Treatment with the glitazone class of diabetes drugs leads to a “modest” increase in the risk of diabetic macular edema (DME)-a common complication that can lead to
Treatment with the glitazone class of diabetes drugs leads to a “modest” increase in the risk of diabetic macular edema (DME)-a common complication that can lead to vision loss, reports a study
Using a database of about 170,000 patients with diabetes, Drs. Donald S. Fong and Richard Contreras of Southern California Permanente Medical Group analyzed the link between glitazones and the development of DME. Diabetic macular edema is a common diabetes complication, with swelling and fluid build-up in the retina leading to progressive visual loss. The researchers identified 996 patients who were diagnosed with DME during 2006.
Overall, patients who took glitazones were 2.6 times more likely to develop DME than patients not taking these drugs. Even after further adjustment for other factors, DME risk remained 60 percent higher for glitazone users.
Previous studies have linked glitazones to problems related to fluid retention and edema (swelling), including heart failure. Fluid retention from heart failure or other diseases can worsen DME. Most of the glitazone users in the study were taking pioglitazone (Actos). Other studies have linked rosiglitazone (Avandia)-the only other approved glitazone drug-to a possible increase in the risk of myocardial infarction.
Although the study is not the first to suggest a link, it provides confirmation in a very large sample of diabetic patients that glitazones are “modestly associated” with DME. Drs. Fong and Contreras concluded, “When treating patients with DME, ophthalmologists should consider the role of the glitazone class of drugs.”
“Ocular complications are an overlooked safety issue of systemic drugs,” commented Dr. Thomas J. Liesegang, Editor-in-Chief of AJO. “Safety is as important as the efficacy of a drug. However, long term safety is not currently monitored because the approval process is based on smaller, shorter term clinical trials. Safety necessarily requires monitoring of treatment in larger groups of people over longer periods of time. This monitoring is often neglected and should be required of all therapies.”
American Journal of Ophthalmology, April 2009
FACT: Enteroviral Infection Implicated in Diabetes Type 1: According to a new report
Enteroviral capsid protein vp1 is commonly found in pancreatic islets from patients with Type 1 diabetes. “The data suggest that a persistent, low level (non-lytic) enteroviral infection of beta-cells could be one of the factors that set in train the series of events that leads to islet cell autoimmunity and insulitis, culminating ultimately in the development of Type 1 diabetes,” states Dr. Morgan from Peninsula Medical School, Plymouth, UK. Dr. Morgan and colleagues investigated the prevalence of immunoreactive vp1 staining in the islets of 72 patients with recent-onset Type 1 diabetes and in 161 relevant controls. More than half (61%) of the recent-onset Type 1 diabetes cases were positive for enteroviral vp1 antigen, with most containing multiple immunopositive cells in a range of islets, the authors report. “It is important to emphasize that the viral protein detected in our studies is expressed in only a minority of beta-cells, suggesting that the infection is not a classical, lytic mechanism,” Dr. Morgan explained. “Rather, it seems likely that a persistent chronic infection may be the mediator of the cellular changes that promote autoimmunity.” He concluded: “If it proves to be the case that one or more enteroviruses is involved in initiation of the events that lead to autoimmunity in Type 1 diabetes, then this opens the possibility that a vaccine might be developed which, in principle, could be useful as a means to prevent the initiation of beta-cell destruction in susceptible individuals.”
Diabetologia, April 2009.