Dr. Wendy Levinbook, MD discusses Bullous Pemphigoid. See much more at www.dermnet.com PLEASE RATE AND COMMENT!!! This disorder typically affects patients over 60 years of age, but it can rarely happen in children. There is no racial or ethnic predilection and the incidence is equal in males and females. Clinically, bullous pemphigoid (BP) is characterized by huge tense bullae that are frequently preceded by red, urticarial patches or plaques. Lesions are most generally located on the lower abdomen, inner thighs, and flexor forearms despite the fact that they might happen anywhere. Mucous membrane involvement is uncommon. Lesions are usually associated with marked pruritus but they do not scar. BP is an acquired autoimmune disorder that occurs secondary to the formation of antibodies that interact with bullous pemphigoid antigen 1 (230 kDa intrahemidesmosomal antigen) and bullous pemphigoid antigen 2 (180 kDa hemidesmosomal transmembrane antigen, also identified as type XVII collagen). This interaction is then followed by an inflammatory response leading to dermal-epidermal separation. On electron microscopic exam, blister formation occurs in the lamina lucida, between the basal cell membrane and the lamina densa. On histopathologic exam, lesions show a subepidermal blister with fluid, fibrin, and inflammatory cells which includes several eosinophils. Direct IF of perilesional skin demonstrates linear C3 and IgG. Indirect IF utilizing normal stratified squamous epithelia (such as human epidermis or monkey ... Video Rating: five / five
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ClassificationClassification is based on cell line of origin. Melanocytic nevi are derived from melanocytes. Epidermal nevi are derived from keratinocytes or derivatives of keratinocytes. Connective tissue nevi are derived from connective tissue cells like adipocyte and fibroblasts. Vascular nevi are derived from structures of the blood vessels. See birthmark for a more complete discussion Melanocytic nevusMain article: Melanocytic nevusCongenital nevus implying a melanocytic nevus present at birth or near birth.Acquired melanocytic nevus. Implies a melanocytic nevus acquired later in life, and not at or near birth. Most melanocytic nevi are of the acquired variety.Melanocytic nevus (nevomelanocytic nevus, nevocellular nevus): benign proliferation of melanocytes, the skin cells that make the brown pigment melanin. Hence, most nevi are brown to black. They are quite common almost all adults have at least one, typically a lot more. They may possibly be congenital or acquired (usually at puberty).Dysplastic nevus usually an acquired melanocytic nevus with abnormal attributes producing it challenging to distinguish from a melanoma. It can be a marker for an individual at risk for creating melanomas. Epidermal nevusEpidermal nevus: congenital, flesh-colored, raised or warty, frequently linear lesion, normally on the upper half of the body.Nevus sebaceus: variant of epidermal nevus on the scalp presenting as a hairless, fleshy or yellowish area. Connective tissue nevusConnective tissue nevus: fleshy, deep nodules. Rare. Vascular nevusHemangioma (strawberry mark or nevus).Nevus flammeus (port-wine stain).Spider angioma (nevus araneus).Blue Rubber Bleb Nevus Syndrome: dilatation of veins anywhere in the body (both skin and internal organs), generally lethal from internal hemorrhage. It is a very rare genetic disorder.The term "venous nevus" has recently been proposed. Diagnosis of neviA dermatoscope.A modern day polarized dermatoscope.Clinical diagnosis of a melanocytic nevus from other nevi can be made with the naked eye using the ABCD guideline, or employing dermatoscopy. The primary concern is distinguishing between a benign nevus, a dysplastic nevus, and a melanoma. Other skin tumors can resemble a melanocytic nevus clinically, such as a seborrheic keratosis, pigmented basal cell cancer, hemangiomas, and sebaceous hyperplasia. A skin biopsy is necessary when clinical diagnosis is inadequate or when malignancy is suspected. Normal Evolution or Maturation of Melanocytic NevusAll melanocytic nevi will alter with time - both congenital and acquired nevi. The "normal" maturation