Eczematous Drug Eruptions: Identification and Management of Pharmacological Culprits in Primary Care

Introduction

Eczematous drug eruptions (EDEs) can mimic common skin conditions like eczema or psoriasis, complicating diagnosis and treatment. These eruptions often present as papular or vesicular lesions, sometimes pruritic, with scaling and crusting. EDEs can manifest anywhere from days to years after initiating medications commonly prescribed in the primary care setting such as calcium channel blockers, ACE inhibitors, ARBs, thiazides, and statins. Misdiagnosis can lead to prolonged patient discomfort and unnecessary treatments. This review emphasizes the importance of accurate differentiation between EDEs and other dermatoses for improved patient outcomes.

Objective

This review aims to aid clinicians in the differentiation of EDEs from clinically similar conditions, such as eczema and psoriasis. It focuses on identifying commonly prescribed medications in primary care settings that trigger EDEs, discusses diagnostic strategies, and explores effective treatment options for managing these eruptions.

Methods

A comprehensive literature review was conducted using databases such as PubMed, Google Scholar, and the Cochrane Library, covering the period from January 1980 to January 2023. The search included terms like “eczematous,” “drug eruption,” “medication,” “drug induced,” “skin reactions,” “adverse cutaneous,” and “side effects.” Studies selected for review included literary reviews, systematic reviews, case reports, and case series focusing on the pharmacological agents responsible for EDEs. Articles were selected based on their focus on primary care medications and their connection to EDEs.

Results

The review identified a broad spectrum of medications implicated in EDEs, including calcium channel blockers, ACE inhibitors, ARBs, thiazides, and statins. Among these, calcium channel blockers were the most frequently associated with chronic, diffuse, and pruritic scaly papules and plaques. Other common offenders include ACE inhibitors and ARBs, which primarily trigger eczema-like rashes in elderly patients. Thiazide diuretics were associated with photosensitivity reactions leading to eczematous eruptions. Statins were found to compromise the skin barrier, contributing to the development of eczematous reactions, particularly in older individuals. The histopathological findings across cases frequently showed spongiosis, eosinophilic infiltrates, and acanthosis, complicating the differentiation from eczema without a thorough medication history.

Conclusions

Early recognition and differentiation of EDEs from common dermatoses, such as eczema or psoriasis, are essential for effective treatment. The review underscores the importance of maintaining a high index of suspicion for drug-induced eruptions in patients on common cardiovascular medications. Prompt discontinuation of the offending drug, combined with alternative treatments, can significantly improve patient outcomes. Dermatologists and primary care providers should collaborate to optimize treatment, particularly when polypharmacy is a factor. Further research is needed to improve the understanding of the mechanisms behind EDEs and to refine diagnostic strategies, thus minimizing patient morbidity.