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

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.

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.

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.

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.