Pancreatic Cell Damage in Children with Fatal Viral Infections

Abstract

The rare fatalities from viral infections most commonly occur in neonates and immunosuppressed older children and adults. With a fatal viremia, pathologic changes in pancreatic acini, interstitium, and islets are frequently subtle and may be overlooked. Islet cell degeneration and necrosis with or without associated inflammation is usually associated with viral infections or ingestion of chemicals that are cytotoxic for islets. Insulitis without degeneration or necrosis of islet cells can probably be attributed to an autoimmune phenomenon. Coxsackievirus B, cytomegalovirus, congenital rubella, and varicella-zoster were the four viruses most frequently associated with islet cell cytopathology. Two of these, Coxsackievirus B and rubella, have been implicated as a trigger for development of IDDM. Insulin degranulation of beta cells in Coxsackievirus infections was greater than expected from the degree of cytopathology in the islets; this was not the case with the other fatal viral infections. Conversely, 50% or fewer beta cells were degranulated in one case each of cytomegalovirus and Coxsackievirus B₄ infections associated with acute-onset IDDM; two patients with congenital rubella syndrome, one with acute-onset IDDM and another with long-standing IDDM had no insulin-producing beta cells. These findings suggest that in some cases of IDDM associated with acute viral infections, insulin-producing beta cells may be initially preserved and potentially amenable to protection by therapeutic measures.