Disclosures: Gorelik reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.
August 09, 2021
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Macrolides, fluoroquinolones reduce risk for anti-drug antibodies in IBD treatment

Disclosures: Gorelik reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.
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Avoidance of cephalosporins and penicillin with beta-lactamase inhibitors during anti-TNF therapy reduced the risk for anti-drug antibodies among patients with inflammatory bowel disease, according to research published in Gut.

“Primary non-response to anti-TNF therapy is seen in 40% of patients with even higher rates of failure to achieve complete remission. Additionally, the rate of secondary loss of response after 12 months of therapy ranges between 23% and 46%,” Yuri Gorelik, Rambam Health Care Campus in Haifa, Israel, and colleagues wrote. “Immunogenicity, which refers to the development of anti-drug antibodies (ADA) is considered as the main factor driving secondary loss of response and is likely involved in primary non-response as well.”

risk for anti-drug antibodies

To assess the implications of antibiotic treatment on immunogenicity to anti-TNF agents, researchers analyzed 1,946 patients with IBD treated with either Humira (adalimumab, AbbVie; 54.7%) or Remicade (infliximab, Janssen; 45.3%) from the epidemiology group of the Israeli IBD research nucleus registry. After a median follow-up of 651 days from anti-TNF treatment, 18.6% of patients had positive serum ADAs. Researchers observed an increased risk for ADA development among patients treated with cephalosporins (HR = 1.97; 95% CI, 1.58-2.44) or penicillin with beta-lactamase inhibitors (HR = 1.4; 95% CI, 1.13-1.74) and a reduced risk for ADA development among patients treated with fluoroquinolones (HR = 0.2; 95% CI, 0.12-1.35), metronidazole (HR = 0.88; 95% CI, 0.7-1.1) and macrolides (HR = 0.38; 95% CI, 0.16-0.86).

“Further studies involving detailed analysis of the antibiotic effects on the human microbiome and immune milieu are needed, as well as comparative experiments with other medications used to reduce immunogenicity,” Gorelik and colleagues concluded.