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题名:Insulin resistance and insulin secretion in renal transplant recipients with hepatitis C.
作者:UCHIDA J; IWAI T; MACHIDA Y; KUWABARA N; KABEI K; KUMADA N; NAKATANI T;
来源:Transplant Proc. 2013 May;45(4):1540-3. doi: 10.1016/j.transproceed.2013.01.053. [ IF= 0.00 ] ]
URL :10.1016/j.transproceed.2013.01.053
日期:20130606
摘要:BACKGROUND: Several reports have suggested an association between hepatitis C
virus (HCV) infection and new-onset diabetes after transplantation (NODAT). NODAT
is a common complication after renal transplantation, and it has been associated
with increased long-term morbidity and mortality. HCV-positive recipients may
have abnormal glucose metabolism, even though NODAT has never been previously
diagnosed. The aim of this study was to analyze the pathogenic factors
responsible for glucose metabolism in a series of HCV-positive renal transplant
recipients. METHODS: The study population comprised 16 renal transplant patients
who received their grafts from deceased or living donors with anti-HCV
antibodies. HCV-negative transplant recipients were individually matched with
these HCV-positive recipients by year of transplantation, sex, age, serum
creatinine levels, and type of calcineurin inhibitors. None of the patients had
been diagnosed with diabetes. Insulin secretion and insulin resistance were
determined by a 75-g oral glucose tolerance test (OGTT) and compared between the
2 groups. Categories of glucose tolerance were defined according to World Health
Organization criteria. RESULTS: Glucose intolerance (impaired fasting glucose,
impaired glucose tolerance, diabetes mellitus) as assessed by OGTT was detected
in 7 of the HCV-positive recipients (43.8%) and 3 of the HCV-negative recipients.
The homeostasis model assessment of insulin resistance was greater in the
HCV-positive recipients than in the HCV-negative recipients. The homeostasis
model assessment of beta-cell function was higher in the HCV-positive recipients
than in the HCV-negative recipients. CONCLUSIONS: The frequency of glucose
intolerance tended to be higher in HCV-positive recipients. Furthermore, insulin
resistance was greater and insulin secretion higher in HCV-positive recipients,
which indicated that the increase in insulin secretion compensated for insulin
resistance observed in these patients. However, HCV-positive renal transplant
recipients may ultimately develop NODAT as this compensation diminishes with
time.

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