Hypomagnesemia and the risk of new-onset diabetes after liver transplantation
β Scribed by Steven Van Laecke; Federico Desideri; Anja Geerts; Hans Van Vlierberghe; Frederik Berrevoet; Xavier Rogiers; Roberto Troisi; Bernard de Hemptinne; Raymond Vanholder; Isabelle Colle
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 279 KB
- Volume
- 16
- Category
- Article
- ISSN
- 1527-6465
- DOI
- 10.1002/lt.22146
No coin nor oath required. For personal study only.
β¦ Synopsis
New-onset diabetes after transplantation (NODAT) is a frequent complication after liver transplantation and has a negative impact on both patient and graft survival. In analogy with the previous finding of an association between posttransplant hypomagnesemia and NODAT in renal transplant recipients, the relation between both pretransplant and posttransplant hypomagnesemia and NODAT was studied in liver transplant recipients (LTRs). One hundred sixty-nine adult LTRs (>18 years old) without diabetes who underwent transplantation between 2004 and 2009 were studied (mean age ΒΌ 52.11 6 12.6 years, proportion of LTRs who were male ΒΌ 67.5%, body mass index ΒΌ 25.5 6 4.4 kg/m 2 , proportion receiving tacrolimus ΒΌ 90.0%). NODAT was defined according to the American Diabetes Association criteria. The association of NODAT with both pretransplant and posttransplant serum magnesium (Mg) was examined. Overall, 52 of 169 patients (30.8%) developed NODAT, and 57.7% of these (30 patients) were treated with antidiabetic drugs. Both pretransplant Mg levels and Mg levels in the first month after transplantation were lower in patients developing NODAT (P ΒΌ 0.008 and P ΒΌ 0.001, respectively). A multivariate regression model (adjusted for weight, pretransplant glucose levels, hyperglycemia in the first week after transplantation, gender, hepatitis C, and corticosteroid dosing) demonstrated both pretransplant Mg levels (hazard ratio ΒΌ 0.844 per 0.1 mg/dL increase, 95% confidence interval ΒΌ 0.764-0.932, P ΒΌ 0.001) and posttransplant Mg levels (hazard ratio ΒΌ 0.659, 95% confidence interval ΒΌ 0.518-0.838, P ΒΌ 0.001) to be independent predictors of NODAT together with age, biopsy-proven acute rejection, and cytomegalovirus (CMV) infection in the first year after transplantation. In conclusion, pretransplant hypomagnesemia and early posttransplant hypomagnesemia are independent predictors of new-onset diabetes after liver transplantation. Other risk factors are age, biopsy-proven acute rejection, and CMV infection.
π SIMILAR VOLUMES
New-onset diabetes mellitus (NODM) develops in approximately 15% of liver transplant recipients, and a similar proportion of patients have diabetes prior to transplantation. Preexisting diabetes and probably NODM are associated with increased mortality and risk of infection. NODM occurs more frequen
Epidemiological studies suggest diabetes mellitus (DM) may be an extrahepatic manifestation of chronic hepatitis C virus (HCV) infection. Since diabetes and HCV are common in liver transplant recipients, we sought to examine the unique contribution of HCV infection to risk of de novo diabetes posttr
New-onset diabetes mellitus (NODM) is seen in 10-30% of renal and 9-21% of liver transplant recipients. [1][2][3][4][5][6][7][8][9][10][11][12][13][14] Older age, black race, obesity, hepatitis C virus (HCV) infection, family history of diabetes mellitus (DM), and use of tacrolimus or corticosteroid
in memoriam
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