Alirocumab may cause scleritis with uveal effusion in susceptible patients

Alirocumab has been linked to scleritis with uveal effusion in patient with autoimmune diseases according to a case study. In the literature alirocumab has not been reported to cause scleritis.

Alirocumab is a human monoclonal antibody that belongs to a novel class of drugs known as proprotein convertase subtilisin/kexin type 9 inhibitors that increase the expression of low-density lipoprotein receptor and decrease levels of low-density lipoprotein cholesterol . It is used  in adults whose high cholesterol is not controlled by diet and statin treatment.

Alirocumab, a newer PCSK9 inhibitor used as a second-line treatment for adults with uncontrolled hypercholesterolemia, may trigger pathologic inflammation including scleritis in susceptible patients. A case report is published in Annals of Internal Medicine.

Clinicians at Columbia University Irving Medical Center, New York-Presbyterian Hospital report the case of a 63-year-old woman who had several weeks of increasing pain, redness, and loss of vision in her right eye that did not resolve with steroid treatment. The patient had a history of Hashimoto thyroiditis and Ménière disease and had been taking an oral statin for hypercholesterolemia, but started alirocumab treatment about 6 weeks before the eye symptoms began. Suspecting a rare reaction from the alirocumab, the clinicians discontinued the medication and treated the patient's scleritis with uveal effusion with prednisone. Within 1 week, the patient reported dramatic improvement in her ocular and systemic symptoms. By 2 months, all of her symptoms and findings had completely resolved. Alirocumab treatment was not resumed.

According to the authors, newer PCSK9 inhibitors will likely bring significant health benefits to many people; however, because they are monoclonal antibodies with immune system interactions, they may also trigger pathologic inflammation in a subset of susceptible patients. Physicians should be on the lookout for idiosyncratic inflammatory responses to these monoclonal antibodies and continue to take good histories to uncover possible links.

For further reference log on to:

http://annals.org/aim/article/doi/10.7326/L19-0815