Immunopathogenesis and risk factors for allopurinol severe cutaneous adverse reactions

@article{Wang2016ImmunopathogenesisAR,
  title={Immunopathogenesis and risk factors for allopurinol severe cutaneous adverse reactions},
  author={Chuang-Wei Wang and Ro-Lan Dao and Wen-Hung Chung},
  journal={Current Opinion in Allergy and Clinical Immunology},
  year={2016},
  volume={16},
  pages={339–345}
}
Purpose of reviewThe article reviews the immunopathogenesis and risk factors related to allopurinol-induced severe cutaneous adverse reactions (SCARs). Recent findingsFor years, allopurinol remains one of the leading cause for SCARs worldwide. The pathogenesis of allopurinol-induced SCARs have been discovered in recent years. HLA-B*58 : 01 has been found to be strongly associated with allopurinol-SCARs with functional interactions between allopurinol/its metabolite-oxypurinol and the T-cell… 
Successful Treatment of Allopurinol-Induced Severe Skin Reactions with Double Filtration Plasmapheresis: A Case Report
TLDR
An 80-year-old female admitted to the authors' hospital after administration of allopurinol in December 2018 developed erythaematous skin of the epidermis of the hips, which rapidly extended over the trunk and limbs, resulting in itching and flaking, which was stopped by double-filtration plasmapheresis (DFPP).
Genetics of Severe Cutaneous Adverse Reactions
TLDR
The findings on genetic factors related to SJS/TEN are summarized, especially for HLA, which indicates advances in identification of multiple genetic alleles associated with specific drugs related SCARS in different populations is an important breakthrough for prevention of SCARs.
Advances in hypersensitivity drug reactions.
  • M. Blanca, B. Thong
  • Biology, Medicine
    Current opinion in allergy and clinical immunology
  • 2016
TLDR
Six reviews dealing with different major topics on drug hypersensitivity reactions (DHRs) are presented, covering a wide spectrum of DHRs mediated by both immunological and nonimmunological mechanisms.
HLA-B*58:01 is not the only risk factor associated with allopurinol-induced severe cutaneous adverse drug reactions.
  • M. Gonçalo
  • Medicine
    Annals of translational medicine
  • 2018
TLDR
There is an urgent need to know the main risk factors in order to establish preventive measures and reduce the number of severe cases.
Hypersensitivity and Cardiovascular Risks Related to Allopurinol and Febuxostat Therapy in Asians: A Population‐Based Cohort Study and Meta‐Analysis
TLDR
The incidence and severity of febuxostat‐hypersensitivity are lower than with allopurinol andFebuxost at did not show an increased risk of CVD and related death.
Structural Elements Recognized by Abacavir-Induced T Cells
TLDR
The data suggest the T cell polyclonal response to abacavir consists of multiple subsets, including T cells that recognize self peptide/HLA-B*57:01 complexes and crossreact with viral peptide/(HLA)-B*,57: 01 complexes due to similarity in TCR contact residues.
An Update On the Immunological, Metabolic and Genetic Mechanisms in Drug Hypersensitivity Reactions.
TLDR
There is still a need of a better understanding of the different aspects related to the immunological mechanism, the drug determinants that are finally presented as well as the genetic factors for increasing the risk of suffering DHRs.
Usefulness of Cutaneous Provocation Tests to Study Drugs Responsible for Cutaneous Adverse Drug Reactions
  • M. Gonçalo
  • Medicine, Biology
    Current Treatment Options in Allergy
  • 2019
TLDR
Patch tests are safe and highly specific when performed according to the recommendations, but sensitivity is highest in exanthemas, DRESS, and fixed drug eruptions and particularly for abacavir, carbamazepine, aminopenicillins and other antibiotics, diltiazem, and tetrazepam.
The Economic Value of Genetic Testing for Tolerance of Allopurinol in Gout
  • G. Shields
  • Medicine
    The Journal of Rheumatology
  • 2017
TLDR
Evidence demonstrates that health-related quality of life (HRQOL) is lower in the gout population when compared with the healthy population, largely attributed to the painful flares and physical disability associated with the disease.
...
1
2
3
...

References

SHOWING 1-10 OF 66 REFERENCES
Positive and negative associations of HLA class I alleles with allopurinol-induced SCARs in Koreans
TLDR
Strong positive association of HLA-B*5801 and negative association ofHLA-A*0201 with the development of allopurinol-induced SCARs in the Korean population is found.
Insights into the poor prognosis of allopurinol-induced severe cutaneous adverse reactions: the impact of renal insufficiency, high plasma levels of oxypurinol and granulysin
TLDR
Impaired renal function and increased plasma levels of oxypur inol and granulysin correlated with the poor prognosis of allopurinol-SCAR, and an early intervention to increase the clearance of plasma oxypURinol may improve the prognosis.
HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol.
TLDR
The results indicated that allopurinol-SCAR is strongly associated with a genetic predisposition in Han Chinese, and in particular, HLA-B*5801 allele is an important genetic risk factor for this life-threatening condition.
Allopurinol Hypersensitivity: A Systematic Review of All Published Cases, 1950–2012
TLDR
All published cases of AH documented in the literature were reviewed in order to better understand the constellation of factors predisposing to this reaction, building on previous reviews by Lupton and Odom, Singer and Wallace and Arellano and Sacristan.
Oxypurinol-Specific T Cells Possess Preferential TCR Clonotypes and Express Granulysin in Allopurinol-Induced Severe Cutaneous Adverse Reactions.
TLDR
Data suggest that, in addition to HLA-B*58:01, clonotype-specific T cells expressing granulysin upon oxypurinol induction participate in the pathogenesis of allopur inol-induced SCAR.
Allopurinol Use and Risk of Fatal Hypersensitivity Reactions: A Nationwide Population-Based Study in Taiwan.
TLDR
The use of allopurinol in patients with asymptomatic hyperuricemia accompanied by renal or cardiovascular diseases statistically significantly increased the risk of hypersensitivity reactions.
Strong association between HLA-B*5801 and allopurinol-induced Stevens–Johnson syndrome and toxic epidermal necrolysis in a Thai population
TLDR
It is suggested that HLA-B*5801 is a valid genetic marker for screening Thai individuals who may be at risk for allopurinol-induced life-threatening SJS and TEN.
HLA-B locus in Japanese patients with anti-epileptics and allopurinol-related Stevens-Johnson syndrome and toxic epidermal necrolysis.
TLDR
While HLA-B*1502 is unlikely to be associated with carbamazepine-related or aromatic anti-epileptic agent-related SJS/TEN in Japanese, HLA*5801 was significantly associated with allopurinol- related S JS/T EN in Japanese.
Febuxostat Hypersensitivity
  • A. Abeles
  • Medicine
    The Journal of Rheumatology
  • 2012
TLDR
The case of a 69-year-old woman with multiple medical problems including gout and moderate renal insufficiency, who developed a hypersensitivity syndrome similar to AHS shortly after initiating febuxostat is described.
Use of HLA-B*58:01 genotyping to prevent allopurinol induced severe cutaneous adverse reactions in Taiwan: national prospective cohort study
TLDR
Prospective screening of the HLA-B*58:01 allele, coupled with an alternative drug treatment for carriers, significantly decreased the incidence of allopurinol induced SCARs in Taiwanese medical centres.
...
1
2
3
4
5
...