is evident as elevation of the lesion from a flat macule to a raised papule. The color alter occurs as the melanocytes clump and migrate from the surface of the skin (epidermis) down deep into the dermis. The color will change from even brown, to speckled brown, and then losing the color and becomes flesh colored or pink. Throughout the evolution, uneven migration can make the nevi look like melanomas, and dermatoscopy can support in differentiation between the benign and malignant lesions. See alsoBecker's nevusDysplastic nevus - a melanocytic nevus with abnormal pigment attributes which can be hard to distinguish from a melanoma. References^ nevus at Dorland's Medical Dictionary^ Zietz S, Happle R, Hohenleutner U, Landthaler M (2008). "The venous nevus: a distinct vascular malformation suggesting mosaicism". Dermatology (Basel) 216 (1): 316. doi:10.1159/000109355. PMID 18032896. http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=000109355. ^ http://www.pathologyresources.com/AFIP/melanocytic/chap02.htm External linksLook up nevus in Wiktionary, the totally free dictionary.Nevus risk elements, symptoms, treatment, and more informationAtlas of Pathology Section of a melanocytic nevuseMedicine: Mole or Melanoma? Tell-Tale Signs in Benign Nevi and Malignant Melanoma: SlideshowNevus Outreach, Inc.v d eDiseases of the skin and appendages by morphologyGrowthsEpidermalwart callus seborrheic keratosis acrochordon molluscum contagiosum actinic keratosis squamous cell carcinoma basal cell carcinoma merkel cell carcinoma nevus sebaceous trichoepitheliomaPigmentedFreckles lentigo melasma nevus melanomaDermal andsubcutaneousepidermal inclusion cyst hemangioma dermatofibroma keloid lipoma neurofibroma xanthoma Kaposi's sarcoma infantile digital fibromatosis granular cell tumor leiomyoma lymphangioma circumscriptum myxoid cystRashesWithepidermalinvolvementEczematouscontact dermatitis atopic dermatitis seborrheic dermatitis stasis dermatitis lichen simplex chronicus Darier's disease glucagonoma syndrome langerhans cell histiocytosis lichen sclerosus pemphigus foliaceus Wiskott-Aldrich syndrome Zinc deficiencyScalingpsoriasis tinea (corporis cruris pedis manuum faciei) pityriasis rosea secondary syphillis mycosis fungoides systemic lupus erythematosus pityriasis rubra pilaris parapsoriasis ichthyosisBlisteringherpes simplex herpes zoster varicella bullous impetigo acute contact dermatitis pemphigus vulgaris bullous pemphigoid dermatitis herpetiformis porphyria cutanea tarda epidermolysis bullosa simplexPapularscabies insect bite reactions lichen planus miliaria keratosis pilaris lichen spinulosus transient acantholytic dermatosis lichen nitidus pityriasis lichenoides et varioliformis acutaPustularacne vulgaris acne rosacea folliculitis impetigo candidiasis gonococcemia dermatophyte coccidioidomycosis subcorneal pustular dermatosisHypopigmentedtinea versicolor vitiligo pityriasis alba postinflammatory hyperpigmentation tuberous sclerosis idiopathic guttate hypomelanosis leprosy hypopigmented mycosis fungoidesWithoutepidermalinvolvementRedBlanchableErythemaGeneralizeddrug eruptions viral exanthems toxic erythema systemic lupus erythematosusLocalizedcellulitis abscess boil erythema nodosum carcinoid syndrome fixed drug eruptionSpecializedurticaria erythema (multiforme migrans gyratum repens annulare centrifugum ab igne)NonblanchablePurpuraMacularthrombocytopenic purpura actinic purpuraPapulardisseminated intravascular coagulation vasculitisInduratedscleroderma/morphea granuloma annulare lichen sclerosis et atrophicus necrobiosis lipoidicaMiscellaneousdisordersUlcersHairtelogen effluvium androgenic alopecia trichotillomania alopecia areata systemic lupus erythematosus tinea capitis loose anagen syndrome lichen planopilaris folliculitis decalvans acne keloidalis nuchaeNailonychomycosis psoriasis paronychia ingrown nailMucousmembraneaphthous stomatitis oral candidiasis lichen planus leukoplakia pemphigus vulgaris mucous membrane pemphigoid cicatricial pemphigoid herpesvirus coxsackievirus syphilis systemic histoplasmosis squamous cell carcinomav d eGonadal tumors, paraganglioma, glomus, nevi and melanomas (ICD-O 8590-8799)Gonadal/sex cord-gonadal stromal (8590-8679)sex