Risk factors In a retrospective case-control study, it was shown that an increased initial dose of
allopurinol was linked to AHS.
Oxypurinol is quickly transformed from
allopurinol and then eliminated by the
kidneys. The mean half-life of
oxypurinol in patients with normal kidney function is 23 hours, although 95% of patients have half-lives between 9 and 38 hours. The half-life of
oxypurinol increases with decreasing kidney function, allowing it to build up over an extended period of time and reach higher steady-state concentrations; among those suffering from
anuria, nearly no
oxypurinol is eliminated. The first report of the link between kidney impairment and AHS was found in a 1984 case series, wherein 58 patients with AHS had demonstrated signs of kidney impairment before starting
allopurinol treatment. Additionally, among the most common co-morbidities in a comprehensive analysis of all 901 reported cases of AHS,
chronic kidney disease was present in 182 out of 376 (48%) patients.
Triggers After beginning
allopurinol, allopurinol hypersensitivity syndrome usually manifests itself in the first few weeks to months. Ninety percent of the 901 documented cases of AHS in the largest review to date began within the first 8 to 9 weeks of starting
allopurinol, with a median time to onset of 3 weeks.
Genetics The
HLA-B gene belongs to the family of genes called the
HLA complex. An
odds ratio of 80–580 has been reported to link the HLA-B*58:01 allele to a higher risk of allopurinol-induced
DRESS and
SJS/
TEN. ==Prevention==