Recently, the attention of the diabetes community has shifted to glycemic management in the inpatient setting, where there has been a rising chorus in support of stricter blood glucose control. We applaud the spirit of the current American College of Endocrinology (ACE) recommendations, which attempt to improve the hospital management of hyperglycemia (1). However, as we examine the very limited evidence upon which these guidelines are based, we are concerned about such prematurely stringent glucose targets. Indeed, there is a paucity of well-controlled randomized trials in which the feasibility and safety of specific insulin strategies in the variety of inpatient settings have been validated. Moreover, few have assessed actual outcomes at different glycemic ranges. We all recognize that several cross-sectional studies have consistently demonstrated that hyperglycemia correlates with increased morbidity and mortality in the acutely ill, particularly in the critically ill and in the perioperative setting (2–4). This association holds for both patients with previously diagnosed diabetes and those with newly recognized hyperglycemia (5). However, the directionality of this relationship remains controversial. Does acute hyperglycemia lead to poor clinical outcomes or is it a reflection of sicker patients, due to increased counterregulatory forces that simply manifest their stress in the form of elevated blood glucose? Is an elevated blood glucose a marker or a pathogenic mechanism of disease in these patients? Experimental evidence has clearly supported a cause-and-effect relationship. Leukocyte action, immunoglobulin production, wound healing, collagen production, endothelial function, cardiac performance, and fluid balance are each impaired in the setting of hyperglycemia, particularly when severe (6,7). Admittedly, most data stem from in vitro observations and from in vivo investigations employing animal models (8–10). Moreover, these studies were typically designed to contrast markedly elevated versus normal ambient glucose concentrations (8–10). And, because insulin …
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Inzucchi et al. (2005) studied this question.
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