Metabolism of Hydralazine: Relevance to Drug-Induced Lupus

Hofstra, Angela H.

doi:10.3109/03602539408998315

Cited by 20 publications

(11 citation statements)

References 76 publications

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“…Three main points are mentioned: genetic factors [31] , drugs or compounds whose metabolites affect various components of the immune system [32][33][34] and interactions of the implicated drugs or their metabolites with nuclear antigens [18,35,36] .…”

Section: Discussionmentioning

confidence: 99%

Acebutolol-Induced Subacute Cutaneous Lupus Erythematosus

Fenniche

Dhaoui

Ammar

et al. 2005

Skin Pharmacol Physiol

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Beta-blocking medications are rarely associated with drug-induced lupus erythematosus syndrome and have never been incriminated as a cause of subacute lupus erythematosus (SCLE). We present herein the first case of SCLE induced by acebutolol. A 57-year-old woman presented with a 1-month history of a cutaneous eruption of the photoexposed areas. One month ago, the patient had started a treatment with oral acebutolol to cure a hypertension of 1-year evolution. Physical examination revealed erythematous scaly annular plaques, involving the face, arms and trunk. Immunologic serology findings revealed a positive titer of antinuclear antibodies up to 1/1,280 with positivity of antihistone and Ro/SSA antibodies. Acebutolol was stopped, and the lesions cleared completely 4 months later. Literature data, along with our case, suggest a link between acebutolol therapy and the onset of a lupus syndrome. Although this is the first report of acebutolol-induced SCLE, we should be aware of this occurrence, and avoidance of acebutolol is recommended in patients with stigmata of lupus erythematosus

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Section: Discussionmentioning

confidence: 99%

Acebutolol-Induced Subacute Cutaneous Lupus Erythematosus

Fenniche

Dhaoui

Ammar

et al. 2005

Skin Pharmacol Physiol

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“…The polymorphic enzyme NAT2 metabolizes both hydralazine and procainamide, and the slow acetylator phenotype appears to be a significant risk factor for drug-induced lupus. The drug-or metabolite-protein complex is recognized as 'foreign' by the immune system (Hofstra, 1994).…”

Section: Anti-arrhythmics Class I (Sodium-channel Blockers)mentioning

confidence: 99%

Oral Adverse Drug Reactions to Cardiovascular Drugs

Torpet

Kragelund

Reibel

et al. 2004

Critical Reviews in Oral Biology & Medicine

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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:

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“…Entretanto, há diversos casos descritos com doses menores dos medicamentos e tempo de exposição variável (18) . O tratamento baseia-se essencialmente no reconhecimento da condição clínica induzida pelo medicamento e imediata suspensão da droga.…”

Section: Características Epidemiológicas E Clínicas Do Lidunclassified

Lúpus induzido por drogas: da imunologia básica à aplicada

Mota

Haddad

Lima

et al. 2007

Rev. Bras. Reumatol.

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RESUMOO lúpus induzido por drogas (LID) é descrito como o desenvolvimento de sintomas semelhantes ao do lúpus eritematoso sistêmico idiopático, temporalmente relacionado à exposição a drogas, havendo, comumente, a resolução do quadro com a suspensão do medicamento desencadeante. A associação mais clássica é feita com a procainamida e a hidralazina. Recentemente, com a introdução de novas drogas na prática clínica, tem sido relatado um aumento no número de medicamentos implicados como causadores da doença, e a lista atual inclui quase uma centena de drogas relacionadas à ocorrência de LID. Embora descrito há mais de 60 anos, o mecanismo imunológico básico do LID ainda não está totalmente compreendido. Há várias hipóteses para o processo de indução de auto-imunidade pelas drogas, e o fenômeno geralmente é interpretado como uma inapropriada ativação do sistema imunitário. Entre as diversas teorias propostas, as mais aceitas são: a inibição da metilação do ácido desoxirribonucléico (DNA) por algumas drogas, o que permitiria a ativação das células T; a oxidação de certas substâncias pelos monócitos, gerando metabólitos ativos que ocasionariam ativação das células apresentadoras de antígenos e/ou a interferência dos metabólitos de determinadas drogas com a tolerância do sistema imune. Novos estudos são necessários para a melhor compreensão da imunopatogenia do LID, objetivando desenvolver tratamentos específicos com base no melhor conhecimento dos mecanismos patogênicos.Palavras-chave: lúpus induzido por drogas, imunologia, lúpus eritematoso sistêmico, droga, auto-imunidade. ABSTRACTDrug-induced lupus (DIL) has been described as the development of idiopathic systemic lupus erythematous-like symptoms, temporarily associated to the exposition to drugs, and as a rule, the condition is improved with the suspension of the triggering medication. The most classical association is with procainamide and hydralazine. Recently, with the introduction of new drugs in the clinical practice, an increase on the number of medications associated with the occurence of the disease has been reported, and the current list includes almost one hundred drugs associated to the occurrence of DIL. The basic DIL immunologic mechanism, although described for more than 60 years, is not yet fully understood. There are several hypotheses for the druginduced autoimmunity process, and the phenomenon is generally interpreted as an inappropriate activation of the immune system. Among the several theories proposed, the most accepted ones are: the inhibition of the DNA methylation by some drugs, what would allow the activation of T-cells; the oxidation of some substances by monocytes, what would generate active metabolites that in turn would lead to the activation of antigen-presenting cells and/or the interference of the metabolites of some drugs with the immune system tolerance. Further studies should be conducted in order to elucidate the DIL immunopathogeny with the objective of developing specific treatments based on the better knowledge on the pathog...

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Metabolism of Hydralazine: Relevance to Drug-Induced Lupus

Cited by 20 publications

References 76 publications

Acebutolol-Induced Subacute Cutaneous Lupus Erythematosus

Acebutolol-Induced Subacute Cutaneous Lupus Erythematosus

Oral Adverse Drug Reactions to Cardiovascular Drugs

Lúpus induzido por drogas: da imunologia básica à aplicada

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