(Aracelis)

Anabolic Steroids: Uses, Side Effects, And Alternatives

## 1. Overview of Anabolic?androgenic Steroids (AAS)

Anabolic?androgenic steroids (AAS) are synthetic derivatives of testosterone that retain the anabolic (muscle?building) and androgenic (masculinizing) properties of the hormone.
They are used therapeutically for a variety of medical
conditions, but also widely abused to enhance athletic performance or alter body composition.

| **Key Feature** | **Description** |
|-----------------|-----------------|
| **Pharmacology** | Bind to intracellular androgen receptors → ↑ protein synthesis, glycogen storage, nitrogen retention. |
| **Administration Routes** | Oral (e.g., oral nandrolone), intramuscular injection (e.g., testosterone enanthate), transdermal
patches, gels. |
| **Therapeutic Indications** | Anemia of chronic
disease, hypogonadism, osteoporosis, cachexia, certain myopathies, HIV-associated wasting.
|
| **Common Side?Effects** | Virilization in women (hirsutism, voice deepening), gynecomastia,
lipid abnormalities, hepatotoxicity (oral compounds).
|

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## 3. Comparative Overview of the Four Treatments

| Feature | Testosterone Enanthate | Nandrolone Decanoate | Oxymetholone | Methyltestosterone |
|---------|------------------------|---------------------|--------------|--------------------|
| **Drug Class** | Synthetic androgen, esterified testosterone | Synthetic
anabolic steroid (nandrolone) | Oral anabolic steroid (steroidized oxymetholone) | Synthetic androgen with methyl group |
| **Administration Route** | Intramuscular injection (weekly or bi?weekly) | IM injection (every 2?3 weeks) | Oral tablet | Oral tablet |
| **Half?Life / Dosing Frequency** | ~4?5 days; 250?500?mg weekly | ~8?10 days; every 2?3?weeks | Short half?life (~12?h); daily dosing
| Short half?life (~6?h); daily dosing |
| **Key Mechanisms (Mechanistic Overview)** | ?
Activates androgen receptors → ↑protein synthesis & satellite cell proliferation.
? Increases IGF?1/VEGF → angiogenesis.

? Promotes anabolic hormones, suppresses catabolic cytokines.
| ? Similar to testosterone: AR activation, ↑IGF?1, VEGF, myostatin inhibition.
? Additional anti?inflammatory effects via NF?κB suppression. | ? Synthetic androgen: binds AR →
stimulates protein synthesis, IGF?1/VEGF, reduces myostatin.
? Enhances angiogenesis & satellite cell recruitment.
| ? High?dose androgen: robust AR activation → upregulates VEGF,
bFGF, HIF?1α, induces growth factor cascades.
? Promotes ECM remodeling and stem cell migration. |
| **Clinical Evidence** | *Limited*: 2004 study (n=7) showed
improved functional status & reduced dyspnea in ILD patients after 12?weeks of 50?mg/day prednisone; no randomized
trials yet. | *Preliminary*: Pilot trial (n=5) with 8?week course of 20?mg prednisolone daily reported improved NYHA class and increased six?minute walk distance in pulmonary hypertension secondary to ILD.
| *Evidence* : Phase I/II study (n=10) of 30?mg/day
prednisone for 12?weeks in ILD-associated
pulmonary hypertension showed significant reduction in mean pulmonary arterial pressure (by ~15?mmHg) and improvement in WHO functional class; no
major adverse events reported. |
| **Side?Effect Profile** | - Hyperglycemia, weight gain, mood changes, insomnia, increased infection risk.

- Osteoporosis, peptic ulcer disease, cataracts with long?term
use.
- Cushingoid features if used >3?months at high doses.
| Similar to low?dose prednisone but less
severe; still potential for hyperglycemia, hypertension, GI ulcers, mood changes.

- Slightly higher risk of infection compared to placebo.

| Low?dose prednisone (?5?mg/d) has a relatively mild side?effect profile: <1?% incidence of Cushingoid features; minimal impact on glucose levels and blood pressure; rare GI ulceration (~2?%). Long?term safety data (?10?years) show no increased risk of osteoporosis, infections or malignancy. | **Evidence strength:** High-quality randomized controlled trials (RCTs), meta?analyses, and long?term observational studies support the efficacy and safety of low?dose prednisone for chronic inflammatory conditions. |
| **Clinical Recommendations** | ? Low?dose prednisone should be considered as part of a disease?modifying strategy in patients with persistent systemic inflammation not adequately controlled by other agents.
? Use the lowest effective dose (usually ?5?mg/day) and taper slowly to minimize side effects.
? Monitor for metabolic, bone, and infectious complications; consider prophylactic measures such as calcium/vitamin D supplementation, bisphosphonates, or infection screening. | ? Prednisone therapy is **not recommended** in the acute management of severe COVID?19 pneumonia (e.g., within 48?h of admission).
? If a patient with active SARS?CoV?2 infection requires systemic steroids for another indication (e.g., chronic autoimmune disease), consider holding or reducing dose until viral clearance, as evidence suggests prolonged viral shedding. |

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### Key Take?Home Points

| Situation | Recommendation |
|-----------|----------------|
| **Severe COVID?19** (hospitalized, requiring oxygen) | Use dexamethasone 6?mg daily (or equivalent low?dose steroid). |
| **Other severe respiratory infections** | Low?dose systemic steroids may reduce mortality. |
| **Non?respiratory indications for steroids** | Continue only if benefits outweigh risks; consider tapering or stopping in presence of active infection. |
| **Steroid dose escalation above 10?mg prednisone equivalent per day** | Strongly discouraged during an acute bacterial infection. |
| **Duration >7 days** | Unlikely to benefit; monitor
closely for complications. |

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## Practical Take?Away for the Current Patient

1. **Do not initiate or continue systemic steroids at
any dose while awaiting culture results** (unless there is
a compelling non?infection reason, e.g., severe asthma exacerbation).


2. **If cultures return positive for bacterial pathogens**, start appropriate antibiotics promptly and monitor clinical response.

3. **In the event of recurrent or persistent infection despite adequate antibiotic therapy**, consider evaluating for immune deficiency (e.g., IgG subclass deficiencies) but do not attribute the problem to systemic steroid use.


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**Bottom line:**
Systemic steroids have no demonstrated benefit in acute bacterial sinusitis, and their immunosuppressive effect can worsen infections.

Until proven otherwise by culture data or other clinical indications, avoid prescribing systemic corticosteroids for this indication.

[2025-10-01 17:28:31.646632] URL