Pathology of primary liver cancer

2021-01-27 12:00 AM

When AFP> 1000ng / ml: Most likely primary liver cancer. A slight increase in ovarian and testicular teratoma, some digestive cancers, necrotizing hepatitis.


The most common organizational forms are:

Hepatocellular Carcinoma.

Cholangio-cellular Carcinoma.

Others: Hepatoblastoma, Angiosarcoma.

Pathogenesis and risk factors

Hepatitis B virus

The frequency of liver cancer in HBsAg (+) is> 200 times higher than in HBsAg (-).

Frequency of HBsAg in liver cancer> 6-20 times the general population (Asia: 60-80%). Protein X in the B genome probably has a role in cancer-causing mutations.

In the high endemic area with hepatitis B virus, there is also a frequency of liver cancer


Liver cancer is caused by 2 mechanisms: directly and indirectly by cirrhosis

Hepatitis C virus

Molecular biology studies, using RT-PCR, have allowed the detection of C virus RNA in 50-70% of serum and in 55-100% of liver structure in patients with TB-free and HBsAg-free.

90% of C-related liver cancers appear on a cirrhotic background.

Anti-HCV-positive liver cancer patients (with or without HBsAg) usually have more severe liver damage (70% cirrhosis, of which 60-70% are in Child B or C) than in patients only HBsAg positive (50% cirrhosis, of which 65% are in Child A) and the liver usually has more tumours


Due to any cause.

Aflatoxin B1

Mycotoxins (Aspergillus), common in mould peanuts; proven to be liver carcinogen in rats and poultry.

Perhaps the carcinogen-mediated role of the metabolite, Epoxide, attaches itself to nucleic acids and changes the transcription of DNA.

Interaction with 53 mutant’s protein.

Other factors

Alcohol: Probably promotes carcinogenesis.

Male hormones: Androgens, oral contraceptive pills.

Chemical (Thorotrast).

Parasites (Schistosoma japonicum, Sch. Mansoni, clonorchis Sinensis).

Alpha 1-antitrypsin deficiency is common in ZZ and MZ phenotypes.

Hémechromatose, H / c Budd-Chiari.


Symptoms of general and physical function


Commonly, a feeling of heaviness in the lower right rib, spreading to the back, rarely severe pain.

Digestive disorders:

Anorexia, nausea, vomiting, diarrhoea.


Continuity, oscillation.

Slim shot clearly in the late stage.

Physical symptoms

Large liver: Visible or palpable under the right rib, stiff, uneven surface, more or less painful, sometimes fixed not moving with breathing. Sometimes the large liver exceeds the midline.

Jaundice: Mainly caused by compression of the biliary tract in the liver.

Ascites: Less or more, can see bloody, rapid regeneration after a puncture.

Listen: T Ieng blow on the liver


Complete blood count: anaemia, sometimes with multiple red blood cells.

Increased blood sedimentation rate.

Liver function: C blowing disturbances in liver cancer or cirrhosis background when tumours account for over 75% of liver volume.

Liver enzymes: Alkaline phosphatase, gamma GT, 5 'Nucl√©otidase, Alpha-2 Globulin, SGOT are usually higher than SGPT.

Cancer markers

Alpha Foto Protein (AFP):

As a glycoprotein produced by the embryonic liver, decreasing 3 weeks postpartum, concentration in adults about 4-10 ng/ml.

When AFP> 1000ng / ml: Most likely primary liver cancer.

A slight increase in ovarian and testicular teratoma, some digestive cancers, necrotizing hepatitis.

AFP with Lectin affinity (AFP - L3) has just been found, more specific than AFP, but the test technique is complicated.

If quantitative conditions are not available, AFP can be quantified using diffuse immunological (Ouchterlony).

DCP (Descarboxy Prothrombin hay PIVKA-II):

Infection in 70% of patients with primary liver cancer and about 50% of patients with liver cancer have normal AFP.

Alpha L-Fucosidase:

This enzyme is elevated in primary liver cancer, with 90% specificity and approximately 75% sensitivity, also increased in benign liver tumours.

Polling images


One or more nodules in the liver. Echo rich, poor, mixed, inlaid with vascular pushing, bile ducts (bending sign), perioral damper.

Hyperplasia of blood vessels in the tumour, often with thrombosis in the portal vein.

Density tomography:

One / more hypodense masses, irregular smoking, the guidance of puncture, biopsy.


Basic preoperative test, which helps locate, perfusion, and potentially remove tumours through a catheter inserted into the trunk artery

The image of tufts to increase blood vessel proliferation (arteries) Perfusion messy organization, lakes of blood vessels (parenchyma tense) early venous blood flow (venous tense)



Biopsy under the guidance of ultrasound, CT scan or laparoscopy.