cord (Granulosa cell tumour, Sertoli cell tumor)stroma (Thecoma, Leydig cell tumor)both (Sertoli-Leydig cell tumour, Luteoma)Paragangliomas AndGlomus tumors (8680-8719)Neuroendocrine tumor: Paraganglioma (Pheochromocytoma)Vascular tissue neoplasm: Glomus tumor (Glomangiosarcoma)Nevi and melanomas (8720-8799)NeviMelanocytic/pigmented nevus (Mongolian spot, Blue nevus, Nevus of Ota, Spitz nevus)location (Junctional nevus, Compound nevus)Halo nevus Dysplastic nevusMelanomas (NE)Superficial spreading melanoma Nodular melanoma lentigo (Lentigo maligna/Lentigo maligna melanoma, Acral lentiginous melanoma)v d eTumors: skin cancer (C43-C44/D22-D23, 172-173/216)EpidermisBasal cell carcinoma Squamous cell carcinoma (Acanthoma)Bowen's diseaseDermisBenign fibrous histiocytoma/dermatofibrosarcoma Dermatofibrosarcoma protuberansNevi and melanomasNevus: Melanocytic nevus Dysplastic nevus Halo nevus Spitz nevusMelanoma: Superficial spreading melanoma Nodular melanoma lentigo (Lentigo maligna/Lentigo maligna melanoma, Acral lentiginous melanoma)integument, SF, LCT navs: anat/physio, noncongen/congen/neoplasia, symptoms+signs/eponymous, procv d eCardiovascular illness: vascular disease Circulatory program pathology (I70-I99, 440-456)Arteries, arteriolesand capillariesInflammationArteritis (Aortitis) Buerger's diseaseArterial occlusive disease/peripheral vascular diseaseArteriosclerosisAtherosclerosis (Foam cell, Fatty streak, Atheroma, Intermittent claudication) Monckeberg's arteriosclerosis Arteriolosclerosis (Hyaline, Hyperplastic, oxycholesterol, cholesterol, LDL, trans fat)StenosisRenal artery stenosis Carotid artery stenosisOtherFibromuscular dysplasia Degos disease Aortoiliac occlusive disease Raynaud's phenomenon/Raynaud's disease ErythromelalgiaAneurysm/dissection/pseudoaneurysmtorso: Aortic aneurysm (Thoracic aortic aneurysm, Abdominal aortic aneurysm) Aortic dissection Coronary artery aneurysmhead/neck: Cerebral aneurysm Intracranial berry aneurysm Carotid artery dissection Vertebral artery dissection Familial aortic dissectionVascular malformationArteriovenous fistula Telangiectasia (Hereditary hemorrhagic telangiectasia)Vascular nevusSpider angioma Halo nevus Cherry hemangiomaVeinsInflammationPhlebitisVenous thrombosis/Thrombophlebitisprimarily lower limb (Deep vein thrombosis)abdomen (Could-Thurner syndrome, Portal vein thrombosis, Budd-Chiari syndrome, Renal vein thrombosis)upper limb/torso (Paget-Schroetter illness, Mondor's disease)head (Cerebral venous sinus thrombosis)Post-thrombotic syndromeVaricose veinsVaricocele Gastric varices Portacaval anastomosis (Hemorrhoid, Esophageal varices, Caput medusae)OtherSuperior vena cava syndrome Inferior vena cava syndrome Venous ulcer Chronic venous insufficiency Chronic cerebrospinal venous insufficiencyArteries or veinsVasculitis Thrombosis Embolism (Pulmonary embolism, Cholesterol embolism, Paradoxical embolism) Angiopathy (Macroangiopathy, Microangiopathy)Blood pressureHypertensionHypertensive heart disease Hypertensive nephropathy Important hypertension Secondary hypertension (Renovascular hypertension) Pulmonary hypertension Malignant hypertension Benign hypertension Systolic hypertension White coat hypertensionHypotensionOrthostatic hypotensionvascular navs: anat/physio/dev, noncongen/systemic vasculitis/congen/neoplasia, symptoms+signs/eponymous, proc Categories: Dermatologic terminology | Oral pathology | Genetic disorders | Disturbances of human pigmentationHidden categories: Articles lacking in-text citations from October 2008 | All articles lacking in-text citations
Bullous pemphigoid usually occurs in older persons and is uncommon in inexperienced folk. Bullous pemphigoid is a rind illness characterized by uneasy blistering eruptions on the surface of the rind. Bullous pemphigoid normally occurs in old adults. Symptoms of bullous pemphigoid contain heavily, stiff blisters on the rind. The rind around the blisters could appear natural, but is regularly crimson and bloated. Itching is well-known this circumstance. It can too impact the mucous membranes, and has been shown to ail dogs, cats, pigs, and horses, as easily as humans. People with BP have a somewhat high than median chance of creating.
