Share on Facebook Share on Twitter Email
Answers.com

List of cutaneous conditions

 
Wikipedia: List of cutaneous conditions
Home > Library > Miscellaneous > Wikipedia
This is an incomplete list, which may never be able to satisfy certain standards for completion.
See also Category:Cutaneous conditions and ICD-10 Chapter XII

There are many conditions of or affecting the human integumentary system—the organ system that covers the entire surface of the body and is composed of skin, hair, nails, and related muscle and glands.[1] The major function of this system is as a barrier against the external environment.[2] The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue.[1] There are two main types of human skin: glabrous skin, the non-hairy skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin.[3] Within the latter type, there are hairs in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle.[4] In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.[5]

Young child with a red rash covering face, chest, shoulders, and arms.
Measles

The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale.[6] Nourishment is provided to these layers via diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and the Merkels cell. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis.[3] This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface.[3] In normal skin, the rate of production equals the rate of loss; it takes about two weeks for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.[7]

The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary and reticular dermis.[8] The superficial papillary dermis interdigitates with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone.[8] Structural components of the dermis are collagen, elastic fibers, and extrafibrillar matrix (previously called ground substance).[8] Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands.[6] The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels.[6] The function of blood vessels within the dermis is twofold: to supply nutrition and regulate temperature.[3]

The subcutaneous tissue is a layer of fat between the dermis and underlying fascia.[9] This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus.[3] The main cellular component of this tissue is the adipocyte, or fat cell.[9] The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance.[6] Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.[9]

Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as several nonpathologic states (like, in certain circumstances, melanonychia and racquet nails).[10] While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described.[9] Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known.[10][11] Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on.[12] Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, while, yellow).[13]

Contents

Acneiform eruptions

See also Category:Acneiform eruptions

Acneiform eruptions are caused by changes in the pilosebaceous unit.[14][15]

Autoinflammatory

See also Category:Autoinflammatory syndromes

Autoinflammatory syndromes are a group of inherited disorders characterized by bouts of inflammatory skin lesions and periodic fevers.[16][17]

Chronic blistering

See also Category:Chronic blistering cutaneous conditions

Chronic blistering cutaneous conditions have a prolonged course and present with vesicles and bullae.[18][19]

Conditions of the mucous membranes

See also Category:Conditions of the mucous membranes

Conditions of the mucous membranes involve the moist linings of the eyes, nose, mouth, and anus.[2]

Conditions of the skin appendages

See also Category:Conditions of the skin appendages

Conditions of the skin appendages are those affecting the glands of the skin, hair, nails, and arrector pili muscles.[1]

Conditions of the subcutaneous fat

See also Category:Conditions of the subcutaneous fat

Conditions of the subcutaneous fat are those affecting the layer of adipose tissue that lies between the dermis and underlying fascia.[20][21][22]

Connective tissue diseases

See also Category:Connective tissue diseases

Connective tissue diseases are caused by a complex array of autoimmune responses that target or affect collagen or ground substance.[23]

Abnormalities of dermal fibrous and elastic tissue

See also Category:Abnormalities of dermal fibrous and elastic tissue

Abnormalities of dermal fibrous and elastic tissue are caused by problems in the regulation of collagen synthesis and/or degradation.[24]

Fuzzy red lines on an abdomen
Striae distensae

Dermal and subcutaneous growths

See also Category:Dermal and subcutaneous growths

Dermal and subcutaneous growths result from (1) reactive or neoplastic proliferation of cellular components of the dermis or subcutaneous tissue, or (2) neoplasms invading or aberrantly present in the dermis.[1]

Dermatitis

See also Category:Dermatitis

Dermatitis is a general term for "inflammation of the skin."[25]

Atopic

See also Category:Atopic dermatitis

Atopic dermatitis is a chronic dermatitis associated with a hereditary tendency to develop allergies to food and inhalant substances.[26][27]

  • Atopic dermatitis (Atopic eczema, Disseminated neurodermatitis, Flexural eczema, Infantile eczema, Prurigo diathsique)

Contact

See also Category:Contact dermatitis

Contact dermatitis is caused by certain substances coming in contact with the skin.[28][29]

Eczema

See also Category:Eczema

Eczema refers to a broad range of conditions that begin as spongiotic dermatitis and may progress to a lichenified stage.[30]

Pustular

See also Category:Pustular dermatitis

Pustular dermatitis is an inflammation of the skin that presents with pustular lesions.[31]