Biopsy: Accurate but bleeding easily.

Small needle aspiration: Fewer complications, but lower accuracy and sensitivity than biopsy.

Para cancerous syndromes

Hypoglycaemia: due to secretory factor cells with activity similar to insulin.

Hypercalcemia: due to the secretory factor-like parathyroid hormone.

Polycythaemia vera: due to a tumour secretion factor similar to Erythropoietin.

Factor V is paradoxically normal.

Progression and complications


Usually severe, poor prognosis, death 6-12 months.


Cervical cancer:

Jaundice: C forced bile sugar in the liver


Upper gastrointestinal bleeding: H SETTLEMENT block the door.

Peritoneum: Broken cancer

Press the vein in the liver or inferior vena cava.

Metastases: T algae, lungs, pleura, bones, lymph nodes, brain.

Differential diagnosis

Painful liver with fever

Liver abscess.

Liver fluke: epidemiological factors + eosinophilia + diagnostic serum.


Compression: Liver and gallbladder are large, differentiated by ultrasound.

Hepatitis: In the pre-jaundice, SGPT increases very high, serum markers of hepatitis virus and scans.

U lower right rib

Chronic hepatitis.

Cannabis, adenoma, lymphosarcoma.

Secondary liver k: Find primary cancer, normal Alpha FP, organize study.


Surgical treatment

Surgery to remove the tumour.

Liver resection is still the most radical treatment for primary liver cancer.


Surgery is often indicated for patients with stage I, II and IIIA liver cancer.

Several criteria are commonly considered in the indication for liver resection.

Size below 5 cm.

One lobe.

The tumour has a shell.

Contraindications to surgery:

Poor liver function due to cirrhosis.

The tumour was invasive in both lobes of the liver.

The tumour invades or blocks the common hepatic duct.

The tumour invades the inferior vena cava 

Door vein thrombosis.

Invasive lymph nodes.

Distal metastases (most commonly lung and bone).

Immediately after surgery, tumour recurrence is possible, sometimes requiring a second or even third resection. A safe distance should be at least 1 cm from the tumour organization.

In Vietnam, Professor Ton Le Tung has done it since the 70s, surgery for isolated small tumours, then supporting the immune system with LH1 with good results. This technique is often applied to solitary tumours less than 5cm in size, under 70 years old. Remaining liver function is the main predictor of prognosis, usually cut in the lobe or segment.

In Japan, postoperative mortality is 3-11%, and survival over 3 years is 46%. The best results when the tumour is less than 2cm, the survival rate is 60.5% over 5 years.

In France, Bismuth performed 35 cases from 1970 to 1984, the survival rate over 2 years was 32%. Survival time dependent on Child-Pudg index over 3 years is 51% for Child A, 12% for B and C.

Complications: The common complications after liver resection are bleeding, infection, groin and liver failure. Rarely is a biliary tract.

Liver transplantation

The main benefit of this approach is the removal of all cancer and lesions that precede it, eliminating the risk of portal hypertension, and the risk of recurrence of hepatitis on the transplanted liver. The results in Hanover showed that 15% of the survival time was over 3 years and 45% in Pittsburgh with solitary tumours over 5 years.

In cases where there is only one tumour less than 5 cm or less than 3 tumours less than 3 cm, the prognosis after transplantation is very good, almost like other transplant patients for non-cancer reasons.

Internally medical treatment

Inject the tincture through the skin directly into the tumour under ultrasound guidance.

In 1982, for the first time in Japan, the authors Ebara M and Okuda K ... studied a treatment method for HCC by injecting Ethanol into a liver tumour and obtained possible results. concerned. After that, there have been many studies in France, Italy, China ... with good results.


Ethanol induces arterial thrombosis in the tumour, which in turn causes tumour clotting necrosis and tumour ischemia.


The patients have been identified as HCC.

The number of tumours should not exceed 3, all are sheathed tumours.

Tumour size is usually smaller than 5 cm, the actual size depends on the number of tumours (1 u ≤ 12 cm, 2 u ≤ 6 cm, 3 u ≤ 4 cm).

Grades Child-Pugh A and B; Prothrombin rate over 60%.


Means and tools:

Ethanol injection technique is performed under the guidance of ultrasound or CT Scan.

Chiba or Terumo needles: 0, 7-0, 9 X 7-15 cm.

Absolute ethanol: 99, 8%, tube 5 cc.

Lidocaine 1%, pain relievers, antiseptic tools.


