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  1. Lichen planus images. Authoritative facts about the skin from DermNet New blessmerp.comg: pokies.:
    Lichen myxoedematosus (lichen myxedematosus) is also known as papular mucinosis. Lichen myxoedematosus has localised and generalised forms. Acral persistent papular blessmerp.comg: pokies. Oral lichen planus. Authoritative facts about the skin from DermNet New blessmerp.comg: pokies. Lichen spinulosus. Authoritative facts about the skin from DermNet New blessmerp.comg: pokies.
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Patients who have widespread skin involvement may be referred to a general physician for assessment of internal organ involvement. Treatment of scleromyxoedema is difficult and disappointing. A variety of treatments have been tried including:. Chemotherapeutic agents which interfere with the development of precursor cells of the bone marrow have been tried but are usually reserved for patients with severe and rapidly progressive disease.

These include ciclophosphamide , melphalan and chlorambucil. In recent years, thalidomide has emerged in as potential treatment due to its immune modulatory effects. Localised lichen myxoedematosus does not require therapy. Topical corticosteroid creams and oral isotretinoin may be of some benefit to reduce the induration hardening of the skin.

Nephrogenic fibrosing dermopathy is a recently recognised fibrosing disorder originally identified as a scleromyxoedema-like cutaneous disease in patients with renal disease. It may also cause fibrosis of internal organs, called nephrogenic systemic fibrosis , which may ultimately prove fatal.

The condition has been linked to exposure to gadolinium-containing contrast material during magnetic resonance imaging. Terms of use Privacy policy Image license. DermNet NZ does not provide an online consultation service. If you have any concerns with your skin or its treatment, see a dermatologist for advice.

References Rongioletti F and Rebora A. Updated Classification of papular mucinosis, lichen myxoedematosus and scleromyxoedema. Lichen spinulosa Dermatoscopic view. Keratosis pilaris Follicular skin conditions Lichenoid disorders Other websites: Lichen Spinulosus — Medscape Reference Books about skin diseases: See the DermNet NZ bookstore.

Email Newsletter Would you like to receive our dermatology updates by email? Submit your images We're seeking high-quality photos of skin diseases. Join the conversation on Twitter. Support Sponsors Advertisers Donations. Terms and conditions Terms of use Privacy policy Image license. Frontal fibrosing alopecia is a form of lichen planopilaris that affects the anterior scalp, forehead and eyebrows. Pseudopelade of Brocq is probably a variant of lichen planus without inflammation or scaling.

Lichen planus affects one or more nails , sometimes without involving the skin surface. It is called twenty-nail dystrophy if all nails are abnormal and nowhere else is affected. Lichen planus thins the nail plate, which may become grooved and ridged. The nail may darken, thicken or lift off the nail bed onycholysis. Sometimes the cuticle is destroyed and forms a scar pterygium.

The nails may shed or stop growing altogether, and they may rarely, completely disappear anonychia. More images of lichen planus of the nails Lichen planus pigmentosus describes ill-defined oval, greyish brown marks on the face and neck or trunk and limbs without an inflammatory phase. It can be provoked by sun exposure but can also arise in sun-protected sites such as the armpits.

It has diffuse, reticulate and diffuse patterns. Lichen planus pigmentosus is similar to erythema dyschromicum perstans and may be the same disease. Lichen planus pigmentosus may rarely affect the lips, resulting in a patchy dark pigmentation on upper and lower lips. Lichenoid drug eruption refers to a lichen planus-like rash caused by medications. Asymptomatic or itchy; pink, brown or purple; flat, slightly scaly patches most often arise on the trunk.

The oral mucosa oral lichenoid reaction and other sites are also sometimes affected. Many drugs can rarely cause lichenoid eruptions. The most common are:. Quinine and thiazide diuretics cause photosensitive lichenoid drug eruption.

Rarely, longstanding erosive lichen planus can result in squamous cell carcinoma squamous cell carcinoma of the mouth oral cancer , vulva vulval cancer or penis penile cancer. This should be suspected if there is an enlarging nodule or an ulcer with thickened edges.

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Vascular abnormalities are also likely to be an early contributor to the pathogenesis of scleroderma. Pericytes, the smooth muscle—like mural cells of capillaries and venules, synthesize matrix components and fibroblast-activating cytokines; thus, they are potential mediators of pathological changes in scleroderma.

