Multidisciplinary management of refractory Kawasaki disease with bilateral giant coronary artery aneurysms and latent tuberculosis infection: a case report focusing on immune-coagulation-infection crosstalk.

A 3.5-year-old boy with refractory Kawasaki disease developed rapid-onset bilateral giant coronary artery aneurysms complicated by latent tuberculosis infection, creating a 'triple challenge' requiring concurrent management of inflammation, cardiovascular risk, and infection.

• The patient was 3.5 years old and male
• Pre-biologic screening identified latent tuberculosis infection (LTBI) prior to initiating biologic therapy
• LTBI strictly contraindicated guideline-recommended TNF-α inhibitors
• The case involved bilateral giant coronary artery aneurysms (CAAs) with rapid onset

TNF-α inhibitors, which are guideline-recommended for refractory Kawasaki disease, were contraindicated due to the confirmed LTBI, necessitating an alternative immunomodulation strategy.

• LTBI was identified through pre-biologic screening
• TNF-α blockade was circumvented to ensure LTBI safety
• Alternative immunomodulation consisted of methylprednisolone and a second IVIG dose
• LTBI prophylaxis with isoniazid/rifampicin was initiated only upon vasculitis remission and hepatic recovery

Rifampicin-induced acceleration of warfarin metabolism created significant anticoagulation management challenges, requiring a 2.5-fold warfarin dose escalation to achieve therapeutic INR.

• Rifampicin caused accelerated warfarin metabolism, termed 'rifampicin-induced warfarin resistance'
• A rapid, percentage-based titration strategy was executed alongside a 'prolonged low-molecular-weight heparin (LMWH) bridge'
• An exact 2.5-fold warfarin dose escalation was required
• A stable, conservative therapeutic INR range of 1.5–2.5 was achieved

At 9-month follow-up, the bilateral giant coronary artery aneurysms demonstrated luminal normalization.

• Follow-up duration was 9 months
• CAAs showed 'luminal normalization' at 9-month follow-up
• The authors noted this necessitates lifelong surveillance for 'vascular pseudonormalization'
• Luminal normalization does not necessarily indicate complete vascular recovery, as pseudonormalization remains a concern

The multidisciplinary team employed a sequential, pathophysiology-driven protocol with three integrated components to manage the immune-coagulation-infection crosstalk.

• The protocol was described as 'sequential' and 'pathophysiology-driven'
• Component 1 involved immunomodulation and LTBI prophylaxis using methylprednisolone and second-dose IVIG
• Component 2 involved precision anticoagulation using a prolonged LMWH bridge and percentage-based warfarin titration
• The MDT approach was described as providing 'a practical clinical paradigm for managing intricate immune-coagulation-infection crosstalk'

The authors identified immune-coagulation crosstalk as a key driver of extreme cardiovascular risk in giant coronary artery aneurysms in Kawasaki disease.

• Giant CAAs were described as driven by 'immune-coagulation crosstalk'
• The case is framed as illustrating the intersection of inflammatory, cardiovascular, and infectious risks
• The concurrent presence of LTBI, refractory KD, and giant CAAs was characterized as a 'formidable triple challenge'
• Managing this crosstalk was identified as 'an urgent and unmet clinical need'