Surveys for diabetes among children and young adults from many geographic locations reveal a spectrum of clinical characteristics. The majority of young European-origin patients appear to fit the clinical picture of Type 1 diabetes, while the prevalence of Maturity-onset Diabetes of Youth (MODY) is estimated at 1-3% (9). In other ethnic groups Type 2-like syndromes are reported more frequently among children, although no consensus on defining characteristics has yet emerged. Winter's classic case-series, published in 1987 (1), described 12 of 129 African American patients with an atypical disease course, an absence of the Type 1 diabetes-associated HLA variants and no detectable islet cell antibodies (ICA). C-peptide levels in these patients were intermediate between those of Type 1 diabetes patients and non-diabetic subjects. Additional characteristics resembling Type 2 diabetes were observed, such as obesity and a high prevalence of diabetes among relatives. These patients were ultimately characterized as having 'atypical' disease.
The possibility that an intermediate form of diabetes is etiologically distinct received an enormous boost in 1997, with the addition of 'Type 1b' to the newly revised WHO/ADA classification scheme for diabetes mellitus as a non-autoimmune, idiopathic form of Type 1 diabetes. In the third NHANES study, conducted between 1988 and 1994, 13 of 2867 subjects aged 12-19 years were considered to have diabetes based on insulin treatment (n = 9), treatment with oral agents, or elevated fasting glucose levels. The overall prevalence of diabetes in this age group was therefore calculated to be 4.1 per 1000, with an estimate that at least 31% of these subjects had Early 2 (10). The NHANES-3 estimate, while based on an extremely small number of cases, included non-Hispanic whites, African Americans and Mexican Americans in the sampling frame. On the other end of the age range, Zimmet and colleagues defined a syndrome, latent autoimmune diabetes of adults (LADA), to distinguish lean, ketosis-prone individuals with diagnosis of diabetes in adulthood that progressed more or less rapidly to insulin dependence (11). Taken as a whole, these developments undermine the conventional practice of categorizing diabetes as either autoimmune Type 1, or insulin-resistant Type 2. Aizawa and colleagues (12) suggest that a combination of many factors, including susceptibility genes, viral infections, immune attack, aging, variation in the beta-cell mass at birth and glucose toxicity, can operate to cause beta-cell damage and insulin resistance. They advocate a comprehensive view of the etiology of diabetes, taking these many factors into account for all patients.
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