Prevalence and Treatment of New-Onset Diabetes Mellitus After Liver Transplantation in Korean Children: A Single-Center Study

Cho, J.M.; Oh, Seok Hee; Kim, K.M.; Namgung, Jung-Man; Kim, D.Y.; Song, Gi‐Won; Ha, Tae Yong; Moon, Deok‐Bog; Ahn, Curie; Hwang, Shin; Lee, S.G.

doi:10.1016/j.transproceed.2013.11.065

Cited by 4 publications

(4 citation statements)

References 11 publications

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“…Measurable c‐peptide levels and high insulin dose requirements have also been described in patients treated with tacrolimus for LT, consistent with insulin resistance . The DM associated with tacrolimus has been reported to be reversible with tapering of tacrolimus dose or selecting an alternative immunosuppressive regimen .…”

Section: Pathogenesis Of Nodatmentioning

confidence: 90%

“…There are no data reporting presenting symptoms for NODAT. As most patients with NODAT still produce some insulin at diagnosis, it is rare for patients to present in diabetic ketoacidosis, although it has been reported in the pediatric literature . The percentage of patients at NODAT diagnosis with frank polyuria and polydipsia, versus asymptomatic hyperglycemia, is unknown.…”

Section: Screening and Diagnosis New‐onset Dm After Liver Transplantmentioning

confidence: 99%

“… reported that 15 of 17 adult patients with NODAT, treated initially with tacrolimus and converted to cyclosporine A for uncontrolled NODAT, had resolution of DM. A pediatric case series reported that seven of 18 patients with NODAT were converted from tacrolimus to cyclosporine, with steroid taper and addition of MMF, and had resolution of NODAT at 1–19 months after diagnosis; the other patients in the series had steroid tapers alone, or with the addition of MMF, with resolution of NODAT at 0.5–2 months . Not all studies have reported positive results, and in another series of adult patients, there was no significant difference in glucose intolerance or frank NODAT when comparing cyclosporine A and tacrolimus immunosuppressive regimens .…”

Section: Pathogenesis Of Nodatmentioning

confidence: 99%

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New‐onset diabetes mellitus after pediatric liver transplantation

Regelmann

Goldis

Arnon

2015

Pediatric Transplantation

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In the first five yr after liver transplant, approximately one in 10 pediatric recipients will develop NODAT. Factors associated with higher risk for NODAT have been difficult to identify due to lack of uniformity in reporting and data collection. Limited studies have reported higher risk in those who are at an older age at transplant, those with high-risk ethnic backgrounds, and in those with particular underlying conditions, such as CF and primary sclerosing cholangitis. Immunosuppressive medications, including tacrolimus, cyclosporine A, GC, and sirolimus, have been implicated as contributing to NODAT, to varying degrees. Identifying those at highest risk, appropriately screening, and diagnosing NODAT is critical to initiating timely treatment and avoiding potential complications. In the pediatric population, treatment is limited primarily to insulin, with some consideration for metformin. Children with NODAT should be monitored carefully for complications of DM, including microalbuminuria, hypertension, hyperlipidemia, and retinopathy.

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Section: Pathogenesis Of Nodatmentioning

confidence: 90%

Section: Screening and Diagnosis New‐onset Dm After Liver Transplantmentioning

confidence: 99%

Section: Pathogenesis Of Nodatmentioning

confidence: 99%

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New‐onset diabetes mellitus after pediatric liver transplantation

Regelmann

Goldis

Arnon

2015

Pediatric Transplantation

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“…For example, NODM has been demonstrated to impact patients' quality of life and possibly to impair graft survival as well as to increase the possibility of infections, neurologic complications, and cardiac events. 1,[3][4][5][6] It appears that both genetic and environmental factors are involved in the pathogenesis of NODM. 7 In large part, the pathophysiology of NODM combines pancreatic β-cell dysfunction with the presence of insulin resistance.…”

Section: Introductionmentioning

confidence: 99%

Glutathione S-Transferase Gene Polymorphisms and the Development of New-Onset Diabetes After Liver Transplant

Musavi

Moasser²,

Zareei³

et al. 2019

Exp Clin Transplant

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Objectives: The association between the glutathione Stransferase polymorphisms and the development of new-onset diabetes mellitus after liver transplant was studied. Materials and Methods: Peripheral blood samples were collected from 106 liver transplant patients divided into 2 groups: 52 with new-onset diabetes mellitus and 54 without new-onset diabetes mellitus; 169 healthy individuals with no clinical evidence of diabetes mellitus were selected as a control group. The multiplex polymerase chain reaction technique was used for genotyping GSTM1 and GSTT1 genes, using the cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) gene as an internal control. The genotype of GSTP1 was determined using the restriction fragment length polymorphism-polymerase chain reaction technique. Results: The frequency of both GSTM1 null and GSTT1 null genotypes was not significantly different in liver transplant patients with new-onset diabetes mellitus compared with the control group (P = .11 for GSTM1; P = .71 for GSTT1). Also, there was no statistically significant association between the frequency of the GSTP1 genotypes in the liver transplant patients with new-onset diabetes mellitus compared with controls. Neither GSTM1 nor GSTT1 null genotypes were associated with the risk of developing new-onset diabetes mellitus (P = .22 for GSTM1; P = .56 for GSTT1). However, the frequency of the heterozygous mutation (AG) in the A313G GSTP1 polymorphism in patients with new-onset diabetes mellitus was significantly higher than in patients without new-onset diabetes mellitus (55.8% vs 7.4%; P = .00). Thus, the risk of developing new-onset diabetes mellitus was significantly higher in patients presenting with heterozygous GSTP1 genotypes (odds ratio = 15.76; 95% confidence interval = 4.53-60.28; P = .00). Conclusions: The GSTP1 AG genotype was associated with an increased susceptibility to the development of new-onset diabetes mellitus after liver transplant.

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