Abstract
IntroductionCritical illness is commonly complicated by hyperglycaemia caused by mediators of stress and inflammation. Severity of disease is the main risk factor for development of hyperglycaemia, but not all severely ill develop hyperglycemia and some do even in mild disease. We hypothesised that acute disease only exposes a latent disturbance of glucose metabolism which puts those patients at higher risk for developing diabetes.MethodsMedical patients with no history of impaired glucose metabolism or other endocrine disorder admitted to an intensive care unit between July 1998 and June 2004 were considered for inclusion. Glucose was measured at least two times a day, and patients were divided into the hyperglycaemia group (glucose ≥7.8 mmol/l) and normoglycaemia group. An oral glucose tolerance test was performed within six weeks after discharge to disclose patients with unknown diabetes or pre-diabetes who were excluded. Patients treated with corticosteroids and those terminally ill were also excluded from the follow-up which lasted for a minimum of five years with annual oral glucose tolerance tests.ResultsA five-year follow-up was completed for 398 patients in the normoglycaemia group, of which 14 (3.5%) developed type 2 diabetes. In the hyperglycaemia group 193 patients finished follow-up and 33 (17.1%) developed type 2 diabetes. The relative risk for type 2 diabetes during five years after the acute illness was 5.6 (95% confidence interval (CI) 3.1 to 10.2).ConclusionsPatients with hyperglycaemia during acute illness who are not diagnosed with diabetes before or during the hospitalization should be considered a population at increased risk for developing diabetes. They should, therefore, be followed-up, in order to be timely diagnosed and treated.
Highlights
Critical illness is commonly complicated by hyperglycaemia caused by mediators of stress and inflammation
Adult patients admitted to the ICU were evaluated for inclusion if they had a negative history of diabetes mellitus (DM), impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or any other endocrine disorder
Diabetes or impaired glucose metabolism was diagnosed after discharge in 76 patients in the hyperglycaemia group which led to their exclusion from the follow-up decreasing hyperglycaemia group to 360 patients
Summary
Critical illness is commonly complicated by hyperglycaemia caused by mediators of stress and inflammation. Mediators of systemic inflammatory response, such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α), cause hyperglycaemia and peripheral insulin resistance by inducing the release of stress hormones. They alter insulin receptor signalling [12,13,14,15,16] and create insulin resistance. Consequent to inhibition of pancreatic beta-cells by cytokines and catecholamines, insulin concentrations may be normal or even decreased [17,18,19] Medical interventions, such as enteral and parenteral nutrition, administration of vasopressors and glucocorticoids, add even further to disturbed glucose homeostasis. We hypothesised that hospital acquired hyperglycaemia reveals this predisposition, that is, those patients are at risk for developing type 2 diabetes in the period subsequent to acute illness
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