Hepatic stellate cell hyperplasia

Introduction The phenomenon that the number of hepatic stellate cells increases by division and reproduction is called hepatic stellate cell hyperplasia, which is a very important key link in the pathogenesis of liver fibrosis. Normally, hepatic stellate cells are at rest. When the liver is damaged by inflammation or mechanical stimulation, the hepatic stellate cells are activated and their phenotype changes from a static type to an activated type. On the one hand, activated hepatic stellate cells participate in the formation of liver fibrosis and the reconstruction of intrahepatic structures by proliferating and secreting extracellular matrix, and on the other hand, the intrahepatic sinus pressure is increased by cell contraction.

Cause

Causes

Hepatic stellate cells (HSCs) have various names, such as fat-storing cells (FSC), lipid cells (1ipocyte), vitamin A-storing cells, and sinusoidal cells. (perisinusoidal cell), Ito cells, etc., it is the main source of ECM, HSC is activated and transformed into myofibroblast-like cells (MFC), and various fibrogenic factors use HSC as the final target cell.

Normally, hepatic stellate cells are at rest. When the liver is damaged by inflammation or mechanical stimulation, the hepatic stellate cells are activated and their phenotype changes from a static type to an activated type. On the one hand, activated hepatic stellate cells participate in the formation of liver fibrosis and the reconstruction of intrahepatic structures by proliferating and secreting extracellular matrix, and on the other hand, the intrahepatic sinus pressure is increased by cell contraction.

Pathogenesis

Hepatic stellate cell hyperplasia has two kinds of physiological hyperplasia and pathological hyperplasia. It occurs because it meets physiological needs and its degree does not exceed the normal limit. It is called physiological hyperplasia. After some tissue damage in the human body, the compensatory hyperplasia of the rest is also physiological hyperplasia. Proliferation beyond the normal range caused by pathological causes is called pathological hyperplasia. Physiological hyperplasia is divided into compensatory hyperplasia and endocrine hyperplasia. The mechanism of physiological hyperplasia is not fully understood. Pathological hyperplasia is mostly related to hormonal stimulation, and tumor hyperplasia caused by tumor cell enlargement also belongs to the pathological hyperplasia range.

However, it is customary for narrowly defined hyperplasia to refer to benign non-neoplastic lesions. Although hyperplasia and hypertrophy are two different concepts, in fact, hyperplasia often has hypertrophy. Compensatory hyperplasia after hyperplasia or injury due to adaptation to physiological needs can enhance or compensate for local metabolic and functional changes, which is beneficial to the body. But pathological hyperplasia is often harmful to the body. Benign prostatic hyperplasia (BPH) is the most common disease in older men and the most common benign tumor in men. BPH is often associated with a range of irritating symptoms and lower urinary tract symptoms (LUTS), which have a negative impact on the patient's quality of life. Untreated BPH can cause some complications, the most common of which are acute urinary retention (AUR), gross hematuria, recurrent urinary tract infections, urinary tract obstruction, bladder stones, and rare renal failure.

The HSC is located in the gap of the Disse, closely adjacent to the sinusoidal endothelial cells (SEC) and hepatocytes. The shape is irregular, the cell body is round or irregular, and a number of stellate cells protrude from the hepatic sinus. In addition, the HSC also protrudes from the cell and contacts the hepatocytes and adjacent stellate cells. There are 1 to 14 lipid droplets rich in vitamin A and triglyceride in the cytoplasm of HSC with a diameter of about 1.0-2.0 m. The cytoplasm is rich in free ribosomes, rough endoplasmic reticulum and developed Golgi complex. The shape of the nucleus is irregular. Due to the extrusion of the lipid droplets, the nucleus often has one or more depressions, and one or two nucleoli are visible in the nucleus. The number of HSCs in normal liver is very small, accounting for only 5% to 8% of the total number of hepatocytes and 1.4% of the total volume, but the stereoscopic distribution and extension of HSC is sufficient to cover the entire hepatic sinus microcirculation.

an examination

Related inspection

MRI examination of liver, gallbladder, pancreas and spleen by liver, gallbladder and spleen

The current diagnostic methods mainly include imaging diagnosis, pathological diagnosis and serological diagnosis.

