The Experts below are selected from a list of 252 Experts worldwide ranked by ideXlab platform
Giampiero Girolomoni - One of the best experts on this subject based on the ideXlab platform.
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drug induced Lupus Erythematosus with emphasis on skin manifestations and the role of anti tnfα agents
Journal Der Deutschen Dermatologischen Gesellschaft, 2012Co-Authors: Camilla Dalle Vedove, Jan C Simon, Giampiero GirolomoniAbstract:Drug-Induced Lupus Erythematosus (DILE) is a Lupus-like syndrome temporally related to continuous drug exposure which resolves upon drug discontinuation. There are currently no standard diagnostic criteria for DILE. Findings include skin manifestations, arthritis, serositis, anti-nuclear and anti-histone antibodies positivity. Similarly to idiopathic Lupus Erythematosus, DILE can be divided into systemic (SLE), subacute cutaneous (SCLE) and chronic cutaneous Lupus (CCLE). Systemic DILE presents as a milder version of idiopathic SLE, and the drugs most frequently implicated are hydralazine, procainamide and quinidine. Anti-TNFα therapies are the latest class of medications found to be associated, although rarely, with a “Lupus-like” syndrome, which is however clinically distinct from classical DILE. Drug-Induced SCLE is the most common form of DILE. It is very similar to idiopathic SCLE in terms of clinical and serologic characteristics. The most commonly implicated drugs are antihypertensive drugs and terbinafine, but in recent years also proton pump inhibitors and chemotherapeutic agents have been associated. Drug-Induced CCLE is very rare and usually caused by fluorouracil agents and NSAIDS, but some cases have induced by pantoprazole and anti-TNFα agents.
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Drug-Induced Lupus Erythematosus
Archives of Dermatological Research, 2009Co-Authors: Camilla Dalle Vedove, Micol Giglio, Donatella Schena, Giampiero GirolomoniAbstract:Drug-Induced Lupus Erythematosus (DILE) is defined as a Lupus-like syndrome temporally related to continuous drug exposure which resolves after discontinuation of the offending drug. There are currently no standard diagnostic criteria for DILE and the pathomechanisms are still unclear. Similarly to idiopathic Lupus, DILE can be diveded into systemic (SLE), subacute cutaneous (SCLE) and chronic cutaneous Lupus (CCLE). Systemic DILE is characterized by typical Lupus-like symptoms including skin signs, usually mild systemic involvement and a typical laboratory profile with positive antinuclear and anti-histone antibodies, while anti-double strand (ds) DNA and anti-extractable nuclear antigens antibodies are rare. High risk drugs include hydralazine, procainamide and isoniazid. Drug-Induced SCLE is very similar to idiopathic SCLE in terms of clinical and serologic characteristic, and it is more common than the systemic form of DILE. Drugs associated with SCLE include calcium channel blockers, angiotensin-converting enzyme inhibitors, interferons, thiazide diuretics and terbinafine. Drug-Induced CCLE is very rarely reported in the literature and usually refers to fluorouracile agents or non steroidal anti-inflammatory drugs. Recently, cases of DILE have been reported with anti-TNFα agents. These cases present with disparate clinical features including arthritis/arthralgia, skin rash, serositis, cytopenia and variable laboratory abnormalities. DILE to anti-TNFα agents differs in several ways to classic DILE. The incidence of rashes is higher compared to classical systemic DILE. In most cases of classic DILE visceral involvement is rare, whereas several cases of anti-TNFα DILE with evidence of renal disease have been reported. Low serum complement levels as well as anti-extractable nuclear antigen antibodies and anti-dsDNA antibodies are rarely present in classic DILE, whereas they are reported in half the cases of anti-TNFα DILE; in contrast, anti-histone antibodies are described in classic DILE more often than in anti-TNFα DILE. Recognition of DILE in patients receiving anti-TNFα therapy can be difficult due to the symptoms of their underlying disease. A temporal association (months to years) of the offending drug with characteristic or suggestive symptoms, and resolution of symptoms on drug withdrawal is the best evidence for this diagnosis of DILE.
Camilla Dalle Vedove - One of the best experts on this subject based on the ideXlab platform.