Pericyte density is increased in the microvasculature of the peripheral zones of active disease. The vasospastic phenomenon of Raynaud is present in most scleroderma patients.

Endothelial cell injury and dysfunction, intimal proliferation, thrombocytosis, elevated factor VIII-von Willebrand factor levels, and vasospasm are found in scleroderma patients and result in vascular compromise. Animal models of scleroderma may help identify abnormalities in human scleroderma. The tight skin mouse model of scleroderma Tsk1 is characterized by increased collagen deposition in the skin and some internal organs, as well as antinuclear antibody ANA production.

The defect is a heterozygous mutation in the fibrillin-1 gene. A haplotype analysis of Choctaw Native Americans who have a fold increase in the prevalence of scleroderma has demonstrated linkage between the fibrillin gene locus and the scleroderma phenotype.

How a defect in fibrillin, an extracellular matrix component, may be involved in the pathogenesis of scleroderma is unclear.

Affected chickens develop vascular occlusion and severe perivascular lymphocytic infiltration of the skin and internal organs. These studies suggest that early pathogenetic events in scleroderma are endothelial abnormalities. Antiendothelial cell antibodies trigger both apoptosis and increased adhesion molecule expression on endothelial cells, resulting in perivascular accumulation of mononuclear cells.

Nelson [ 24 ] has suggested the role of microchimerism in the pathogenesis of scleroderma, because of the similarity of scleroderma to chronic graft versus host disease and the frequent onset of scleroderma in women after their childbearing years.

Microchimerism indeed occurs to a greater degree in persons with scleroderma or other autoimmune disorders than in healthy patients. A causal linkage between microchimerism and autoimmune disorders has not been demonstrated. The incidence of systemic sclerosis approximates 2. The prevalence is cases per million persons. In other countries, the incidence of systemic sclerosis is slightly lower than in the United States.

In Iceland, systemic sclerosis occurs In 3. The incidence in Russia is 7 cases per million adults per year, in England is 3. Disease prevalence is slightly lower in other countries compared with the United States; in Greece it is cases per million, in the United Kingdom is it 82 cases per million, in France it is cases per million, and in Australia it is cases per million. Both the prevalence and incidence of systemic sclerosis is higher in blacks than in whites.

The prevalence of diffuse disease among black patients is nearly twice that of white patients. Survival for black patients versus nonblack patients is marginally worse during the first 12 years after diagnosis, but, in general, survival for both groups is comparable. Some Choctaw Native American and Thai populations are more likely to have diffuse disease, while some European and white Australian groups have more limited disease.

Females have a greater incidence of scleroderma than males. This difference appears greater during childbearing years. Mayes et al [ 25 ] reported an overall female-to-male ratio of 4. The usual age of onset of scleroderma is approximately years. Black women tend to present at an earlier age. In a large US study by Mayes et al, [ 25 ] the survival rate from time of diagnosis was computed to be The extent of skin involvement is a good predictor of survival in patients with scleroderma. Limited cutaneous disease as defined by Medsger [ 34 ] in is associated with a better survival rate than diffuse disease.

Renal involvement is responsible for half of all scleroderma-related deaths in patients with widespread skin changes, while patients with sclerodactyly alone do not tend to develop any type of renal disease. The mortality in patients with limited skin involvement results from cardiac, pulmonary, and GI causes. Adigun R, Bhimji S. Clinical and biological features of scleroderma]. Ann Med Interne Paris. Multiple telangiectasia, Raynaud's phenomenon, sclerodactyly, and subcutaneous calcinosis: A syndrome mimicking hereditary hemorrhagic telangiectasia.

Bull Johns Hopkins Hosp. A reevaluation of the CRST syndrome, abstracted. Comparison with systemic sclerosis scleroderma. Classification and nomenclature of progressive systemic sclerosis scleroderma.

A survival study of patients with scleroderma diagnosed over 30 years A comparison with acrosclerosis. Predicting mortality in systemic sclerosis: Rheum Dis Clin North Am. A proposal of criteria for the classification of systemic sclerosis. Maricq HR, Valter I. A working classification of scleroderma spectrum disorders: Classification of systemic sclerosis. Enhanced expression of the receptor for granulocyte macrophage colony stimulating factor on dermal fibroblasts from scleroderma patients.

