Background and importance Acute graft versus host disease of the gastrointestinal tract (aGVHD-GI) is one of the most common complications in patients undergoing allogeneic haematopoietic stem cell transplantation (HSCT).

Vedolizumab is proposed as a therapeutic alternative in patients with aGVHD-GI resistant to multiple lines of treatment.

Aim and objectives To describe the usefulness of therapeutic drug monitoring (TDM) of vedolizumab to optimise treatment in one patient with aGVHD-GI.

Material and methods A 42-year-old with acute lymphoblastic B leukaemia admitted for allogeneic HSCT developed grade 4 aGVHD-GI. Vedolizumab was administered as sixthline treatment after corticosteroid therapy, mesenchymal stem cells plus mycophenolate mofetil, infliximab, and extracorporeal photopheresis plus ruxolitinib.

Response was measured by clinical criteria (resolution of diarrhoea), imaging tests (gastroscopy and colonoscopy) and inflammatory biochemical markers (faecal calprotectin). Partial response to treatment (PR) was defined as resolution of overall aGVHD in one or more organs without worsening of others, and complete response (CR) as resolution of symptoms in all organs.

Trough vedolizumab serum concentrations (VSC) were determined by ELISA. Vedolizumab clearance (CL) and volume of distribution (Vd) were estimated using a Bayesian population pharmacokinetic approach that incorporated a validated population pharmacokinetic model in patients with inflammatory bowel disease, due to the lack of population data in aGVHD-GI. VSC >30 µg/mL in the induction phase and >14 µg/mL in the maintenance phase were considered therapeutic.

Results Vedolizumab 300 mg was administered as an intravenous infusion during the induction phase at weeks 0, 1, 4 and 6, based on the estimated pharmacokinetic parameters (CL=0.159 L/day; Vd=3.19 L). VSC measured at week 3 was 44 µg/mL. The patient presented a PR and initiated oral tolerance that week. He achieved CR of his grade 4 aGVHD in week 6. The maintenance phase was initiated administering vedolizumab every 4 weeks. VSC measured at weeks 10, 14 and 26 were 3.8, 31.3 and 53.4 µg/mL, respectively. Starting on week 26, vedolizumab was administered every 6 weeks, obtaining a VSC of 22.4 µg/mL. The patient maintained CR during this phase.

Conclusion and relevance TDM of vedolizumab is a valid tool for individualising treatment in patients with aGVHD-GI, avoiding early therapeutic failure.

References and/or acknowledgements No conflict of interest.