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drug induced Lupus Erythematosus with emphasis on skin manifestations and the role of anti tnfα agents
Journal Der Deutschen Dermatologischen Gesellschaft, 2012Co-Authors: Camilla Dalle Vedove, Jan C Simon, Giampiero GirolomoniAbstract:Drug-Induced Lupus Erythematosus (DILE) is a Lupus-like syndrome temporally related to continuous drug exposure which resolves upon drug discontinuation. There are currently no standard diagnostic criteria for DILE. Findings include skin manifestations, arthritis, serositis, anti-nuclear and anti-histone antibodies positivity. Similarly to idiopathic Lupus Erythematosus, DILE can be divided into systemic (SLE), subacute cutaneous (SCLE) and chronic cutaneous Lupus (CCLE). Systemic DILE presents as a milder version of idiopathic SLE, and the drugs most frequently implicated are hydralazine, procainamide and quinidine. Anti-TNFα therapies are the latest class of medications found to be associated, although rarely, with a “Lupus-like” syndrome, which is however clinically distinct from classical DILE. Drug-Induced SCLE is the most common form of DILE. It is very similar to idiopathic SCLE in terms of clinical and serologic characteristics. The most commonly implicated drugs are antihypertensive drugs and terbinafine, but in recent years also proton pump inhibitors and chemotherapeutic agents have been associated. Drug-Induced CCLE is very rare and usually caused by fluorouracil agents and NSAIDS, but some cases have induced by pantoprazole and anti-TNFα agents.
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Drug-Induced Lupus Erythematosus
Archives of Dermatological Research, 2009Co-Authors: Camilla Dalle Vedove, Micol Giglio, Donatella Schena, Giampiero GirolomoniAbstract:Drug-Induced Lupus Erythematosus (DILE) is defined as a Lupus-like syndrome temporally related to continuous drug exposure which resolves after discontinuation of the offending drug. There are currently no standard diagnostic criteria for DILE and the pathomechanisms are still unclear. Similarly to idiopathic Lupus, DILE can be diveded into systemic (SLE), subacute cutaneous (SCLE) and chronic cutaneous Lupus (CCLE). Systemic DILE is characterized by typical Lupus-like symptoms including skin signs, usually mild systemic involvement and a typical laboratory profile with positive antinuclear and anti-histone antibodies, while anti-double strand (ds) DNA and anti-extractable nuclear antigens antibodies are rare. High risk drugs include hydralazine, procainamide and isoniazid. Drug-Induced SCLE is very similar to idiopathic SCLE in terms of clinical and serologic characteristic, and it is more common than the systemic form of DILE. Drugs associated with SCLE include calcium channel blockers, angiotensin-converting enzyme inhibitors, interferons, thiazide diuretics and terbinafine. Drug-Induced CCLE is very rarely reported in the literature and usually refers to fluorouracile agents or non steroidal anti-inflammatory drugs. Recently, cases of DILE have been reported with anti-TNFα agents. These cases present with disparate clinical features including arthritis/arthralgia, skin rash, serositis, cytopenia and variable laboratory abnormalities. DILE to anti-TNFα agents differs in several ways to classic DILE. The incidence of rashes is higher compared to classical systemic DILE. In most cases of classic DILE visceral involvement is rare, whereas several cases of anti-TNFα DILE with evidence of renal disease have been reported. Low serum complement levels as well as anti-extractable nuclear antigen antibodies and anti-dsDNA antibodies are rarely present in classic DILE, whereas they are reported in half the cases of anti-TNFα DILE; in contrast, anti-histone antibodies are described in classic DILE more often than in anti-TNFα DILE. Recognition of DILE in patients receiving anti-TNFα therapy can be difficult due to the symptoms of their underlying disease. A temporal association (months to years) of the offending drug with characteristic or suggestive symptoms, and resolution of symptoms on drug withdrawal is the best evidence for this diagnosis of DILE.
M Deschauer - One of the best experts on this subject based on the ideXlab platform.
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efalizumab induced isolated cerebral Lupus like syndrome
Neurology, 2009Co-Authors: M Wendt, Johannes Wohlrab, S Zierz, M DeschauerAbstract:Drug-Induced Lupus Erythematosus has been recognized as a side effect of more than 80 drugs since its first description in association with sulfadiazine in 1945.1 Novel bioengineered agents for treatment of autoimmune disorders can also induce Lupus-like syndromes. This is especially described for tumor necrosis factor alpha (TNFα) antagonists.2,3 Efalizumab is an immunosuppressive recombinant humanized IgG1 kappa isotype monoclonal antibody that binds to human CD11a. It is indicated for the treatment of adult patients with chronic moderate to severe plaque type psoriasis.4 Although efalizumab was been used for treatment of refractory subacute cutaneous Lupus Erythematosus,5 this drug can also induce the cutaneous form of this disease.6 However, a cerebral Lupus-like syndrome has not been reported in association with efalizumab. We report a 56-year-old man who was admitted to the hospital because of psychosyndrome and movement disorder. His wife reported a change of his character 2 weeks before. A few days previously he developed uncontrolled movements of all limbs, so that he could not walk alone. There was a history of a severe recalcitrant plaque type psoriasis, which was futilely treated …
