HPE Grunenthal handbook - Page 9

Optimising treatment The patient journey and optimising treatment Patients often only present to specialised care at an advanced stage, and then only a few treatment options remain, so the earlier GPs are involved in the patient journey, the more options for individualised pharmacotherapeutic regimens there will be Tim Jansen MD PhD Matthijs Janssen MD PhD VieCuri MC, Venlo, The Netherlands Gout is a highly prevalent disorder in the general population and in rheumatology practices. Its pathophysiology is based on monosodium urate accumulation and on activation of the inflammasome, which results in an auto- inflammatory syndrome. Gout predominantly affects males, but it might also affect females, particularly after menopause. 1 Serum urate concentrations in patients (normal value in females: 0.12–0.34mmol/l (2–6mg/dl) and males: 0.20–0.42mmol/l (3–7mg/dl)) vary greatly, with a diurnal and annual rhythm. The urate level is a result of genetic predisposition and environmental factors, and the presence of comorbidities such as cardio-renal diseases, diabetes mellitus and the metabolic syndrome. Hyperuricaemia is an elevated serum urate concentration above normal limits and is associated with gout. Gout is associated with sleep apnoea syndrome, non-alcoholic fatty liver disease, congestive heart disease, stroke and hyperlipidaemia. Gout is not only an unpleasant or invalidating disease but is also associated with premature cardiovascular death and probably increased death due to cancer and infectious diseases. Data from the USA categorised gout patients into groups, with hypertension in 74% of patients, chronic kidney disease (stage 2 or more) in 71%, obesity in 53%, diabetes in 26%, and heart failure in 11%. 2 Aggregation of comorbidities in gout is common but complex. Cluster analysis in a French gout population of over 2750 patients revealed a similar picture. This study divided the patients into five different clusters with, interestingly, Cluster 1 comprising 12% of the total French gout population and consisting of only males with neither comorbidities nor cardiovascular disease. 3 A total table 1 Gout subdivided into phases in a patient journey and potential actions taken General practitioner Rheumatologist 0 Asymptomatic hyperuricaemia No actions/considerations No actions/considerations unless high cardiovascular risk, then lifestyle advice 1 First arthritic attack Metatarsophalangeal joint Ankle Knee NSAIDs; most frequently diclofenac Obtain crystal proof and dietary advice with five days prednisolone 2 Second arthritic attack NSAID/colchicine/ five days prednisolone scheme (any inflammasome inhibitor) Prednisolone/colchicine scheme plus XOI 3 Third and following arthritic attack or ongoing attack and/or in between gout arthropathy with double contour at ultrasonography Tophaceous accumulation NSAID/colchicine /prednisolone scheme; Consider: referral to rheumatologist or start XOI [any inflammasome inhibitor plus ULT?] ULT indicated if two attacks within one year OR tophi Consider: Prednisolone and/colchicine scheme with escalating dose XOi 4 Negative urate balance with potentially some short attacks Treatment focusing on attack rate annihilation Personalised XOI and/or US aiming for pre-defined target 5 Debulked and on stable low serum urate levels, lacking attacks Continue chronic ULTs Continue chronic ULT aiming at serum urate <360 micromolar (<6mg/dl) Consider stopping ULT when the patient is in complete remission (first-choice NSAID etoricoxib or naproxen) Consider: interleukin-1 blockade when NSAID/colchicine/prednisolone are failing XOi, xanthine oxidase inhibitor (allopurinol/febuxostat); ULT, urate-lowering therapies; US, uricosuric (benzbromarone/ lesinurad/ probenecid) hospitalpharmacyeurope.com | 2018 | 9