Immunohistochemical expression of transforming growth factor beta3 in calcinosis in a patient with systemic sclerosis and CREST syndrome. Effect of granulocyte macrophage-colony stimulating factor on extracellular matrix deposition by dermal fibroblasts from patients with scleroderma.

Tissue inhibitor of metalloproteinase 1 TIMP-1 may be an autocrine growth factor in scleroderma fibroblasts. Protease nexin-1 messenger RNA levels are not affected by serum or interferon beta in cultured systemic sclerosis fibroblasts. Hyperplasia of dermal microvascular pericytes in scleroderma.

Increased expression of platelet-derived growth factor type B receptors in the skin of patients with systemic sclerosis. Microchimerism and the pathogenesis of systemic sclerosis. Prevalence, incidence, survival, and disease characteristics of systemic sclerosis in a large US population. Increased prevalence of systemic sclerosis in a Native American tribe in Oklahoma. Association with an Amerindian HLA haplotype.

Patch tests may be recommended for patients with oral lichen planus affecting the gums, to assess for contact allergy to mercury.

Treatment is not always necessary. Local treatments for symptomatic cutaneous or mucosal disease are:. Systemic treatment for widespread or severe local disease often includes a 1—3 month course of oral prednisone , while commencing another agent from the following list:.

In cases of oral lichen planus affecting the gums with contact allergy to mercury, the lichen planus may resolve on replacing the fillings with composite material. If the lichen planus is not due to mercury allergy, removing amalgam fillings is very unlikely to result in cure.

Lichen planopilaris is reported to improve with pioglitazone. Cutaneous lichen planus tends to clear within a couple of years in most people, but mucosal lichen planus is more likely to persist for a decade or longer. Spontaneous recovery is unpredictable, and lichen planus may recur at a later date. Scarring is permanent, including balding of the scalp. Lichenoid drug eruptions clear up slowly when the responsible medication is withdrawn. Terms of use Privacy policy Image license.

DermNet NZ does not provide an online consultation service. If you have any concerns with your skin or its treatment, see a dermatologist for advice. Cutaneous lichen planus Classical violaceous polygonal plaques Wickham's striae Guttate plaques Hypertrophic plaques Provided by Hypertrophic plaques. Lichen planus affecting the scalp. Email Newsletter Would you like to receive our dermatology updates by email?

Submit your images We're seeking high-quality photos of skin diseases. Join the conversation on Twitter. Support Sponsors Advertisers Donations. Terms and conditions Terms of use Privacy policy Image license. New Zealand Dermatological Society. Oral lichenoid lesions are also part of the spectrum of chronic graft-versus-host disease that occurs after bone marrow transplantation.

The diagnosis of oral lichen planus is often made by its clinical appearance. However tissue biopsy may be helpful, when characteristic features of lichen planus may be observed.

Under the microsope, the pathologist may observe a characteristic lichenoid reaction. Direct immunofluorescence may reveal positive staining for fibrinogen, immunoglobulins and complement. Biopsy is often performed to rule out oral cancer.

Oral lichen planus can be very painful and ulceration may lead to scarring. Sometimes eating is so uncomfortable that affected person is unable to maintain adequate nutrition.

Lichen planus may rarely lead to oral cancer squamous cell carcinoma. Persistent ulcers and enlarging nodules should undergo biopsy. It is important to identify and remove any potential agent that might have caused a lichenoid reaction, such as drugs that have been started in recent months and contact allergens identified by patch testing.

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Oral lichenoid lesions are also part of the spectrum of chronic graft-versus-host disease that occurs after bone marrow transplantation. The diagnosis of oral lichen planus is often made by its clinical appearance. However tissue biopsy may be helpful, when characteristic features of lichen planus may be observed. Under the microsope, the pathologist may observe a characteristic lichenoid reaction.

Direct immunofluorescence may reveal positive staining for fibrinogen, immunoglobulins and complement. Biopsy is often performed to rule out oral cancer. Oral lichen planus can be very painful and ulceration may lead to scarring. Sometimes eating is so uncomfortable that affected person is unable to maintain adequate nutrition. Lichen planus may rarely lead to oral cancer squamous cell carcinoma.

