Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors describes four cases of lupus erythematosus (LE) diagnosed during the course of a medication toxicodermia, which was always acute and variable in its severity (in one case it concerned a Lyell's syndrome). The lupus affection was made evident by the toxicodermia and lupic manifestations may regress spontaneously after recovery from the skin disorder. This emphasizes the value of clinical and biological testing for the presence of LE in severe cases of toxicodermia in women, more particularly immunofluorescent studies of the basal structures in the cutaneous lesions.
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PMID:[Lupos erythematosus discovered during the course of a toxicodermia (author's transl)]. 4 63

Subepidermal bullous dermatoses are a heterogenous group of disorders characterized by loss of tissue adhesion in the dermoepidermal junction and formation of a vesicle or bulla in the lamina lucida or under the lamina densa. These diseases can be classified into the following: 1. Subepidermal autoimmune bullous dermatoses. These are characterized by circulating autoantibodies against normal constituents of the basement membrane zone and include the following: Epidermolysis bullosa acquisita, bullous pemphigoid, dermatitis herpetiformis Duhring, linear IgA disease, herpes gestationis, cicatricial pemphigoid and bullous systemic lupus erythematosis (SLE). II. Subepidermal bullous dermatoses, due to mutation of the basement membrane zone proteins. These are epidermolysis bullosa junctionalis and epidermolysis bullosa dystrophicans. III. Subepidermal bullous dermatoses due to metabolic disorders: Porphyria cutanea tarda (PCT). IV. Drug induced Lyell-Syndrome Due to space limitation it is not possible to discuss the histology of all these dermatoses. I will therefore choose the most important of them and display their histology in detail.
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PMID:[Histology of supepidermal bullous dermatoses]. 906 14

Toxic epidermal necrolysis (TEN), or Lyell's syndrome, is a fulminant bullous dermatitis. TEN is often a drug-induced reaction and virtually any drug class appears capable of provoking it. We report here a case of TEN after administration of ciprofloxacin. Systemic lupus erythematosus (SLE) was suspected as a possible etiologic or modifying cofactor in TEN in this case.
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PMID:Ciprofloxacin-induced toxic epidermal necrolysis in a patient with systemic lupus erythematosus. 1473 88

A great many cardiovascular drugs (CVDs) have the potential to induce adverse reactions in the mouth. The prevalence of such reactions is not known, however, since many are asymptomatic and therefore are believed to go unreported. As more drugs are marketed and the population includes an increasing number of elderly, the number of drug prescriptions is also expected to increase. Accordingly, it can be predicted that the occurrence of adverse drug reactions (ADRs), including the oral ones (ODRs), will continue to increase. ODRs affect the oral mucous membrane, saliva production, and taste. The pathogenesis of these reactions, especially the mucosal ones, is largely unknown and appears to involve complex interactions among the drug in question, other medications, the patient's underlying disease, genetics, and life-style factors. Along this line, there is a growing interest in the association between pharmacogenetic polymorphism and ADRs. Research focusing on polymorphism of the cytochrome P450 system (CYPs) has become increasingly important and has highlighted the intra- and inter-individual responses to drug exposure. This system has recently been suggested to be an underlying candidate regarding the pathogenesis of ADRs in the oral mucous membrane. This review focuses on those CVDs reported to induce ODRs. In addition, it will provide data on specific drugs or drug classes, and outline and discuss recent research on possible mechanisms linking ADRs to drug metabolism patterns. Abbreviations used will be as follows: ACEI, ACE inhibitor; ADR, adverse drug reaction; ANA, antinuclear antigen; ARB, angiotensin II receptor blocker; BAB, beta-adrenergic blocker; CCB, calcium-channel blocker; CDR, cutaneous drug reaction; CVD, cardiovascular drug; CYP, cytochrome P450 enzyme; EM, erythema multiforme; FDE, fixed drug eruption; I, inhibitor of CYP isoform activity; HMG-CoA, hydroxymethyl-glutaryl coenzyme A; NAT, N-acetyltransferase; ODR, oral drug reaction; RDM, reactive drug metabolite; S, substrate for CYP isoform; SJS, Stevens-Johnson syndrome; SLE, systemic lupus erythematosus; and TEN, toxic epidermal necrolysis.
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PMID:ORAL ADVERSE DRUG REACTIONS TO CARDIOVASCULAR DRUGS. 1476 98

