A dermal hypersensitivity reaction (DHR) is an exaggerated immune response in the skin, resulting in visible inflammation and tissue damage. This happens when the immune system mistakenly identifies a typically harmless substance, known as an allergen or hapten, as a threat. Skin reactions, such as rashes or hives, are caused by this inappropriate response rather than a toxic effect. Understanding the immune processes and reaction timing helps identify the triggers.
The Role of the Immune System
A dermal hypersensitivity reaction is fundamentally different from a simple skin irritation. An irritant causes immediate damage to the skin’s outer layer, affecting nearly everyone exposed to a high enough concentration. In contrast, a hypersensitivity reaction, or sensitization, involves a specific immune response that only develops in certain individuals after repeated exposure.
This process involves two distinct stages: the sensitization phase and the elicitation phase. During the initial, asymptomatic sensitization phase, the skin is exposed to the allergen, and specialized immune cells recognize it as foreign. This first contact creates a specific immune memory, involving the development of T-cells or the production of antibodies. The elicitation phase is the subsequent exposure, which triggers the rapid activation of these memory cells and antibodies, resulting in the visible skin reaction.
Classification by Reaction Timing
Dermal hypersensitivity reactions are classified into four main types based on the immune mechanism involved and the time it takes for the symptoms to appear, known as the Gell and Coombs classification. Type I, or immediate hypersensitivity, is mediated by Immunoglobulin E (IgE) antibodies and appears within minutes of exposure. IgE antibodies bind to mast cells; re-exposure causes these cells to rapidly release inflammatory chemicals like histamine, leading to hives or swelling.
Type II reactions are cytotoxic, involving Immunoglobulin G (IgM) antibodies binding directly to antigens on cell surfaces, leading to cell destruction. While less common as a primary dermal reaction, this mechanism is relevant in certain drug-induced skin disorders. Type III reactions involve the formation of immune complexes—clusters of circulating antigens and IgG/IgM antibodies that deposit in tissues. These complexes activate the complement system, causing inflammation that can manifest as vasculitis, often appearing several hours after exposure.
Type IV hypersensitivity, or delayed-type hypersensitivity, is mediated by T-cells rather than antibodies and is the slowest to develop, appearing 48 to 72 hours after contact. T-cells recognize the allergen and release signaling molecules called cytokines, which recruit other immune cells to the site. This causes the characteristic inflammation seen in allergic contact dermatitis, a mechanism responsible for many common skin reactions caused by topical substances.
Common Causes of Contact Hypersensitivity
Many dermal hypersensitivity reactions are caused by direct contact with external substances, triggering the delayed Type IV pathway. These contact allergens are small molecules called haptens that penetrate the skin and bind to skin proteins. This reaction is localized to the area of contact, though it can sometimes spread.
The metal nickel, commonly found in jewelry and belt buckles, is one of the most frequent causes. Plant oils, such as the urushiol found in poison ivy and poison oak, are notorious for inducing a blistering, itchy allergic contact dermatitis. Chemicals used in everyday products are also common culprits, including formaldehyde, which acts as a preservative in cosmetics and other goods.
Ingredients in personal care products, such as fragrances and preservatives, can cause sensitization with repeated use. Materials like latex rubber, frequently used in gloves, can trigger a Type IV reaction, or sometimes an immediate Type I response. Identifying and avoiding these specific substances is the main way to manage this form of skin reaction.
Systemic Triggers: Medications and Diet
Hypersensitivity reactions can also be triggered by substances that enter the body systemically through ingestion or injection, often leading to more widespread skin symptoms. Medications are a significant cause of such reactions, which can manifest through any of the four hypersensitivity types. For instance, certain antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs) may cause widespread morbilliform rashes or hives.
Drug eruptions can range from mild, generalized rashes to severe, life-threatening conditions involving systemic symptoms like fever and organ inflammation. The timing of drug reactions is highly variable, sometimes occurring within minutes (Type I) or developing days to weeks after starting the medication (Type IV). A severe reaction with systemic involvement is referred to as Drug Hypersensitivity Syndrome (DHS).
Dietary factors, including food allergies, are another source of systemic triggers that cause cutaneous symptoms. Foods like peanuts, eggs, or shellfish can provoke rapid IgE-mediated Type I reactions, resulting in generalized urticaria (hives). Ingesting an allergen like nickel or Balsam of Peru can sometimes lead to systemic contact dermatitis, a delayed T-cell-mediated reaction causing a flare-up of existing dermatitis or new lesions.