Hyperresponsiveness

Hyperresponsiveness refers to the abnormal amplification of a tissue's or organ's response to a stimulus, producing an effect that exceeds the normal range. It can result from heightened receptor sensitivity, increased signal transduction, persistent inflammation, neural sensitization, or genetic factors that predispose toward stronger responses. The concept is used across disciplines but is most commonly discussed in respiratory and immunological contexts.

In the respiratory system, airway hyperresponsiveness is a central feature of asthma. The airways constrict more readily in response to triggers such as pharmacologic provocants (for example methacholine or histamine), cold air, exercise, or environmental irritants, leading to symptoms like coughing, wheeze, and shortness of breath. Similar exaggerated reactivity can occur in other tissues, including skin and the gastrointestinal tract, where stimuli that are benign in typical individuals provoke disproportionate responses.

Mechanisms behind hyperresponsiveness are multifactorial. They include increased mediator release by inflammatory cells, altered receptor expression, heightened sensitivity of nerve fibers, and structural changes in tissue, all of which may be driven by genetics, prior sensitization, and ongoing pathology.

Assessment depends on the affected organ. Airway hyperresponsiveness is assessed with provocation tests such as methacholine challenge, often alongside measures of baseline lung function and inflammation. In other tissues, provocative testing and biomarkers of inflammation or neural activity may be used.

Management focuses on reducing the amplified response and its triggers. In asthma-like airway hyperresponsiveness, this commonly involves anti-inflammatory medications (eg, inhaled corticosteroids), bronchodilators, trigger avoidance, and, in selected cases, targeted biologics or neuromodulatory approaches. Treatment is tailored to the underlying condition producing hyperresponsiveness.