title: Normoglycemia in nondiabetic African Americans hospitalized with heart failure.
abstract: BACKGROUND
  In nondiabetic patients hospitalized with multiorgan failure, neurohormonal activation can lead to stress-induced hyperglycemia (>140 mg/dL), as could Mg(2+) and Zn(2+) deficiencies. However, it is currently uncertain whether nondiabetic African Americans (AA) hospitalized with either chronic, decompensated biventricular failure (DecompHF) having hepatic and splanchnic congestion, ionized hypomagnesemia and hypozincemia, or acute left heart failure (LHF) would exhibit hyperglycemia at admission.
  
  
  METHODS
  We retrospectively examined admission serum glucose in 77 AA patients without a history of diabetes, who were hospitalized with heart failure. This examination included 41 patients admitted during a 4-month period with chronic DecompHF and whose clinical presentation included findings of expanded intra- and extravascular volumes, together with echocardiographic evidence of marked tricuspid regurgitation and distended inferior vena cava, without respiratory variation. These patients were compared with 14 nondiabetic patients hospitalized during the same time period with acute LHF. We also studied admission serum glucose in 22 patients who were admitted with DecompHF having documented hypomagnesemia and hypozincemia.
  
  
  RESULTS
  Admission serum glucose (mean +/- standard error of mean) in patients with chronic DecompHF was 105.41 +/- 4.08 mg/dL and was modestly elevated (140-160 mg/dL) in 3 patients. In those with acute LHF, glucose was 94.86 +/- 3.96 mg/dL and did not exceed 140 mg/dL in any patient. Glucose (103.2 +/- 4.3 mg/dL) was not elevated in patients having chronic DecompHF and reduced ionized Mg(2+) and serum Zn(2+) (0.44 +/- 0.01 mmol/L and 69.6 +/- 3.2 mug/dL, respectively).
  
  
  CONCLUSIONS
  Hyperglycemia at admission was infrequent in nondiabetic AA patients hospitalized with either acute LHF or chronic DecompHF, which may have also included hypomagnesemia and hypozincemia. This calls into question the need for intensive insulin therapy in these patients.
authors.affiliation: From the Division of Cardiovascular Diseases, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.
authors.forename: Marshall S
authors.initials: MS
authors.lastname: Shook
authors.forename: Haris
authors.initials: H
authors.lastname: Zafarullah
authors.forename: Maeda D
authors.initials: MD
authors.lastname: Nelson
authors.forename: Syamal K
authors.initials: SK
authors.lastname: Bhattacharya
authors.forename: Richard C
authors.initials: RC
authors.lastname: Davis
authors.forename: Kevin P
authors.initials: KP
authors.lastname: Newman
authors.forename: Karl T
authors.initials: KT
authors.lastname: Weber
mesh_terms: D001741:Black or African American; D001786:Blood Glucose / Q000032:analysis*; D003920:Diabetes Mellitus; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000208:ethnology; D006801:Humans; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies
chemical_list: D001786:Blood Glucose