Persistent ulcers and enlarging nodules should undergo biopsy. It is important to identify and remove any potential agent that might have caused a lichenoid reaction, such as drugs that have been started in recent months and contact allergens identified by patch testing.

In severe cases systemic corticosteroids may be used. Terms of use Privacy policy Image license. DermNet NZ does not provide an online consultation service. If you have any concerns with your skin or its treatment, see a dermatologist for advice.

Oral lichen planus Plaque lichen planus Reticular lichen planus Erosive lichen planus Ulcerative lichen planus Lichenoid reaction to amalgam Graft versus host disease Lichenoid drug reaction Alveolar cancer. References Lopez Jornet, P.

Several possible causes have been postulated but none have been confirmed. Diagnosis is made by clinical assessment alone. At present, no specific laboratory or diagnostic tests have been identified to make or confirm a diagnosis of lichen spinulosus.

Histological findings of lichen spinulosus are similar to those found in keratosis pilaris. There is no specific treatment for lichen spinulosus and in most cases it resolves spontaneously within 1—2 years, although it can persist for decades in some patients.

Some patients may find the following useful:. Terms of use Privacy policy Image license. DermNet NZ does not provide an online consultation service. If you have any concerns with your skin or its treatment, see a dermatologist for advice. Lichen spinulosa Dermatoscopic view. Keratosis pilaris Follicular skin conditions Lichenoid disorders Other websites: Lichen Spinulosus — Medscape Reference Books about skin diseases: See the DermNet NZ bookstore.

Email Newsletter Would you like to receive our dermatology updates by email?

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Each subtype of the localised form differs in distribution and course. The skin does not harden and the disease is usually stable. There are no abnormal protein levels in the blood. Skin biopsy is the main diagnostic test to assess for suspected lichen myxoedematosus and shows characteristic pathological features.

If paraprotein is present, referral to a haematologist and a bone marrow biopsy may be considered. Patients who have widespread skin involvement may be referred to a general physician for assessment of internal organ involvement.

Treatment of scleromyxoedema is difficult and disappointing. A variety of treatments have been tried including:. Chemotherapeutic agents which interfere with the development of precursor cells of the bone marrow have been tried but are usually reserved for patients with severe and rapidly progressive disease.

These include ciclophosphamide , melphalan and chlorambucil. In recent years, thalidomide has emerged in as potential treatment due to its immune modulatory effects. Localised lichen myxoedematosus does not require therapy. Topical corticosteroid creams and oral isotretinoin may be of some benefit to reduce the induration hardening of the skin. Nephrogenic fibrosing dermopathy is a recently recognised fibrosing disorder originally identified as a scleromyxoedema-like cutaneous disease in patients with renal disease.

It may also cause fibrosis of internal organs, called nephrogenic systemic fibrosis , which may ultimately prove fatal.

The condition has been linked to exposure to gadolinium-containing contrast material during magnetic resonance imaging. Terms of use Privacy policy Image license. DermNet NZ does not provide an online consultation service. If you have any concerns with your skin or its treatment, see a dermatologist for advice. References Rongioletti F and Rebora A. Updated Classification of papular mucinosis, lichen myxoedematosus and scleromyxoedema.

J Am Acad Dermatol Lichen myxoedematosus Papular Mucinosis: New Concepts and Perspectives for an Old Disease. Semin Cutan Med Surg It tends to have a sudden onset and is not accompanied by other signs and symptoms. The follicular papules are small rough bumps that appear in round or oval patches, which extend and spread rapidly over a few days to affect large areas of skin.

When a patch is rubbed gently with the fingers, it has been likened to the feel of brushing your fingers over a nutmeg grater. The lesions do not cause any pain but some patients may complain of pruritus itching. The cause of lichen spinulosus is unknown. Several possible causes have been postulated but none have been confirmed. Diagnosis is made by clinical assessment alone. At present, no specific laboratory or diagnostic tests have been identified to make or confirm a diagnosis of lichen spinulosus.

Histological findings of lichen spinulosus are similar to those found in keratosis pilaris. There is no specific treatment for lichen spinulosus and in most cases it resolves spontaneously within 1—2 years, although it can persist for decades in some patients. Some patients may find the following useful:. Terms of use Privacy policy Image license.

DermNet NZ does not provide an online consultation service. If you have any concerns with your skin or its treatment, see a dermatologist for advice.

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