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Drug-induced eosinophilia and systemic symptoms
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Rajesh Verma, Pradeesh Arumugam
Drug reaction with eosinophilia and systemic symptoms (DRESS) is an idiosyncratic, potentially life-threatening, multisystem drug hypersensitivity disorder [1,2]. It is a peculiar syndrome historically described by various names such as phenytoin hypersensitivity, sulfone syndrome, anticonvulsant hypersensitivity syndrome, allopurinol hypersensitivity syndrome, drug-induced pseudolymphoma, drug-induced hypersensitivity syndrome (DIHS), hypersensitivity syndrome (HSS), and drug-induced delayed multiorgan hypersensitivity syndrome (DIDMOHS). The variable presentations that mimic many other diseases, prolonged latency period, and waves of the disease occurring over prolonged periods can make the diagnosis difficult. Early identification of this syndrome and active management are crucial in preventing serious complications and mortality.
Crystal deposition disorders
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Paul Creamer, Dimitris Kassimos
Febuxostat is an alternative inhibitor of xanthine oxidase, metabolized and excreted by the liver, so no dose adjustment appears to be necessary in patients with mild-to-moderate renal impairment. Side-effect profile and the risk of gout flares are similar to allo-purinol. It may be useful in patients with intolerance to allopurinol or who develop allopurinol hypersensitivity syndrome.
Recent approaches to gout drug discovery: an update
Published in Expert Opinion on Drug Discovery, 2020
Naoyuki Otani, Motoshi Ouchi, Hideo Kudo, Shuichi Tsuruoka, Ichiro Hisatome, Naohiko Anzai
Allopurinol is associated with several adverse effects, including gastrointestinal effects, rash, and Stevens-Johnson’s syndrome [14], as well as the rare but potentially fatal adverse event – allopurinol hypersensitivity syndrome (AHS). AHS is characterized by rash (e.g., Stevens‐Johnson syndrome, toxic epidermal necrolysis), eosinophilia, leukocytosis, fever, increased risk of hepatitis, and renal failure [15]. Risk factors for the development of AHS include the HLA–B*5801 genotype. The prevalence of HLA-B*5801 is as low as 1–2% in Japanese people, but as high as 20–30% in Chinese people; thus, adverse reactions are also associated with a genetic background [16]. Caution should be applied for using allopurinol with other drugs due to drug interactions, because allopurinol is prone to causing aplastic anemia when used in combination with drugs that cause bone marrow suppression, such as cyclophosphamide. Also, the interaction between allopurinol and azathioprine, a thiopurine drug, and its metabolite, 6‐mercaptopurine (6‐MP), is among the clinically significant drug interactions known. This combination of drugs can result in significant myelosuppression, and in some instances, death. In summary, the XOR inhibitor allopurinol, which is reportedly limited to use in patients with renal failure and due to drug interactions, has long been the basis for managing hyperuricemia.
Prescribing patterns of allopurinol and febuxostat according to directives on the reimbursement criteria and clinical guidelines: analysis of a primary care database
Published in Current Medical Research and Opinion, 2019
Ettore Marconi, Alessandra Bettiol, Niccolò Lombardi, Giada Crescioli, Luca Parretti, Alfredo Vannacci, Gerardo Medea, Claudio Cricelli, Francesco Lapi
In our study, more than 10% of patients switching to febuxostat had experienced at least one acute gout attack during previous allopurinol treatment. Adherence to ULT is, therefore, a key issue in the management of gout. According to a study by Mantarro et al.21 conducted in this same setting, only 3.2% of patients were adherent to allopurinol over 1-year follow-up. Poor adherence to allopurinol seems mainly related to its tolerability profile22, given that allopurinol causes adverse reactions in 2–8% of users23–26. According to a case-control study conducted on patients prescribed with allopurinol for either symptomatic gout, asymptomatic hyperuricemia, or tumor lysis syndrome, 5% of patients experienced adverse events, after a mean time of 6 weeks since treatment initiation27. Most common adverse reactions included skin rash, gastrointestinal events, neurologic events, fever, musculoskeletal events, and allopurinol hypersensitivity syndrome (AHS). Of note, AHS causes death in up to 27% of cases23–26. Risk of severe adverse events, including AHS, such as Stevens–Johnson syndrome and toxic epidermal necrolysis, is known to increase in renal disease28,29. In our study, ∼ 9% of cases of switch from allopurinol to febuxostat were related to intolerance or contraindication to previous allopurinol treatment.
Switching from allopurinol to febuxostat: efficacy and safety in the treatment of hyperuricemia in renal transplant recipients
Published in Renal Failure, 2019
Yanchun Li, Min Liu, Xuelei Zhang, Yuewu Lu, Juan Meng
Allopurinol is a first-line medication commonly used to treat gout and/or hyperuricemia [11]. However, allopurinol is associated with multiple side-effects, including increased toxicity with low glomerular filtration rate resulting in increased risk of allopurinol hypersensitivity syndrome (AHS), hepatotoxicity, and Stevens-Johnson syndrome. Febuxostat is a new nonpurine selective xanthine oxidase inhibitor well tolerated in patients with Gout and in those with mild or moderate chronic kidney disease [12–15]. However, the long-term efficacy and tolerability of febuxostat after switching from allopurinol in renal transplant recipients have not been assessed. The aim of this study was to evaluate the efficacy and safety of switching from allopurinol to febuxostat in management of hyperuricemia and the progression of renal function in stable renal transplant recipients.