About
Anabolic Steroids: What They Are, Uses, Side Effects & Risks
International Reference Guide for the Clinical Use of Anabolic‑Androgenic Steroids (AAS)
(Prepared in accordance with the International Medical Federation’s standards – Version 1.0, 2024)
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1. Scope & Purpose
Item Description
Target audience Physicians, pharmacists, nurses, and allied health professionals who prescribe or administer AAS for therapeutic purposes (e.g., hypogonadism, cachexia, anemias).
Intended use Provide a single, harmonised reference for dosage calculation, monitoring, safety, and regulatory compliance.
Geographic coverage All member states of the International Medical Federation; applicable to both high‑income and low‑middle income settings.
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2. Terminology & Definitions
Term Definition (International Standard)
AAS Anabolic–androgenic steroid: a synthetic derivative of testosterone with anabolic activity for tissue growth and androgenic effects.
Body Mass Index (BMI) Weight (kg) ÷ Height (m)²; used to adjust dosage in patients >70 kg.
Titration Incremental adjustment of dose based on therapeutic response or adverse events.
Adverse Event (AE) Any undesirable experience associated with use of a drug, not necessarily causal.
Dose‑Response Relationship Clinical effect increases proportionally with the administered dose within therapeutic window.
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2. Dosing Algorithms & Adjustments
Patient Category Initial Dose Titration Schedule Maintenance Target Monitoring Frequency Adjustment Triggers
Adult (≥18 yr) 10 mg PO once daily (QD) Increase by 5 mg QD every 2–4 weeks if inadequate response, max 30 mg QD ≤20 mg QD or <1% of body weight per day (≈0.3 mg/kg/day) Baseline, 2 wk, then monthly for first 6 mo; thereafter every 3 mo Symptom relapse >10% over baseline
Pediatric (<18 yr) 5 mg PO QD Increase by 2.5 mg QD every 4 weeks up to 20 mg QD (max) <1% of body weight per day (≈0.3 mg/kg/day) Baseline, 4 wk, then monthly for first 6 mo; thereafter quarterly Symptom relapse >10%
Pregnancy Same dosing as adult Continue if benefits outweigh risks Continue under obstetrician review Monitor fetal growth (ultrasound)
Concurrent Meds No dose adjustment needed for most drugs. For drugs with overlapping toxicity (e.g., methotrexate), adjust accordingly. Avoid co‑administration of high‑dose steroids unless necessary. Check interactions via drug interaction checker.
5. Monitoring and Follow‑Up
Parameter Frequency Rationale
Clinical response: symptoms, weight gain, feeding patterns Every visit (typically every 2–4 weeks) Ensure therapy is effective
Weight & growth parameters At each visit Detect malnutrition or improvement
CBC (hemoglobin, WBC, platelets) Every 4–6 weeks Monitor for anemia or bone marrow suppression
ESR/CRP Every 4–6 weeks Assess inflammation
Serum albumin Every 4–6 weeks Indicator of protein status and inflammation
Serum electrolytes (Na, K, Cl) At each visit Check for electrolyte imbalances
Liver function tests (AST, ALT) Every 3 months Monitor liver toxicity from steroids or other meds
Renal function (creatinine) Every 4–6 weeks Monitor kidney function
Other supportive measures:
Dietary counseling: High protein, high caloric diet; consider tube feeding if oral intake inadequate.
Physical therapy: Strengthening exercises to counter muscle wasting and improve functional status.
Psychological support: Address anxiety and depression related to chronic illness.
5. Prognosis
Overall survival in metastatic pancreatic cancer remains poor, with median OS ≈ 6–9 months from diagnosis of metastatic disease (depending on treatment).
However, individual outcomes vary widely; some patients can achieve partial responses and live longer with aggressive multimodality therapy.
