-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Author: Tanyou Wen subsidiary of Zhenjiang, Jiangsu University Hospitals This article is the author's permission NMT Medical publish, please do not reprint without authorization.
The diagnosis of liver cancer in the clinic mainly relies on imaging, clinical history, and laboratory tests such as alpha-fetoprotein (AFP).
But for lesions smaller than 2 cm, imaging diagnosis is still quite difficult.
Many small lesions are precancerous lesions.
Precancerous lesions of liver cancer, this name is not used as a standardized disease diagnosis, and there is no clear internationally recognized definition, but it continues to appear in authoritative specifications and guidelines.
The author analyzes such a disease state together based on the following case.
Case introduction: Male, 63 years old, with hepatitis B liver cirrhosis.
Entecavir has been antiviral standard for several years.
Adhere to ultrasound, liver function, HBV DAN, AFP and other testing and follow-up.
Recently, ultrasound found a suspicious malignant lesion about 1.
3 cm in size in the right anterior lobe.
Magnetic resonance and Pumex showed that T1 low signal, T2 high signal, limited diffusion, Gd-EOB-DTPA specific enhancement, arterial phase and other signals, portal vein phase slightly higher signal, hepatobiliary phase did not see the transfer.
The possibility of malignant lesions is high (Figure 1).
AFP is normal, and the upper limit of abnormal prothrombin 2 times the normal value is increased.
Figure 1 MRI and Gd-EOB-DTPA specific enhancer imaging According to the judgment of the patient's liver function, coagulation function, etc.
, radiofrequency ablation and pathological puncture are selected.
The operation process is shown in Figure 2.
Figure 2 The operation process of radiofrequency ablation and pathological puncture was smooth, the ablation was complete, there was a low fever one day after the operation, and there was no obvious discomfort during and after the operation.
Figure 3 Pathological description of the patient's pathological examination results: See local liver cells arranged in 2-3 layers, some liver cells have different nuclei in size, heterosexual, large hepatocytes and small hepatocytes can be seen, and a few unpaired arteries are seen in the portal area.
Heppar-1 is negative, GLC-3 is suspiciously positive, CD34, CD10 is negative, and HBsAg is positive.
Pathological diagnosis: liver cirrhosis with high-grade dysplasia.
What is precancerous lesion of liver cancer? The precancerous lesions of liver cancer have always been a problem of debate between clinicians and pathologists.
The occurrence and development of liver cancer is a long clinical process of multi-factor and multi-step carcinogenesis, which mostly follows "chronic hepatitis-cirrhosis-dysplasia-low-grade dysplastic nodules (LGDN)- High-grade dysplastic nodules (HGDN)-early-early liver cancer-early liver cancer-medium-advanced liver cancer" multi-part pattern.
Moreover, the development pattern of liver cancer shows a law that the size of the tumor (usually regarded as the cut-off value of 20 mm) doubles with time.
Atypical hyperplasia refers to a cluster of atypical hyperplastic cells with a diameter of less than 1 mm.
If the diameter is greater than 1 mm, it is called an atypical hyperplastic nodule.
Therefore, in recent years, studies have suggested that the precancerous lesions of the liver are mainly dysplastic nodules and dysplastic nodules (DN) in the background of liver cirrhosis.
Pathological features of precancerous lesions Precancerous lesions of hepatocellular carcinoma (HCC) are usually accompanied by large cell changes (LCC) and small cell changes (SCC).
LCC is characterized by an increase in the volume of hepatocytes and nuclei to 2-3 times the normal size, and at the same time, the nucleus has an atypia, with enlarged nucleoli, polynuclear and dense nuclear chromatin.
In the early years, it was believed to be closely related to human HCC.
However, in recent years, studies have shown that this view lacks evidence of transition to HCC.
