Preliminary findings on outcomes for JAK inhibitors from a novel pharmacy-led clinic at a specialist IBD centre

Introduction

Janus kinase (JAK) Inhibitors are targeted small molecules recently approved for moderate to severe ulcerative colitis (UC). They regulate proinflammatory cytokines involved in the pathogenesis of immune-mediated diseases. We monitored the clinical response and blood results in a specialist pharmacist-led clinic (PLC).

Methods

37 patients were prescribed JAK inhibitors between May 2019 and January 2023 at our specialist tertiary centre. 18/37 (48.6%) were on Tofacitinib, the remainder were on newer selective JAK inhibitors: 15 on Filgotinib and 4 on Upadacitinib. All patients received prior counselling in the specialist PLC and suitability confirmed depending on patient’s characteristics and clinical status. Treatment was closely monitored with clinical assessment and blood results after starting therapy for 32 patients (5 were omitted due to: 2 FU local team, 1 moved residence, 1 pancreatic cancer, 1 emergency surgery)

Results

Data was available for 32/37 patients (reasons for omission were: 2 FU local team, 1 moved residence, 1 pancreatic cancer, 1 emergency surgery). The mean age of the patients observed was 39. 22 (69%) patients were male and 10 (31%) were female. No patients observed were E1, 8 (25%) were E2 and 24 (75%) were E3. The mean Mayo scores decreased from 8 to 0 for Tofacitnib and 8 to 3 for Filgotinib. Upadacitinib mean Mayo score pre-treatment was 8 and follow-up is still pending. Tofacitinib therapy was associated with increase in both fasting cholesterol (median change from 4.3 mmol/L to 5.3 mmol/L; increase in IQR from 0.6 to 1.8), and HDL (median change from 1.7 mmol/L to 1.8 mmol/L; increase in the IQR from 0.3 to 0.5). Likewise, Upadacitinib therapy was associated with an increase in both Cholesterol (median change from 5.1 mmol/L to 6.1 mmol/L) and HDL (median change from 1.2 mmol/L to 2.3 mmol/L). Fasting cholesterol levels on Filgotinib were not affected by therapy, but HDL levels increased (median of 1.6 mmol/L to 1.7 mmol/L) post treatment.

Conclusion

As prescribing of JAK inhibitors is expected to increase, demand for treatment counselling and monitoring will follow. Our PLC offers a valuable service with the appropriate skill sets for these purposes. We report good clinical response and differential changes in lipids in this small preliminary cohort seen in a newly set-up PLC. The set-up offer potential for collaborative data collection to further understand implications of lipid changes. Evidence-based guidance on measures to address lipid changes are warranted. Figure 1: Effect on clinical response and lipid profile