M. Eric Gershwin - One of the best experts on this subject based on the ideXlab platform.
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Drug-Induced Lupus Erythematosus
Drug Safety, 2011Co-Authors: Christopher Chang, M. Eric GershwinAbstract:The generation of autoantibodies and autoimmune diseases such as systemic Lupus Erythematosus has been associated with the use of certain drugs in humans. Early reports suggested that procainamide and hydralazine were associated with the highest risk of developing Lupus, quinidine with a moderate risk and all other drugs were considered low or very low risk. More recently, Drug-Induced Lupus has been associated with the use of the newer biological modulators such as tumour necrosis factor (TNF)-α inhibitors and interferons. The clinical features and laboratory findings of TNFα inhibitor-induced Lupus are different from that of traditional Drug-Induced Lupus or idiopathic Lupus, and standardized criteria for the diagnosis of Drug-Induced Lupus have not been established. The mechanism(s) responsible for the development of Drug-Induced Lupus may vary depending on the drug or even on the patient. Besides Lupus, other autoimmune diseases have been associated with drugs or toxins. Diagnosis of Drug-Induced Lupus requires identification of a temporal relationship between drug administration and symptom development, and in traditional Drug-Induced Lupus there must be no pre-existing Lupus. Resolution of symptoms generally occurs after cessation of the drug. In this review, we will discuss those drugs that are more commonly associated with Drug-Induced Lupus, with an emphasis on the new biologicals and the difficulty of making the diagnosis of Drug-Induced Lupus against a backdrop of the autoimmune diseases that these drugs are used to treat. Stimulation of the immune system by these drugs to cause autoimmunity may in fact be associated with an increased effectiveness in treating the pathology for which they are prescribed, leading to the dilemma of deciding which is worse, the original disease or the adverse effect of the drug. Optimistically, one must hope that ongoing research in drug development and in pharmacogenetics will help to treat patients with the maximum effectiveness while minimizing side effects. Vigilance and early diagnosis are critical. The purpose of this review is to summarize the most recent developments in our understanding of the incidence, pathogenesis, diagnosis and treatment of Drug-Induced Lupus.
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Drug-Induced Lupus Erythematosus: incidence, management and prevention.
Drug Safety, 2011Co-Authors: Christopher Chang, M. Eric GershwinAbstract:The generation of autoantibodies and autoimmune diseases such as systemic Lupus Erythematosus has been associated with the use of certain drugs in humans. Early reports suggested that procainamide and hydralazine were associated with the highest risk of developing Lupus, quinidine with a moderate risk and all other drugs were considered low or very low risk. More recently, Drug-Induced Lupus has been associated with the use of the newer biological modulators such as tumour necrosis factor (TNF)-α inhibitors and interferons. The clinical features and laboratory findings of TNFα inhibitor-induced Lupus are different from that of traditional Drug-Induced Lupus or idiopathic Lupus, and standardized criteria for the diagnosis of Drug-Induced Lupus have not been established. The mechanism(s) responsible for the development of Drug-Induced Lupus may vary depending on the drug or even on the patient. Besides Lupus, other autoimmune diseases have been associated with drugs or toxins. Diagnosis of Drug-Induced Lupus requires identification of a temporal relationship between drug administration and symptom development, and in traditional Drug-Induced Lupus there must be no pre-existing Lupus. Resolution of symptoms generally occurs after cessation of the drug.
M Wendt - One of the best experts on this subject based on the ideXlab platform.
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efalizumab induced isolated cerebral Lupus like syndrome
Neurology, 2009Co-Authors: M Wendt, Johannes Wohlrab, S Zierz, M DeschauerAbstract:Drug-Induced Lupus Erythematosus has been recognized as a side effect of more than 80 drugs since its first description in association with sulfadiazine in 1945.1 Novel bioengineered agents for treatment of autoimmune disorders can also induce Lupus-like syndromes. This is especially described for tumor necrosis factor alpha (TNFα) antagonists.2,3 Efalizumab is an immunosuppressive recombinant humanized IgG1 kappa isotype monoclonal antibody that binds to human CD11a. It is indicated for the treatment of adult patients with chronic moderate to severe plaque type psoriasis.4 Although efalizumab was been used for treatment of refractory subacute cutaneous Lupus Erythematosus,5 this drug can also induce the cutaneous form of this disease.6 However, a cerebral Lupus-like syndrome has not been reported in association with efalizumab. We report a 56-year-old man who was admitted to the hospital because of psychosyndrome and movement disorder. His wife reported a change of his character 2 weeks before. A few days previously he developed uncontrolled movements of all limbs, so that he could not walk alone. There was a history of a severe recalcitrant plaque type psoriasis, which was futilely treated …
