In the medical world, drug eruption is an adverse drug reaction to the skin. Most of the drug-induced skin reactions are mild and disappear when the offending drug is withdrawn. This is called a "simple" drug eruption. However, more serious drug eruptions may be associated with organ injuries such as liver or kidney damage and are categorized as "complex". Drugs can also cause hair and nail changes, affect mucous membranes, or cause itching without external skin changes.
The use of synthetic drugs and biopharmaceuticals in medicine has revolutionized human health, allowing us to live longer. As a result, the average adult human is exposed to a large number of drugs during a longer treatment period throughout life. This unprecedented increase in pharmaceutical use has led to an increase in the number of drug reactions observed.
There are two broad categories of adverse drug reactions. Type A reaction is a side effect of a highly predictable drug called, pharmatoxicologic. While Type B or a hypersensitivity reaction, often immune-mediated and reproducible with repeated exposure to the normal dose of the given drug. Unlike type A reactions, the mechanism of type B drug reactions or hypersensitivity is not fully explained. However, there is a complex interaction between the genetics of patient inheritance, pharmacokloricology of the drug and the immune response that eventually leads to manifestations of drug eruption.
Because the manifestations of drug eruption are complex and highly individualized, there are many sub areas in medicine that study this phenomenon. For example, the pharmacogenomic field aims to prevent severe heavy drug reactions by analyzing a person's innate genetic risk. Thus, there are clinical examples of derived genetic alleles that are known to predict drug hypersensitivity and for available diagnostic testing.
Video Drug eruption
Classification
Some of the most serious and life-threatening examples of drug eruption are erythema multiforme, Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), hypersensitivity vasculitis, drug induced hypersensitivity syndrome (DIHS), erythroderma and generalized whole eczematic pustulosis (AGEP). These severe skin lesions are categorized as hypersensitivity and immune-mediated reactions. There are four types of hypersensitivity reactions and many drugs can induce one or more hypersensitivity reactions.
With appearance
The most common types of eruption are morbilliform or erythematous rash (about 90% of cases). Less commonly, appearance may also be urticarial, papulosquamous, pustular, purpuric, bullous (with abrasions) or lichenoid. Angioedema can also be drug induced (mainly, by angiotensin converting enzyme inhibitor).
With the
mechanismThe underlying mechanism may be immunological (as in drug allergy) or non-immunologic (eg, in photodermatitis or as anticoagulant side effects). A fixed drug eruption is a term for drug eruption that occurs in the same skin area every time the person is exposed to the drug. Eruptions can often occur with certain drugs (eg, by phenytoin), or very rarely (eg, Sweet syndrome after colony-stimulating factor).
With drugs
The culprit can be a prescription or over-the-counter medication.
Examples of common drugs that cause drug eruption are antibiotics and other antimicrobial drugs, sulfa drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), biopharmaceuticals, chemotherapy agents, anticonvulsants, and psychotropic drugs. Common examples include photodermatitis due to local NSAIDs (such as piroxicam) or due to antibiotics (such as minocycline), drug eruptions remain due to acetaminophen or NSAID (Ibuprofen), and rash after ampicillin in case of mononucleosis.
Certain drugs are less likely to cause drug eruptions (estimated rate <= 3 per 1000 exposed patients). These include: digoxin, aluminum hydroxide, multivitamins, acetaminophen, bisacodyl, aspirin, thiamine, prednisone, atropine, codeine, hydrochlorothiazide, morphine, insulin, warfarin, and spironolactone.
Maps Drug eruption
Diagnostic and Filtering Tests
Drug eruptions are diagnosed mainly from medical history and clinical examination. However, they can replicate other conditions, thus delaying the diagnosis (eg, drug-induced lupus erythematosus, or erlotinib-induced rashes). Skin biopsy, blood tests, or immunological tests can also be beneficial.
Drug reactions have a unique time. The amount of typical time required for the appearance of a rash after exposure to the drug may help categorize the type of reaction. For example, exhaustive acute exanthematous pustulosis usually occurs within 4 days of starting anesthetic. Drug Reactions with Eosinophilia and Systemic Symptoms usually occur between 15 and 40 days after exposure. Toxic epidermal necrolysis and Stevens-Johnson syndrome usually occur 7-21 days after exposure. Anaphylaxis occurs within minutes. A simple eksanthematous eruption occurs between 4 and 14 days after exposure.
TEN and SJS are severe skin reactions involving skin and mucous membranes. To accurately diagnose this condition, detailed drug history is essential. Often, some medications can be the cause and allergy tests can help. Sulfa drugs are notorious for inducing TEN or SJS in certain people. For example, HIV patients have an increased incidence of SJS or TEN compared with the general population and have been found to express low levels of drug metabolic enzymes responsible for detoxifying sulfa drugs. Genetics plays an important role in predisposing a particular population to TEN and SJS. Thus, there are some FDA-recommended genetic screening tests available for certain drugs and ethnic populations to prevent drug eruptions. The most famous example is carbamezepine (anti-convulsant used to treat seizures) hypersensitivity associated with the presence of HLA-B * 5801 genetic alleles in Asian populations.
DIHS is a delayed onset of the drug, often occurring several weeks to 3 months after initiation of the drug. Interestingly, the worsening of systemic symptoms occurs 3-4 days after discontinuation of the offending drug. There is a genetic risk allele that predicts the development of DIHS for certain drugs and ethnic populations. Most importantly, abacavir (anti-viral used in the treatment of HIV) hypersensitivity is associated with the presence of HLA-B * 5701 alleles in European and African populations in the United States and Australia.
AGEP is often caused by antimicrobial, anti-fungal or antimalarial drugs. Diagnosis is often done with a patch test. This test should be done within a month after the resolution of the rash test results and patches interpreted at different time points: 48 hours, 72 hours and even later at 96 hours and 120 hours to increase the sensitivity.
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External links
Source of the article : Wikipedia
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