Posted by Therese B. on February 05, 2001 at 13:23:37:
Don't have any stats, but isn't this on the rise? (onset under age 5)
Wouldn't the lack of autoimmunity make a *huge* difference in a cure like, for example, INGAP?
Sometimes I see autoimmunity downplayed by researchers as a hurdle, (success in preventing rejection of non-self islets would be sufficient in also stopping autoimmune reaction.)
other times it is seemingly at the forefront of concern (like INGAP.)
How might one be able to prove autoimmunity or nonautoimmunity?
Therese
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Early-Onset Type 1 Diabetes Has Different Cause Than Later Childhood Onset
A DGReview of :"Diabetic autoimmunity in infants and pre-schoolers with type 1 diabetes"
Pediatric Diabetes
01/29/2001
By Mark Greener
While the increase in the incidence of type 1 diabetes is most pronounced among children under five years of age, the demographics and autoimmune markers in this age group are poorly characterised. However, researchers from Loma Linda University Children's Hospital, CA, USA, recently identified several factors in patients who develop the disease as babies or toddlers that might suggest a different mechanism to that responsible in older children.
The authors compared 47 children who were diagnosed as suffering from type 1 diabetes before five years of age with a representative cohort of 49 children diagnosed after the age of five years.
Compared to those diagnosed after the age of five years, children with early-onset diabetes had higher incidence of symptoms of viral illnesses and diabetic ketoacidosis at diagnosis.
On the other hand, haemoglobin A1C (HbA1c) levels at diagnosis were higher among the later-onset group. The authors commented the lower HbA1c values in the younger age group may indicate a shorter pre-clinical phase. Indeed, the authors reported that 14.8 percent of children diagnosed before five years of age experience a honeymoon period compared to 42.1 percent of those diagnosed when aged over five years.
Moreover, researchers found that the titres of antibodies against Islet-cells and glutamic acid decarboxylase differed between the groups. For example, Islet-cell antibody titers were positive in 35.29 and 70.83 percent of the early and late onset groups respectively. The proportions positive for antibodies against glutamic acid decarboxylase were 41.38 and 71.74 percent respectively. Titers of insulin autoantibodies after insulin treatment began did not differ significantly between the groups.
The authors suggested that the antibody results suggest a relative lack of immune markers in infants and toddlers with new-onset diabetes. This observation, as well as the shorter pre-clinical phase, might suggest age-related differences in the autoimmunity that promotes type 1 diabetes. Alternatively, the authors suggest that younger children might develop diabetes from non-autoimmune mechanisms.