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Drug-induced liver injury (DILI) is a serious, potentially life-threatening complication of anti-tuberculosis therapy, often leading to treatment interruption, hepatic failure, or death. Management is challenging, especially where liver transplantation is not readily available. The Direct Plasma Molecular Adsorption System (DPMAS) is an extracorporeal liver support therapy designed to remove bilirubin, bile acids, and inflammatory mediators using dual adsorptive cartridges (BS330 and HA330-II). By clearing toxic metabolites and modulating systemic inflammation, DPMAS can act as a bridge therapy in patients with reversible liver injury. This report describes the successful use of DPMAS in a patient with pancreaticobiliary tuberculosis who developed severe DILI after resuming anti-tuberculosis medications, highlighting its potential as a life-saving intervention.
A 66-year-old female with pancreaticobiliary tuberculosis presented with acute hepatic failure two weeks after restarting isoniazid and rifampicin, showing progressive jaundice, coagulopathy, and hepatic encephalopathy. Laboratory evaluation revealed severe liver dysfunction: total bilirubin 498 µmol/L, AST 85.9 U/L, ALT 39 U/L, INR 15.09, prothrombin activity 5%, and serum creatinine 209.6 µmol/L, corresponding to a MELD score of 36, indicating high short-term mortality. Imaging revealed a 5.9 × 7.8 × 6.2 cm peripancreatic mass encasing the hepatic vessels. Histopathology confirmed granulomatous inflammation with Langerhans-type giant cells, consistent with pancreatic tuberculosis.
The patient underwent three DPMAS sessions every other day via an internal jugular catheter using BS330 and HA330-II cartridges. Supportive care included intravenous N-acetylcysteine, vitamin K, and albumin infusion. Therapy was well-tolerated, with no adverse events.
After each DPMAS session, the patient’s clinical and biochemical status improved. Encephalopathy resolved, jaundice decreased, and renal function normalized, with serum creatinine dropping from 209.6 µmol/L to 68.1 µmol/L. Coagulopathy improved: INR decreased from 15.09 to 1.51 and prothrombin activity increased from 5% to 64%. Liver enzymes declined, with AST from 85.9 U/L to 37 U/L and ALT from 39 U/L to 15 U/L, while total bilirubin fell to 180 µmol/L. Platelet count rose from 85 ×10⁹/L to 118 ×10⁹/L, reflecting recovery of hepatic synthetic function. The MELD score improved from 36 to 17. The patient remained hemodynamically stable and was discharged fully alert, ambulatory, and clinically well.
Parameter
Baseline
Post-1st Session
Post-3rd Session
Total Bilirubin (µmol/L)
498
320
180
AST (U/L)
85.9
58
37
ALT (U/L)
39
25
15
INR
15.09
3.21
1.51
Prothrombin Activity (%)
5
30
64
Plasma Ammonia (µg/dL)
85
59
Serum Creatinine (µmol/L)
209.6
110
68.1
Platelet Count (×10⁹/L)
95
118
Table 1. Biochemical parameters at baseline and after the first and third DPMAS sessions
This case demonstrates that DPMAS can reverse severe hepatic dysfunction due to anti-tuberculosis DILI, leading to rapid clinical and biochemical recovery without complications. The dual-cartridge system effectively clears bilirubin, bile acids, and inflammatory mediators, supports hepatic synthetic recovery, including platelet improvement, and maintains hemodynamic stability. Early recognition of reversible hepatic injury and timely initiation of DPMAS may improve outcomes in high-risk patients, particularly in resource-limited settings or where transplantation is not immediately available. This case highlights the feasibility of using DPMAS as a bridge to recovery in severe DILI.
