Drug Eruptions in Dermatology

Abstract and Introduction

Abstract

Adverse drug reactions are common and can range from benign and self-limiting to life-threatening with a high morbidity and mortality. Prompt identification and accurate diagnosis of an adverse drug reaction is therefore essential in order to optimally manage the patient, averting possible significant complications. Many adverse reactions to drugs involve the skin, and therefore essential knowledge of such reactions by both dermatologists and nondermatologists is of paramount importance. In this article a comprehensive review is given on a wide range of cutaneous adverse drug reactions encompassing both benign and more serious reactions, in addition to some less common adverse reactions. The article provides a tabular summary of some of the main features of such reactions, in addition to a separate table with a list of the common culprit drugs identified for each cutaneous adverse reaction.

Introduction

Cutaneous adverse drug reactions (ADRs) are the most common and most reported form of adverse reactions to drugs, representing approximately 30% of all reported cases.^[1] Its incidence in hospitalized patients has been estimated to be approximately 2%.^[2] In the USA alone, it is estimated that ADRs (both cutaneous and noncutaneous) affect nearly 2 million patients each year, leading to nearly 100,000 deaths.^[3] Several factors predispose to ADRs and include: advanced age, polypharmacy, female gender, concomitant infection (particularly HIV) and genetic predisposition.^[4] ADRs are often wrongly termed allergic; both immune-mediated and non-immune-mediated mechanisms are involved, and many are poorly understood. All four classical Gell and Coombs types of hypersensitivity reactions play a role in drug eruptions; in some cases it is the reactive drug metabolites acting as a hapten rather than the parent drug that acts as an antigen for T-cell activation.^[5] Drug-specific CD4 and CD8 positive T cells recognize drugs through their T-cell receptors in an MHC-dependent way.

The classical – and still widely accepted – pharmacological classification of ADRs was described by Rawlins and Thompson who divided ADRs into two types; type A reactions are dose dependent and predictable on the basis of the drug's known pharmacological action, and type B reactions are idiosyncratic and not necessarily dose dependent.^[6]

Intrinsic factors, such as genetic variation in drug metabolism or HLA associations, can increase the risk of ADRs.^[5] More detailed examples of the pharmacogenetics of ADRs will be discussed in this article.

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