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Immunization Safety Review: Multiple Immunizations and Immune Dysfunction
development of clinical disease is preceded by an asymptomatic period of progressive islet destruction that may last for many years. As understanding of type 1a diabetes increases, the preclinical period may provide a window for interventions that can delay or prevent clinical onset (Knip, 1997).
The etiology of type 1a diabetes and other autoimmune diseases is multifactorial, involving genetics and environmental exposures. Genetic susceptibility, arising from combinations of multiple genetic factors, appears to be a necessary but not sufficient risk factor for the disease. Monozygotic twins of persons with type 1a diabetes are at increased risk compared with other family members, but as few as 23 percent of these twins developed the disease in one report (Abiru and Eisenbarth, 2000). Although the disease can cluster in families, more than 80 percent of type 1 diabetes cases are reported to occur in persons with no family history of the disease (Dorman et al., 1995). Certain genetic factors may also provide protection from type 1 diabetes.
Environmental factors are thought to serve as triggers or promoters of the autoimmune process in genetically susceptible individuals. In particular, dietary and viral exposures have been suspected in type 1 diabetes. Some studies found that early exposure to cow’s milk was associated with increased risk (Gerstein, 1994), as was breastfeeding for less than 3 months (Gerstein, 1994). Newer prospective studies, however, have found no association with these factors (Graves et al., 1999; Hummel et al., 2000; Norris et al., 1996). Congenital rubella syndrome (CRS) shows a clear association with type 1 diabetes, with about 20 percent of CRS patients in the United States also having diabetes (Menser et al., 1978; Rubinstein et al., 1982). Studies of Coxsackie B virus infections have produced conflicting evidence regarding their possible contribution to type 1 diabetes (Robles and Eisenbarth, 2001). Atkinson and Eisenbarth (2001) described a model of progression to clinical disease that depends not on exposure to a single triggering environmental agent but rather on the cumulative effect of various exposures over time.
Worldwide, estimates of the incidence of type 1 diabetes4 in children under 14 years of age range from 0.1 per 100,000 in parts of China and Venezuela to 36.8 per 100,000 in Sardinia and 36.5 per 100,000 in Finland (Karvonen et al., 2000). As reported by Karvonen and colleagues (2000), estimated incidence for the early 1990s for United States locations range from 11.7 per 100,000 in Chicago to 17.8 per 100,000 in Allegheny County, Pennsylvania. In most populations, incidence is highest in the oldest age group (10–14 years). The disease is also diagnosed in adults, but incidence data are limited. Data from Rochester, Minnesota, for 1945–1969 suggest an incidence rate of 9.2 per 100,000 among persons age 20 and older (Melton et al., 1983).
Rates have generally been lower in more tropical countries and higher in populations of European origin. These patterns may be related to differences
Most population-based studies do not distinguish between types 1a and 1b diabetes.