Drug delays type-1 diabetes in individuals at high risk: Study

DiabetesWashington: Scientists have developed a treatment that can delay type-1 diabetes by two or more years among individuals at high risk. Published in the New England Journal of Medicine, the Yale University research involved treatment with teplizumab, an anti-CD3 monoclonal antibody.

The researchers enrolled 76 participants aged 8 to 49, who were relatives of people with type-1 diabetes, had at least two types of diabetes-related autoantibodies (proteins made by the immune system), and abnormal glucose (sugar) tolerance.



Participants were randomly assigned to either the treatment group, which received a 14-day course of teplizumab, or the control group, which received a placebo. Regular glucose tolerance tests were done on the all participants till the completion of the study or until the participants developed clinical type-1 diabetes—whichever happened first.

During the study period, clinical diabetes developed in 72 per cent of individuals in the control group, while in only 43 per cent of those in the treatment group.

The median time for the participants in the control group to develop clinical diabetes was just over 24 months, whereas for those in the teplizumab group, the median time was 48 months before progressing to diagnosis.

Type-1 diabetes develops when the T cells of the immune system destroy the cells in the pancreas called beta cells. Beta cells make insulin which is required to convert glucose into energy. Teplizumab targets T cells to reduce beta cells destruction.

According to Kevan C. Herold of Yale University, “Previous clinical research found that teplizumab effectively slows the loss of beta cells in people with recent onset clinical type-1 diabetes, but the drug had never been tested in people who did not have clinical disease.” He further said, “We wanted to see whether early intervention would have a benefit for people who are at high risk but do not yet have symptoms of type-1 diabetes.”

The drug was most effective in the first year after it was given, when 41 per cent of the people, mainly in the placebo group, developed clinical diabetes. Factors, such as age, could have played a role in the ability of teplizumab to delay clinical disease, because at-risk children and adolescents are known to progress to type-1 diabetes faster than adults.

Quicker progression of type-1 diabetes is related to a highly active immune system, which may explain the impact of immune system-modulating drugs like teplizumab.

The study may also help researchers understand why certain people responded to the drug teplizumab. People who responded to the treatment tended to have certain autoantibodies and other immune system characteristics.

The study team, however, warned that the study had limitations, such as the small number of participants, their lack of ethnic diversity, and that all participants were relatives of people with type-1 diabetes, which potentially restrains the ability to interpret the study broadly.

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