It is now generally considered to be the result of chronic liver injury and liver cell degeneration. SCC is characterized by reduced cytoplasm and moderately enlarged nucleus, increased nuclear/plasma ratio, between normal hepatocytes and hepatocarcinoma cells; heterotypic nucleus, dense chromatin, may be multinucleated, and cytoplasmic basophilic The thickness of the liver plate can increase by 2-3 layers of cells, the density of the nucleus increases, and the formation of pseudo-adenoid structures can sometimes be seen; it is mostly nodular and focal, which can squeeze the surrounding liver parenchyma.
SCC has a high proliferative activity, its morphology is similar to that of liver cancer cells, its immunophenotype is similar to that of liver progenitor cells, and it has similar chromatin changes with neighboring liver cancer cells.
In combination with the above pathological manifestations, most scholars believe that SCC is a true dysplasia and a precancerous lesion of the liver.
The important sign of the progression of dysplastic nodules into HCC is the appearance and increase of unmatched arterioles, while the portal area gradually decreases.
Normal hepatocytes are supplied with oxygen by the portal vein and hepatic artery.
HCC grows many new arterioles, which are supplied with oxygen by the arteries.
They do not accompany the small bile ducts and are not part of the portal area.
They are called non-matching arterioles.
The portal area can be seen in LGDN, and unmatched arterioles are relatively rare, while HGDN has more unmatched arterioles, and the portal area may still exist.
LGDN has a clear boundary, surrounded by fibrous tissue, and liver cells have tiny atypia, which is manifested by increased cell density.
LCC may be present, but SCC is rare.
The liver plate is 1-2 layers of cells thick and does not contain pseudo-adenoid arrangement.
There is no obvious thickening of the liver plate.
The boundary of HGDN is clear under the naked eye and under the microscope, and it can be seen under the microscope: the local hepatocyte density increases, forming a boundary, and the boundary of HGDN under high magnification is not clear.
Irregular trabecular hepatocytes are often arranged in the nodules, the cell density is ≥ 2 times the normal, and the thickness of the liver can reach 3 layers of cells.
Occasionally false adenoid arrangement.
LCC rarely occurs, SCC is more common, more obvious, and easier to distinguish from regenerative nodules.
The imaging findings of precancerous lesions.
The blood supply change of the nodule (from the portal vein to the artery) is an important pathophysiological change of cancer.
CT or MRI also judges the nature of the nodule based on this change. CT is slightly lower or iso-density.
13%-31% of dysplastic nodules appear to be enhanced in the arterial phase of CT, which may be due to the increased blood supply of the hepatic artery.
Most dysplastic nodules are in the arterial phase and portal vein.
No enhancement during the period.
MRI manifestations of high signal on T1WI are more common, and can also be expressed as isointensity, and low signal on T2WI.
This is a characteristic manifestation of distinguishing dysplastic nodules from HCC.
The appearance of dysplastic nodules enhanced by gadolinium contrast agent in the three-phase scan is generally not significantly different from that of the surrounding liver parenchyma.
MRI with SPIO and disodium gadolinium oxide as a contrast agent is helpful to make accurate diagnosis of dysplastic nodules and HCC in the liver.
Studies have shown that double-enhanced MRI with gadolinium contrast agent and SPIO improves the diagnostic accuracy, and the sensitivity for detecting liver cancers with diameters of <1 cm, 1-2 cm, and> 2 cm reaches 38%, 92%, 91 %, but a second MRI is required.
Principles for the treatment of precancerous lesions In precancerous lesions, the risk of HGDN progressing to HCC within 5 years is as high as 60%-80%.
Therefore, many scholars currently believe that aggressive radical treatments such as surgery and minimally invasive ablation treatment are needed for HGDN.
Minimally invasive ablation may be more accepted by patients due to less damage to normal liver tissue, low complications, and cost-benefit advantages.
.
References: 1.
He Lingling, Zhao Yalin, Du Linlin, et al.
Pathological and imaging manifestations of liver nodular lesions.
Journal of Clinical Hepatobiliary Diseases.
31(9):1547-52.
2.
Stratified screening and primary liver cancer Monitoring Guide (2020 Edition).
Tan Youwen, Chief Physician, Ph.
D.
