P98 A pilot pharmacist led carvedilol titration service leads to sustained doses of high dose carvedilol in patients with clinically significant portal hypertension

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Non-selective beta blockers (NSBBs) reduce the risk of hepatic decompensation in patients with cirrhosis and clinically significant portal hypertension (CSPH). However, prescribed doses in real-world practice are frequently below those used in clinical studies and sub-therapeutic doses risk beneficial effects not manifesting as improved clinical outcomes for patients. To address this implementation challenge, we set up a pharmacist led supervision service to initiate and carefully titrate carvedilol to therapeutic doses. Eligible patients included those meeting the Baveno VII criteria for CSPH without contraindications to NSBB who were on a dose of carvedilol of <25mg per day. Patients with decompensated liver disease (defined as Child-Pugh (CP) B8 or above) or previous variceal haemorrhage episodes remained in the consultant led service. Patients were seen at a single face to face appointment where eligibility was confirmed or reassessed. 1–2 weekly telephone follow up calls were undertaken to assess adverse events and review ambulatory blood pressure (BP) and pulse monitoring results. Statistical analysis was performed using Wilcoxon signed-rank test and paired t-test. In 12 weeks (September to December 2023), 29 patients were reviewed at a community hepatology clinic in Southampton (UK). Mean age was 59 (standard deviation 11), 69% were male, and MASLD was the most common underlying aetiology (58%). All patients met criteria for CSPH with the following biochemical values (mean ± SD); platelet count (157.2 ± 75.3 x 109/L), liver stiffness (37.7 ± 22.8 kPa), ELF (11.4 ± 1.1). 4 (14%) were CPB7. 22 (76%) completed dose optimisation. Median time to maximum tolerated dose was 2 weeks (range 1–6). Median dose at the first appointment was 6.25 mg (range, 0–25 mg) with 10 (38%) not taking any carvedilol as baseline. Post follow up dose (median = 25 mg, range 6.25–25 mg), was significantly higher than pre-intervention dose (median = 6.25 mg, range 0–25 mg) (Wilcoxon, p < 0.001). No significant change was observed for mean arterial pressure (p = 0.13) or pulse rate (p = 0.162) before and after dose optimisation. 4 experienced fatigue, but no significant adverse events requiring treatment cessation occurred. Our pharmacist led carvedilol optimisation service was well attended by patients and able to offer rapid, sustained, and safe dose titration. Although NSBBs are not universally recommended, wherever the practice is implemented we must ensure doses match trials as closely as possible. An intensive pharmacist led service is a feasible approach to achieve this.

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