Autoimmune polyglandular syndrome Type I (APS I) is a disorder defined by the presence of at least two of the following diseases: Addison's disease, hypoparathyroidism, and chronic mucocutaneous candidiasis. We present the case of a 45-yr-old woman, affected by APS I, in chronic treatment with betamethasone. She was referred to a Division of General Medicine for jaundice, ascites and peripheral edema attributed to worsening of pre-existing autoimmune chronic hepatitis. During hospitalization, the following drugs were given: Amoxicillin/Clavulanic acid and Levofloxacin for bronchopneumonia, Furosemide and Canreonate for renal impairment, Pantoprazole for gastric protection, and Itraconazole for oral candidiasis. After about a month, she developed widespread, sheet-like, epidermal detachment, with painful lesions of the conjunctiva, lips and mouth. Toxic epidermal necrolysis (TEN) was diagnosed, and the patient was transferred to a Burn Center, where she died 10 days after the first onset of cutaneous rash. Autoptic and histopathological findings (epidermal necrosis and detachment, lymphomonocytic infiltration of the dermis) confirmed the clinical diagnosis. TEN is a usually drug-induced cutaneous inflammatory disorder characterized by extensive epidermal detachment and frequent mucosal involvement. It has also been associated with immuno-mediated disorders (HIV infection, graft-vs-host disease, systemic lupus erythematosus, mixed essential cryoglobulinemia), in keeping with immuno-mediated pathogenesis. We present, to our knowledge, the first report of TEN in a patient with APS I, and suggest that some pathogenetic mechanisms of APS I are shared with TEN. We stress how such a disease can occur in an autoimmune syndrome, even during corticosteroid treatment.
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PMID:Fatal toxic epidermal necrolysis in autoimmune polyglandular syndrome type I. 1527 83

Toxic epidermal necrolysis (TEN) is an acute, rapidly evolving mucocutaneous reaction with a high mortality rate characterized by extensive painful cutaneous and mucosal exfoliation and systemic involvement that is frequently associated with medication use. The treatment of this condition is controversial. Systemic lupus erythematosus (SLE) is a generalized autoimmune disease of unknown etiology characterized by the production of autoantibodies to self antigens. Several case reports in the literature have demonstrated an association between SLE and TEN, and it has been postulated that lupus-associated TEN may exist. In this review, we will explore the association of SLE and TEN, and its diagnosis and treatment.
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PMID:Toxic epidermal necrolysis in systemic lupus erythematosus. 1643 52

Toxic epidermal necrolysis (TEN) is a severe, life-threatening disease appearing after certain drugs, characterized by keratinocyte necrosis, which shows with painful cutaneous and mucosal exfoliation and systemic involvement. TEN mortality rate is between 30% to 70%, so patients need early administration of medical care. We report a case of a 40-year old woman with TEN-like symptoms, who received treatment with sulphasalazine for 3 weeks because of arthritis. Various diagnostic procedures were performed which caused many doubts about diagnosis. In differential diagnosis we thought about: firstly TEN after treatment with sulphasalazine--patient with systemic lupus erythematosus, secondly toxic epidermal necrolisis like lupus erythematosus, finally TEN and LE after treatment with sulpasalazine--patient with rheumatoid arthritis. Final diagnosis needs more investigation and further diagnostic procedures. The patient stays under our control.
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PMID:[Toxic epidermal necrolysis during therapy with sulphasalazine in a patient with arthritis. Case report]. 2253 53

