Clinical research studyHypoglycemia-associated Mortality Is Not Drug-associated but Linked to Comorbidities
Section snippets
Study Population
We examined a retrospective cohort of patients hospitalized at Montefiore Medical Center in Bronx, New York, from January 1 to December 31, 2007. The data assembled were restricted to nonpregnant patients aged 21 years or more and included those with and without the concurrent diagnosis of diabetes who were admitted to the general units. Patients admitted or transferred to medical or surgical intensive care units and patients discharged from the emergency department were excluded from this
Baseline Characteristics
We identified 31,970 patients with at least 1 blood glucose determination during their hospitalization (mean age 61 ± 17.8 years, 58% were female). Self-designated race/ethnicity was available in 92.6% of patients (whites: 23.6%, blacks: 32.2%, Hispanics: 36.8%, unknown: 7.4%). Table 1 presents baseline patient characteristics of those subjects who did (n = 3349) and did not (n = 28,621) develop hypoglycemia during their hospital stay. The proportion of female patients was similar between the 2
Discussion
In this large group of patients hospitalized in the general wards, hypoglycemia was associated with greater risk of in-hospital mortality, but this association only occurred in those who developed it spontaneously. In contrast, hypoglycemia that occurred with initiation of antidiabetic medications was not associated with higher in-hospital mortality. These findings suggest that hypoglycemia in hospitalized patients may be a marker of disease burden rather than a direct cause of death, results
Conclusions
Our study shows that although hypoglycemia is associated with increased in-hospital mortality among patients admitted to the general wards, this risk is confined to patients with spontaneous hypoglycemia. In contrast, drug-associated hypoglycemia is not associated with higher in-hospital mortality. Although hypoglycemia remains an undesirable event and should be avoided when possible, these data suggest that hypoglycemia behaves as a marker of disease burden rather than as a direct cause of
Acknowledgments
The authors thank Drs Harry Shamoon, Norman Fleischer, and Martin I. Surks, Albert Einstein College of Medicine, for critically reading the manuscript and providing helpful suggestions.
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Cited by (0)
Funding: This publication was made possible by the Clinical and Translational Science Award Grant UL1 RR025750 and KL2 RR025749 and TL1 RR025748 from the National Center for Research Resources, a component of the National Institutes of Health (NIH), and NIH Roadmap for Medical Research. Its contents are solely the responsibility of the authors and do not necessary represent the official view of the National Center for Research Resources or NIH.
Conflict of Interest: LB, WNS, and JZ have not received any support from any organization for the submitted work. LB and WNS have no financial relationships with any organizations that might have an interest in the submitted work in the previous 3 years. JZ serves on an advisory panel for Takeda Pharmaceutical North America and on the speakers bureau for Amylin Pharmaceuticals, Eli Lilly, Merck, Novo Nordisk, and Sanofi-Aventis.
Authorship: LB, WNS, and JZ had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. LB designed the study, researched the data, wrote, reviewed, and edited the manuscript. WNS contributed to data collection, researched the data, and contributed to writing, reviewing, and editing the manuscript. JZ contributed to designing the study, writing, reviewing, and editing the manuscript.