1/29. 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'.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/29. Drug-induced cholestasis.The spectrum of drug-induced cholestasis ranges from 'bland' reversible cholestasis to chronic forms due to the vanishing bile duct syndrome. Agents known for many years to cause cholestasis include estrogens and anabolic steroids, chlorpromazine, erythromycin, and the oxypenicillins; structurally similar congeners of these drugs (tamoxifen, newer macrolides) may also cause cholestasis. Contemporary drugs linked to cholestastic liver injury include ticlopidine, terfenadine, terbinafine, nimesulide, irbesartan, fluoroquinolones, cholesterol-lowering 'statins,' and some herbal remedies (greater celandine, glycyrrhizin, chaparral). Amoxillin-clavulanate, ibuprofen, and pediatric cases of the vanishing bile duct syndrome are recent additions to a long list of drugs associated with the vanishing bile duct syndrome. Particular human leukocyte antigen profiles have recently been identified among those who have developed cholestasis with specific drugs (tiopronin and amoxicillin-clavulanate), and the mechanistic relevance of these genetic associations is being explored. The treatment of drug-induced cholestasis is largely supportive. The offending drug should be withdrawn immediately. Cholestyramine or ursodeoxycholic acid are used to alleviate pruritus, with rifampicin and opioid antagonists being reserved for those who fail first line therapy. nutritional support is essential for those with prolonged cholestasis, a subgroup who are at risk of developing biliary cirrhosis and liver failure. Timely referral for liver transplant assessment is crucial in these patients.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
3/29. vancomycin-induced linear IgA disease with autoantibodies to BP180 and LAD285.Linear IgA disease (LAD) is an acquired autoimmune subepidermal bullous disease characterized by the linear deposition of IgA at the basement membrane zone. A minority of cases are induced by drugs, of which the most frequently implicated is vancomycin. The target antigens in idiopathic LAD are heterogeneous, but have not previously been reported in vancomycin-induced LAD. We report three cases, and in two of these we investigated the target antigens. In both we identified IgA antibodies to LAD285 and IgA and IgG antibodies (dual response) to BP180.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
4/29. Papulonodular lichenoid and pseudolymphomatous reaction at the injection site of hepatitis b virus vaccination.immunization with the hepatitis b virus (HBV) is effective and safe with an estimated incidence of adverse reactions, either local or systemic, of less than 0.1%. Cutaneous side effects are rare and include lichen planus (LP) and lichenoid reactions. We report the case of a 21-year-old female, in whom a persistent, papulonodular lesion developed at the site of the injection, 6 weeks after the second dose of the HBV. Histological examination revealed lichenoid and pseudolymphomatous features. In addition, sensitization to thiomersal, a vaccine constituent, was documented by patch testing. The association of LP with chronic liver disease is well established. Furthermore, less than 20 cases of lichen or lichenoid reactions, following HBV vaccination, have been reported. Although several arguments have been presented, it is still debated whether there is a causal association or the occurrence of LP following HBV vaccination is a simple coincidence. It has been speculated that a T-cell-mediated, graft-versus-host-like reaction, triggered by a sensitizing protein, is directed against keratinocytes expressing an epitope of hepatitis B surface antigen or a similar epitope. Our case may represent a localized lichenoid reaction to HBV vaccination, a local reactive hyperplasia or a persisting delayed hypersensitivity reaction to a vaccine constituent. This is the first case of a local lichenoid reaction at the injection site of the HBV vaccine, providing further documentation for a causal association linking the HBV vaccine with LP.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
5/29. Development of an idlike reaction during treatment for acute pulmonary histoplasmosis: a new cutaneous manifestation in histoplasmosis.Id reactions often occur secondary to release of antigens after initiation of antimicrobial therapy. This reaction commonly occurs during treatment of trichophyton infections. The diagnosis is usually made clinically and is supported in the presence of an infection and/or initiation of therapy. We report an idlike reaction during therapy for pulmonary histoplasmosis.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
6/29. Allergic contact dermatitis caused by idoxuridine. Patterns of cross reactivity with other pyrimidine analogues.idoxuridine has been used for many years in the treatment of herpex simplex infections of the eye. Use of the drug for herpes simplex infection of the skin is increasing. Ophthalmologists have noted occasional conjunctival and corneal irritant reactions, but no true delayed cutaneous hypersensitivity has been verified. We report four cases of allergic contact dermatitis from idoxuridine, sensitized by both eye and skin applications. Cross reactivity to brominated and chlorinated, but not fluorinated, pyrimidine analogues is noted. Extensive patch testing indicates the general relationship between the structure of pyrimidine compounds and their antigenic cross reactivity.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
