Metabolic risk factors in southern Taiwanese with impaired fasting glucose of 100 to 109 mg/dL

Hung, Wei‐Wen; Chang, Chun‐Chi; lee, Yau-Jiunn; Hsin, Shih-Chieh; Lin, Kun‐Der; Hsieh, Ming‐Chia; Hsiao, Pi‐Jung; Shin, Shyi–Jang

doi:10.1016/j.metabol.2006.11.013

Cited by 4 publications

(2 citation statements)

References 33 publications

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“…However, this practice is based on the relative convenience and lower cost of FPG compared with a 75‐g oral glucose tolerance test (OGTT) [32,33]. It was estimated that 19.3–59.3% of glucose abnormalities remained undetected using the current IFG criteria alone [34].…”

Section: Clinical Viewmentioning

confidence: 99%

Glucose abnormalities in hepatitis C virus infection

Huang¹,

Yu²,

Yu³

et al. 2012

The Kaohsiung J of Med Scie

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Hepatitis C virus (HCV) infection is one of the most important causes of cirrhosis and hepatocellular carcinoma and has a tremendous impact on public health worldwide. HCV is both hepatotropic and lymphotropic. Replication of HCV in diseased extrahepatic organs and tissues may either trigger latent autoimmunity or induce autoimmune disorders. In addition to established liver injury, type 2 diabetes mellitus (T2DM) is an important feature of extrahepatic metabolic disorders which is attributed to HCV infection. It also has some impact on the disease activity, disease course, clinical outcomes, and treatment efficacy of antiviral therapy. Previous experimental and clinical findings have highly suggested that HCV per se is diabetogenic. The cause-effect interaction between a common endocrine disorder and an infectious disease is an important issue to elucidate. Although the precise mechanisms whereby HCV infection leads to insulin resistance (IR) and glucose abnormalities are not entirely clear, it differs from the usual pathogenesis of T2DM in those with non-HCV liver diseases. This review initially highlights epidemiological and pathophysiological studies addressing the mutual link between chronic HCV infection (CHC) and T2DM. The characteristics of glucose abnormalities in this special population are depicted from the current evidence. The mutual roles of IR and CHC with respect to the prediction of treatment efficacy, how treatment response affects IR, and the role of pancreatic beta cell function in the entire suite are discussed. With the rapid progression of antiviral therapy for CHC in the past decade, we have also listed some points of future perspective in this issue.

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Section: Clinical Viewmentioning

confidence: 99%

Glucose abnormalities in hepatitis C virus infection

Huang¹,

Yu²,

Yu³

et al. 2012

The Kaohsiung J of Med Scie

View full text Add to dashboard Cite

show abstract

“…DM history and coadministration of oral hypoglycemic agents or insulin were reviewed by the physicians and recorded by trained coordinators in the outpatient department before, during, and after antiviral therapy. Because glucose abnormalities might be underestimated by measuring fasting plasma glucose (FPG) alone, particularly in CHC patients, [ 25 ] 75 g oral glucose tolerance tests (OGTT) were performed in patients without DM history before and 6 months after completing treatment, as previously described. [ 15 , 26 ] The judgment of glucose abnormality was based on the definition established by the American Diabetes Association.…”

Section: Methodsmentioning

confidence: 99%