neurogenic inflammation. Arch Dermatol 139:1479, 2003.
91. Egan CL, et al: Characterization of unmyelinated axons uniting epidermal and dermal immune cells in primate and murine skin. J Cutan Pathol 25:20, 1998.
92. Murphy GF, et al: Reaction patterns in the skin and special dermatologic techniques. In Moschella S (ed): Dermatology. Philadelphia, WB Saunders, 1984, p 104.
93. Sackstein R, Messina JL, Elfenbein GJ: In vitro adherence of lymphocytes to dermal endothelium under shear stress: implications in pathobiology and steroid therapy of acute
cutaneous GVHD. Blood 101:771, 2003.
94. Binet I, Wood KJ: In vivo models of inflammation: immune rejection and skin transplantation in vivo. Methods Mol Biol 225:239, 2003.
95. Murphy GF, et al: Cytotoxic T lymphocytes and phenotypically abnormal epidermal dendritic cells in fixed cutaneous eruptions. Hum Pathol 16:1264, 1985.
96. Gilliam A, et al: Apoptosis is the predominant form of epithelial target cell injury in acute experimental graft-versus-host disease. J Invest Dermatol 107:377, 1996.
97. Kim JC, et al: Novel expression of vascular cell adhesion molecule-1 (CD106) by squamous epithelium in experimental acute graft-versus-host disease. Am J Pathol 161:763, 2002.
98. de Jong EM: Psoriasis of the nails associated with disability in a large number of patients: results of a recent interview with 1,728 patients. Dermatology 193:300, 1996.
99. Gudjonsson JE, et al: Immunopathogenic mechanisms in psoriasis. Clin Exp Immunol 135:1, 2004.
100. Bowcock AM, Cookson WO: The genetics of psoriasis, psoriatic arthritis and atopic dermatitis. Hum Mol Genet 13 (Suppl 1):R43, 2004.
101. Kreuger G, Callis K: Potential of tumor necrosis factor inhibitors in psoriasis and psoriatic arthritis. Arch Dermatol 140:218, 2004.
102. Schechtman RC, et al: HIV and Malassezia yeasts: a quantitative study of patients presenting with seborrheic dermatitis. Br J Dermatol 133:694, 1995.
103. Gupta A, Bluhm R: Seborrheic dermatitis. J Eur Acad Dermatol Venereol 18:13, 2004.
104. Hay RJ, Graham-Brown RA: Dandruff and seborrheic dermatitis: causes and management. Clin Exp Dermatol 22:3, 1997.
105. Fischer M, et al: Skin function and skin disorders in Parkinson's disease. J Neural Transm 108:205, 2001.
106. Franck JM, Young AW Jr: Squamous cell carcinoma in situ arising within lichen planus of the vulva. Dermatol Surg 21:890, 1995.
107. Iijima W, et al: Infiltrating CD8+ T cells in oral lichen planus predominantly express CCR5 and CXCR3 and carry respective chemokine ligands RANTES/CCL5 and IP-10/
CXCL10 in their cytolytic granules: a potential self-recruiting mechanism. Am J Pathol 163:261, 2003.
108. Maddison PJ: Is it SLE? Best Pract Res Clin Rheumatol 16:167, 2002.
109. Boumpas DT, et al: Systemic lupus erythematosus: emerging concepts. Part 2: Dermatologic and joint disease, the antiphospholipid antibody syndrome, pregnancy and hormonal
therapy, morbidity and mortality, and pathogenesis. Ann Intern Med 123:42, 1995.
110. Hashimoto T: Recent advances in the study of the pathophysiology of pemphigus. Arch Dermatol Res 295 (Suppl 1):S2, 2003.
111. Hacker-Foegen MK, et al: Pathogenicity and epitope characteristics of anti-desmoglein-1 from pemphigus foliaceus patients expressing only IgG1 autoantibodies. J Invest Dermatol
112. Koch PJ, et al: Targeted disruption of the pemphigus vulgaris antigen (desmoglein 3) gene in mice causes loss of keratinocyte cell adhesion with a phenotype similar to pemphigus
vulgaris. J Cell Biol 137:1091, 1997.
113. Xue W, Hashimoto K, Toi Y: Functional involvement of urokinasetype plasminogen activator receptor in pemphigus acantholysis. J Cutan Pathol 25:469, 1998.
114. Seishima M, et al: Pemphigus IgG induces expression of urokinase plasminogen activator receptor on the cell surface of cultured keratinocytes. J Invest Dermatol 10:650, 1997.
115. Hanakawa Y, et al: Expression of desmoglein 1 compensates for genetic loss of desmoglein 3 in keratinocyte adhesion. J Invest Dermatol 119:27, 2002.
116. Yeh SW, et al: Blistering disorders: diagnosis and treatment. Dermatol Ther 16:214, 2003.
117. Imber MJ, et al: The immunopathology of bullous pemphigoid. In Ahmed AR (ed): Clinics in Dermatology-Bullous Pemphigoid. Philadelphia, JB Lippincott, 1987, p 81.
118. Liu Z, et al: A major role for neutrophils in experimental bullous pemphigoid. J Clin Invest 100:1256, 1997.
119. Duhring L: Dermatitis herpetiformis. JAMA 250:212, 1983.
120. Bickle K, Roark TR, Hsu S: Autoimmune bullous dermatoses: a review. Am Fam Physician 65: 1861, 2002.
121. Mitsuhashi Y, Hashimoto I: Genetic abnormalities and clinical classification of epidermolysis bullosa. Arch Dermatol Res 295:529, 2003.
122. Mallipeddi R, et al: Dilemmas in distinguishing between dominant and recessive forms of dystrophic epidermolysis bullosa. Br J Dermatol 149:810, 2003.
123. Harper JC, Thiboutot DM: Pathogenesis of acne: recent research advances. Adv Dermatol 19:1–10, 2003.
124. Walton S, et al: Clinical, ultrasound and hormonal markers of androgenicity in acne vulgaris. Br J Dermatol 133:249, 1995.
125. Leyden JJ: New understandings of the pathogenesis of acne. J Am Acad Dermatol 32(pt 3):S15, 1995.
126. Miskin JE, et al: Propionibacterium acnes, a resident of lipid-rich human skin, produces a 33 kDa extracellular lipase encoded by gehA. Microbiology 143:1745, 1997.
127. Berson DS, Shalita AR: The treatment of acne: the role of combination therapies. J Am Acad Dermatol 32(pt 3):S31, 1995.
128. de Villiers EM: Papillomavirus and HPV typing. Clin Dermatol 15:199, 1997.
129. Hart WR: Vulvar intraepithelial neoplasia: historical aspects and current status. Int J Gynecol Pathol 20:16, 2001.
130. Majewski S, Jablonska S: Human papillomavirus-associated tumors of the skin and mucosa. J Am Acad Dermatol 36(pt 1):659, 1997.
131. Harris AJ, et al: A novel human papillomavirus identified in epidermodysplasia verruciformis. Br J Dermatol 136:587, 1997.
132. Sadick NS: Current aspects of bacterial infections of the skin. Dermatol Clin 15:341, 1997.
133. Darmstadt GL, Lane AT: Impetigo: an overview. Pediatr Dermatol 11:293, 1994.
134. Hanakawa Y, et al: Molecular mechanisms of blister formation in bullous impetigo and staphylococcal scalded skin syndrome. J Clin Invest 110:53, 2002.
135. Leyden JJ, Aly R: Tinea pedis. Semin Dermatol 12:280, 1993.
Date: 2016-04-22; view: 412