Seborrheic

See also Category:Seborrheic dermatitis

Seborrheic dermatitis is a chronic, superficial, inflammatory disease characterized by scaling on an erythematous base.[32]

Disturbances of pigmentation

See also Category:Disturbances of human pigmentation

Disturbances of human pigmentation, either loss or reduction, may be related to loss of melanocytes or the inability of melanocytes to produce melanin or transport melanosomes correctly.[33][34]

Drug eruptions

See also Category:Drug eruptions

Drug eruptions are adverse drug reactions that present with cutaneous manifestations.[35][36]

Endocrine-related

See also Category:Endocrine-related cutaneous conditions

Endocrine conditions often present with cutaneous findings as the skin interacts with the endocrine system in many ways.[37]

Epidermal nevi, neoplasms, cysts

See also Category:Epidermal nevi, neoplasms, cysts

Epidermal nevi, neoplasms, cysts are skin lesions that develop from the epidermal layer of the skin.[6]

Erythemas

See also Category:Erythemas

Erythemas are reactive skin conditions in which there is blanchable redness.[1][7]

Genodermatoses

See also Category:Genodermatoses

Genodermatoses are inherited genetic skin conditions often grouped into three categories: chromosomal, single gene, and polygenetic.[38][39]

Infection-related

See also Category:Infection-related cutaneous conditions

Infection-related cutaneous conditions may be caused by bacteria, fungi, yeast, viruses, and/or parasites.[40]

Bacterium-related

See also Category:Bacterium-related cutaneous conditions

Bacterium-related cutaneous conditions often have distinct morphologic characteristics that may be an indication of a generalized systemic process or simply an isolated superficial infection.[40][41]

Mycobacterium-related

See also Category:Mycobacterium-related cutaneous conditions

Mycobacterium-related cutaneous conditions are caused by mycobacterium infections.[40]

Mycosis-related

See also Category:Mycosis-related cutaneous conditions

Mycosis-related cutaneous conditions are caused by fungi or yeasts, and may present as either a superficial or deep infection of the skin.[40]

Parasitic infestations, stings, and bites

See also Category:Parasitic infestations, stings, and bites of the skin

Parasitic infestations, stings, and bites in humans are caused by several groups of animals belonging to the following phyla: Arthropoda, Chordata, Cnidaria, Nemathelminthes, Platyhelminthes, Annelida, and Protozoa.[40]

Virus-related

See also Category:Virus-related cutaneous conditions

Virus-related cutaneous conditions are caused by two main groups of viruses–DNA and RNA types–both of which are obligatory intracellular parasites.[40]

Lichenoid eruptions

See also Category:Lichenoid eruptions

Lichenoid eruptions are dermatoses related to the unique, common inflammatory disorder lichen planus, which affects the skin, mucous membranes, nails, and hair.[42][43]

Lymphoid-related

See also Category:Lymphoid-related cutaneous conditions

Lymphoid-related cutaneous conditions are a group of disorders characterized by collections of lymphocyte cells within the skin.[44]

Melanocytic nevi and neoplasms

See also Category:Melanocytic nevi and neoplasms

Melanocytic nevi and neoplasms are caused by either a proliferation of (1) melanocytes, or (2) nevus cells, a form of melanocyte, but which lack dendritic processes.[45]

Monocyte- and macrophage-related

See also Category:Monocyte- and macrophage-related cutaneous conditions

Monocyte- and macrophage-related cutaneous conditions are characterized histologically by infiltration of the skin by monocyte and/or macrophage cells.[8]

Mucinoses

See also Category:Mucinoses

Mucinoses are a group of conditions caused by dermal fibroblasts producing abnormally large amounts of mucopolysaccharides.[2]

Multiple, brownish colored patches of skin on an adult arm
Scleroderma

Neurocutaneous

See also Category:Neurocutaneous conditions

Neurocutaneous conditions are due organic nervous system disease or are psychiatric in etiology.[46][47]

Noninfectious immunodeficiency-related

See also Category:Noninfectious immunodeficiency-related cutaneous conditions

Noninfectious immunodeficiency-related cutaneous conditions are caused by T-cell and/or B-cell dysfunction.[48][49]

Nutrition-related

See also Category:Malnutrition

Nutrition-related cutaneous conditions are caused by malnutrition due to an improper or inadequate diet.[50][51]

