Severe Adverse Reaction to Carbamazepine: Significance of Humoral and Cellular Reactions to the Drug

Horneff, Gerd; Lenard, H. G.; Wahn, V.

doi:10.1055/s-2008-1071357

Cited by 31 publications

(15 citation statements)

References 3 publications

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“…Additionally, in spite of elevated levels of CYP2E1-specific IgG4 autoantibodies, significantly elevated levels of immune complexes were not demonstrated. Low levels of complement components have been previously reported in persons with drug-induced liver injury (13,15,38,50). Finding elevated levels of IgG4 autoantibodies in AH or any other form of IDDIH to our knowledge has not previously been demonstrated.…”

Section: Discussionmentioning

confidence: 69%

Role of CYP2E1 Immunoglobulin G4 Subclass Antibodies and Complement in Pathogenesis of Idiosyncratic Drug-Induced Hepatitis

Njoku

Mellerson

Talor

et al. 2006

Clin Vaccine Immunol

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Idiosyncratic drug-induced hepatitis (IDDIH) is the third most common cause for acute liver failure in the United States. Previous studies have attempted to identify susceptible patients or early stages of disease with various degrees of success. To determine if total serum immunoglobulin subclasses, CYP2E1-specific subclass autoantibodies, complement components, or immune complexes could distinguish persons with IDDIH from others exposed to drugs, we studied persons exposed to halogenated volatile anesthetics, which have been associated with IDDIH and CYP2E1 autoantibodies. We found that patients with anesthetic-induced IDDIH had significantly elevated levels of CYP2E1-specific immunoglobulin G4 (IgG4) autoantibodies, while anesthetic-exposed healthy persons had significantly elevated levels of CYP2E1-specific IgG1 autoantibodies. Anesthetic IDDIH patients had significantly lower levels of C4a, C3a, and C5a compared to anesthetic-exposed healthy persons. C1q-and C3d-containing immune complexes were significantly elevated in anesthetic-exposed persons. In conclusion, our data suggest that anesthetic-exposed persons develop CYP2E1-specific IgG1 autoantibodies which may form detectable circulating immune complexes subsequently cleared by classical pathway activation of the complement system. Persons susceptible to anesthetic-induced IDDIH develop CYP2E1-specific IgG4 autoantibodies which form small, nonprecipitating immune complexes that escape clearance because of their size or by direct inhibition of complement activation.

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Section: Discussionmentioning

confidence: 69%

Role of CYP2E1 Immunoglobulin G4 Subclass Antibodies and Complement in Pathogenesis of Idiosyncratic Drug-Induced Hepatitis

Njoku

Mellerson

Talor

et al. 2006

Clin Vaccine Immunol

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“…Interestingly, it is known that the treatment with anticonvulsants sometimes induces hypogammaglobulinaemia in patients with epilepsy [18,19,20]. Recently, Kano et al [21] have demonstrated that hypogammaglobulinaemia is an important laboratory abnormality in DIHS.…”

Section: Discussionmentioning

confidence: 99%

Drug-Induced Hypersensitivity Syndrome Associated with Transient Hypogammaglobulinaemia and Increase in Serum IgE Level

Nakashima¹,

Yamane²,

Ihn³

et al. 2005

Dermatology

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Drug-induced hypersensitivity syndrome (DIHS) is a rare but severe disease with multiorgan failure. Recently, the association of the human herpesvirus (HHV) family, particularly of HHV-6, with DIHS has been reported. We report a 43-year-old female diagnosed as having DIHS based on the clinical course and laboratory examinations. The HHV-6 reactivation was demonstrated by significantly increased levels of the specific antibody in her paired sera and by polymerase chain reaction of HHV-6 DNA. Notably, transient hypogammaglobulinaemia was detected in the early stage of the disease, which was associated with the disease activity. By contrast, the serum IgE level and eosinophils were increased 2 or 3 weeks later. In addition, serum levels of interferon γ, interleukin (IL)-4 and soluble IL-2 receptor, which were increased in the early phase of the disease, decreased gradually after the corticosteroid therapy.

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“…Nevertheless, leukopenia or lymphopenia have also been reported [20] and this occasionally precedes leukocytosis. A leukemoid reaction may occur in some patients.…”

Section: Laboratory Findingsmentioning

confidence: 95%

Drug-Induced Hypersensitivity Syndrome and Viral Reactivation

Shiohara¹,

Takahashi²,

Kano³

2007

Drug Hypersensitivity

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Drug-induced hypersensitivity syndrome (DIHS), often referred to as drug reaction with eosinophilia and systemic symptoms (DRESS), is a life-threatening multi-organ system reaction characterized by rash, fever, lymphadenopathy, hepatitis, and leukocytosis with eosinophilia. DIHS has a worldwide distribution but is undoubtedly underdiagnosed in many countries probably due to a lack of awareness. This syndrome has several unique features that cannot be solely explained by drug etiology: they include delayed onset, a paradoxical worsening of clinical symptoms after withdrawal of the causative drugs and unexplained crossreactivity to multiple drugs with different structures. These unique features suggest the additional role of viral infections. Indeed, we demonstrated that not only human herpesvirus 6 (HHV-6) but also other herpesviruses (EpsteinBarr virus, cytomegalovirus and HHV-7) can be reactivated in a sequential manner during the course of DIHS, as demonstrated in graft-versus-host disease. In this review, we will discuss recent work including our own, focusing on the interactions among what we considered the main players of inflammatory responses in DIHS: cross-reactive memory T cells and various herpesviruses.In 1938, Merritt and Putnam [1] reviewed the toxic symptoms caused by therapy with phenytoin and noted that the symptoms could be divided into two cutaneous reactions: the first one being a mild, morbilliform eruption that healed when phenytoin was withdrawn and often did not re-

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Severe Adverse Reaction to Carbamazepine: Significance of Humoral and Cellular Reactions to the Drug

Cited by 31 publications

References 3 publications

Role of CYP2E1 Immunoglobulin G4 Subclass Antibodies and Complement in Pathogenesis of Idiosyncratic Drug-Induced Hepatitis

Role of CYP2E1 Immunoglobulin G4 Subclass Antibodies and Complement in Pathogenesis of Idiosyncratic Drug-Induced Hepatitis

Drug-Induced Hypersensitivity Syndrome Associated with Transient Hypogammaglobulinaemia and Increase in Serum IgE Level

Drug-Induced Hypersensitivity Syndrome and Viral Reactivation

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