Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management


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Autoimmune diseases of the skin : pathogenesis, diagnosis, management. Autoimmune diseases of the skin pathogenesis, diagnosis, management. All rights reserved. Remember me on this computer. Cancel Forgot your password? Showing all editions for 'Autoimmune diseases of the skin : pathogenesis, diagnosis, management'. Year 11 2 17 6 Language English 36 Undetermined 1. Pemphigus vulgaris is the most severe of the pemphigus diseases in the dog and has a predilection for the mucocutaneous junctions and oral mucosa. Bullae formation in pemphigus vulgaris results from autoantibody production against desmoglein-3, a protein in desmosomes which is responsible for squamous cell adhesion.

The bullae in pemphigus vulgaris are localized to the suprabasilar region of the lower epidermis. Pemphigus vegetans is a rare, mild variant of pemphigus vulgaris. Pemphigus foliaceous is the most common autoimmune skin disease in the dog and is characterized by superficial subcorneal bullae. The autoantibody in pemphigus foliaceous is directed against desmoglein-1, a protein found in squamous cell desmosomes.

Unlike pemphigus vulgaris, pemphigus foliaceous does not have a predilection for mucocutaneous junctions in the dog. It usually involves the head and nose, but may become generalized. Pemphigus erythematosus is a hybrid between pemphigus foliaceous and systemic lupus erythematosus with immunological features of both diseases. It is confined primarily to the face and ears.


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Direct immunofluorescence of skin lesions shows intercellular immunofluorescence typical of the pemphigus disease and also concomitant immune complex deposition at the dermoepidermal junctions. Some dogs may have antinuclear antibodies. Bullous pemphigoid is a bullous autoimmune skin disease that clinically resembles pemphigus vulgaris. Although the disease has a predilection for mucocutaneous junctions, the groin, and axilla, it differs from pemphigus vulgaris in that the bullae are located in the subepidermis.

The autoantibody in bullous pemphigoid are directed against desmoplakins — proteins in hemidesmosomes that attach cells to the basement membrane of the skin. A breed predilection for collies, Shetland sheepdogs, and Doberman pinschers has been reported. Discoid lupus erythematosus DLE clinically resembles the cutaneous manifestation of SLE in dogs, but there is no internal organ involvement, and antinuclear antibody tests are negative.


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  5. The lesions are primarily isolated to the face and are exacerbated by sunlight. Direct immunofluorescence reveals immune complex deposition at the dermoepidermal junction that are usually restricted to involved skin only which is in contrast to SLE in which the immune complex deposition extends to adjacent normal skin.

    Frontiers | Diagnosis of Autoimmune Blistering Diseases | Medicine

    A breed predilection for DLE has been observed for collies, Shetland sheepdogs, German shepherds, and Siberian huskies. Christine A. Bullous pemphigoid is a rare autoimmune skin disease of horses characterized by the development of vesicles and ulceration of the oral mucosa and occasionally the skin. Bullous pemphigoid is caused by production of an autoantibody pemphigoid antibody against a component in the basement membrane of the skin and mucous membranes. These cells release proteolytic enzymes that disrupt the dermal-epidermal cohesion, separation occurs, and a vesicle forms.

    In horses, vesicles and bullae develop at the mucocutaneous junction in the axillary or inguinal regions or in the oral cavity. Vesicles and bullae rupture easily and often are crusted and secondarily infected with bacteria. Pain, pruritus, anorexia, fever, and salivation are common. Definitive diagnosis is by eliminating other causes of vesicular lesions from the differential list and by skin biopsy. Biopsy of a vesicle or intact bullae is essential; biopsy of crusted or ulcerative lesions will be nondiagnostic. Bullous pemphigoid is characterized by subepidermal vacuolar alterations and subepidermal clefts and vesicles.

    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management, Third Edition

    If one performs direct immunofluorescence testing and the results are positive, one observes a linear deposition of immunoglobulin at the basement membrane zone. Direct immunofluorescence testing is not recommended. Few reports exists of treatment of bullous pemphigoid in horses. After the arrest of new lesion development and healing, one institutes maintenance therapy with alternate-day administration of glucocorticoids at the smallest effective dose.

    Therapy must be individualized and most likely will be lifelong.

    ISBN 13: 9783709119051

    The use of adjuvant therapy e. Psoriatic arthritis is a fascinating disease in combining features of an autoimmune skin disease see Chapter 58 with those of a seronegative arthritis.

    Despite the quite different clinical expressions, common features include skin lesions of psoriasis, absence of rheumatoid factor RF , similar HLA associations and characteristic radiologic findings. Men and women are affected with equal frequency, and the peak incidence is in the fourth through sixth decades. Especially in these cases, a thorough family history is of prime importance. Mark C. Ballow, in Clinical Immunology Fourth Edition , Anti-idiotypic neutralization of autoimmune antibodies in autoimmune mucocutaneous blistering diseases.

