Successful Treatment of Refractory Gout Using Combined Therapy Consisting of Febuxostat and Allopurinol in a Patient with Chronic Renal Failure

Maekawa, Michitaka; Tomida, Hidetaka; Aoki, Takafumi; Hishida, Manabu; Morinaga, Takatoshi; Tamai, Hirofumi

doi:10.2169/internalmedicine.53.0698

Cited by 11 publications

(10 citation statements)

References 15 publications

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“…Using the search terms as outlined in Supplementary Table 1, 1678 studies of glucocorticoid use were initially identified, as summarised in a PRISMA flowchart summary (Supplementary Figure 4). After a sequential review of the title, abstract and full-text, a final total of 12 studies were included for data extraction [57,64,[87][88][89][90][91][92][93][94][95][96]. Eleven out of these 12 studies were of case reports (n = 10) and of case series (n = 1) [57,[87][88][89][90][91][92][93][94][95][96].…”

Section: Glucocorticoidsmentioning

confidence: 99%

Efficacy and safety of gout flare prophylaxis and therapy use in people with chronic kidney disease: a Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN)-initiated literature review

et al. 2021

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Gout flare prophylaxis and therapy use in people with underlying chronic kidney disease (CKD) is challenging, given limited treatment options and risk of worsening renal function with inappropriate treatment dosing. This literature review aimed to describe the current literature on the efficacy and safety of gout flare prophylaxis and therapy use in people with CKD stages 3–5. A literature search via PubMed, the Cochrane Library, and EMBASE was performed from 1 January 1959 to 31 January 2018. Inclusion criteria were studies with people with gout and renal impairment (i.e. estimated glomerular filtration rate (eGFR) or creatinine clearance (CrCl) < 60 ml/min/1.73 m2), and with exposure to colchicine, interleukin-1 inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs), and glucocorticoids. All study designs were included. A total of 33 studies with efficacy and/or safety analysis stratified by renal function were reviewed—colchicine (n = 20), anakinra (n = 7), canakinumab (n = 1), NSAIDs (n = 3), and glucocorticoids (n = 2). A total of 58 studies reported these primary outcomes without renal function stratification—colchicine (n = 29), anakinra (n = 10), canakinumab (n = 6), rilonacept (n = 2), NSAIDs (n = 1), and glucocorticoids (n = 10). Most clinical trials excluded study participants with severe CKD (i.e. eGFR or CrCl of < 30 mL/min/1.73 m2). Information on the efficacy and safety outcomes of gout flare prophylaxis and therapy use stratified by renal function is lacking. Clinical trial results cannot be extrapolated for those with advanced CKD. Where possible, current and future gout flare studies should include patients with CKD and with study outcomes reported based on renal function and using standardised gout flare definition.

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Section: Glucocorticoidsmentioning

confidence: 99%

Efficacy and safety of gout flare prophylaxis and therapy use in people with chronic kidney disease: a Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN)-initiated literature review

et al. 2021

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“…Hatoum et al ( 27 ) examined a database of adults with newly diagnosed gout and concluded that febuxostat was effective in the management of gout. Maekawa et al ( 28 ) reported that allopurinol, febuxostat, and benzbromarone therapy reduced serum urate levels to below 6 mg/dL in the treatment of refractory gout. Huang et al ( 29 ) reported that the urate-lowering efficacy of febuxostat at 80 mg QD was greater than that of febuxostat at 40 mg QD and allopurinol at 300 mg QD.…”

Section: Discussionmentioning

confidence: 99%

Safety and efficacy of oral febuxostat for treatment of HLA-B*5801-negative gout: a randomized, open-label, multicentre, allopurinol-controlled study

Hsu

et al. 2016

Scandinavian Journal of Rheumatology

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Objectives: This phase IIIB study compared the efficacy and safety of febuxostat and allopurinol in gout patients with or without tophi who were HLA-B*5801 negative. Method: Eligible patients were randomized to a febuxostat group (80 mg QD) or an allopurinol group (300 mg QD). Following an initial 2-week washout period, over the next 12 weeks we made five measurements of serum urate levels along with assessments of adverse events (AEs). Results: Forty-three out of 152 screened subjects (28.3%) were ineligible either because of the presence of the HLA-B*5801 allele or for various other reasons. The febuxostat group (n = 54) and the allopurinol group (n = 55) had no significant differences in demographic or baseline characteristics. From week 2 to week 12, the febuxostat group had a significantly lower serum urate level than the allopurinol group (p ≤ 0.001 for all comparisons) and significantly more patients with serum urate levels less than 6.0 mg/dL. The serum urate levels of the febuxostat group declined by more than 40% from week 2 to week 12 and this decrease was greater than that in the allopurinol group (~30%). The two groups were similar in terms of AEs. Conclusions: Febuxostat was more effective than allopurinol in reducing the serum urate levels of Han Chinese patients with gout or tophaceous gout who were HLA-B*5801 negative, without causing any serious skin reactions. Febuxostat should be considered for treatment of Han Chinese patients with gout who are HLA-B*5801 negative.

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“…Next-generation sequencing and comparable in vitro experiments were not performed in any of the previous studies. Studies of molybdenum cofactor deficiency (MoCD) made use of knockout mice to study the molecular basis and treatment of human MoCD [26,27]. To confirm our hypothesis, we next intend to establish animal models, namely homozygous MCSU −/− and heterozygous MCSU −/+ mice.…”

Section: In Vitro Study Quantitative Rt-pcr Examination Of the Mcsu Imentioning

confidence: 99%

Using Next-Generation Sequencing to Identify a Mutation in Human MCSU that is Responsible for Type II Xanthinuria

Zhou

Zhang

Ding

et al. 2015

Cell Physiol Biochem

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Background: Hypouricemia is caused by various diseases and disorders, such as hepatic failure, Fanconi renotubular syndrome, nutritional deficiencies and genetic defects. Genetic defects of the molybdoflavoprotein enzymes induce hypouricemia and xanthinuria. Here, we identified a patient whose plasma and urine uric acid levels were both extremely low and aimed to identify the pathogenic gene and verify its mechanism. Methods: Using next-generation sequencing (NGS), we detected a mutation in the human molybdenum cofactor sulfurase (MCSU) gene that may cause hypouricemia. We cultured L02 cells, knocked down MCSU with RNAi, and then detected the uric acid and MCSU concentrations, xanthine oxidase (XOD) and xanthine dehydrogenase (XDH) activity levels, and xanthine/hypoxanthine concentrations in cell lysates and culture supernatants. Results: The NGS results showed that the patient had a mutation in the human MCSU gene. The in vitro study showed that RNAi of MCSU caused the uric acid, human MCSU concentrations, the XOD and XDH activity levels among cellular proteins and culture supernatants to be extremely low relative to those of the control. However, the xanthine/hypoxanthine concentrations were much higher than those of the control. Conclusions: We strongly confirmed the pathogenicity of the human MCSU gene.

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Successful Treatment of Refractory Gout Using Combined Therapy Consisting of Febuxostat and Allopurinol in a Patient with Chronic Renal Failure

Cited by 11 publications

References 15 publications

Efficacy and safety of gout flare prophylaxis and therapy use in people with chronic kidney disease: a Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN)-initiated literature review

Efficacy and safety of gout flare prophylaxis and therapy use in people with chronic kidney disease: a Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN)-initiated literature review

Safety and efficacy of oral febuxostat for treatment of HLA-B*5801-negative gout: a randomized, open-label, multicentre, allopurinol-controlled study

Using Next-Generation Sequencing to Identify a Mutation in Human MCSU that is Responsible for Type II Xanthinuria

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