Annals of gastroenterology · 2014
Insulin resistance in euglycemic cirrhosis.
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Goswami Amitava, Bhargava Narendra, Dadhich Sunil, Kulamarva Ganaraj
Аннотация
BACKGROUND: Insulin resistance (IR) is associated with hepatic fibrosis and cirrhosis, regardless of its etiology but the mechanism of hyperinsulinemia in cirrhosis is still unclear. The current study was designed to assess hyperinsulinemia and pancreatic β-cell function in euglycemic cirrhosis of varied etiology.
METHODS: A cross sectional case control study of 100 subjects. IR was assessed by the Homeostasis Model Assessment (HOMA) and quantitative insulin sensitivity check index in euglycemic cirrhosis of varied etiology and in different stages of cirrhosis. HOMA-β was calculated for insulin secretion ability of pancreatic β-cells in different stages of cirrhosis.
RESULTS: Overall IR in euglycemic cirrhosis was seen in 68.5%. IR was seen in the order hepatitis C (100%), non-alcoholic fatty liver disease (100%), autoimmune hepatitis (100%), hepatocellular carcinoma (80%), alcoholic liver disease (72%) and hepatitis B (45%). HOMA-IR value was raised in Child Turcotte Pugh (CTP) score >9 (P value 0.0004) and model of end stage liver disease (MELD) score >15 (P value 0.02). HOMA-β was raised in CTP score >9 (P value 0.02) and MELD score >15 (P value 0.0003). HOMA-β level among diabetic controls was 27.1±7.7 compared to 154.6±80.7 in euglycemic cases (P value <0.0001).
CONCLUSION: IR is common in euglycemic cirrhosis and with advancement of liver disease; there is a compensatory increase in pancreatic β-cell insulin secretion to overcome the IR. However, over a period of time with fall in β-cell function development of hepatogenous diabetes may occur.
METHODS: A cross sectional case control study of 100 subjects. IR was assessed by the Homeostasis Model Assessment (HOMA) and quantitative insulin sensitivity check index in euglycemic cirrhosis of varied etiology and in different stages of cirrhosis. HOMA-β was calculated for insulin secretion ability of pancreatic β-cells in different stages of cirrhosis.
RESULTS: Overall IR in euglycemic cirrhosis was seen in 68.5%. IR was seen in the order hepatitis C (100%), non-alcoholic fatty liver disease (100%), autoimmune hepatitis (100%), hepatocellular carcinoma (80%), alcoholic liver disease (72%) and hepatitis B (45%). HOMA-IR value was raised in Child Turcotte Pugh (CTP) score >9 (P value 0.0004) and model of end stage liver disease (MELD) score >15 (P value 0.02). HOMA-β was raised in CTP score >9 (P value 0.02) and MELD score >15 (P value 0.0003). HOMA-β level among diabetic controls was 27.1±7.7 compared to 154.6±80.7 in euglycemic cases (P value <0.0001).
CONCLUSION: IR is common in euglycemic cirrhosis and with advancement of liver disease; there is a compensatory increase in pancreatic β-cell insulin secretion to overcome the IR. However, over a period of time with fall in β-cell function development of hepatogenous diabetes may occur.