    Enhanced degradation of autoantibodies through the FcRn receptor pathway. The autoimmune neurologic diseases and inflammatory myopathies provide a broad group of immunologically mediated diseases in which many inflammatory and immune-mediated effector pathways lead to tissue destruction.

    These neurological and myopathic diseases provide models for the study of the mechanisms of action by which IVIG modulates these autoimmune and inflammatory processes. Several mechanisms have been proposed for the immune-modulating effects of IVIG.

    Patients with Autoimmune Disorders

    IVIG may modulate the inflammatory response by the suppression of cytokine production. Pro-inflammatory cytokines, e. As discussed above for ITP, the administration of large amounts of IgG could saturate the FcRn receptor and accelerate the degradation of the IgG autoantibodies found in many of the autoimmune neuropathies.

    The principal inflammatory mechanism in DM is complement C -dependent microangiopathy with activation of C3 and deposition of the complement C5b-9 membranolytic attack complex MAC on the endomysial capillaries. Lela A.

    way2sell.com/meizu-x8-kik-spy.php Lee, Victoria P. Infections frequently occur on the skin and can mimic autoimmune skin diseases. Skin biopsies can help confirm some types of skin infections, and some require a skin biopsy for culture to determine the organism and drug sensitivity. Patients with many infectious diseases present with both skin and rheumatologic findings. Borrelia burgdorferi, the causative agent of Lyme disease in North America, is associated with erythema migrans EM. The relationship between markers and specific genes can be controversial.

    Only common variants are currently detected, many with a limited impact on disease susceptibility.

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    Further progress may come not only from technology improvement e. Ward: For genetic markers to gain use in clinical applications, these markers should provide unique information about prognosis or treatment response not provided by other more readily available and less expensive sources, be it the clinical history or examination, or more commonly used laboratory tests.

    Observational studies showing the differences in patient outcomes by genotype should be followed by randomized controlled trials showing that a strategy of screening for genetic markers, and clinical management based on the screen, results in patient outcomes superior to those obtained with a strategy of not screening. Ideally, treatment based on screening would also result in more-efficient and cost-effective care, so these outcomes should also be measured.

    At present, markers of potential drug toxicity glucosephosphate dehydrogenase and thiopurine- S -methyltransferase are used, but no genetic markers are used clinically for prognosis or to guide treatment decisions. Heterogeneity in symptoms, signs, and responses to treatment among patients of the same genotype will complicate these efforts. Can you briefly discuss current treatment strategies specific for different stages of autoimmune disease? Are there any markers that are clinically used to assess treatment response and predict outcome?

    These 2 groups show very similar clinical presentations in the early phase of the disease, but ACPA-positive patients develop a much more erosive disease. Rik Lories: My main expertise is ankylosing spondylitis and related spondyloarthritides.

    What is the immune system?

    I have learned that besides nonsteroidal antiinflammatory drugs, anti-TNF drugs are now essential in the treatment algorithm. The widespread use of magnetic resonance imaging, a technique that can visualize inflammation, has changed clinical practice. Outcome prediction is still more difficult but increasingly successful in other diseases, such as RA. Studies of other systemic diseases, such as SLE, are currently also exploring the use of biologics, and new clinical discoveries are eagerly awaited.

    Ward: This is difficult to answer because there are many different autoimmune diseases. In general, the treatment approach is to quickly control symptoms and inflammation to limit the potential for permanent organ damage, whether in the joints, skin, vessel wall, kidney, or other organs, and improve quality of life. A similar remission-induction and remission-maintenance paradigm has been used in recent trials of proliferative lupus nephritis.

    Although the validity of stages of treatment responsiveness is questionable, the idea of initial aggressive treatment to limit inflammation and then reducing treatment intensity has good clinical merit. In granulomatosis with polyangiitis Wegener disease , there are conflicting data on the ability of anti—proteinase 3 antibody levels to predict clinical relapses.

    Can you speculate on how the diagnosis and clinical management of autoimmune diseases will change in the next 10 years? What will be the main factors driving this change? Unfortunately, most research money is directed toward the discovery of new therapeutics. New and early serologic predictors of autoimmune diseases can possibly be found when detailed studies of aberrant chemical modifications of proteins in disease e. Rik Lories: Better knowledge will lead to more-personalized medicine.

    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management
    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management
    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management
    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management
    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management
    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management
    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management
    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management
    Autoimmune Diseases of the Skin: Pathogenesis, Diagnosis, Management

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