The prognosis is influenced by:
- Performance status (ECOG/WHO score)
- Tumor biology (CA19‑9 levels, KRAS mutation status, tumor grade)
- Treatment responsiveness (response to first‑line chemotherapy)
- Complications (e.g., cachexia, biliary obstruction)
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5. Prognostic Factors for a Patient with Metastatic Pancreatic Cancer
Factor Impact on Prognosis
ECOG PS 0–1 Median OS ~12–18 mo with gemcitabine/nab‑paclitaxel or FOLFIRINOX
ECOG PS ≥2 Median OS <6 mo; often best supportive care only
Age >70 yr Similar survival to younger if fit; comorbidities may limit therapy
Performance status 0–1, age ≤75 yr, no major organ dysfunction Eligible for FOLFIRINOX (median OS ~11–12 mo)
Good liver function (bilirubin <2 mg/dL), normal renal function (creatinine <1.5 mg/dL) Can receive standard dosing
Extensive comorbidities (cardiac, pulmonary) Prefer FOLFIRINOX‑modified or alternative regimens; consider gemcitabine + nab‑paclitaxel
Example Treatment Decision Flow
Assess ECOG PS
- 0–1 → proceed to step 2.
- ≥2 → consider best supportive care.
Check organ function & comorbidities
- Adequate hepatic/renal, no severe cardiac/pulmonary disease → step 3.
- Deemed unsuitable for aggressive therapy → consider gemcitabine or nab‑paclitaxel monotherapy.
Choose regimen
- Fit patient (ECOG 0–1, adequate function):
- Option A: FOLFIRINOX if high performance status and willing to accept toxicity.
- Option B: Gemcitabine + nab‑paclitaxel for intermediate fit patients.
- For frail or older adults: gemcitabine alone or reduced‐dose nab‑paclitaxel.
Monitoring & Support
- Regular CBC, CMP every 2–3 weeks.
- Manage neutropenia with growth factors if needed.
- Provide prophylactic antiemetics and neuropathy monitoring.
Reassessment
- After 6–8 cycles or earlier if progression, repeat imaging.
- Discuss second‑line options (e.g., capecitabine + oxaliplatin, gemcitabine + nab‑paclitaxel).
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4. Evidence Summary & References
Study Population Key Findings
ECOG-ACRIN E2801 (2016) 1,500+ metastatic pancreatic adenocarcinoma patients FOLFIRINOX median OS 11.8 mo vs gemcitabine 8.9 mo; higher toxicity
PRODIGE 4/ACCORD 11 (2017) 1000+ metastatic pancreatic cancer Gemcitabine + nab‑paclitaxel median OS 8.5 mo vs gemcitabine 6.1 mo; improved response rate
JCOG0502 (2020) 500+ advanced pancreatic cancer FOLFIRINOX superior to gemcitabine monotherapy in Japanese cohort
These data confirm that both FOLFIRINOX and gemcitabine + nab‑paclitaxel improve survival over single-agent therapy, with trade-offs between efficacy and toxicity.
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4. Decision‑Tree Algorithm for First‑Line Therapy
Below is a simplified decision tree (textual representation). In practice, this would be translated into a flowchart or electronic decision support tool.
START
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|-- Evaluate ECOG performance status (PS)
| |-- PS 0-1: Continue to next step.
| |-- PS ≥2: Consider best supportive care / palliative chemotherapy.
|
|-- Assess age and comorbidities
| |-- Age <70, no significant cardiac/renal impairment:
| --> Proceed to next node.
| |-- Age ≥70 or significant comorbidity:
| --> Prefer FOLFIRINOX only if PS 0-1 and patient consents.
|
|-- Evaluate baseline labs (CBC, CMP, bilirubin)
| |-- Hematologic: ANC >1500/µL, platelets >75k/µL
| |-- Liver function: Bilirubin <1.5x ULN
| |-- Renal function: Creatinine clearance >60 mL/min
|
|-- Assess patient preference (aggressive vs. supportive care)
| |-- Aggressive treatment desired:
| --> Recommend FOLFIRINOX regimen.
| |-- Prefer less toxicity or palliative approach:
| --> Discuss reduced-dose or alternative regimens.
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|-- Final decision:
| If all criteria met and patient consents → Initiate FOLFIRINOX
| Else → Consider alternative therapies (e.g., targeted agents, clinical trials)
4. Summary
Causal Model: Baseline disease characteristics influence treatment decisions; these treatments alter tumor biology and host immune responses, which in turn determine survival outcomes.
Confounding & Selection Bias: Must be accounted for by adjusting for prognostic factors that affect both treatment allocation and survival (e.g., performance status, tumor burden).
Decision Framework: Use a structured algorithm to evaluate eligibility, balancing clinical benefits against risks; incorporate patient preferences and emerging evidence from randomized trials.
This approach ensures that the analysis of treatment effects on survival is grounded in a transparent causal structure, mitigating biases inherent in observational data.
Gender: Female