ABSTRACT
Background/Aims Research has shown nurse-led gout clinics provide better outcomes compared to usual care. This District General Hospital set up a pilot nurse-led gout clinic in autumn 2019. This aimed to improve patients' understanding of their condition, achieve better control of serum uric acid levels (SUA), reduce flares and prevent Emergency Department attendances. Methods A modified clinic protocol, closely modelled on BSR guidance was agreed within the department. With consultant supervision, one nurse specialist provided a mix of in-person and telephone appointments. Targets were set aiming for SUA <360mumol/L for most patients and <300mumol/L for those with erosive change or tophi. All patients were offered prophylaxis. Patients required a rheumatologist's diagnosis of gout or crystal confirmation for enrolment. Exclusion criteria were significant renal or hepatic derangement. Within 3 months of the service starting SARS-CoV-2 impacted the operation of healthcare worldwide and led to the closure of routine outpatient clinics in Northern Ireland. A decision was made to switch the gout clinic to run entirely by telephone. Blood testing was facilitated through primary care and phlebotomy hubs. Results Over a 19-month period, 78 patients were treated and audited through this clinic: 69 men and 9 women. Average age was 57, mean SUA 509 mumol/L at referral and 322 mumol/L on discharge. 69 patients received allopurinol and 9 received febuxostat. No patients required uricosuric drugs. All patients were offered and agreed to take prophylaxis with a majority (85.8%) remaining on it for 3-6 months. Patients required a mean of 3.38 appointments prior to discharge from the clinic. The mean dose of urate lowering therapy on discharge was 315.9mg allopurinol and 93.3mg febuxostat. 95% experienced >=2 flares during their enrolment in the clinic with no patients requiring Emergency Department attendance due to gout flare. Conclusion The nurse-led gout clinic was well received by patients and was effective as a telephone service during the pandemic when so many services were stood down. The clinic was able to continue to provide education, deliver effective reductions in uric acid as well as reduce incidence of flares and Emergency Department attendances. Lower doses of urate lowering therapy than expected were needed to achieve target. A small number of patients were discharged prior to enrolment for initial non-engagement which may have been exacerbated by the lack of face-to-face appointments. Our COVID-19 model did struggle with those patients needing an interpreter. In-person initial appointments have since been restarted;however, a greater proportion of reviews will continue to be offered by telephone given the unexpected success of the model. This audit showed that a nurse-led gout clinic can run successfully, even during a pandemic with a significant reliance on telephone consultations.
ABSTRACT
Rationale: In severe COVID-19 patients, decrease of ATP production caused by mitochondrial dysfunction thought to induce the lung injury. Febuxostat, which is a therapeutic medicine for hyperuricemia, is thought to have the effect of improving mitochondrial dysfunction and enhances the production of ATP. The purpose of this study is to investigate the effect of febuxostat in LPS induced lung injury mouse model. Methods: C57BL/6 WT mice (8-12 wk-old males) were exposed to lipopolysaccharide (LPS) intratracheally to develop the murine model of LPS-induced lung injury. For the treatment, 100 μg of febuxostat was administered twice a day from 2 days before the exposure of LPS. Bronchial lavage fluid (BALF) and lung tissue were collected 24 hours and 7 days after the LPS exposure. The BALF were analyzed for total and differential cell counts. The lung tissues were stained with Masson's trichrome staining and analyzed for lung fibrosis. Results: Twenty-four hours after the LPS exposure, the number of total cells and neutrophils in the BALF was increased. In the group receiving febuxostat, the number of total cells and neutrophils were significantly decreased at 24 hours after the LPS exposure. At 7 days after the LPS exposure, the number of total cells and neutrophils in both LPS and LPS + Febuxostat group returned to almost the same level as control group. Additionally, the percentage of collagen deposition area representing lung fibrosis in the entire lung field was enhanced in LPS group compared to control group at 7 days after the LPS exposure. Moreover, the treatment of febuxostat inhibited the fibrosis in LPS group. Conclusions: Administration of febuxostat inhibited the lung inflammation in the acute phase and improved the lung fibrosis in LPS-induced lung injury model. This study suggests that the treatment of febuxostat may inhibit the lung injury caused in severe COVID-19 patients.