Other auto-immune diseases such as pernicious anaemia, rheumatoid arthritis, and vitiligo. Treatment is focused on relief of symptoms and prevention of infection. Tetracycline and Minocycline antibiotics are really beneficial for mild to moderate illness. Oral steroids (prednisone, prednisolone) are the treatment of selection for severe cases. Niacin (a B complex vitamin) is sometimes given along with tetracycline. Steroids decrease inflammation and suppress the immune system. A high dose is usually needed at 1st. The dose is decreased once new blisters have stopped forming. A lower daily dose is normally then necessary to stop blisters forming.
Do not stop taking a corticosteroid drug suddenly. These kinds of drugs should be tapered off slowly under a doctor’s supervision. Immunosuppressive agents are employed in combination with the oral steroids to enable a lower dose. BP is a self-limiting disease that is in most cases ultimately entirely clears up and the treatment can be stopped. Treatment is generally necessary for several years, but usually right after a few months it is achievable to lessen the dose of medications to reasonably low levels. There's no prevention for bullous pemphigoid. Certain drugs provoke a reaction that produces blisters similar to those of bullous pemphigoid in some individuals.
Conventional medical remedies may possibly aid relieve the symptoms of bullous pemphigoid but they do not address the root of the dilemma BP also usually has a pattern of remissions and flare-ups. If you have blisters in your mouth, stay away from consuming challenging and crunchy foods, such as chips and raw fruits and vegetables. Your skin is fragile, both from bullous pemphigoid and the medication used to treat it, so take care to prevent trauma. If you accidentally break a blister on your skin, cover it with a dry. At least 30 minutes before you head outdoors winter or summer generously apply sunscreen with a sun protection factor (SPF) of 15 or greater.
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Epidemiology The condition affects 0.1%0.2% of humans, occurring in both males and females, though far more females than males.[citation needed] Alopecia areata occurs in people who are apparently healthy and have no skin disorder. Initial presentation most commonly occurs in the late teenage years, early childhood, or young adulthood, but can happen with people of all ages. Types The most common type of alopecia areata involves hair loss in one or more round spots on the scalp. Hair may also be lost more diffusely over the whole scalp, in which case the condition is called diffuse alopecia areata. Alopecia areata monolocularis describes baldness in only one spot. It may occur anywhere on the head. Alopecia areata multilocularis refers to multiple areas of hair loss. The disease may be limited only to the beard, in which case it is called Alopecia areata barbae. If the patient loses all the hair on his/her scalp, the disease is then called Alopecia areata totalis. If all body hair, including pubic hair, is lost, the diagnosis then becomes Alopecia areata universalis. Alopecia areata totalis and universalis are rare. Causes Alopecia areata is noncommunicable, or not contagious. It occurs more frequently in people who have affected family members, suggesting that heredity may be a factor. Strong evidence that genes may increase risk for alopecia areata was found by studying families with two or more affected members. This study identified at least four regions in the genome that are likely to contain alopecia areata genes. In addition, it is slightly more likely to occur in people who have relatives with autoimmune diseases. The condition is thought to be an autoimmune disorder in which the body attacks its own hair follicles and suppresses or stops hair growth. There is evidence that T cell lymphocytes cluster around these follicles, causing inflammation and subsequent hair loss. An unknown environmental trigger such as emotional stress or a pathogen is thought to combine with hereditary factors to cause the condition. There are a few recorded cases of babies being born with congenital alopecia areata; however, these are not cases of autoimmune disease because an infant is born without a fully developed immune system. Diagnosis Alopecia areata First symptoms are small, soft, bald patches which can take