Abstract
In 1976, in a letter to the editor of Lancet, Cox et al1 reported a study of the pancreas in 25 so-called cot deaths, infants who had died of the sudden infant death syndrome (SIDS). Those authors claimed that 9 of the 25 (36%) had islet cell hyperplasia and nesidioblastosis. They attributed those nine deaths to hypoglycemia secondary to pancreatic lesions. They defined nesidioblastosis as multifocal budding of endocrine cells from ductal or ductular epithelium, or interposition of endocrine cells in the midst of ductal or ductular epithelium, together with diffuse proliferation of single endocrine cells or small cell nests in the midst of parenchyma and apart from clearly defined islets. The conviction of these investigators was apparently supported, at least in part, by an earlier report that many SIDS victims have abnormally low levels of glucose in the vitreous humor.2