Corticosteroids are medications that mimic natural adrenal hormones like cortisol, distinct from anabolic steroids used for muscle building. A “steroid responder” is an individual who exhibits a noticeable, sometimes heightened, physiological reaction to corticosteroids, including both desired therapeutic effects and unintended side effects.
How Corticosteroids Work
Corticosteroids primarily reduce inflammation and suppress the immune system. They achieve this by binding to specific receptors inside cells, influencing gene expression. This process leads to decreased production of pro-inflammatory substances and increased production of anti-inflammatory mediators.
These medications can be fast-acting, making them useful for sudden, severe symptoms like allergic reactions. Genomic actions, which take hours to days, are mediated through glucocorticoid receptors that stimulate gene expression, ultimately reducing inflammation. Individual genetic or physiological differences can influence how effectively these processes occur, explaining why some people may exhibit a stronger or different response.
Recognizing a Steroid Responder
Steroid responders are identified through careful observation of their reactions to corticosteroid treatment, often by monitoring for exaggerated side effects. A common sign is a significant rise in intraocular pressure (IOP) in the eye, which can lead to steroid-induced glaucoma. This increase is defined as an IOP above 21-24 mmHg, or an increase of more than 5-10 mmHg from baseline.
Eye pressure elevation appears three to six weeks after starting topical steroid eye drops, though it can occur sooner. Other signs include pronounced skin thinning (dermal atrophy) from topical corticosteroid creams, resulting from inhibited collagen production and keratinocyte proliferation. Identification relies on these clinical observations, as no single diagnostic test exists.
Managing Treatment as a Steroid Responder
Steroid responders require close medical supervision and regular monitoring to manage potential adverse effects. If increased intraocular pressure is observed, the first step is often to discontinue the steroid if medically feasible. IOP returns to normal within about two weeks after stopping eye drops, though injections may take longer.
If steroid treatment must continue, strategies include reducing the dosage or switching to a less potent steroid, such as fluorometholone 0.1% or rimexolone 1%. Medications used for primary open-angle glaucoma, such as beta-blockers, prostaglandin analogs, alpha-2 agonists, and carbonic anhydrase inhibitors, can also be prescribed to help lower intraocular pressure. Laser trabeculoplasty may be considered if medications are insufficient or cause undesirable side effects.
For skin thinning, discontinuing the topical steroid is the primary management strategy. Epidermal thinning may be reversible, but deeper dermal damage, like stretch marks, can be permanent. Patient-provider communication is important to tailor treatment plans, ensuring benefits outweigh risks for sensitive individuals.