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Hemoglobin A1 in cirrhosis of the liver
Insights
Patients with liver cirrhosis show similar HbA1 levels to healthy individuals, despite higher fasting plasma glucose. This suggests caution when interpreting HbA1 in liver cirrhosis due to glucose intolerance.
Area of Science:
- Hepatology
- Endocrinology
- Clinical Chemistry
Background:
- Liver cirrhosis frequently causes glucose intolerance due to hepatic dysfunction.
- Accurate assessment of glycemic control is crucial for managing patients with liver disease.
Purpose of the Study:
- To compare Hemoglobin A1c (HbA1) levels and blood sugar control in patients with liver cirrhosis (LC) against healthy controls (N), diabetes mellitus (DM), and chronic hepatitis (CH) groups.
- To investigate the relationship between HbA1 and fasting plasma glucose (FPG) across different patient cohorts.
Main Methods:
- Collected HbA1 and FPG data from patients with liver cirrhosis (n=12), healthy controls (n=43), diabetes mellitus (n=36), and chronic hepatitis (n=12).
- Analyzed correlations between HbA1 and various glucose measures, including FPG, daily glucose profiles, and oral glucose tolerance test (OGTT) results.
- Compared regression lines of HbA1 against glucose levels between the study groups.
Main Results:
- HbA1 levels in the liver cirrhosis group (6.40%) were similar to healthy controls (6.52%), but FPG was significantly higher (130 mg/dl vs 83 mg/dl).
- All groups demonstrated positive correlations between HbA1 and glucose measures.
- The regression of HbA1 on glucose differed significantly between the LC group and the DM/CH groups.
Conclusions:
- Hemoglobin A1c levels in liver cirrhosis patients may underestimate glycemic control compared to diabetes mellitus or chronic hepatitis patients.
- Caution is advised when interpreting HbA1 levels in the context of hepatic cirrhosis due to underlying glucose intolerance.
- Further research is needed to refine glycemic monitoring in liver cirrhosis.
Abstract:
Patients with cirrhosis of the liver (LC group, n = 12) frequently have glucose intolerance secondary to hepatic dysfunction. We compared HbA1 levels and other measures of blood sugar control in the LC group with those in healthy controls (N group, n = 43), patients with diabetes mellitus (DM group, n = 36), or patients with chronic hepatitis without evidence of cirrhosis (CH group, n = 12). HbA1 levels and the mean values of fasting plasma glucose for the past month (FPG) were as follows: LC group 6.40 +/- 0.36 (mean +/- SEM)% and 130 +/- 20 mg/dl, DM group 10.29 +/- 0.45% and 172 +/- 11 mg/dl, CH group 10.70 +/- 0.86% and 176 +/- 21 mg/dl, N group 6.52 +/- 0.11% and 83 +/- 1 mg/dl, respectively. HbA1 in the LC group was similar to that in the N group, although FPG in the former was higher (p less than 0.05). All groups showed statistically significant positive correlations between HbA1 levels and (a) FPG, (b) the daily profile of plasma glucose values, (c) the total or peak plasma glucose values during a 50 g-OGTT. The regression line in the LC group, however, was statistically different from that in DM or CH group. Thus, HbA1 in the LC group is lower than that in DM or CH in spite of equivalent glucose intolerance. Therefore, we suggest caution in the interpretation of HbA1 levels in hepatic cirrhosis.