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Abstract
Difficult-to-treat depression (DTD) may involve a biologically distinct inflammatory endotype characterized by low-grade systemic inflammation (hs-CRP ≥3 mg/L).
- Treatment failure in DTD may result from a mismatch between neuroinflammation and conventional antidepressant therapies.
- A precision stratification workflow is proposed, starting with screening for inflammation using hs-CRP levels.
- Confirmation and characterization of inflammation can be achieved through a cytokine panel measuring IL-6, TNF-α, and IL-1β.
- Therapeutic options could include targeted anti-inflammatory agents, neuromodulation, psychotherapy, lifestyle changes, and digital monitoring.
- Patient-centered outcomes, such as functioning, quality of life, and cognition, should be prioritized alongside symptom reduction.
- Implementation of this approach may improve outcomes for patients with depression that does not respond to standard treatments.
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