HUS is a condition well known to have multi-systemic effects. Whilst the predominant organ to be affected is the kidneys, it is also well recognised that the pancreas can be affected during the acute phase of the illness, causing a transient diabetes mellitus. Less well documented, however, is that HUS has been linked to long-term diabetes, with patients developing insulin deficiency, years after contracting HUS. We report on the case of a twelve-year-old girl who developed insulin dependent diabetes by the age of ten, with a past medical history of haemolytic uraemic syndrome at the age of two. She displayed transient hyperglycaemia requiring insulin during recovery from HUS. Autoimmune antibody testing was negative in this patient when she presented with diabetes, as described in similar cases. The literature suggests up to one third of survivors may develop permanent diabetes as late as eleven years after the acute illness. The pathophysiology is very different to immune-mediated type one diabetes mellitus, with testing for autoantibodies being negative in case reports of these patients. The full extent of the mechanism by which insulin deficiency occurs is unknown, however, it is recognised that the pathological processes occurring in the body during the acute illness can lead to physical destruction of the pancreas. Fibrosis, pancreatic arteriolar thrombosis and microangiopathy of the pancreatic microvasculature leading to beta cell death have all been described. Whilst absolute numbers of patients developing diabetes secondary to HUS remain small, the literature supports the theory that diabetes may be a lasting consequence in patients who have had HUS and that these patients may benefit from routine follow up screening or increased awareness of this possible long-term complication.
Keywords: Haemolytic uraemic syndrome; E. coli O157:H7; diabetes mellitus; long-term complications.
07 - 09 Nov 2018
British Society for Paediatric Endocrinology and Diabetes