Supervisor of Master's Candidates of Jiangsu University, Director of the Department of Liver, Zhenjiang Third Hospital of Jiangsu University, columnist of Yi Maitong
The diagnosis of liver cancer in the clinic mainly relies on imaging, clinical history, and laboratory tests such as alpha-fetoprotein (AFP).
But for lesions smaller than 2 cm, imaging diagnosis is still quite difficult.
Many small lesions are precancerous lesions.
Precancerous lesions of liver cancer, this name is not used as a standardized disease diagnosis, and there is no clear internationally recognized definition, but it continues to appear in authoritative specifications and guidelines.
The author analyzes such a disease state together based on the following case.
Case introduction: Male, 63 years old, with hepatitis B liver cirrhosis.
Entecavir has been antiviral standard for several years.
Adhere to ultrasound, liver function, HBV DAN, AFP and other testing and follow-up.
Recently, ultrasound found a suspicious malignant lesion about 1.
3 cm in size in the right anterior lobe.
Magnetic resonance and Pumex showed that T1 low signal, T2 high signal, limited diffusion, Gd-EOB-DTPA specific enhancement, arterial phase and other signals, portal vein phase slightly higher signal, hepatobiliary phase did not see the transfer.
The possibility of malignant lesions is high (Figure 1).
AFP is normal, and the upper limit of abnormal prothrombin 2 times the normal value is increased.
Figure 1 MRI and Gd-EOB-DTPA specific enhancer imaging According to the judgment of the patient's liver function, coagulation function, etc.
, radiofrequency ablation and pathological puncture are selected.
The operation process is shown in Figure 2.
Figure 2 The operation process of radiofrequency ablation and pathological puncture was smooth, the ablation was complete, there was a low fever one day after the operation, and there was no obvious discomfort during and after the operation.
Figure 3 Pathological description of the patient's pathological examination results: See local liver cells arranged in 2-3 layers, some liver cells have different nuclei in size, heterosexual, large hepatocytes and small hepatocytes can be seen, and a few unpaired arteries are seen in the portal area.
Heppar-1 is negative, GLC-3 is suspiciously positive, CD34, CD10 is negative, and HBsAg is positive.
Pathological diagnosis: liver cirrhosis with high-grade dysplasia.
What is precancerous lesion of liver cancer? The precancerous lesions of liver cancer have always been a problem of debate between clinicians and pathologists.
The occurrence and development of liver cancer is a long clinical process of multi-factor and multi-step carcinogenesis, which mostly follows "chronic hepatitis-cirrhosis-dysplasia-low-grade dysplastic nodules (LGDN)- High-grade dysplastic nodules (HGDN)-early-early liver cancer-early liver cancer-medium-advanced liver cancer" multi-part pattern.
Moreover, the development pattern of liver cancer shows a law that the size of the tumor (usually regarded as the cut-off value of 20 mm) doubles with time.
Atypical hyperplasia refers to a cluster of atypical hyperplastic cells with a diameter of less than 1 mm.
If the diameter is greater than 1 mm, it is called an atypical hyperplastic nodule.
Therefore, in recent years, studies have suggested that the precancerous lesions of the liver are mainly dysplastic nodules and dysplastic nodules (DN) in the background of liver cirrhosis.
Pathological features of precancerous lesions Precancerous lesions of hepatocellular carcinoma (HCC) are usually accompanied by large cell changes (LCC) and small cell changes (SCC).
LCC is characterized by an increase in the volume of hepatocytes and nuclei to 2-3 times the normal size, and at the same time, the nucleus has an atypia, with enlarged nucleoli, polynuclear and dense nuclear chromatin.
In the early years, it was believed to be closely related to human HCC.
However, in recent years, studies have shown that this view lacks evidence of transition to HCC.
It is now generally considered to be the result of chronic liver injury and liver cell degeneration. SCC is characterized by reduced cytoplasm and moderately enlarged nucleus, increased nuclear/plasma ratio, between normal hepatocytes and hepatocarcinoma cells; heterotypic nucleus, dense chromatin, may be multinucleated, and cytoplasmic basophilic The thickness of the liver plate can increase by 2-3 layers of cells, the density of the nucleus increases, and the formation of pseudo-adenoid structures can sometimes be seen; it is mostly nodular and focal, which can squeeze the surrounding liver parenchyma.