The nosology of bullous lesions or equivalents (vesicles, erosions, and crusts) in patients with lupus erythematosus (LE) is rarely addressed.The primary aim of this study was to draw up a precise phenotypic inventory of such skin lesions; the secondary objective was to assess a potential relationship between the different types of loss of epidermis and extracutaneous lupus manifestations.We conducted a retrospective multicenter study including 22 patients with definite LE and bullous lesions or equivalents. All biopsies were reviewed. Patients were recruited in the dermatology departments of 6 centers. Patients were included if they met the diagnosis of systemic LE according to American College of Rheumatology and/or Systemic Lupus International Collaborating Clinics criteria or diagnosis of cutaneous LE based on classic clinical criteria and/or histological ascertainment of LE. Patients were recruited through clinician's memory and photographic collections.Three clinico-pathological patterns could be individualized. First, toxic epidermal necrolysis (TEN)-like, sheet-like, skin detachment; sun-exposure, mild mucosal involvement, and dermal mucin deposition allow differential diagnosis with classical Lyell syndrome. Second, vesiculo-bullae and/or crusting occurring on typical lesions of subacute cutaneous lupus erythematosus or chronic cutaneous lupus erythematosus. Third, tense vesicles and/or blisters with an underlying neutrophilic dermatosis and a usual response to dapsone.A careful analysis of 22 LE patients with epidermal detachment reveals 2 main pathomechanisms: a classic LE interface dermatitis, which can be hyperacute and lead to TEN-like skin detachment; and a neutrophilic dermatosis, with tense vesicles and/or blisters, including classic bullous LE.
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PMID:Blisters and Loss of Epidermis in Patients With Lupus Erythematosus: A Clinicopathological Study of 22 Patients. 2657 26

This case report describes a patient with arthritis of the large joints, bilateral sacroiliitis, and positive anti-SSA and anti-dsDNA antibody, who received sulfasalazine and shortly thereafter became critically ill. He developed toxic epidermal necrolysis, hemolytic anemia, lymphopenia, markedly elevated ferritin, and muscle wasting. A diagnosis of systemic lupus erythematosus was made, and mycophenolate mofetil and systemic glucocorticoids brought this severe disease under control. Toxic epidermal necrolysis-like lesions and hemophagocytic syndrome have been reported as manifestations of systemic lupus erythematosus. This patient possibly had spondyloarthritis or an undifferentiated connective tissue disease at presentation, and we suggest, based on the timing of events, that sulfasalazine may have acted as a trigger of the severe disease manifestations.
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PMID:Toxic Epidermal Necrolysis-Like Lesions and Systemic Lupus Erythematosus Possibly Triggered by Sulfasalazine. 2747 75

Based on their immunomodulatory properties, high-dose intravenous immunoglobulins (IVIGs) are successfully used in the treatment of various dermatological autoimmune diseases, in particular pemphigus vulgaris and dermatomyositis. In autoimmune bullous diseases, IVIGs can be used in an adjuvant setting (second- or third-line therapy) once combined immunosuppressive regimens have failed. In dermatomyositis, IVIGs may already be employed as an adjuvant second-line therapy after failure of corticosteroid monotherapy. In scleromyxedema, IVIGs may be considered as first-line treatment, given the lack of effective and safe alternatives. Other potential indications for IVIGs may include severe recalcitrant cases of systemic vasculitis and systemic lupus erythematosus. Toxic epidermal necrolysis may be an indication for high-dose IVIGs if administered early. Common, readily manageable side effects include nausea, headache, fatigue, and febrile infusion reactions. Severe adverse events such as thromboembolic events, anaphylaxis, and acute renal failure are very uncommon. The risk of viral transmission is very low. Potential mechanisms of action include upregulation of inhibitory Fc receptors, reduction of the half-life of endogenous immunoglobulins due to displacement from protective receptor sites, neutralization of autoantibodies by anti-idiotypic antibodies, as well as inhibition of complement activation.
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PMID:High-dose intravenous immunoglobulins for the treatment of dermatological autoimmune diseases. 2922 99


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