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Insulin resistance in euglycemic cirrhosis
#MMPMID24974878
Goswami A
; Bhargava N
; Dadhich S
; Kulamarva G
Ann Gastroenterol
2014[]; 27
(3
): 237-243
PMID24974878
show ga
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 ?-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-? was calculated for insulin secretion
ability of pancreatic ?-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-? was raised in CTP score >9 (P value 0.02) and MELD score >15 (P value
0.0003). HOMA-? 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 ?-cell insulin secretion to overcome the IR. However, over a period
of time with fall in ?-cell function development of hepatogenous diabetes may
occur.