Injection Into Lymph Nodes May Slow Progression of Type 1 Diabetes

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New study shows potential to slow the progression of type 1 diabetes

A new research study, which looked at the preservation of beta cell function in people with type 1 diabetes, has been published in the New England Journal of Medicine.

Researchers from Linköping University in Sweden trialed an experimental therapy in six patients with type 1 diabetes to halt the destruction of insulin-producing cells. The study was small, but the research team says the outcome of the study shows promise.

Johnny Ludvigsson, senior professor at Linköping University and principal investigator for the study, told EurekaAlert, “The results for these six patients are very promising. Type 1 diabetes usually progresses gradually as the patient loses the ability to produce insulin, but this has not happened in these patients.”

In people with type 1 diabetes, beta cells, or insulin-producing cells, are destroyed. However, not all of these cells are eliminated by the time a person is diagnosed with type 1 diabetes. “…some cells manage to dodge the attacks and continue to produce some insulin. That’s why several research teams have been working on finding ways to rescue the remaining cells, or delay their destruction in people who have been recently diagnosed with the condition,” reports LiveScience.

The new technique attempted by Linköping University researchers involves an injection of the protein GAD directly into a patient’s lymph nodes (intralymphatic injection). This is similar to a method used to treat certain allergies by introducing the body to small amounts of a substance to build tolerance.

LiveScience writes, “Lymph nodes contain many immune cells, and the idea behind the treatment is that exposing the body’s immune cells to larger amounts of GAD than they normally encounter will cause the immune cells to become more tolerant of GAD, and halt their attack on it.”

The study results note that, “Direct injection of GAD-alum into the lymph node with administration of oral vitamin D was associated with preservation of residual beta-cell function in six patients with type 1 diabetes, as compared with historical age-matched patients with type 1 diabetes who received vitamin D alone or, in other immune-intervention trials, placebo.” 

According to LiveScience, Ludvigsson’s team had previously attempted the same treatment, but had injected the protein under the skin instead of into a lymph node, which was not as effective.

The team looks forward to expanding the study to a larger number of patients. Dr. Ludvigsson told EurekaAlert: “We must follow them for a longer period and we must include more patients before we can say anything about the effectiveness of the treatment, but the results so far are extremely exciting.”

If the positive effects of this treatment are confirmed in larger trials, it could mean reduced risk of complications for people with type 1 diabetes. Preserving insulin-producing cells and, thus, the body’s ability to secrete even small amounts of insulin, would make treatment and management of type 1 diabetes much easier. It is also likely to reduce extreme high and low blood sugars, which could increase a patient’s quality of life.

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