7/29. jaundice and rash associated with the use of phenobarbital and hydrochlorothiazide.Rash, lymphadenopaty, splenomegaly, periorbital edema, and hepatitis occurred in an 18-year-old woman who was taking phenobarbital and hydrochlorothiazide. Tests for fluorescent antinuclear antibody and hepatitis-associated antigen and antibody were negative. Liver biopsy was not characteristic of viral hepatitis. Clinical recovery occurred within two weeks. Treatment consisted of withdrawal of the above drugs plus the administration of methylprednisolone and diphenhydramine.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
8/29. Exacerbation of paraneoplastic pemphigus by cyclophosphamide treatment: detection of novel autoantigens and bronchial autoantibodies.A 48-year-old woman with a follicular, grade III, B-cell non-Hodgkin lymphoma developed clinical, immunopathological and histological features of paraneoplastic pemphigus. The skin symptoms flared after repeated cyclophosphamide infusions, and were preceded and accompanied by a progressive dyspnoea. Although the skin and oral mucosal disease went into remission with high-dose steroid and intravenous immunoglobulin therapy, the severe alveolitis led to death. immunoblotting of human epidermal extracts showed that the patient's serum IgG reacted with the 210-kDa envoplakin, 190-kDa periplakin, as well as the recombinant protein of BP180 NC16a domain. IgG and IgA enzyme-linked immunosorbent assays for desmoglein 3 were positive, too. Indirect immunofluorescence studies on COS-7 cells transiently transfected with desmocollin 1-3 cDNAs showed that the patient's serum contained IgG and IgA antibodies to desmocollin 3 as well as IgG antibodies to desmocollin 2. serum IgG and IgA strongly stained rat bronchial epithelium, corresponding to autoantibodies possibly involved in the pathomechanism of the severe lung disease. In this case, which was characterized by a mixed IgA/IgG antibody panel displaying known and unique antigenicity, the serious episodes of paraneoplastic pemphigus flared after cyclophosphamide treatment.- - - - - - - - - - ranking = 5keywords = antigen (Clic here for more details about this article) |
9/29. Granulocyte colony-stimulating-factor-induced psoriasiform dermatitis resembles psoriasis with regard to abnormal cytokine expression and epidermal activation.psoriasis is a chronic inflammatory skin disorder characterized by accumulation of Th1-type T cells and neutrophils, regenerative keratinocyte proliferation and differentiation, and enhanced epidermal production of antimicrobial peptides. The underlying cause is unknown, but there are some similarities with the immunologic defense program against bacteria. Development of psoriasiform skin lesions has been reported after administration of granulocyte colony-stimulating factor (G-CSF), a cytokine induced in monocytes by bacterial antigens. To further investigate the relation between this type of cytokine-induced dermatitis and psoriasis, we analyzed the cutaneous cytokine profile [tumor necrosis factor-alpha (TNF-alpha), interferon-gamma, transforming growth factor-beta1 (TGF-beta1), interleukin-10 (IL-10), IL-12p35 and p40, and IL-8] and expression of markers of epidermal activation [Ki-67, cytokeratin-16, major histocompatibility complex (MHC) class II, intercellular adhesion molecule-1 (ICAM-1)] in a patient who developed G-CSF-induced psoriasiform dermatitis by using quantitative real-time reverse transcriptase-polymerase chain reaction and immunohistology. The histologic picture resembled psoriasis with regard to epidermal hyperparakeratosis and the accumulation of lymphocytes in the upper corium. CD8( ) T cells were found to infiltrate the epidermis which was associated with an aberrant expression of Ki-67, cytokeratin-16, MHC class II, and ICAM-1 on adjacent keratinocytes. As compared to normal skin (n = 7), there was an increased expression of TNF-alpha, IL-12p40, and IL-8, a decreased expression of TGF-beta1, and a lack of IL-10, similar to the findings in active psoriasis (n = 8). Therefore, G-CSF may cause a lymphocytic dermatitis that, similar to psoriasis, is characterized by a pro-inflammatory Th1-type cytokine milieu and an epidermal phenotype indicative of aberrant maturation and acquisition of non-professional immune functions.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
10/29. Localized linear IgA disease induced by ampicillin/sulbactam.We describe a patient who developed an exclusively perianal-intergluteal vesicular eruption after receiving a course of ampicillin/sulbactam. Direct immunofluorescence microscopy of perilesional skin demonstrated linear deposits of IgA along the dermal-epidermal junction. Circulating IgA autoantibodies against the 120-kd soluble ectodomain of bullous pemphigoid antigen 180 (LAD-1 autoantigen) were detected by immunoblotting. Discontinuation of the antibiotics resulted in a rapid resolution of the skin lesions. This is a most unusual case of localized drug-induced linear IgA disease.- - - - - - - - - - ranking = 2keywords = antigen (Clic here for more details about this article) |
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