Papulosquamous hyperkeratotic

See also Category:Papulosquamous hyperkeratotic skin diseases

Papulosquamous hyperkeratotic skin conditions are those that present with papules and scales caused by a thickening of the stratum corneum.[7]

Pruritic

See also Category:Pruritic skin conditions

Pruritus, commonly known as itchiness, is a sensation exclusive to the skin, and characteristic of many skin conditions.[52][53]

Psoriasis

See also Category:Psoriasis

Psoriasis is a common, chronic, and recurrent inflammatory disease of the skin characterized by circumscribed, erythematous, dry, scaling plaques.[54][55][56]

Large, red, scaly plaque
Psoriasis

Reactive neutrophilic

See also Category:Reactive neutrophilic cutaneous conditions

Reactive neutrophilic cutaneous conditions constitute a spectrum of disease mediated by neutrophils, and typically associated with underlying diseases, such as inflammatory bowel disease and hematologic malignancy.[57][58]

Multiple ulcerations with undermined edges on the adult back and upper, posterior arm
Pyoderma gangrenosum

Recalcitrant palmoplantar eruptions

See also Category:Recalcitrant palmoplantar eruptions

Recalcitrant palmoplantar eruptions are skin conditions of the palms and soles which are resistant to treatment.[2]

  • Dermatitis repens (Acrodermatitis continua, Acrodermatitis continua of Hallopeau, Acrodermatitis continua suppurativa Hallopeau, Acrodermatitis perstans, Dermatitis repens Crocker, Hallopeau's acrodermatitis, Hallopeau's acrodermatitis continua, Pustular acrodermatitis)
  • Infantile acropustulosis (Acropustulosis of infancy)
  • Palmoplantar pustulosis (Persistent palmoplantar pustulosis, Pustular psoriasis of the Barber type, Pustular psoriasis of the extremities, Pustulosis palmaris et plantaris)
  • Pustular bacterid

Resulting from errors in metabolism

See also Category:Skin conditions resulting from errors in metabolism

Skin conditions resulting from errors in metabolism are caused by enzymatic defects that lead to an accumulation or deficiency of various cellular components, including, but not limited to, amino acids, carbohydrates, and lipids.[10]

Resulting from physical factors

See also Category:Skin conditions resulting from physical factors

Skin conditions resulting from physical factors occur due to a number of causes, including, but not limited to, hot and cold temperatures, friction, moisture, and ionizing radiation.[2]

Urticaria and angioedema

See also Category:Urticaria and angioedema

Urticaria is a vascular reaction of the skin characterized by the appearance of wheals, which are firm, elevated swelling of the skin.[59] Angioedema, which can occur alone or with urticaria, is characterized by a well-defined, edematous swelling that involves subcutaneous tissues, abdominal organs, and/or upper airway.[60]

Raised, edematous, red skin lesions on the abdomen
Urticaria

Vascular-related

See also Category:Vascular-related cutaneous conditions

Vascular-related cutaneous conditions result from dysfunction of the blood and/or blood vessels in the dermis, or lymphatics in the subcutaneous tissues.[7]

Footnotes

  1. ^ Parentheticals are used to indicate other names by which a condition is known. If there are multiple alternative names for a condition, they are separated by commas within the parenthetical.