just about any shape but are most usually round. It most often affects the scalp and beard but may occur on any hair-bearing part of the body. There may be different skin areas with hair loss and regrowth in the same body at the same time. It may also go into remission for a time, or permanently. The area of hair loss may tingle or be very slightly painful. The hair tends to fall out over a short period of time, with the loss commonly occurring more on one side of the scalp than the other. Another presentation of the condition are exclamation point hairs. Exclamation point hairs are hairs that become narrower along the length of the strand closer to the base, producing a characteristic "exclamation point" appearance. One diagnostic technique applied by medical professionals is to gently tug at a handful of hair along the edge of a patch with less strength than would be required to pull out healthy hair. In healthy hair, no hair should fall out or ripped hair should be distributed evenly across the tugged portion of the scalp. In cases of alopecia areata hair will tend to pull out more easily along the edge of the patch where the follicles are already being attacked by the body's immune system than away from the patch where they are still healthy. Professionals usually remind patients that the hair that is pulled out would eventually fall naturally. The test is conducted only once to identify the condition and rule out a simple localized hair loss condition. Nails may have pitting or trachyonychia. Treatment About 50% of patients' hair will regrow in one year without any treatment. If the affected region is small, it is reasonable to observe the progression of the illness as the problem often spontaneously regresses and the hair grows back. In 90% of cases, the hair will, ultimately, grow back. In the other 10%, only some or no hair will regrow.[citation needed] In cases where there is severe hair loss, there has been limited success treating alopecia areata with clobetasol or fluocinonide, steroid injections, or cream. Steroid injections are commonly used in sites where there are small areas of hair loss on the head or especially where eyebrow hair has been lost. Some other medications used are minoxidil, irritants (anthralin or topical coal tar), and topical immunotherapy cyclosporine, each of which are sometimes used in different combinations. Oral corticosteroids decrease the hair loss, but only for the period during which they are taken, and these drugs have adverse side effects. For small patches on the beard or head it is possible to suppress with topical tacrolimus ointments like Protopic. Symptoms may remain suppressed until aggravated by stress or other factors. Treatment with tacrolimus is recommended only for short periods of time due to adverse side effects.[citation needed] Initial stages may be kept from increasing by applying topical corticosteroids. However, topical corticosteroids frequently fail to enter the skin deeply enough to affect the hair bulbs, which are the treatment target. In terms of adapting to the disease rather than treating in an effort to cure, there are also many options available. Wigs are often used by those with Alopecia, particularly Alopecia Totalis, in which hair is entirely lost from the scalp. Wigs are available at many levels of development and technology, including wigs with suction mechanisms to keep it firmly attached to the scalp. Most of the wigs available are so well made that it is impossible without close investigation to tell whether they are a person's actual hair, or a wig. Prognosis In most cases that begin with a small number of patches of hair loss, hair grows back after a few months to a year. In cases with a greater number of patches, hair can either grow back or progress to alopecia totalis or, in rare cases, universalis. -Effects of alopecia areata are mainly psychological (loss of self image due to hair loss). However, patients also tend to have a slightly higher incidence of asthma, allergies, atopic dermal ailments, and even hypothyroidism. Loss of hair also means that the scalp burns more easily in the sun. Loss of nasal hair increases severity of hay fever and similar allergic conditions. Patients may also have aberrant nail formation because keratin forms both hair and nails. Hair may grow back and then fall out again later. This may not indicate a recurrence of the condition, however, but rather a natural cycle of growth-and-shedding from a relatively synchronised start; such a pattern will fade over time. Episodes of alopecia areata before puberty predispose chronic recurrence of the condition. Pitting of the fingernails can hint at a more severe or prolonged course.