[Clinicopathologic features of hepatic diabetic microangiopathy]

Zhonghua Bing Li Xue Za Zhi. 2012 Oct;41(10):676-80. doi: 10.3760/cma.j.issn.0529-5807.2012.10.007.
[Article in Chinese]

Abstract

Objective: To study the clinicopathological features of diabetic microangiopathy in liver and diabetic hepatosclerosis (DHS) of elderly male with type 2 diabetes mellitus (T2DM).

Methods: One hundred and twenty autopsy cases with T2DM (diabetic group) and contemporary 48 cases, non-diabetic and glucose tolerance abnormal, matched by gender and age (control group) were selected in the study. Cases with the cirrhosis and fibrosis of liver caused by other foregone etiological factors were excluded. The histopathological changes of microangiopathy in liver, hepatic portal areas and hepatic sinusoid were investigated by HE staining, histochemical and immunohistochemical stain methods. The clinical data of diagnostic DHS cases were analyzed.

Results: (1) Microangiopathy was observed in 54.2% (65/120) cases of diabetic group. Histological features: microangiopathy was found in interlobular arteries (especially in arteriole, the lumen diameter < 100 µm), which included endothelial denudation, eosinophilic material deposition in the tunica intima of artery, and eccentric intimal thickening. The smooth muscle fibers of tunica media were hyperplastic or atrophy. Fibroplasia and collagen deposition were found in the tunica adventitia of artery. Arterial lumina showed stenosis and occlusion. Microangiopathy was seen in 16.7% (8/48) cases of the control group. There was statistically significant difference between the two groups (χ(2) = 19.622, P < 0.01). (2) The fibrosis and sclerosis of portal areas were detected in 55.8% (67/120) cases of T2DM group. Hyaline collagen fiber tissues was deposited around interlobular arteries, interlobular veins and interlobular bile ducts, resulting in enlargement of the portal area and the secondary atrophy and disappearance of portal triad. The fibrosis and sclerosis of portal areas were detected in 22.9% (11/48) cases of the control group. There was a statistically significant difference between the two groups (χ(2) = 14.936, P < 0.01). (3) The pathological features of 14.2% (17/120) cases were consistent with the diagnosis of DHS. The fibrous tissue extended from fibrosis or sclerosis of portal areas, or eosinophilic material deposition in the hepatic sinusoid in non-zonal pattern. The results of histochemical staining showed collagen fiber deposition in hepatic sinusoid. Stainings for Collagen IV, SMA, CD34 were found in the hepatic sinusoid. The sclerosis of hepatic sinusoid was not detected in any case in the control group.Overall, 13/17 and 11/17 DHS cases had liver microangiopathy and portal areas sclerosis respectively. Diabetic nephropathy was seen in 10 of 17 DHS cases. Among the 17 cases, 7 cases showed ALP elevation, of which there were 3 cases with ALT and AST mild elevation.

Conclusions: Diabetic microangiopathy is common in the liver of elderly men with T2DM. And DHS is associated with diabetic microangiopathy. Fibrosis and sclerosis of portal areas may be the early or concomitant changes of DHS on histological ground. DHS is one of the complications of T2DM.

Publication types

  • English Abstract

MeSH terms

  • Actins / metabolism
  • Aged
  • Aged, 80 and over
  • Alanine Transaminase / blood
  • Alkaline Phosphatase / blood
  • Antigens, CD34 / metabolism
  • Aspartate Aminotransferases / blood
  • Collagen Type IV / metabolism
  • Diabetes Mellitus, Type 2 / complications*
  • Diabetic Angiopathies / blood
  • Diabetic Angiopathies / etiology
  • Diabetic Angiopathies / metabolism
  • Diabetic Angiopathies / pathology*
  • Diabetic Nephropathies / complications
  • Diabetic Nephropathies / pathology
  • Humans
  • Liver / blood supply
  • Liver / pathology*
  • Liver Cirrhosis / complications*
  • Male
  • Middle Aged
  • Sclerosis

Substances

  • ACTA2 protein, human
  • Actins
  • Antigens, CD34
  • Collagen Type IV
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Alkaline Phosphatase