Written by Dr. Emma Dorris (Scientist, UCD), Mariosa Kieran (Pharmacist, Mater Misericordiae University Hospital), Professor Nicola Dalbeth (Consultant Rheumatologist, University of Auckland) and Professor Geraldine McCarthy (Consultant Rheumatologist, Mater Misericordiae University Hospital/UCD)
Gout is the most common form of inflammatory arthritis in adults. The incidence of gout is rising. People with gout have an increased risk of cardiovascular disease, and gout is associated with a number of comorbidities including diabetes and renal impairment. The increased incidence of gout together with increased cardiovascular risk and comorbidities is a significant public health challenge.
Unlike other common rheumatic diseases, the underlying cause of gout is well understood. Gout is caused by hyperuricaemia, too much uric acid in the body. This can occur due an underexcretion and/or overproduction of urate, which leads to monosodium urate (MSU) crystal formation and deposition in joints and tissues in susceptible individuals (figure 1). Acute gout flares occur as an inflammatory response to the MSU crystals. The goal of urate lowering therapy is to reduce serum urate to a therapeutic target level, thereby permitting MSU crystals to dissolve, in addition to preventing further crystal formation and deposition.
An important issue in urate lowering therapy is that paradoxically, initiation of urate lowering therapy can actually induce a gout attack. This happens because the urate lowering therapy causes MSU crystals to be shed from the articular cartilage into the joint space, resulting in acute inflammation. To prevent this, a low dose of anti-inflammatory prophylaxis, such as colchicine, is recommended for at least the first three to six months following initiation of urate lowering therapy.
Community pharmacists are the most easily accessible members of a patient’s health care team. Pharmacists are often a key source of information on disease management and patients have confidence in them. Pharmacists act as a critical resource for effective management of disease, particularly when chronic such as gout. Thus, open communication and education between the pharmacy and prescriber communities is essential to provide the most up-to-date and appropriate patient care. However, pharmacists frequently report a lack of patient treatment plan information and clinical connection to other healthcare professionals as barriers to providing optimal care to patients.
The use of low dose colchicine as a prophylaxis is an example of this gap in knowledge translation. Colchicine use in gout is most commonly used in the treatment of acute gout flares in a strictly time limited fashion. Legacy prescribing, whereby short or intermediate-term medications are not appropriately discontinued, is prevalent. Patients, and indeed pharmacists, can be unsure whether the prescribed colchicine is intended as a prophylaxis or is a legacy prescription that was previously prescribed in case of flare. This confusion can be magnified by lack of clear, definitive statements on updated best practices from national bodies and the time lag in incorporating professional body recommendations into readily accessible drug information sources, e.g. the product Summary of Product Characteristics, the British National Formulary. Pharmacists have reported that the advice on use of colchicine as a prophylaxis in their typical reference manuals is poorly defined in comparison to its use for acute flares. This can lead to conflicting advice being given to patients from their pharmacists and rheumatologists about gout management, particularly in relation to colchicine use. This prompted research into the pharmacist knowledge of gout management, leading to the development of an educational intervention for pharmacists.
Our research showed that pharmacist-knowledge of gout management in Ireland was not in line with current European (EULAR) gout management guidelines. However, we also demonstrated that pharmacists do not typically use disease management guidelines as standard sources of information. As such, there is a knowledge gap in the most up to date recommendations for gout management. Given the wide number of conditions encountered on a daily basis in community pharmacy, this is somewhat understandable. As such, a dedicated effort must be made by prescribers and professional societies to communicate treatment standards to pharmacists.
In response to our initial findings, an education intervention was co-developed by two consultant rheumatologists and gout specialists, a pharmacist and general practitioner. We worked closely with the site founder of Pharmabuddy, the eLearning platform designed for and used by pharmacists. A thirteen minute video tutorial on the pharmaceutical management of gout was produced and is hosted on the Pharmabuddy eLearning platform. Nine months after the initial launch of the video, the impact of the educational intervention was assessed. Pharmacists who had watched the tutorial had significantly greater knowledge of gout management than the pharmacists who had not. Importantly, pharmacists who had watched the tutorial had greater knowledge about colchicine and its use as prophylaxis following initiation of ULT. This demonstrates that low-cost educational interventions can greatly improve pharmacist knowledge of gout management.
Gout management recommendations can be impeded if translation into pharmacy practice is neglected. Our research acts as a proof of concept that a co-designed educational intervention on gout management is effective. The Pharmacy Act 2007 requires that all pharmacists in Ireland undertake continuing professional development (CPD). For wider implementation, our intervention could be integrated into a CPD for gout management. This could increase the reach of this information to pharmacists. Pharmacists, particularly community pharmacists, have a hugely broad remit. The onus is on the rheumatology community to communicate to pharmacists and other health care providers about up-to-date recommendations for gout management. Improved pharmacist knowledge can in turn empower patients to assume self-management of gout.
The original research paper is available open access at BMC Rheumatology: Pharmacist knowledge of gout management: impact of an educational intervention. ER Dorris, M. Kieran, N. Dalbeth & G. McCarthy. BMC Rheumatol 6, 30 (2022). https://doi.org/10.1186/s41927- 022-00259-x
Figure 1: Pathophysiology of Gout
Both the overproduction of urate and the underexcretion of urate can contribute to hyperuricaemia, leading to gout.
The goal of urate lowering therapy is to reduce serum uric acid levels below its saturation point, thereby preventing crystal formation and deposition. The rate of crystal reduction is dependent upon both the total crystal load and reduction in serum uric acid. Urate lowering therapy initiation can cause rapid dissolution of crystal deposits and may lead to increased flare rate and associated pain due to the removal of protein deposits protecting the underlying surface from attack by inflammatory cells. Thus an anti-inflammatory prophylaxis, such as Colchicine, is recommended for the first six months following initiation of urate lowering therapy.
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