[citation needed] Psychosocial issues Alopecia can certainly be the cause of psychological stress. Because hair loss can lead to significant appearance changes, individuals may experience social phobia, anxiety, and depression. Some psychologists have even gone as far as to describe the feelings of loss and depression felt at the onset of the disease as being similar to those felt by people afflicted with terminal illness. In severe cases where the chance of hair regrowth is slim, individuals need to adapt to the condition, rather than look for a cure. A UK charity named The Little Princess Trust provides wigs to children with hair loss. This has been shown to increase their self-confidence. See also Alopecia totalis Alopecia universalis Noncicatricial alopecia Baldness Locks of Love List of cutaneous conditions References This page may also be able to help find problematic links. Several templates are available for formatting. (January 2010) ^ Odom, Richard B.; Davidsohn, Israel; James, William D.; Henry, John Bernard; Berger, Timothy G.; Clinical diagnosis by laboratory methods; Dirk M. Elston (2006). Andrews' diseases of the skin: clinical dermatology. Saunders Elsevier. ISBN 0-7216-2921-0. [page needed] ^ a b c d e f g h i j k Zoe Diana Draelos (August 30, 2007), Alopecia Areata. MedicineNet.com. Retrieved on December 2, 2007 ^ McElwee KJ, Boggess D, Olivry T, et al. (1998). "Comparison of alopecia areata in human and nonhuman mammalian species". Pathobiology 66 (2): 90107. doi:10.1159/000028002. PMID 9645633. ^ a b c d e f g Alopecia Areata at Merck Manual of Diagnosis and Therapy Professional Edition ^ Marks, James G; Miller, Jeffery (2006). Lookingbill and Marks' Principles of Dermatology (4th ed.). Elsevier Inc. ISBN 1-4160-3185-5. ^ a b c d Skin Conditions: Alopecia Areata. WebMD. Retrieved on December 2, 2007. ^ Martinez-Mir A, Zlotogorski A, Gordon D, et al. (February 2007). "Genomewide scan for linkage reveals evidence of several susceptibility loci for alopecia areata". American Journal of Human Genetics 80 (2): 31628. doi:10.1086/511442. PMID 17236136. ^ Freedberg, Irwin M.; Fitzpatrick, Thomas B. (2003). Fitzpatrick's dermatology in general medicine. New York: McGraw-Hill, Medical Pub. Division. ISBN 0-07-138076-0. [page needed] ^ a b c American Osteopathic College of Dermatology. Alopecia Areata. Dermatologic Disease Database. Aocd.org. Retrieved on December 3, 2007. ^ BBC News article about a girl receiving a wig. External links National Institute of Arthritis and Musculoskeletal and Skin Diseases at NIH DermAtlas 42 Dermpedia Alopecia areata v d e Diseases of the skin and appendages by morphology Growths Epidermal wart callus seborrheic keratosis acrochordon molluscum contagiosum actinic keratosis squamous cell carcinoma basal cell carcinoma merkel cell carcinoma nevus sebaceous trichoepithelioma Pigmented Freckles lentigo melasma nevus melanoma Dermal and subcutaneous epidermal inclusion cyst hemangioma dermatofibroma keloid lipoma neurofibroma xanthoma Kaposi's sarcoma infantile digital fibromatosis granular cell tumor leiomyoma lymphangioma circumscriptum myxoid cyst Rashes With epidermal involvement Eczematous contact dermatitis atopic dermatitis seborrheic dermatitis stasis dermatitis lichen simplex chronicus Darier's disease glucagonoma syndrome langerhans cell histiocytosis lichen sclerosus pemphigus foliaceus Wiskott-Aldrich syndrome Zinc deficiency Scaling psoriasis tinea (corporis cruris pedis manuum faciei) pityriasis rosea secondary syphillis mycosis fungoides systemic lupus erythematosus pityriasis rubra pilaris parapsoriasis ichthyosis Blistering herpes simplex herpes zoster varicella bullous impetigo acute contact dermatitis pemphigus vulgaris bullous pemphigoid dermatitis herpetiformis porphyria cutanea tarda epidermolysis bullosa simplex Papular scabies insect bite reactions lichen planus miliaria keratosis pilaris lichen spinulosus transient acantholytic dermatosis lichen nitidus pityriasis lichenoides et varioliformis acuta Pustular acne vulgaris