Elevated serum cobalamin in patients with decompensated biventricular failure

Haris Zafarullah, Atta U. Shahbaz, Ragheed Alturkmani, Stephen P. Laguardia, Basil M. Paulus, David L. Battin, M. Omer Afzal, Richard C. Davis, J. Lacey Smith, Karl Weber

Research output: Contribution to journalArticle

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Abstract

BACKGROUND: Serum cobalamin (vitamin B12), bound to transcobalamin II, is taken up by the endothelium of the hepatic vasculature via a receptor-mediated membrane transport process. We hypothesized hepatic congestion is associated with elevated serum B12 without hepatocyte necrosis. METHODS AND RESULTS: Serum B12, aspartate and alanine transaminases, alkaline phosphatase, bilirubin (Bili), and brain natriuretic peptide (BNP) were monitored at the time of admission in 91 hospitalized patients: (a) 38 with decompensated biventricular failure having systemic venous distention, tricuspid regurgitation (TR), and echocardiographic evidence of inferior vena cava dilation and moderate to marked TR; (b) 18 with acute left heart failure having a myocardial infarction, an ischemic cardiomyopathy, or hypertensive heart disease; and (c) 35 without clinical evidence of failure despite myocardial infarction, pericarditis, or atrial arrhythmia. Serum cobalamin (normal 180-600 pg/mL) was elevated with biventricular failure (861.4 ± 53.0 pg/mL) compared with (P < 0.0001) left heart or no failure, where B12 remained normal. Serum aspartate, alanine, and alkaline phosphatase were normal in each group whereas Bili was increased (1.8 ± 0.2 mg/dL; P < 0.05) with biventricular failure. Plasma BNP was elevated in each group. CONCLUSIONS: Elevated cobalamin and Bili are respective biomarkers of hepatocellular dysfunction and cholestasis in patients having decompensated biventricular failure with systemic venous distention and TR without hepatocyte necrosis vis-à-vis left heart failure or in the absence of clinical failure. Elevated plasma BNP did not distinguish between the presence or absence of systemic venous congestion.

Original languageEnglish (US)
Pages (from-to)383-388
Number of pages6
JournalAmerican Journal of the Medical Sciences
Volume336
Issue number5
DOIs
StatePublished - Jan 1 2008

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Vitamin B 12
Tricuspid Valve Insufficiency
Brain Natriuretic Peptide
Bilirubin
Serum
Alkaline Phosphatase
Hepatocytes
Necrosis
Heart Failure
Myocardial Infarction
Transcobalamins
Pericarditis
Liver
Cholestasis
Hyperemia
Inferior Vena Cava
Aspartate Aminotransferases
Alanine Transaminase
Cardiomyopathies
Aspartic Acid

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Zafarullah, H., Shahbaz, A. U., Alturkmani, R., Laguardia, S. P., Paulus, B. M., Battin, D. L., ... Weber, K. (2008). Elevated serum cobalamin in patients with decompensated biventricular failure. American Journal of the Medical Sciences, 336(5), 383-388. https://doi.org/10.1097/01.MAJ.0000310651.34229.73

Elevated serum cobalamin in patients with decompensated biventricular failure. / Zafarullah, Haris; Shahbaz, Atta U.; Alturkmani, Ragheed; Laguardia, Stephen P.; Paulus, Basil M.; Battin, David L.; Afzal, M. Omer; Davis, Richard C.; Smith, J. Lacey; Weber, Karl.

In: American Journal of the Medical Sciences, Vol. 336, No. 5, 01.01.2008, p. 383-388.

Research output: Contribution to journalArticle

Zafarullah, H, Shahbaz, AU, Alturkmani, R, Laguardia, SP, Paulus, BM, Battin, DL, Afzal, MO, Davis, RC, Smith, JL & Weber, K 2008, 'Elevated serum cobalamin in patients with decompensated biventricular failure', American Journal of the Medical Sciences, vol. 336, no. 5, pp. 383-388. https://doi.org/10.1097/01.MAJ.0000310651.34229.73
Zafarullah H, Shahbaz AU, Alturkmani R, Laguardia SP, Paulus BM, Battin DL et al. Elevated serum cobalamin in patients with decompensated biventricular failure. American Journal of the Medical Sciences. 2008 Jan 1;336(5):383-388. https://doi.org/10.1097/01.MAJ.0000310651.34229.73
Zafarullah, Haris ; Shahbaz, Atta U. ; Alturkmani, Ragheed ; Laguardia, Stephen P. ; Paulus, Basil M. ; Battin, David L. ; Afzal, M. Omer ; Davis, Richard C. ; Smith, J. Lacey ; Weber, Karl. / Elevated serum cobalamin in patients with decompensated biventricular failure. In: American Journal of the Medical Sciences. 2008 ; Vol. 336, No. 5. pp. 383-388.
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abstract = "BACKGROUND: Serum cobalamin (vitamin B12), bound to transcobalamin II, is taken up by the endothelium of the hepatic vasculature via a receptor-mediated membrane transport process. We hypothesized hepatic congestion is associated with elevated serum B12 without hepatocyte necrosis. METHODS AND RESULTS: Serum B12, aspartate and alanine transaminases, alkaline phosphatase, bilirubin (Bili), and brain natriuretic peptide (BNP) were monitored at the time of admission in 91 hospitalized patients: (a) 38 with decompensated biventricular failure having systemic venous distention, tricuspid regurgitation (TR), and echocardiographic evidence of inferior vena cava dilation and moderate to marked TR; (b) 18 with acute left heart failure having a myocardial infarction, an ischemic cardiomyopathy, or hypertensive heart disease; and (c) 35 without clinical evidence of failure despite myocardial infarction, pericarditis, or atrial arrhythmia. Serum cobalamin (normal 180-600 pg/mL) was elevated with biventricular failure (861.4 ± 53.0 pg/mL) compared with (P < 0.0001) left heart or no failure, where B12 remained normal. Serum aspartate, alanine, and alkaline phosphatase were normal in each group whereas Bili was increased (1.8 ± 0.2 mg/dL; P < 0.05) with biventricular failure. Plasma BNP was elevated in each group. CONCLUSIONS: Elevated cobalamin and Bili are respective biomarkers of hepatocellular dysfunction and cholestasis in patients having decompensated biventricular failure with systemic venous distention and TR without hepatocyte necrosis vis-{\`a}-vis left heart failure or in the absence of clinical failure. Elevated plasma BNP did not distinguish between the presence or absence of systemic venous congestion.",
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T1 - Elevated serum cobalamin in patients with decompensated biventricular failure

