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1/32. Pseudoporphyria induced by propionic acid derivatives.

    BACKGROUND: Pseudoporphyria is a photosensitive bullous skin disease that is distinguished from porphyria cutanea tarda (PCT) by its normal porphyrin profile. Drugs are a major cause of this disease, and the list of culprits is continually expanding. Nonsteroidal antiinflammatory agents (NSAIDs), especially naproxen and other propionic acid derivatives, appear to be the most common offenders. OBJECTIVE: The study was carried out to increase awareness about the etiology and characteristic features of pseudoporphyria. methods: We report two cases of pseudoporphyria caused by naproxen and oxaprozin. We review the current English language literature on this entity and discuss its clinical features, histology, ultrastructure, etiology, and pathophysiology. RESULTS: A 44-year-old man taking naproxen for chronic low back pain and a 20-year-old woman on oxaprozin for rheumatoid arthritis presented with tense bullae and cutaneous fragility on the face and the back of the hands. In both, skin biopsy showed a cell-poor subepidermal vesicle with festooning of the dermal papillae. Direct immunofluorescence revealed staining at the dermal-epidermal junction and around blood vessels with IgG in the first case and with IgG, IgA, and fibrin in the second case. urine collections and serum samples yielded normal levels of uro- and coproporphyrins. CONCLUSIONS: Most cases of pseudoporphyria are drug-induced. naproxen, the most common offender, has been associated with a dimorphic clinical pattern: a PCT-like presentation and one simulating erythropoietic protoporphyria in the pediatric population. Other NSAIDs of the propionic acid family can also cause pseudoporphyria.
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ranking = 1
keywords = skin disease
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2/32. Subepidermal autoimmune bullous skin diseases associated with B-cell lymphoproliferative disorders.

    The development of several types of autoimmune disorders is well known in the course of B-cell lymphoproliferative diseases. In order to investigate whether these autoimmune diseases may target cutaneous antigens, especially those of the dermal-epidermal junction, we conducted a retrospective analysis of all cutaneous direct immunofluorescence studies performed in patients with B-cell neoplasia who presented with cutaneous lesions requiring a skin biopsy. patients with linear deposits of immunoglobulin or C3 molecules at the dermal-epidermal junction were studied further, using immunoblotting and immunoelectron microscopy. patients with no overt hematologic malignancies but with cutaneous lesions requiring direct immunofluorescence were studied as a control population. During the study period, the diagnosis of autoimmune blistering diseases of the dermal-epidermal junction was established in 9/102 (8.9% /- 2%) patients with a B-cell lymphoid disorder, compared with 288/8,189 (3.5% /- 0.04%) patients without underlying hemopathy (p < 0.01). Among the 9 patients, 7 were studied in detail. Immunologic studies demonstrated epidermolysis bullosa acquisita in 6 patients and cicatricial pemphigoid in 1. Autoimmune blistering diseases, especially epidermolysis bullosa acquisita, are part of the spectrum of autoimmune disorders associated with B-cell neoplasia.
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ranking = 4
keywords = skin disease
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3/32. A paraneoplastic mixed bullous skin disease: breakdown in tolerance to multiple epidermal antigens.

    We report a new type of paraneoplastic mixed bullous skin disease in a patient with a B-cell lymphoma associated with monoclonal IgM kappa paraproteinaemia. The patient's clinical and histological features were reminiscent of bullous pemphigoid. Characterization of antiepidermal antibodies by immunoblotting and indirect immunoelectron microscopy demonstrated a novel pattern of reactivity: IgG antibodies were directed against desmoplakins I-II and BPAG2, and were associated with antidesmoglein 3 polyclonal IgM antibodies. Such an autoreactive pattern involving antidesmoplakins, anti-BPAG2 and antidesmoglein 3 antibodies has not been previously reported. It reflects the breakdown of tolerance to multiple epidermal antigens observed in some patients with malignancy.
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ranking = 5
keywords = skin disease
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4/32. autoantibodies in anti-p200 pemphigoid stain skin lacking laminin 5 and type VII collagen.

    We report the case of a patient with a widespread bullous skin disease and linear deposits of IgG and C3 at the dermal-epidermal junction using direct immunofluorescence microscopy. Indirect immunofluorescence analysis demonstrated circulating IgG autoantibodies that stained, like autoantibodies to laminin 5 and type VII collagen, the dermal side of 1 mol L-1 NaCl-split human skin. By immunoblotting dermal extracts, the patient's serum, like serum samples from two control patients, reacted with a 200-kDa protein. Using immunoelectron microscopy, the serum labelled a component of the lower lamina lucida, but not the lamina densa/sublamina densa region, distinguishing this from the type VII collagen localization pattern. By immunofluorescence microscopy on skin sections from patients lacking either laminin 5 (Herlitz's epidermolysis bullosa) or type VII collagen (recessive dystrophic epidermolysis bullosa of Hallopeau-Siemens), the patient's serum retained reactivity with these test substrates. The patient's disease responded rapidly to the use of topical corticosteroids and lesions healed without scarring or milia formation. Our results provide strong evidence for the hypothesis that the 200 kDa autoantigen is different from laminin 5 and type VII collagen. For this new disease, we propose the designation 'anti-p200 pemphigoid'.
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keywords = skin disease
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5/32. Acute generalized exanthematic pustulosis (AGEP) in a patient treated with furosemide.

