Hepatic injuries resulting from chronic alcohol abuse identified by forensics

Abstract

Alcohol intake is largely spread all over the world, although it is well-known that it causes important changes of the liver, from liver steatosis, hepatitis to liver cirrhosis. The study we performed on 93 patients deceased in suspicious circumstances and brought to the Institute of Forensic Medicine, Iaşi, Romania, confirmed through the determination of Ethyl glucuronide, that these were alcohol consumers. The macroscopic analysis during necropsy highlighted the presence of alcoholic liver disease (ALD), while microscopy studies confirmed the macroscopic observations. The immunohistochemical studies showed the existence of a chronic liver inflammation, the transdifferentiation of stellate hepatic cells, the activation of Kupffer cells, important changes of the hepatic vascular network, hepatocyte necrosis, lipid loadings and the progression of liver fibrosis process.

Figure 1

Distribution of patients according to age

Figure 2

Distribution of deceased patients with ALD according to sex (n; %). ALD: Alcoholic liver disease

Figure 3

Distribution of patients with ALD according to the environment (n; %). ALD: Alcoholic liver disease

Figure 4

Mean levels of EtG [ng/mL] in blood samples depending on the associated hepatic pathology. EtG: Ethyl glucuronide

Figure 5

Image of macrovascular steatosis associated with perilobular fibrosis. HE staining, ×100. HE: Hematoxylin–Eosin

Figure 6

Image of liver with macro- and microvacuolar steatosis. HE staining, ×100

Figure 7

Image of alcoholic hepatitis characterized by vacuolar degenerescence of hepatocytes, moderated hepatocyte necrosis and the presence of a moderate inflammatory infiltrate in the Kiernan space, associated with a deposit of collagen fibers. HE staining, ×100

Figure 8

Liver parenchyma in a case of alcoholic hepatitis, where we may observe the ballooning of hepatocytes, vacuolar degenerescence, associated with a microvascular steatosis. HE staining, ×200

Figure 9

Image of liver cirrhosis, characterized by the abundant development of the fibrous conjunctive tissue in the Kiernan spaces, and also in the intralobular spaces, associated with hepatocyte necrosis and macrovacuolar steatosis. GS trichrome staining, ×200. GS: Goldner–Szekely

Figure 10

Liver cirrhosis: regeneration nodule. GS trichrome staining, ×40

Figure 11

Area of liver steatosis with a moderate inflammatory infiltrate in the Kiernan space. Anti-CD3 antibody immunomarking, ×200. CD3: Cluster of differentiation 3

Figure 12

Image of liver steatosis with rare B-lymphocytes in the Kiernan portal space. Anti-CD20 antibody immunomarking, ×200. CD20: Cluster of differentiation 20

Figure 13

Abundant inflammatory infiltrate in the Kiernan space, mainly formed of T-lymphocytes, in a case of alcoholic hepatitis. Anti-CD3 antibody immunomarking, ×200

Figure 14

Alcoholic hepatitis with rare B-lymphocytes in the Kiernan space. Anti-CD20 antibody immunomarking, ×200. CD20: Cluster of differentiation 20

Figure 15

Area of steatohepatitis with numerous hypertrophied Kupffer cells, with vacuolar cytoplasm. Anti-CD68 antibody immunomarking, ×200. CD68: Cluster of differentiation 68

Figure 16

Kiernan space with numerous small-sized macrophages, in a case of alcoholic hepatitis. Anti-CD68 antibody immunomarking, ×200

Figure 17

Intense reaction of liver stellate cells to anti-α-SMA antibody in a case of liver steatosis. Anti-α-SMA antibody immunomarking, ×200. α-SMA: Alpha-smooth muscle actin

Figure 18

Numerous myofibroblast cells arranged in the Kiernan space, in a case of alcoholic liver cirrhosis. Anti-α-SMA antibody immunomarking, ×200

Figure 19

Macrovascular liver steatosis associated with a low number of intralobular sinusoidal capillaries. Anti-CD31 antibody immunomarking, ×200. CD31: Cluster of differentiation 31

Figure 20

Image of steatohepatitis where we may observe the reduction of the intralobular sinusoidal capillaries and the increase of the number of blood vessels in the Kiernan space and the porto–portal conjunctive septa. Anti-CD34 antibody immunomarking, ×100. CD34: Cluster of differentiation 34