Daniel J. Brotman

BACKGROUND:Risk factors for hospital‐acquired gastrointestinal bleeding in the intensive care unit are established, and acid‐suppressive prophylaxis has been advocated for certain subsets of critically ill patients. In contrast, risk factors and appropriate prevention strategies are not yet established for general medical patients. The objective of this study was to identify risk factors for nosocomial gastrointestinal bleeding (GIB) in non–critically ill medical patients, to evaluate the utility of prophylactic gastric acid suppression, and to characterize the endoscopic lesions.METHODS:This was a retrospective case–control study that took place at a U.S. tertiary care center. All patients admitted to the General Medicine ward for nongastrointestinal disorders who developed clinically relevant gastrointestinal bleeding during admission or within 4 weeks of discharge were considered cases. Clinically relevant bleeding was defined as any bleeding requiring esophagogastroduodenoscopy (EGD). Random controls were matched to cases by date of hospitalization in a 1:1 ratio. Clinical information was extracted by chart review.RESULTS:Of 17,707 patients admitted to the General Medicine ward over a 4‐year period, 73 (0.41%) met the case definition. The main risk factor for nosocomial GIB was treatment with full dose anticoagulants or clopidogrel (OR = 5.4; 2.6–11.7; P < .0001). Use of aspirin, nonsteroidal anti‐inflammatory medications, and glucocorticoids did not differ significantly between cases and controls. De novo acid‐suppressive prophylaxis was not protective (OR = 1.0; 95% CI: 0.4–2.4; P = 0.97). Endoscopic abnormalities were noted in 74% of patients; many cases had lesions unlikely to be prevented by acid blockade.CONCLUSIONS:Hospital‐acquired gastrointestinal bleeding is uncommon in non–critically ill patients. Anticoagulation appears to be the most important risk factor for nosocomial GIB. Routine use of acid suppressant medications for prophylaxis is unnecessary in most hospitalized patients. Journal of Hospital Medicine 2006;1:13–20. © 2006 Society of Hospital Medicine.

Glucocorticoids are known to acutely increase blood pressure, suppress inflammation, and precipitate insulin resistance. However, the short-term effects of glucocorticoids on other cardiovascular risk factors remain incompletely characterized. Our objective was to determine the effects of a short course of dexamethasone on multiple cardiovascular biomarkers and to determine whether suppression of morning cortisol in response to low-dose dexamethasone is correlated with cardiovascular risk markers in healthy volunteers. We conducted a randomized, double-blind, placebo-controlled study. The study took place in a tertiary care hospital. Twenty-five healthy male volunteers, ages 19-39 yr, participated in the study. Subjects received either 3 mg dexamethasone twice daily or placebo for 5 d. Subjects also underwent a low-dose (0.5 mg) overnight dexamethasone suppression test. Parameters examined before and after the 5-d intervention included heart rate, blood pressure, weight, fasting lipid variables, homocysteine, renin, aldosterone, insulin resistance (homeostasis model assessment), high-sensitivity C-reactive protein, B-type natriuretic peptide, flow-mediated and nitroglycerin-mediated brachial artery dilatation, and heart rate recovery after exercise. All measurements were done in the morning hours in the fasting state. Dexamethasone increased systolic blood pressure, weight, B-type natriuretic peptide, and high-density-lipoprotein-cholesterol. Dexamethasone decreased resting heart rate, high-sensitivity C-reactive protein, and aldosterone and tended to attenuate nitroglycerin-mediated vasodilatation. There was no effect on flow-mediated vasodilatation, diastolic blood pressure, triglycerides, low-density-lipoprotein-cholesterol, nonesterified fatty acids, homocysteine, or heart rate recovery. The response of circulating cortisol to low-dose dexamethasone had no significant correlation with any of the cardiovascular risk markers. Short-term glucocorticoids elicits both favorable and unfavorable effects on different cardiovascular risk factors. Manipulation of specific glucocorticoid-responsive physiological pathways deserves further study.