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Corresponding author: dengxin, dx8848@126.com

DOI: 10.12201/bmr.202610.00009

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  Abstract: Collateral disease theory emphasizes the pathological evolution of chronic disease involving the collaterals, obstruction of the collaterals by phlegm and blood stasis, and the eventual formation of accumulation due to persistent collateral obstruction. These concepts are consistent, at the level of pathological evolution, with the progression of liver fibrosis from functional dysregulation to microcirculatory disturbance and structural remodeling. Based on collateral disease theory and current understanding of the pathological mechanisms of liver fibrosis, this article explores the dynamic interactions among phlegm, blood stasis, and collateral dysfunction during disease progression. It proposes that “binding of phlegm and blood stasis followed by collateral obstruction and accumulation formation” represents a key pathological process in the evolution of liver fibrosis. Accordingly, a stage-oriented therapeutic approach is proposed, including eliminating pathogenic factors while regulating the liver and strengthening the spleen, simultaneously resolving phlegm and activating blood circulation, removing blood stasis and unblocking the collaterals, and softening accumulation while supporting healthy qi and nourishing the collaterals. This article provides a collateral disease–based perspective for understanding the dynamic pathogenesis of liver fibrosis and may offer a theoretical basis for syndrome differentiation, stage-oriented treatment, and clinical intervention in traditional Chinese medicine.

  Key words: : Liver fibrosis; Collateral disease theory; Phlegm and blood stasis binding; Collateral obstruction and accumulation formation; Stage-oriented treatment

  Submit time: 8 October 2026

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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• ID	Submit time	Number	Download
  2	2026-09-22	10.12201/bmr.202610.00009V2	Download
  1	2026-09-22	10.12201/bmr.202610.00009V1	Download

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