1, imaging diagnosis, mainly B-ultrasound and CI1, widely used in clinical, but only in the advanced stage of liver fibrosis, cirrhosis and portal hypertension can occur abnormal images, can not make an early diagnosis.

2. Although the gold index for liver fibrosis is a liver biopsy, there are also many problems in itself, such as the blindness of liver puncture, insufficient sampling, and sampling error caused by heterogeneity of liver lesions, although it is a minimally invasive examination. However, most patients still have concerns and are unwilling to accept, and can not repeatedly take materials for dynamic observation. There is no reliable way to determine the collagen content of liver tissue. It is necessary to further quantify liver fiber tissue based on the estimation of intrahepatic fiber proliferation.

3. Serological diagnosis is the most widely used diagnostic method for liver fibrosis. Easy to take, low price, early diagnosis. Serological indicators include extracellular matrix (ECM) components, collagenases and cytokines. ECM components are more commonly used.

Differential diagnosis

Identification:

1. Histiocytosis: Langerhans cell histiocytosis or Langerhans' cell disease, also known as Histiocytosis X, is a rare group. a disease characterized by Langerhans cell proliferation. The etiology and pathogenesis of this disease are still unclear. Some people think it is a reactive disease, not a true tumor. Some people think that this disease is caused by abnormal immune system, but more positive cells can be seen by PCNA immunohistochemistry, and the common mitotic figures in lesions are considered to be proliferative diseases, which may be neoplastic hyperplasia.

2. Excessive accumulation of fat in liver cells: refers to lesions caused by excessive accumulation of fat in liver cells due to various reasons. Fatty liver disease is a serious threat to the health of Chinese people and has become the second largest liver disease after viral hepatitis. It has been recognized as a common cause of occult cirrhosis. Fatty liver is a common clinical phenomenon, not an independent disease. Its clinical manifestations are asymptomatic, and the severe cases are fierce. In general, fatty liver is a reversible disease, which can be restored to normal after early diagnosis and timely treatment. Normal human liver total fat, about 5% of liver weight, contains phospholipids, triglycerides, fatty acids, cholesterol and cholesterol. More than 5% of fat is mild fatty liver, more than 10% is moderate fatty liver, and more than 25% is severe fatty liver. When the total amount of fat in the liver exceeds 30%, it can be detected by B-ultrasound and diagnosed as "fatty liver" by B-ultrasound. In patients with fatty liver, the total fat can reach 40%-50%, and some of them are more than 60%, mainly triglycerides and fatty acids, while phospholipids, cholesterol and cholesterol esters increase only slightly.

3, hepatic cell fatty changes: dystrophic cirrhosis clinical manifestations of hepatic steatosis. Malnutration Cirrhosis is caused by chronic nutrient deficiencies. The causes of malnutrition, in addition to the lack of intake of individual patients, mostly due to other diseases limit food intake and absorption, such as small bowel bypass surgery, Birroth II type surgery. Patients can supplement various vitamins and vitamins CE and B vitamins, improve liver cell metabolism, prevent fatty changes and protect liver cells, and take yeast tablets, supplemented with vitamin KB12 and folic acid as appropriate.

diagnosis:

The current diagnostic methods mainly include imaging diagnosis, pathological diagnosis and serological diagnosis. Imaging diagnosis, mainly B-ultrasound and CI1, is widely used in clinical practice, but only in the advanced stage of liver fibrosis, abnormal images can occur when cirrhosis and portal hypertension occur, and early diagnosis cannot be made. Although the gold index for liver fibrosis is a liver biopsy, there are many problems in itself, such as blindness of liver puncture, insufficient sampling, and sampling error caused by heterogeneity of liver lesions. Although it is a minimally invasive examination, it is a minimally invasive examination. Most patients still have concerns and are unwilling to accept, and can not repeatedly take materials for dynamic observation. There is no reliable way to determine the collagen content of liver tissue. It is necessary to further quantify liver fiber tissue based on the estimation of intrahepatic fiber proliferation. Serological diagnosis is currently the most widely used diagnostic method for liver fibrosis. Easy to take, low price, early diagnosis. Serological indicators include extracellular matrix (ECM) components, collagenases and cytokines. ECM components are more commonly used.

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