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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.
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Objective To explore the occurrence and influencing factors of serum uric acid elevation in patients with coronavirus disease 2019 (COVID-19) treated with favipiravir. Methods Medical records of patients with COVID-19 who were hospitalized in Beijing Ditan Hospital between June 1, 2020 and June 30, 2021 and treated with the 5- or 10-day regimen of favipiravir were collected and retrospectively analyzed. After favipiravir withdrawal, if the elevation in serum uric acid was >=30% of baseline level, it was defined as serum uric acid elevation. Then patients were divided into serum uric acid elevation group and non-serum uric acid elevation group. The clinical characteristics such as gender, age, body mass index, comorbidities, smoking and drinking behavior, COVID-19 grade, favipiravir regimen, and serum uric acid level and renal function before treatment in patients between the 2 groups were compared. Influencing factors of favipiravir-associated serum uric acid elevation was analyzed using multivariate logistic regression method. Results A total of 179 patients were included in the analysis, including 104 (58.1%) males and 75 (41.9%) females, aged from 19 to 70 years with a median age of 43 years. The level of serum uric acid in 179 patients after favipiravir treatment was significantly higher than before [(451+/-119) mumol/L vs. (332+/-94) mumol/L, P<0.001]. The change rate of serum uric acid from baseline level ranged from -57.1% to 157.8% with the median of 38.6%. The elevation in serum uric acid of >= 30% of baseline level occurred in 108 (60.3%) patients. The incidences of serum uric acid elevation in patients treated with 5-day and 10-day regi- mens of favipiravir were 46.8% (36/77) and 70.6% (72/102), respectively, and the difference between them was significant (P=0.001). Multivariate logistic regression analysis showed that body mass index 24.0 to <28.0 kg/m2 (OR=3.109, 95%CI: 1.209-7.994, P=0.019) and 10-day regimen of favipiravir (OR=3.017, 95%CI: 1.526-5.964, P=0.001) were independent risk factors for favipiravir-associated serum uric acid elevation. Conclusions More than half of COVID-19 patients treated with favipiravir can develop serum uric acid elevation. Overweight and 10-day regimen of favipiravir are independent risk factors for serum uric acid elevation in patients.Copyright © 2022 Adverse Drug Reactions Journal.
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In the absence of respiratory system involvement, COVID-19 patients developing ARDS can clinically mimic other diseases including acute leukemia due to presence of atypical lymphocytes in peripheral blood smear and increased serum lactate dehydrogenase and serum uric acid levels. Herein, we report a case who was initially suspected to have acute leukemia based on his atypical symptoms without any respiratory system involvement and deranged laboratory parameters and finally, diagnosed with COVID-19. Our patient presented with fever, myalgia, gum bleed, and petechiae. On clinical and laboratory evaluation, he was suspected to have acute leukemia based on markedly deranged serum lactate dehydrogenase and serum uric acid and the presence of atypical cells in peripheral blood smear and bone marrow. On day 3 of hospitalization, he developed respiratory symptoms, breathing difficulty which progressed to ARDS, and subsequently, he succumbed to his illness. His real-time reverse transcriptase-polymerase chain reaction test for severe acute respiratory syndrome coronavirus-2 yielded positive results. Also, Flow cytometry and fluorescence in situ hybridization studies for leukemia workup did not show any abnormalities. Although we are reporting the findings of only a single case, we aim to enhance and contribute further to the understanding of this novel infection.Copyright © 2021 Necati Ozpinar. All right reserved.