AU - Zafarullah, Haris

AU - Shahbaz, Atta U.

AU - Alturkmani, Ragheed

AU - Laguardia, Stephen P.

AU - Paulus, Basil M.

AU - Battin, David L.

AU - Afzal, M. Omer

AU - Davis, Richard C.

AU - Smith, J. Lacey

AU - Weber, Karl

PY - 2008/1/1

Y1 - 2008/1/1

N2 - BACKGROUND: Serum cobalamin (vitamin B12), bound to transcobalamin II, is taken up by the endothelium of the hepatic vasculature via a receptor-mediated membrane transport process. We hypothesized hepatic congestion is associated with elevated serum B12 without hepatocyte necrosis. METHODS AND RESULTS: Serum B12, aspartate and alanine transaminases, alkaline phosphatase, bilirubin (Bili), and brain natriuretic peptide (BNP) were monitored at the time of admission in 91 hospitalized patients: (a) 38 with decompensated biventricular failure having systemic venous distention, tricuspid regurgitation (TR), and echocardiographic evidence of inferior vena cava dilation and moderate to marked TR; (b) 18 with acute left heart failure having a myocardial infarction, an ischemic cardiomyopathy, or hypertensive heart disease; and (c) 35 without clinical evidence of failure despite myocardial infarction, pericarditis, or atrial arrhythmia. Serum cobalamin (normal 180-600 pg/mL) was elevated with biventricular failure (861.4 ± 53.0 pg/mL) compared with (P < 0.0001) left heart or no failure, where B12 remained normal. Serum aspartate, alanine, and alkaline phosphatase were normal in each group whereas Bili was increased (1.8 ± 0.2 mg/dL; P < 0.05) with biventricular failure. Plasma BNP was elevated in each group. CONCLUSIONS: Elevated cobalamin and Bili are respective biomarkers of hepatocellular dysfunction and cholestasis in patients having decompensated biventricular failure with systemic venous distention and TR without hepatocyte necrosis vis-à-vis left heart failure or in the absence of clinical failure. Elevated plasma BNP did not distinguish between the presence or absence of systemic venous congestion.

AB - BACKGROUND: Serum cobalamin (vitamin B12), bound to transcobalamin II, is taken up by the endothelium of the hepatic vasculature via a receptor-mediated membrane transport process. We hypothesized hepatic congestion is associated with elevated serum B12 without hepatocyte necrosis. METHODS AND RESULTS: Serum B12, aspartate and alanine transaminases, alkaline phosphatase, bilirubin (Bili), and brain natriuretic peptide (BNP) were monitored at the time of admission in 91 hospitalized patients: (a) 38 with decompensated biventricular failure having systemic venous distention, tricuspid regurgitation (TR), and echocardiographic evidence of inferior vena cava dilation and moderate to marked TR; (b) 18 with acute left heart failure having a myocardial infarction, an ischemic cardiomyopathy, or hypertensive heart disease; and (c) 35 without clinical evidence of failure despite myocardial infarction, pericarditis, or atrial arrhythmia. Serum cobalamin (normal 180-600 pg/mL) was elevated with biventricular failure (861.4 ± 53.0 pg/mL) compared with (P < 0.0001) left heart or no failure, where B12 remained normal. Serum aspartate, alanine, and alkaline phosphatase were normal in each group whereas Bili was increased (1.8 ± 0.2 mg/dL; P < 0.05) with biventricular failure. Plasma BNP was elevated in each group. CONCLUSIONS: Elevated cobalamin and Bili are respective biomarkers of hepatocellular dysfunction and cholestasis in patients having decompensated biventricular failure with systemic venous distention and TR without hepatocyte necrosis vis-à-vis left heart failure or in the absence of clinical failure. Elevated plasma BNP did not distinguish between the presence or absence of systemic venous congestion.

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