1 in 5 with IBD Have High Retinal Drusen Counts

Retinal drusen are more common in patients with inflammatory bowel disease (IBD) and are linked with longer disease duration and increased complications, according to a study published in Scientific Reports.

“Retinal drusen are deposits of inflammatory proteins that are found in macular degeneration and glomerulonephritis and result, in part, from complement activation,” explained a research team from Australia.

The cross-sectional observational study investigated retinal drusen in consecutive patients with IBD from a metropolitan teaching hospital’s gastroenterology clinic over a 6-month period. For the study, patients underwent nonmydriatic retinal photography, and investigators examined deidentified images for drusen.

Among the 63 patients in the final cohort, 65% had Crohn’s disease, 30% had ulcerative colitis, and 5% had indeterminate colitis. The patients were matched for age and gender with control subjects without systemic inflammatory disease recruited simultaneously from general medical and preoperative surgical clinics.

According to the findings, drusen counts were higher in participants with IBD (12 ± 34 on average) compared with control subjects (3 ± 8). Some 22% of participants with IBD, and 6% of controls, had abnormal drusen counts of 10 or higher.

Drusen counts of 10 or higher in patients with IBD were associated with longer disease duration (researchers reported a 1.06 odds ratio), increased likelihood of complications (6.90 odds ratio), and higher C-reactive protein levels at recruitment (1.02 odds ratio).

“The identification of drusen in IBD suggests that complement activation is important in IBD pathogenesis,” researchers advised. “Treatments used for drusen including those targeting the complement pathway in macular degeneration may be relevant in IBD.”

—Jolynn Tumolo

Reference:
Nicklason E, Ham Y, Ng D, et al. Retinal drusen counts are increased in inflammatory bowel disease, and with longer disease duration, more complications and associated IgA glomerulonephritis. Sci Rep. 2022;12(1):11744.