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Purpose: Gout in kidney transplant (KT) recipients can be severe and particularly challenging to manage. Pegloticase co-therapy with immunomodulators improved urate lowering therapy (ULT) response rates over phase 3 monotherapy trials by reducing anti-drug antibodies.1,2 This open-label trial (PROTECT NCT04087720) examined pegloticase safety and efficacy in KT patients with uncontrolled gout. Method(s): KT recipients with uncontrolled gout (serum urate [SU]>=7 mg/dL, intolerance/ inefficacy to ULT and >=1 of the following: tophi, chronic gouty arthritis, >=2 flares in past year) and functioning KT graft (eGFR>=15 ml/min/l.73m2) on stable immunosuppressive (IS) therapy (KT>l year earlier) received pegloticase (8 mg every 2 weeks for 24 weeks). SU response during Month 6 (SU <6 mg/dL for >=80% of time) and Health Assessment Questionnaire (HAQ) pain (most severe: 100) and Disability Index (HAQ-DI, max: 3) scores were evaluated. Patients discontinuing treatment before Month 6 were considered nonresponders. Patients discontinuing due to COVID-19 concerns were excluded from analysis if no data points were available in Month 6. Result(s): 20 patients enrolled (mean+/-SD;age: 53.9+/-10.9 years, 85% male, time since KT: 14.7+/-6.9 years, SU: 9.4+/-1.5 mg/dL, gout duration: 7.9+/-11.6 years;all on >=2 IS) and 14/20 completed treatment. 16/18 (88.9% [95% CI: 65.3, 98.6]) were SU responders vs 43.5% previously reported3 without immunomodulation. Substantial SU reductions during treatments were reported in 18/20 patients completing or discontinuing for non-SU monitoring rule reasons (pre-dose SU>6 mg/dL at 2 consecutive visits). No notable eGFR changes were observed up to 3 months follow-up. In patients completing treatment, HAQ-pain and HAQ-DI mean scores improved by 35.5+/-31.5 and 0.3+/-0.6, respectively, at Week 24 (n=13 and n=14). 7 serious adverse events, deemed unrelated to pegloticase, were reported in 5 patients. No anaphylaxis or infusion reaction events occurred. Conclusion(s): Pegloticase was safe and effective in treated KT patients with uncontrolled gout, achieving a higher durable response rate than in previously-reported patients not on IS therapy along with improved HAQ scores indicative of quality of life impact. These findings are consistent with other reports of immunomodulation with pegloticase.
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Background: Data on the course and outcomes of the coronavirus disease 2019 (COVID-19) in patients with gout are scarce, as gout is underrepresented in leading COVID-19 and rheumatological Scientific publications [1]. Objectives: To describe clinical changes, quality of life, therapy of gout before and after COVID-19, and the clinical course of severe acute respiratory syndrome-related coronavirus 2 (SARS-Cov-2) infection in the cohort of patients with gout. Methods: In total, 84 males with gout were examined before the pandemic, during COVID-19 (March 2020 to December 2021) and 6 months after SARS-Cov-2 infection. The severity of COVID-19 in our cohort was determined. We conducted a comparative analysis of clinical and laboratory data, Gout Activity Score (GAS), urate-lowering (UST) and symptomatic therapy, Physical Component Summary (PCS) and Mental Component Summary (MCS) of the Short Form 36 (SF-36) Health Survey Questionnaire. Statistical difference of qualitative indicators was carried out using the Pearson Chi-square test (χ2), quantitative indicators using the Student's or the Wilcoxon test between groups. Results: The mean age (mean±SD) of the study patients was 51.07±7.45 years and the disease duration was 9.84±6.02 years. Most SARS-CoV-2 infected patients with gout exhibited a moderate illness (40.48%), almost every third (28.57%) had mild, 21.43% had severe and 9.52% had critical illness. Comparison of pre-COVID-19 vs 6-month post-COVID-19 data demonstrated an increase of gout fares in preceding 6 months (0.7±0.59 vs 4.35±2.25, p<0.001), serum uric acid level (5.9±1.54 vs 7.62±1.99, p<0.01), GAS (3.83±0.4 vs 6.1±1.63, p<0.01), non-steroidal anti-infammatory drug intake (19.05% vs 72.62%, p<0.001), colchicine (27.38% vs 53.6%, p<0.001), and corticosteroid use (5.95% vs 34.52%, p<0.001), but decreased intake of ULT (88.09% vs 77.38%, p>0.05), SF-36 PCS (43.7 ± 6.19 vs 36.08±6.54, p<0.01) and SF-36 MCS (48.35±5.89 vs 40.13±6.84, p<0.01). Conclusion: The current study identifed the majority of patients with gout had a moderate course, every ffth had a severe course and 9.52% had a critical course of COVID-19. In the post-COVID-19 period, we found a six-fold increase in gout fares, rising gout activity by 59.3%, more frequent medication use for symptomatic therapy of gout, decreased physical and mental health in the cohort of patients with gout.