References

  1. ^ a b c d e Miller, Jeffrey H.; Marks, James G. (2006). Lookingbill and Marks' Principles of Dermatology. Saunders. ISBN 1-4160-3185-5. 
  2. ^ a b c d e James, William D.; et al. (2006). Andrews' Diseases of the Skin: Clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0. 
  3. ^ a b c d e Burns, Tony; et al. (2006) Rook's Textbook of Dermatology CD-ROM. Wiley-Blackwell. ISBN 1405131306.
  4. ^ Paus R, Cotsarelis G (1999). "The biology of hair follicles". N Engl J Med 341 (7): 491–7. doi:10.1056/NEJM199908123410706. PMID 10441606. 
  5. ^ Goldsmith, Lowell A. (1983). Biochemistry and physiology of the skin. Oxford University Press. ISBN 0-19-261253-0. 
  6. ^ a b c d e Freedberg, Irwin M.; et al. (2003). Fitzpatrick's Dermatology in General Medicine. McGraw-Hill. ISBN 0-07-138076-0. 
  7. ^ a b c d Bolognia, Jean L.; et al. (2007). Dermatology. St. Louis: Mosby. ISBN 1-4160-2999-0. 
  8. ^ a b c d Rapini, Ronald P. (2005). Practical dermatopathology. Elsevier Mosby. ISBN 0-323-01198-5. 
  9. ^ a b c d Lynch, Peter J. (1994). Dermatology. Williams & Wilkins. ISBN 0-683-05252-7. 
  10. ^ a b c Bluefarb, Samuel M. (1984). Dermatology. Upjohn Co. ISBN 0-89501-004-6. 
  11. ^ Lambert WC, Everett MA (October 1981). "The nosology of parapsoriasis". J. Am. Acad. Dermatol. 5 (4): 373–95. PMID 7026622. 
  12. ^ Jackson R (1977). "Historical outline of attempts to classify skin diseases". Can Med Assoc J 116 (10): 1165–8. PMID 324589. 
  13. ^ Fitzpatrick, Thomas B.; Klauss Wolff; Wolff, Klaus Dieter; Johnson, Richard R.; Suurmond, Dick; Richard Suurmond (2005). Fitzpatrick's color atlas and synopsis of clinical dermatology. McGraw-Hill Medical Pub. Division. ISBN 0-07-144019-4. 
  14. ^ Rustin MH (1990). "Dermatology". Postgrad Med J 66 (781): 894–905. doi:10.1136/pgmj.66.781.894. PMID 2148371. 
  15. ^ Feldman S, Careccia RE, Barham KL, Hancox J (2004). "Diagnosis and treatment of acne". Am Fam Physician 69 (9): 2123–30. PMID 15152959. 
  16. ^ Fietta P (2004). "Autoinflammatory diseases: the hereditary periodic fever syndromes". Acta Biomed 75 (2): 92–9. PMID 15481697. 
  17. ^ Centola M, Aksentijevich I, Kastner DL (1998). "The hereditary periodic fever syndromes: molecular analysis of a new family of inflammatory diseases". Hum Mol Genet 7 (10): 1581–8. doi:10.1093/hmg/7.10.1581. PMID 9735379. http://hmg.oxfordjournals.org/cgi/content/full/7/10/1581. 
  18. ^ Yeh SW, Ahmed B, Sami N, Razzaque Ahmed A (2003). "Blistering disorders: diagnosis and treatment". Dermatol Ther 16 (3): 214–23. doi:10.1046/j.1529-8019.2003.01631.x. PMID 14510878. 
  19. ^ Eming R, Hertl M (2006). "Autoimmune bullous disorders". Clin Chem Lab Med 44 (2): 144–9. doi:10.1515/CCLM.2006.027. PMID 16475898. 
  20. ^ Requena L, Yus ES (2001). "Panniculitis. Part I. Mostly septal panniculitis". J Am Acad Dermatol 45 (2): 163–83; quiz 184–6. doi:10.1067/mjd.2001.114736. PMID 11464178. 
  21. ^ Requena L, Sánchez Yus E (2001). "Panniculitis. Part II. Mostly lobular panniculitis". J Am Acad Dermatol 45 (3): 325–61; quiz 362–4. doi:10.1067/mjd.2001.114735. PMID 11511831. 
  22. ^ Phelps RG, Shoji T (2001). "Update on panniculitis". Mt Sinai J Med 68 (4–5): 262–7. PMID 11514913. http://www.mssm.edu/msjournal/68/6845262.shtml. 
  23. ^ Crofford, Leslie J.; Klippel, John H.; Weyand, Cornelia M.; Stone, John F. (2001). Primer on the rheumatic diseases. Atlanta, GA: Arthritis Foundation. ISBN 0-912423-29-3. 