acne rosacea folliculitis impetigo candidiasis gonococcemia dermatophyte coccidioidomycosis subcorneal pustular dermatosis Hypopigmented tinea versicolor vitiligo pityriasis alba postinflammatory hyperpigmentation tuberous sclerosis idiopathic guttate hypomelanosis leprosy hypopigmented mycosis fungoides Without epidermal involvement Red Blanchable Erythema Generalized drug eruptions viral exanthems toxic erythema systemic lupus erythematosus Localized cellulitis abscess boil erythema nodosum carcinoid syndrome fixed drug eruption Specialized urticaria erythema (multiforme migrans gyratum repens annulare centrifugum ab igne) Nonblanchable Purpura Macular thrombocytopenic purpura actinic purpura Papular disseminated intravascular coagulation vasculitis Indurated scleroderma/morphea granuloma annulare lichen sclerosis et atrophicus necrobiosis lipoidica Miscellaneous disorders Ulcers Hair telogen effluvium androgenic alopecia trichotillomania alopecia areata systemic lupus erythematosus tinea capitis loose anagen syndrome lichen planopilaris folliculitis decalvans acne keloidalis nuchae Nail onychomycosis psoriasis paronychia ingrown nail Mucous membrane aphthous stomatitis oral candidiasis lichen planus leukoplakia pemphigus vulgaris mucous membrane pemphigoid cicatricial pemphigoid herpesvirus coxsackievirus syphilis systemic histoplasmosis squamous cell carcinoma v d e Diseases of the skin and subcutaneous tissue (integumentary system) (L, 680-709) Infections Bacterial skin disease Staphylococcus (Staphylococcal scalded skin syndrome, Impetigo, Boil, Carbuncle) Strep (Impetigo) Corynebacterium (Erythrasma) Viral skin disease Wart Molluscum contagiosum Erythema infectiosum Exanthema subitum Herpes simplex (Herpetic whitlow, Eczema herpeticum) General Cellulitis (Paronychia) Acute lymphadenitis Pilonidal cyst Pimple (Pustule) Bullous disorders acantholysis (Pemphigus, Transient acantholytic dermatosis) Pemphigoid (Bullous, Cicatricial, Gestational) Dermatitis herpetiformis Inflammatory Dermatitis and eczema Atopic dermatitis Seborrhoeic dermatitis (Dandruff, Cradle cap) Contact dermatitis (Diaper rash, Urushiol-induced contact dermatitis) Erythroderma Lichen simplex chronicus/Prurigo nodularis Itch (Pruritus ani, Pruritus scroti, Pruritus vulvae) Nummular dermatitis Dyshidrosis Pityriasis alba Papulosquamous disorders Psoriasis (Psoriatic arthritis) Parapsoriasis (Pityriasis lichenoides et varioliformis acuta, Pityriasis lichenoides chronica, Lymphomatoid papulosis) other pityriasis (Pityriasis rosea, Pityriasis rubra pilaris) other lichenoid (Lichen planus, Lichen nitidus) Urticaria Dermatographic urticaria Cold urticaria Cholinergic urticaria Solar urticaria Erythema Erythema multiforme/ drug eruption Stevens-Johnson syndrome Toxic epidermal necrolysis Erythema nodosum Acute generalized exanthematous pustulosis Other eryth
Dr. Wendy Levinbook, MD discusses Cicatricial Pemphigoid. See more at www.dermnet.com PLEASE RATE AND COMMENT!!! Cicatricial pemphigoid (CP) is a rare blistering disease characterized by erosive lesions of the mucous membranes and skin that result in scarring. The mean age of onset is in the early 60's and there is a slight female predominance. There is no known racial or geographic clustering. Other names for this disorder include benign mucous membrane pemphigoid, desquamative gingivitis, and ocular pemphigus. Clinically, oral and conjunctival mucous membranes are most frequently affected and are typically the first sites of involvement. In the mouth, the gingiva, buccal mucosa, and palate are typically involved and patients may present with mucosal erosions or tense blisters. Adhesions may develop in severe disease and gingival involvement can result in loss of teeth. Ocular involvement typically manifests as unilateral or bilateral conjunctivitis or as burning, dryness, or foreign body sensation. Severe disease can lead to scarring and vision loss. Other mucosal sites that may be affected include the nasopharyngeal, laryngeal, esophageal, genital, and rectal mucosa. Cutaneous lesions are present in about one third of patients. The head, neck and upper trunk are most frequently involved. Typically, patients have a few scattered erosions or tense blisters on a red or urticarial base. However, the extent and number of cutaneous lesions is usually small. On electron ... Video Rating: 0 / 5