SCC has a high proliferative activity, its morphology is similar to that of liver cancer cells, its immunophenotype is similar to that of liver progenitor cells, and it has similar chromatin changes with neighboring liver cancer cells.
In combination with the above pathological manifestations, most scholars believe that SCC is a true dysplasia and a precancerous lesion of the liver.
The important sign of the progression of dysplastic nodules into HCC is the appearance and increase of unmatched arterioles, while the portal area gradually decreases.
Normal hepatocytes are supplied with oxygen by the portal vein and hepatic artery.
HCC grows many new arterioles, which are supplied with oxygen by the arteries.
They do not accompany the small bile ducts and are not part of the portal area.
They are called non-matching arterioles.
The portal area can be seen in LGDN, and unmatched arterioles are relatively rare, while HGDN has more unmatched arterioles, and the portal area may still exist.
LGDN has a clear boundary, surrounded by fibrous tissue, and liver cells have tiny atypia, which is manifested by increased cell density.
LCC may be present, but SCC is rare.
The liver plate is 1-2 layers of cells thick and does not contain pseudo-adenoid arrangement.
There is no obvious thickening of the liver plate.
The boundary of HGDN is clear under the naked eye and under the microscope, and it can be seen under the microscope: the local hepatocyte density increases, forming a boundary, and the boundary of HGDN under high magnification is not clear.
Irregular trabecular hepatocytes are often arranged in the nodules, the cell density is ≥ 2 times the normal, and the thickness of the liver can reach 3 layers of cells.
Occasionally false adenoid arrangement.
LCC rarely occurs, SCC is more common, more obvious, and easier to distinguish from regenerative nodules.
The imaging findings of precancerous lesions.
The blood supply change of the nodule (from the portal vein to the artery) is an important pathophysiological change of cancer.
CT or MRI also judges the nature of the nodule based on this change. CT is slightly lower or iso-density.
13%-31% of dysplastic nodules appear to be enhanced in the arterial phase of CT, which may be due to the increased blood supply of the hepatic artery.
Most dysplastic nodules are in the arterial phase and portal vein.
No enhancement during the period.
MRI manifestations of high signal on T1WI are more common, and can also be expressed as isointensity, and low signal on T2WI.
This is a characteristic manifestation of distinguishing dysplastic nodules from HCC.
The appearance of dysplastic nodules enhanced by gadolinium contrast agent in the three-phase scan is generally not significantly different from that of the surrounding liver parenchyma.
MRI with SPIO and disodium gadolinium oxide as a contrast agent is helpful to make accurate diagnosis of dysplastic nodules and HCC in the liver.
Studies have shown that double-enhanced MRI with gadolinium contrast agent and SPIO improves the diagnostic accuracy, and the sensitivity for detecting liver cancers with diameters of <1 cm, 1-2 cm, and> 2 cm reaches 38%, 92%, 91 %, but a second MRI is required.
Principles for the treatment of precancerous lesions In precancerous lesions, the risk of HGDN progressing to HCC within 5 years is as high as 60%-80%.
Therefore, many scholars currently believe that aggressive radical treatments such as surgery and minimally invasive ablation treatment are needed for HGDN.
Minimally invasive ablation may be more accepted by patients due to less damage to normal liver tissue, low complications, and cost-benefit advantages.
.
References: 1.
He Lingling, Zhao Yalin, Du Linlin, et al.
Pathological and imaging manifestations of liver nodular lesions.
Journal of Clinical Hepatobiliary Diseases.
31(9):1547-52.
2.
Stratified screening and primary liver cancer Monitoring Guide (2020 Edition).
Tan Youwen, Chief Physician, Ph.
D.
Supervisor of Master's Candidates of Jiangsu University, Director of the Department of Liver, Zhenjiang Third Hospital of Jiangsu University, columnist of Yi Maitong