What are steroids and how are they classified in medicine?

What Are Steroids and How Are They Classified in Medicine?

Steroids are lipophilic molecules derived from cholesterol that function as hormones regulating cellular, tissue, and organ functions throughout the body, with medical classifications based on their chemical structure, potency, and clinical application. 1

Basic Definition and Structure

Steroids are complex molecules synthesized from cholesterol in specialized endocrine cells located in the adrenal gland, ovary, and testis. 1 These compounds move freely across cell membranes to activate intracellular nuclear receptors that function as ligand-dependent transcriptional regulators, modifying expression of hundreds to thousands of specific target genes. 1

Major Medical Classifications

1. Endogenous Steroid Hormones

Natural steroid hormones produced by the body include:

• Glucocorticoids (cortisol): Essential stress hormones secreted with ACTH in response to corticotropin-releasing hormone from the hypothalamus, maintaining vascular tone, endothelial integrity, and metabolic functions. 2
• Mineralocorticoids (aldosterone): Regulate electrolyte and water balance. 1
• Sex steroids (estradiol, testosterone): Control reproductive functions and secondary sexual characteristics. 1

2. Synthetic Corticosteroids by Potency

The American Academy of Dermatology classifies topical corticosteroids into 7 classes based on vasoconstrictor potency:

• Class 1 (Ultra-high/Superpotent): Clobetasol propionate 0.05%, halobetasol propionate 0.05% with 58-92% efficacy, limited to 2-4 weeks continuous use. 3, 4
• Class 2 (High potency): Amcinonide 0.1%, betamethasone dipropionate 0.05%, fluocinonide 0.05% with 68-74% efficacy. 3
• Classes 3-4 (Medium potency): 68-72% efficacy for moderate inflammatory conditions. 3
• Classes 5-7 (Low potency): Hydrocortisone 1-2.5% with 41-83% efficacy, safest for face, genitals, and intertriginous areas. 3, 4

3. Systemic Corticosteroids by Route

• Oral corticosteroids: Prednisone doses >20 mg/day for >3 months associated with HBV reactivation (OR 4.9), while <10 mg/day considered low immunosuppressive risk. 5
• Intravenous corticosteroids: Used for acute rejection episodes and severe inflammatory conditions. 5
• Intramuscular corticosteroids: Methotrexate 15-25 mg IM weekly effective for chronic inflammatory bowel disease. 5
• Inhaled corticosteroids: Lower systemic absorption with 3.2% HBV reactivation rate versus 11.1% with oral steroids. 5
• Intranasal corticosteroids: Mometasone furoate, fluticasone propionate with minimal systemic effects, requiring 8-12 weeks for optimal benefit. 6

4. Anabolic-Androgenic Steroids (AAS)

Synthetic derivatives of testosterone designed to enhance muscle growth and athletic performance, producing 5-20% strength gains and 2-5 kg bodyweight increases but associated with cardiovascular risks, liver effects, and psychological disturbances. 7 Designer steroids are manufactured to evade detection with unknown safety profiles. 8

Clinical Application Algorithm

For anatomical site selection:

• Face, genitals, intertriginous areas → Classes 5-7 only due to increased absorption and atrophy risk. 4
• Trunk and extremities → Classes 2-5 for moderate-severe disease. 4
• Thick chronic plaques → Class 1 for maximum 2-4 weeks. 4

For duration considerations:

• Class 1: Never exceed 2-4 weeks continuous use or 50 grams weekly. 4
• Classes 2-5: Up to 4 weeks for plaque psoriasis. 3
• Intranasal steroids: Minimum 8-12 weeks for full therapeutic effect. 6

Critical Safety Considerations

Common pitfalls to avoid:

• Clobetasol (Class 1) caused skin atrophy in 100% of users after only 8 weeks of facial application. 4
• Continuous oral corticosteroids >3 months significantly increase infection reactivation risk. 5
• Premature discontinuation of intranasal steroids before 8-12 weeks prevents adequate assessment of benefit. 6
• Systemic steroids should be avoided in diabetic patients when possible due to glucose dysregulation. 6

Mechanism of Action

Corticosteroids exert effects through multiple pathways: converting to dihydrotestosterone via 5-alpha-reductase, aromatization to estrogens, competitive antagonism of glucocorticoid receptors, and direct anti-inflammatory effects by reducing leukocyte migration and neutrophil-mediated tissue injury. 7, 2