Identify liver tumour need puncture under ultrasound or CT Scan.

Locate needle puncture, anaesthesia.

Insert a needle through the skin into the tumour centre under the guidance of an ultrasound or CT scan.

Inject Ethanol slowly into the tumour, both injecting and observing the diffusion of Ethanol in place.

Draw cum close to the liver shell, replace the syringe with lidocaine to numb the liver shell.

Draw needle, bandage in place.

Dosage: 1-2 injection sites / time x 2 times per week; Each injection 2-12 cc.

The total dose of Ethanol to be injected is calculated according to the formula Sugiura N (Japan) 1983. V = 4/3 (r + 0.5) 3.

In which: V is the total dose of Ethanol.

R: Tumour radius.

Preliminary results of some studies: according to many studies by many foreign authors (Livraghi, Ebara ...) and in the country (Mai Hong Bang), the results are very positive, the survival rate after 3 years is 71% (Child A), and 41% (Child B), some patients live more than 7 years. The majority of patients improved clinically, AFP decreased significantly, the rate of complete tumour necrosis on ultrasound was more than 60%. This technique can also help treat haemostasis in case of liver cancer rupture.

Methods of causing embolism

The embolism method was first used in 1975 in the United States. Nakamura treated 200 patients with primary liver cancer and gave 2 months, 12 months and 24 months of survival respectively 71%, 48, 1% and 20.8%. The embolism group combined with lipiodol had a significantly longer survival time


Normally, the liver receives 2 blood supply sources, the hepatic artery and the portal vein, in which the tumours receive blood mainly from the hepatic artery, thus causing embolism by injecting into the selected arterial branch. The tumour contributes to tumour necrosis but does not interrupt perfusion to the healthy liver. The combination of necrotic anaemia effects with the effects of anti-cancer chemicals will increase the therapeutic effect.

Techniques of blocking circuits:

Stuck the selected hepatic artery with gelatine tank foam, inserted into the artery branch nourishing the tumour through the femoral and visceral artery.

Super selective hepatic artery occlusion

Hepatic artery blockage combined with injecting anti-tumour chemicals (TACE), commonly used chemicals is doxorubicin, cisplatin ...

Petrochemical occlusion of the hepatic artery (TOCE)

Side effects after shutdown are Fever, abdominal pain, vomiting, bedside, liver coma, increased transaminases.

In addition, it can cause complications of extra-hepatic vessel shut down or cause an abscess. These techniques can be repeated after a period of 3-6 months.


Liver tumours cannot be removed by surgery.

Emergency treatment of peritoneal haemorrhage caused by a rupture of liver tumour.

Causing preoperative embolism to reduce tumour size and increase postoperative survival.

In all cases, the portal vein should not contain thrombosis.

Other temporary treatments

Radiation therapy:

In the past, external radiation therapy for patients with primary liver cancer has been used. But due to limited results, is currently rarely indicated. The radioactive substances used were I131-antiferritin, an I 131-anti HCC monolithic antibody. Currently, in Europe there is also research on the treatment of selective radiation to the tumour with initial results that prolong the survival of the patient.


The commonly used chemicals are 5 FU, cisplatin, doxorubicin, Mitomycin C ...

Rich routes of use: oral, intravenous, injection into the circular ligament, portal vein ...


The most commonly used immunological means are means of microbiological origin (BCG, Corynebacterium,.), chemicals (levamisole, Isoprinosine ...) or cytokine group (IL2, IFN-beta, IFN-gamma ...). However, there is no completely specific method.

Some authors recommend subcutaneous BCG after tumour resection in the hope of nonspecific immunization. Lai et al. Using the combination of Doxorubicin + IFN- alpha 2 showed a decrease in tumour stimulation and a reduction in complications compared to the control group.

Genetic engineering: delivers specific therapeutic genes to destroy malignant cells without damaging the healthy liver. Viral vectors such as adenovirus are often used. Tumour-responsive monoclonal antibodies have also been used to deliver genes to cancer cells.


Hormonal dependence and the presence of endocrine receptors in liver cancer suggest that tumour development is due to hormones, but preliminary studies with Tamoxifen have been controversial.

Heat therapy:

Often used radiofrequency ablation (RFA) emits heat through a needle plugged in the tumour, high temperature helps to destroy cancer cells. Initial results are quite good.


Primary liver cancer is quite common in our country, the symptoms are diverse and often start silently, diagnosis is mostly in the late stage so treatment is difficult, the prognosis is often very bad.

Prevention of liver cancer is mainly based on vaccination against the hepatitis B virus and the treatment of chronic viral hepatitis.