Aim: To compare lansoprazole 30 mg daily with ranitidine 150 mg b.d. in the treatment of acid‐related dyspepsia in general practice. Methods: In a double‐blind, parallel group, randomized, multicentre study conducted in 32 general practices in the UK, 213 patients were randomized to receive lansoprazole 30 mg daily, and 219 to receive ranitidine 150 mg b.d., for 4 weeks. All patients had experienced symptoms of reflux‐like or ulcer‐like dyspepsia on at least 4 of the 7 days prior to the study; 75% had experienced dyspepsia in the past, and 74 of the lansoprazole patients and 77 of the ranitidine patients had documented histories of acid‐related disorders, investigated by either radiology or endoscopy. Results: After 2 weeks 55% of the lansoprazole patients and 33% of the ranitidine group were symptom‐free (P = 0.001, χ2 = 7.12) with corresponding 4‐week figures of 69% and 44%, respectively (P = 0.001, χ2 = 18.03). Similar figures were found at both 2 and 4 weeks for daytime and night‐time heartburn and epigastric pain scores; in the lansoprazole group, at 4 weeks, 80% of patients were free of daytime heartburn and 81% of night‐time epigastric pain, compared with 55% (P = 0.001, χ2 = 15.44) and 65% (P = 0.01, χ2 = 6.10) in the ranitidine group. Conclusion: Superior symptom relief for patients presenting with ulcer‐like and reflux‐like symptoms in general practice is provided by lansoprazole 30 mg daily compared with ranitidine 150 mg twice daily.

This model found the licensed dose regimen of etanercept 50 mg biw to be cost effective in the U.K. This regimen was particularly appropriate for patients with severe disease or poor quality of life at baseline.

Objectives Real-world secukinumab gastrointestinal related adverse events (GIRAE) data as treatment for ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are lacking. We aimed to achieve this through baseline evaluation of pre-existing inflammatory bowel disease (IBD), rates and predictors of GIRAE. Methods Patient electronic and paper records commencing secukinumab from ten UK hospitals between 2016–2019 were reviewed. GIRAE after initiation were defined as: definite (objective evidence of IBD (biopsy proven), clear temporal association, resolution of symptoms on drug withdrawal, no alternative explanation felt more likely), probable (as per definite, but without biopsy confirmation) or possible (gastrointestinal symptoms not fulfilling definite or probable criteria). Results Data for all 306 patients started on secukinumab were analysed: 124 (40.5%) AS and 182 (59.5%) PsA. 24/306 (7.8%) experienced GIRAE after starting secukinumab. Amongst patients who developed GIRAE, 4 (1.3%) had definite, 7 (2.3%) probable and 13 (4.2%) possible IBD. All definite cases were patients with AS and stopped secukinumab; two had pre-existing IBD and two (0.7%) were de-novo cases of which one required surgical intervention. Seven patients (2.3%) had pre-existing diagnoses of IBD prior to initiation of which 5 patients experienced GIRAE. Conclusion Absolute rates of new IBD in patients starting secukinumab are low. The majority of patients developing new GIRAE did not develop objective evidence of IBD or stop therapy. For patients with pre-existing IBD and AS the risk of GIRAE is much higher, and prescribing alternatives should be considered.

Background Secukinumab is a selective interleukin-17a inhibitor (anti-IL17) and an effective treatment option for psoriatic arthritis (PsA) and ankylosing spondylitis (AS). Phase III study safety data indicate a possible risk of inflammatory bowel disease (IBD), a link which is biologically plausible as IL-17 is known to influence intestinal immunopathology. Real world data for secukinumab gastrointestinal safety are limited. We set out to describe the post-licensing experience of secukinumab in routine care, evaluating both baseline evaluation of pre-existing IBD as well as incident gastrointestinal adverse effects. Methods We undertook a retrospective cohort study. Ten centres from the South East of England participated. All records for patients commencing secukinumab at each centre between 2016-2019 were reviewed. A fully anonymised data collection form was used to collate patient information. Questions sought to answer whether IBD screening had occurred prior to secukinumab initiation. All gastrointestinal adverse events were reviewed. IBD-related adverse events after initiation were defined as: definite (biopsy confirmed, objective inflammation from biomarkers, clear temporal association, improvement on drug withdrawal), probable (as per definite, but without biopsy confirmation) or possible (gastrointestinal symptoms not fulfilling definite or probable criteria). Results Data for 306 patients were available: 124 (40.5%) with AS and 182 (59.5%) with PsA. 106 (34.6%) of patients had documented assessment for IBD prior to initiation; 7 of which already had pre-existing diagnoses of IBD. 24 (7.8%) patients experienced gastrointestinal related adverse events after starting secukinumab; 18 of which were formally investigated for bowel disease due to symptoms. Amongst patients who developed gastrointestinal symptoms, 4 (1.3%) had definite, 7 (2.3%) probable and 13 (4.2%) possible IBD. Out of the 4 with definite IBD; all were AS patients, all stopped secukinumab, three had pre-existing IBD and one (0.3%) case of de-novo IBD required surgical management for an inflammatory perianal abscess. All 7 patients with probable IBD had symptom resolution on withdrawal of secukinumab. Of these, 4/7 were PsA and 3/7 were AS. For the 13 patients that fulfilled possible IBD criteria, symptoms resolved without intervention and continued secukinumab treatment. Conclusion Absolute rates of new IBD in patients starting secukinumab are low. In addition, a majority of patients developing new gastrointestinal symptoms did not develop objective evidence of IBD or stop therapy. However, our experience suggests that in people with pre-existing IBD the risk is much higher. Only one-third of patients had documented evidence of screening for IBD at baseline. Given that only one patient developed de-novo IBD in the cohort, our experience would not support the practice of pre-screening for IBD prior to starting anti-IL17 therapy. Further research to evaluate this would be wise to focus specifically on the characteristics of AS patients, stratifying IBD risk prior to anti-IL17 initiation. Disclosures I.A. Onac: Other; Education support to attend conference from Abbvie. C. Tacu: Honoraria; Novartis Pharmaceutical UK - Speaker Fee. Other; education support- course - Novartis. B.D. Clarke: None. M. Lloyd: Other; departmental support from Novartis. V. Hajela: None. T. Batty: None. J. Thoroughgood: None. S. Smith: None. H. Irvine: None. D. Hill: None. G. Baxter: None. N. Horwood: Other; attend conferences from Lilly and Abbvie. S. Mahendrakar: Other; Education support to attend conferences from Lilly. R. Rajak: Honoraria; Honoraria for speaker: Eli Lilly, Amgen, Internis, Roche, UCB, Abbvie. Honoraria for chairing: Roche, Novartis, Eli Lilly, UCB. S. Griffith: Other; None declared. P. Kiely: Honoraria; Abbvie, BMS, Gilead, Lilly, Novartis, Sanofi. Member of speakers’ bureau; Abbvie, BMS, Lilly, Novartis, Sanofi. J.B. Galloway: Honoraria; Speaker fees, travel support and grants from Lilly, Abbvie, BMS, Celgene, Janssen, Pfizer, UCB, Sanofi.