  24. ^ Ushiki T (2002). "Collagen fibers, reticular fibers and elastic fibers. A comprehensive understanding from a morphological viewpoint" (PDF). Arch Histol Cytol 65 (2): 109–26. doi:10.1679/aohc.65.109. PMID 12164335. http://www.jstage.jst.go.jp/article/aohc/65/2/109/_pdf. 
  25. ^ Alsaad KO, Ghazarian D (2005). "My approach to superficial inflammatory dermatoses". J Clin Pathol 58 (12): 1233–41. doi:10.1136/jcp.2005.027151. PMID 16311340. 
  26. ^ Wüthrich B, Cozzio A, Roll A, Senti G, Kündig T, Schmid-Grendelmeier P (2007). "Atopic eczema: genetics or environment?". Ann Agric Environ Med 14 (2): 195–201. PMID 18247450. 
  27. ^ Roosterman D, Goerge T, Schneider SW, Bunnett NW, Steinhoff M (2006). "Neuronal control of skin function: the skin as a neuroimmunoendocrine organ". Physiol Rev 86 (4): 1309–79. doi:10.1152/physrev.00026.2005. PMID 17015491. 
  28. ^ Saint-Mezard P, Rosieres A, Krasteva M, et al. (2004). "Allergic contact dermatitis". Eur J Dermatol 14 (5): 284–95. PMID 15358566. http://www.john-libbey-eurotext.fr/en/revues/medecine/ejd/e-docs/00/04/05/5F/article.phtml. 
  29. ^ Krasteva M, Kehren J, Sayag M, et al. (1999). "Contact dermatitis II. Clinical aspects and diagnosis". Eur J Dermatol 9 (2): 144–59. PMID 10066966. http://www.john-libbey-eurotext.fr/en/revues/medecine/ejd/e-docs/00/01/88/1A/article.phtml. 
  30. ^ Buxton PK (1987). "ABC of dermatology. Eczema and dermatitis". Br Med J (Clin Res Ed) 295 (6605): 1048–51. doi:10.1136/bmj.295.6605.1048. PMID 3120868. 
  31. ^ Mengesha YM, Bennett ML (2002). "Pustular skin disorders: diagnosis and treatment". Am J Clin Dermatol 3 (6): 389–400. doi:10.2165/00128071-200203060-00003. PMID 12113648. 
  32. ^ Schwartz RA, Janusz CA, Janniger CK (2006). "Seborrheic dermatitis: an overview". Am Fam Physician 74 (1): 125–30. PMID 16848386. 
  33. ^ Costin GE, Hearing VJ (2007). "Human skin pigmentation: melanocytes modulate skin color in response to stress". FASEB J 21 (4): 976–94. doi:10.1096/fj.06-6649rev. PMID 17242160. 
  34. ^ Yamaguchi Y, Brenner M, Hearing VJ (2007). "The regulation of skin pigmentation". J Biol Chem 282 (38): 27557–61. doi:10.1074/jbc.R700026200. PMID 17635904. 
  35. ^ Goolamali SK (1985). "Drug eruptions". Postgrad Med J 61 (720): 925–33. doi:10.1136/pgmj.61.720.925. PMID 2932688. 
  36. ^ Svensson CK, Cowen EW, Gaspari AA (2001). "Cutaneous drug reactions". Pharmacol Rev 53 (3): 357–79. PMID 11546834. http://pharmrev.aspetjournals.org/cgi/content/full/53/3/357. 
  37. ^ Slominski A, Wortsman J (2000). "Neuroendocrinology of the skin". Endocr Rev 21 (5): 457–87. doi:10.1210/er.21.5.457. PMID 11041445. http://edrv.endojournals.org/cgi/content/full/21/5/457. 
  38. ^ Joel L. Spitz (2005). Genodermatoses: a clinical guide to genetic skin disorders. Lippincott Williams & Wilkins. ISBN 0-7817-4088-6. 
  39. ^ McLean WH (2003). "Genetic disorders of palm skin and nail". J Anat 202 (1): 133–41. doi:10.1046/j.1469-7580.2003.00141.x. PMID 12587928. 
  40. ^ a b c d e f Habif, Thomas P. (2001). Skin disease: diagnosis and treatment. Mosby. ISBN 0-8151-3762-1. 
  41. ^ Stulberg DL, Penrod MA, Blatny RA (2002). "Common bacterial skin infections". Am Fam Physician 66 (1): 119–24. PMID 12126026. http://www.aafp.org/afp/20020701/119.html. 
  42. ^ Ismail SB, Kumar SK, Zain RB (2007). "Oral lichen planus and lichenoid reactions: etiopathogenesis, diagnosis, management and malignant transformation" (PDF). J Oral Sci 49 (2): 89–106. doi:10.2334/josnusd.49.89. PMID 17634721. http://www.jstage.jst.go.jp/article/josnusd/49/2/89/_pdf. 
  43. ^ Katta R (2000). "Lichen planus". Am Fam Physician 61 (11): 3319–24, 3327–8. PMID 10865927. 