    BACKGROUND: Although they appear more rarely than electrolyte disturbances, cutaneous reactions are important adverse effects of furosemide. This is particularly true for bullous skin eruptions, because they may be life-threatening. CASE REPORT: We describe a patient who developed acute generalized exanthematic pustulosis (AGEP) during treatment with furosemide. Because the patient had developed similar skin eruptions during treatment with furosemide years before, furosemide was considered the most likely cause of this reaction. The short period of time between exposure to furosemide and the appearance of the skin reaction, as well as a positive lymphocyte transformation test, suggest an immunological mechanism of the skin disease. CONCLUSION: AGEP is a possible cutaneous side effect of furosemide.
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keywords = skin disease
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6/32. linear iga bullous dermatosis induced by atorvastatin.

    linear iga bullous dermatosis (LABD) is an autoimmune blistering skin disease characterized by circulating IgA antibodies binding the basement membrane zone. In most cases the origin is not clear, but in a minority of cases LABD is drug induced. We describe a patient in whom linear IgA disease developed shortly after beginning therapy with atorvastatin. In Western blotting analysis we detected IgA and IgG class antibodies targeting a 97-kd protein. To our knowledge this is the first reported case of atorvastatin-induced LABD.
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ranking = 1
keywords = skin disease
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7/32. Bullous skin disease: an unusual allergic reaction to vancomycin.

    Severe reactions due to vancomycin are uncommon. We describe a case of vancomycin-induced linear immunoglobulin a bullous disease and review the literature pertinent to this entity. This is a rare subepidermal blistering disorder, with a heterogenous clinical presentation. It is characterized by IgA deposition in a linear pattern along the basement membrane zone. It seems to be autoantibody-mediated and is not dose-dependent. Spontaneous and complete skin healing follows vancomycin withdrawal; rechallenge reproduces the disease with a more rapid and severe onset. Because vancomycin is almost never suspected to be the cause of such manifestations, awareness of this rare autoimmune reaction is crucial. early diagnosis through direct immunofluorescence of the perilesional skin would avoid unnecessary laboratory investigations and therapeutic measures and would shorten significantly the pain and suffering of these patients.
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ranking = 4
keywords = skin disease
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8/32. Pseudoverrucous papules: an aspect of incontinence in children.

    Pseudoverrucous papules and nodules can be observed on skin surrounding urostomies and colostomies. These lesions appear to be uncommon, and sometimes can be misdiagnosed, even leading to surgical removal. We report the case of a 12-year-old boy whose lesions appeared in crops in an area subjected to urine leakage and spontaneously regressed in time. In this patient, anogenital warts had to be ruled out, but many skin diseases must be considered in the differential diagnosis of these misunderstood lesions. We stress the importance of a skin examination by a trained professional aware of these problems to avoid unnecessary investigations and treatments.
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ranking = 1
keywords = skin disease
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9/32. A bullous skin disease patient with autoantibodies against separate epitopes in 1 mol/L sodium chloride split skin.

    BACKGROUND--We describe a patient with a subepidermal bullous skin disease associated with autoantibodies recognizing separate epitopes in 1 mol/L sodium chloride (NaCl) split skin. OBSERVATIONS--Direct immunofluorescence microscopy showed deposits of immunoglobulins and C3 in a continuous pattern in the patient's epidermal basement membrane zone. Direct immunoelectron microscopy demonstrated thick deposits of IgG overlying the lamina lucida and the lamina densa in a unique pattern. The patient had circulating IgG anti-basement membrane zone antibodies that bound both sides of 1 mol/L NaCl split skin, exhibited at least a fourfold-higher titer against the dermal side of this test substrate, and bound basal keratinocyte hemidesmosomes as well as focal sites along the superior portion of the lamina densa on indirect immunoelectron microscopy. Affinity purification of anti-basement membrane zone antibodies against epidermal or dermal strips of 1 mol/L NaCl split skin yielded IgG that only bound the side of split skin from which it was eluted. The patient's serum contained IgG that immunoprecipitated and immunoblotted the 230- and 170-kd bullous pemphigoid antigens. Affinity purification of patient antibody against bullous pemphigoid antigen immobilized on nitrocellulose paper yielded IgG that bound only the epidermal side of 1 mol/L NaCl split skin. The patient showed no evidence of reactivity against type VII collagen by direct immunoelectron microscopy, indirect immunoelectron microscopy, or immunoblot. CONCLUSIONS--This patient's bullous skin disease is associated with IgG anti-basement membrane zone antibodies with two specificities: one recognizing the bullous pemphigoid antigen in the epidermal side of 1 mol/L NaCl split skin, and another binding a distinct, yet presently unidentified, epitope in the superior aspect of the lamina densa.
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ranking = 6
keywords = skin disease
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10/32. UV light-induced linear IgA dermatosis.

    Various exogenous factors (eg, drugs, dietary antigens, trauma, infections, radiographs, and UV radiation) are known to induce or aggravate skin diseases. UV radiation in particular is known to induce or aggravate the autoimmune bullous diseases of pemphigus foliaceus, pemphigus vulgaris, and bullous pemphigoid. Its role in linear IgA dermatosis, however, is not well recognized. We report the second case of linear IgA dermatosis induced by intense sun exposure in which blistering was induced by UVA radiation. Furthermore, a review of the literature on photoinduced autoimmune bullous diseases and the wavelengths responsible for the induction of blistering is presented and several proposed mechanisms of action for the blister induction, including release or unmasking of antigens, promotion of antibody fixation by UV radiation, and launching of an inflammatory process, are discussed. We conclude that linear IgA dermatosis should be added to the list of autoimmune bullous diseases induced and/or aggravated by UV radiation.
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ranking = 1
keywords = skin disease
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