TBA (18A110)

Effects of Baricitinib on Haematological Laboratory Parameters in Patients with Rheumatoid Arthritis

Author(s)

Thomas W Huizinga1, Jonathan Kay2, Masayoshi Harigai3, Edward Keystone4, Josef Smolen5, José Rosas6, Paul Emery7, Stephen Hall8, Filip van den Bosch9, Morton Scheinberg10, Jean Dudler11, Ran Liao12, Gabriella Meszaros13, Jane Barry14, Joel Kremer15, Erica Tierney (Presenter only)16

Department(s)/Institutions

1Leiden University Medical Center, Leiden, Netherlands; 2Division of Rheumatology, UMass Memorial Medical Center and University of Massachusetts Medical School, Worcester, Massachusetts; 3Institute of Rheumatology, Tokyo Women’s Medical University, Tokyo; 4The Rebecca MacDonald Centre For Arthritis, Mount Sinai Hospital, Toronto, Ontario; 5Medical University of Vienna, Vienna, Austria; 6Marina Baixa Hospital, Villajoyosa, Alicante, Spain; 7Leeds MSK Biomed/Chapel Allerton Hospital, UK; 8Cabrini Medical Centre, Malvern, Australia ; 9University Hospital Ghent, Belgium; 10Albert Einstein Hospital, Brazil; 11Hôpital Cantonal, Fribourg, Switzerland; 12Eli Lilly & Company, Indianapolis, USA; 13Eli Lilly & Company, Vienna, Austria; 14 Eli Lilly and Company, Basingstoke, UK; 15Albany Medical College, USA; 16Presenting on behalf of the authors

Introduction

Baricitinib (BARI) is a reversible oral JAK inhibitor with selectivity for JAK1/JAK2 for active Rheumatoid Arthritis.

Aims/Background

Rheumatoid arthritis is associated with an increased neutrophil and platelet count, and decreased lymphocyte count.

Method

To summarise changes in absolute neutrophil counts (ANC), absolute lymphocyte counts (ALC), platelet counts, and haemoglobin (Hgb), and associated adverse events, with baricitinib (BARI [JAK1/2 inhibitor]) treatment. Data were pooled from completed Phase 1/2/3 studies and an extension study.

Results

BARI treatment was associated with a decrease in ANC and an increase in ALC and platelets, which stabilized and returned to baseline with prolonged treatment or treatment discontinuation. Neutropaenia (<1000 cells/mm3) was rare (<1%) and was not associated with higher risk of overall or serious infections. Lymphopaenia was associated with slightly higher rate of overall infections. Incidence of overall and serious infections in ALL BARI-RA set was 29.9 and 2.9 per 100 patient-years, respectively.
More BARI 4-mg (2.3%) as compared to placebo-treated (1.3%) patients had platelet count ≥600x109/L. In 6-study placebo-controlled set (0-24 weeks), 5 BARI 4-mg-treated patients (vs 0 placebo-treated) had “deep vein thrombosis” (DVT) and/or “pulmonary embolism” (PE). Incidence of overall and serious DVT/PE in ALL BARI-RA set remained low at 0.5 and 0.3 per 100 patient-years, respectively. The proportion of patients with high platelet levels (≥600x109/L) was comparable between patients with DVT/PE vs those without DVT/PE (at baseline: 0 vs 0.5%; post-baseline: 6.5% vs 3.3%).
With long-term BARI treatment, Hgb levels decreased transiently before returning to levels slightly higher than baseline at Week-52. Incidence of severe treatment-emergent shifts in Hgb (grade <3 to grade ≥3: <8 and ≥6.5 g/dL) was low across all treatment groups (<0.5%).

Conclusions

No associations were observed between ANC decrease and infections or thrombocytosis and DVT/PE. BARI treatment was not associated with an increased incidence of erythropaenia-related events or anaemia as compared to placebo. Few patients interrupted/discontinued BARI due to TE laboratory abnormalities.