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Background: Coronavirus disease causes a proximal tubule dysfunction of kidneys, inducing uric acid loss [1]. It has been established that several changes in laboratory markers (C-reactive protein (CRP), ferritin, interleukin-6 (IL-6)) can predict the severity of Covid-19 [2]. The purpose of this retrospective study was to analyze whether uric acid could act as another predictor of severe Covid-19. Objectives: To evaluate the relationship between the severity of Covid-19 and uric acid levels on admission to the hospital. Methods: This retrospective study included 150 hospitalized patients with con-frmed Covid-19 (mean age 60.3±14.6 years;52% were men), the severity of which was determined by the presence and type of oxygen support: (1) without O2, (2) O2 by mask or nasal cannula, (3) continuous positive airway pressure, (4) positive bi-pressure in the airways or high-fow oxygen, (5) invasive ventilation. Among them, 90 subjects required oxygen support, and 60 people didn't. The mortality rate in our study was 9.3%. The average uric acid level was compared with patients without Covid-19 (40 subjects). The study included patients who didn't receive urate-lowering therapy. Levels of CRP, ferritin, IL-6, D-dimer were also determined on admission. The Spearman's rank coefficient was used for measuring correlation. Results: The mean uric acid level in patients with coronavirus disease was 251.5±104.1 μ mol/L;without Covid-19 it was signifcantly higher - 328.6±96.9 μ mol/L (p<0.001). Approximately one in four (24.6%) Covid-19 patients had uric acid levels below the lower limit of normal (208 μ mol/L for men, 155 μ mol/L for women). A decrease in serum uric acid levels was also observed in patients suffering from asymptomatic hyperuricemia or gout. However, there was no correlation between uric acid levels and disease severity (r=0.01, p=0.88). Also, uric acid levels did not correlate with other laboratory markers of severe Covid-19 (CRP: r=0.07, p=0.73;ferritin: r=0.15, p=0,07;IL-6: r=0.11, p=0,22;D-dimer: r=0.02, p=0,79). Conclusion: Low uric acid levels are common in patients with Covid-19, but are not predictive of a more severe course of this disease. A correlation between uric acid and the level of other laboratory markers of severe Covid-19 was not found.
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Background: When uncontrolled gout cannot be managed with oral urate-lower-ing therapies, pegloticase is one of the few remaining treatment options. Patients receiving infusion therapies experienced treatment interruptions due to the COVID-19 pandemic. As with other biologic therapies, patients can develop antidrug antibodies (ADAs) against pegloticase, and longer infusion intervals can result in higher rates of pegloticase immunogenicity.1 The literature suggests that co-administering an immunomodulator with pegloticase can markedly decrease the proportion of patients who develop ADAs,2 increasing the proportion with sustained urate-lowering response.3 Objectives: This case series reports one rheumatologists' experience with a gap in pegloticase therapy during the COVID-19 pandemic. Methods: Uncontrolled gout patients who underwent pegloticase treatment during 2019/2020 and had a gap in therapy of ≥28 days were identifed. Patient, clinical, and treatment (number post-gap infusions, immunomodulation co-therapy) characteristics were retrospectively examined, along with urate-lowering response following therapy interruption. Patients who had a serum urate (SU) <6 mg/dL after the last post-gap pegloticase infusion were considered to have recaptured response. Results: 7 patients (5 men, 64.3±13.5 years, pretherapy sUA: 7.76±2.47 mg/dL, 6 had tophi) were included with 2 remaining on therapy at data collection. Eleven gaps were noted with an average gap duration of 11.4±9.3 weeks (median: 9 weeks). For the last gap in therapy, patients received 13.9±7.0 infusions (range: 4-22) before the gap and 7.0±4.1 infusions (range: 2-14) after (Figure 1). Four patients (57%;Patients 1, 2, 5, 7) had recaptured urate-lowering at last pegloticase infusion, all of whom began immunomodulation (3 methotrexate, 1 mycophenolate mofetil/hydroxychloroquine) prior to resuming pegloticase. Of the 3 patients without response recapture, 2 initiated MTX after resuming pegloticase. 4 patients (57%) experienced ≥1 AE, including mild infusion reaction (n=1), acute gout flare (n=2), clinically meaningful decrease in eGFR (14.8 ml/min/1.73m2, n=1), heart attack (n=1), and anemia (n=1). Conclusion: These cases suggest that it may be possible to recapture urate-low-ering response to pegloticase in some patients, particularly in the presence of immunomodulation. These preliminary fndings are important to this vulnerable patient population, particularly during the COVID-19 pandemic. Further study is needed to confrm our fndings.