  44. ^ Connors JM, Hsi ED, Foss FM (2002). "Lymphoma of the skin". Hematology Am Soc Hematol Educ Program: 263–82. PMID 12446427. http://asheducationbook.hematologylibrary.org/cgi/content/full/2002/1/263. 
  45. ^ Alan N. Houghton; Balch, Charles M. (1992). Cutaneous melanoma. J.B. Lippincott. ISBN 0-397-51052-7. 
  46. ^ Jafferany M (2007). "Psychodermatology: a guide to understanding common psychocutaneous disorders". Prim Care Companion J Clin Psychiatry 9 (3): 203–13. PMID 17632653. 
  47. ^ Harth W, Hermes B, Niemeier V, Gieler U (2006). "Clinical pictures and classification of somatoform disorders in dermatology". Eur J Dermatol 16 (6): 607–14. PMID 17229599. http://www.john-libbey-eurotext.fr/en/revues/medecine/ejd/e-docs/00/04/28/31/article.phtml. 
  48. ^ Sillevis Smitt JH, Wulffraat NM, Kuijpers TW (2005). "The skin in primary immunodeficiency disorders". Eur J Dermatol 15 (6): 425–32. PMID 16280293. http://www.john-libbey-eurotext.fr/en/revues/medecine/ejd/e-docs/00/04/12/B8/article.phtml. 
  49. ^ Cooper MD, Lanier LL, Conley ME, Puck JM (2003). "Immunodeficiency disorders". Hematology Am Soc Hematol Educ Program: 314–30. PMID 14633788. http://asheducationbook.hematologylibrary.org/cgi/content/full/2003/1/314. 
  50. ^ Miller SJ (1989). "Nutritional deficiency and the skin". J Am Acad Dermatol 21 (1): 1–30. doi:10.1016/S0190-9622(89)70144-4. PMID 2663932. 
  51. ^ Heath ML, Sidbury R (2006). "Cutaneous manifestations of nutritional deficiency". Curr Opin Pediatr 18 (4): 417–22. doi:10.1097/01.mop.0000236392.87203.cc. PMID 16914997. 
  52. ^ Greaves MW (2007). "Recent advances in pathophysiology and current management of itch" (PDF). Ann Acad Med Singap 36 (9): 788–92. PMID 17925991. http://www.annals.edu.sg/pdf/36VolNo9Sep2007/V36N9p788.pdf. 
  53. ^ Steinhoff M, Bienenstock J, Schmelz M, Maurer M, Wei E, Bíró T (2006). "Neurophysiological, neuroimmunological, and neuroendocrine basis of pruritus". J Invest Dermatol 126 (8): 1705–18. doi:10.1038/sj.jid.5700231. PMID 16845410. 
  54. ^ Langley RG, Krueger GG, Griffiths CE (2005). "Psoriasis: epidemiology, clinical features, and quality of life". Ann Rheum Dis 64 (Suppl 2): ii18–23; discussion ii24–5. doi:10.1136/ard.2004.033217. PMID 15708928. 
  55. ^ Luba KM, Stulberg DL (2006). "Chronic plaque psoriasis". Am Fam Physician 73 (4): 636–44. PMID 16506705. 
  56. ^ Krueger JG, Bowcock A (2005). "Psoriasis pathophysiology: current concepts of pathogenesis". Ann Rheum Dis 64 (Suppl 2): ii30–6. doi:10.1136/ard.2004.031120. PMID 15708932. 
  57. ^ Callen JP (2002). "Neutrophilic dermatoses". Dermatol Clin 20 (3): 409–19. doi:10.1016/S0733-8635(02)00006-2. PMID 12170875. 
  58. ^ Wallach D, Vignon-Pennamen MD (2006). "From acute febrile neutrophilic dermatosis to neutrophilic disease: forty years of clinical research". J Am Acad Dermatol 55 (6): 1066–71. doi:10.1016/j.jaad.2006.07.016. PMID 17097401. 
  59. ^ Clarke P (2004). "Urticaria". Aust Fam Physician 33 (7): 501–3. PMID 15301166. http://www.racgp.org.au/afp/200407/14489. 
  60. ^ Muller BA (2004). "Urticaria and angioedema: a practical approach". Am Fam Physician 69 (5): 1123–8. PMID 15023012. 

Further reading

External links


This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)

Search unanswered questions...

Enter a question here...
Search: All sources Community Q&A Reference topics

 
 

 

Copyrights:

Wikipedia. This article is licensed under the Creative Commons Attribution/Share-Alike License. It uses material from the Wikipedia article "List of cutaneous conditions".  Read more