How do oral and transdermal menopausal hormone therapies compare in terms of fracture risk and breast cancer risk?

Current evidence suggests that oral and transdermal menopausal hormone therapies (MHT) show no significant differences in their effects on fracture risk reduction or breast cancer risk. Both administration routes appear to provide comparable skeletal protection and similar levels of breast cancer risk elevation when used under equivalent hormonal conditions. This indicates that the choice between oral and transdermal MHT should primarily consider other factors like patient preference, side effect profiles, and metabolic impacts rather than these specific risks.

Key Points Explained:

1. Fracture Risk Reduction

   • Both oral and transdermal MHT demonstrate similar efficacy in reducing fracture risk among postmenopausal women.
   • The mechanisms involve estrogen's role in maintaining bone mineral density by inhibiting osteoclast activity.
   • Since fracture protection is systemic, the route of administration (oral vs. skin absorption) does not significantly alter outcomes.

2. Breast Cancer Risk

   • Current data shows no major difference in breast cancer risk between oral and transdermal estrogen when combined with the same type of progestogen.
   • Risk elevation is more influenced by:
     • Duration of therapy (longer use correlates with higher risk).
     • Progestogen type (synthetic progestins may pose greater risk than micronized progesterone).
   • Transdermal estrogen avoids first-pass liver metabolism, but this does not translate to a clinically meaningful difference in breast cancer incidence compared to oral forms.

3. Clinical Considerations Beyond These Risks

   • Metabolic Differences: Oral estrogen affects liver metabolism (increasing clotting factors and SHBG), while transdermal has minimal hepatic impact.
   • Patient-Specific Factors: Transdermal routes may be preferred for those with gastrointestinal issues or a history of thrombosis.
   • Progestogen Choice: This often matters more than estrogen route for breast cancer risk.

4. Research Limitations

   • Most studies compare MHT to placebo, not oral vs. transdermal head-to-head.
   • Long-term data on transdermal estrogen (especially with progesterone) is less robust than for oral formulations.

In summary, while oral and transdermal MHT differ in pharmacokinetics, their net effects on fracture protection and breast cancer risk are comparable. Decisions should prioritize individual health profiles and practical administration preferences.

Summary Table:

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