Case Report: Liangxue Jiedu Huayu Formula as adjunctive therapy for leptospirosis with Weil's syndrome.

BACKGROUND: Leptospirosis is a global zoonotic disease with over one million cases annually worldwide. Approximately 5%-10% of patients progress to Weil's syndrome, characterized by multi-organ failure and high mortality, but treatment options remain limited. This report describes a patient with severe leptospirosis who showed marked improvement following treatment with Liangxue Jiedu Huayu Formula (LXJDHYF), a traditional Chinese medicine formula, and explores potential mechanisms. CASE PRESENTATION: A 54-year-old male farmer developed high fever, jaundice, acute kidney injury, and early disseminated intravascular coagulation after working in a lotus pond. Leptospirosis was confirmed by a four-fold rise in MAT titer from 1:50 to 1:200. Despite initial treatment with conventional therapies including antibiotics, continuous renal replacement therapy, and plasma infusion, the patient remained febrile with persistently elevated white blood cell and bilirubin levels. From day 5 of hospitalization, LXJDHYF was added. Fever gradually subsided, total bilirubin progressively decreased, serum creatinine eventually normalized, and coagulation function returned to normal. At 6-month follow-up, the patient had fully recovered. MECHANISTIC EXPLORATION: Network pharmacology identified 14 common targets, including ICAM1, SELE, TLR4, and SERPINE1. KEGG enrichment revealed pathways related to TLR4/NF-κB signaling, cytokine-cytokine receptor interaction, and complement/coagulation cascades. Molecular docking showed strong binding affinities (≤ -7.0 kcal/mol) between core components (cryptotanshinone, nortanshinone, rhein, naringenin) and core targets (TLR4, ICAM1, ALB). These computational findings are hypothesis-generating and require experimental validation. CONCLUSION: This case suggests that adjuvant treatment with LXJDHYF may be beneficial for leptospirosis complicated by Weil's syndrome, based on conventional therapy. Network pharmacology has generated testable hypotheses regarding multi-target modulation of inflammatory, adhesion, and coagulation pathways. These computational findings require experimental validation.