6 Imaging Examinations

The grading of liver tissue inflammation and necrosis (G) and the staging of fibrosis (S) can be referenced in the pathological diagnosis section of the “Viral Hepatitis Prevention and Treatment Guidelines” issued in 2001. Today, the internationally recognized Knodell HAI scoring system is commonly used, though scoring systems developed by Ishak, Scheuer, Chevallier, and other experts can also be employed to assess the degree of liver inflammation and fibrosis, as well as evaluate drug efficacy. Immunohistochemical techniques can also be used to detect viral particles or antigens within hepatocytes.

(6) Imaging Examinations Ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) can be performed on the liver, gallbladder, and spleen. The primary purpose of imaging examinations is to aid in differential diagnosis, monitor the progression of chronic hepatitis B, and detect space-occupying lesions in the liver, such as hepatocellular carcinoma (HCC).

II. Diagnosis

Viral hepatitis is a highly prevalent disease caused by multiple pathogens. With advances in social civilization, improvements in people’s material and cultural lives, and changes in hygiene habits, hepatitis A and hepatitis E—transmitted via the fecal-oral route—are becoming less common, with sporadic local outbreaks occurring. At present, hepatitis B has a greater impact on public health, followed by hepatitis C. The Liver Disease Branch of the Chinese Medical Association and the Infectious Diseases and Parasitology Branch jointly formulated the “Hepatitis C Prevention and Treatment Guidelines” in 2004 and the “Chronic Hepatitis B Prevention and Treatment Guidelines” in 2005, setting forth the following diagnostic criteria:

(1) Classification and Diagnosis of Hepatitis B

1. Chronic Hepatitis B is divided into HBeAg-positive chronic hepatitis B and HBeAg-negative chronic hepatitis B. The former shows positive serum HBsAg, HBV DNA, and HBeAg, while anti-HBe is negative; the latter exhibits positive serum HBsAg and HBV DNA, with persistent negative HBeAg and either positive or negative anti-HBe. Both types often show persistently or repeatedly elevated serum ALT levels, or hepatocellular lesions as revealed by liver tissue examination. Based on biochemical tests and other clinical and auxiliary examination results, these two types of hepatitis can further be categorized as mild, moderate, or severe.

2. Hepatic Cirrhosis: Hepatic cirrhosis is a result of the progression of chronic hepatitis B. According to the stage of the disease, it can be divided into compensated cirrhosis and decompensated cirrhosis. The former may present with mild fatigue, loss of appetite, or abdominal distension, with abnormal ALT and AST levels, but without obvious signs of liver dysfunction. The latter often leads to severe complications such as esophageal and gastric variceal rupture bleeding, hepatic encephalopathy, and ascites. Many patients experience significant liver dysfunction, such as serum albumin levels below 35 g/L, bilirubin levels above 35 µmol/L, and ALT and AST levels rising to varying degrees, with prothrombin activity (PTA) below 60%.

3. Carriers: These include chronic HBV carriers and inactive HBsAg carriers. In the latter group, HBeAg and HBV DNA are not detected in the serum (using PCR).

4. Latent Chronic Hepatitis B: Serum HBsAg is negative, but HBV DNA is positive in both serum and/or liver tissue, with clinical manifestations consistent with chronic hepatitis B.

(2) Diagnosis of Hepatitis C

Individuals with a history of blood transfusion, blood product use, or clear exposure to HCV—such as intravenous drug users or those who have undergone tattooing—may also be diagnosed. Clinical manifestations include general fatigue, loss of appetite, nausea, and right upper quadrant pain, occasionally accompanied by low-grade fever and mild hepatosplenomegaly; some patients may develop splenomegaly, while a few may experience jaundice. However, most patients do not exhibit obvious symptoms, instead presenting as latent infections, often discovered only when ALT levels rise during routine health checkups. Hepatitis C can be classified into acute and chronic forms.

1. Acute Hepatitis C (1) Epidemiological History: Individuals with a history of blood transfusion, blood product use, or clear HCV exposure. The incubation period for acute hepatitis C after blood transfusion is 2–16 weeks (with an average of 7 weeks), though the incubation period for sporadic acute hepatitis C remains under study. (2) Clinical Manifestations: General fatigue, loss of appetite, nausea, and right upper quadrant pain—occasionally accompanied by low-grade fever, mild hepatosplenomegaly, and in some cases, splenomegaly; a few patients may develop jaundice. Some patients exhibit no obvious symptoms, instead presenting as latent infections. (3) Laboratory Examinations: ALT levels are often mildly or moderately elevated, with positive anti-HCV and HCV-RNA ≥1×10³. HCV-RNA often turns negative before ALT returns to normal, though there are also cases where ALT returns to normal while HCV-RNA remains positive. Those who meet any of the above three criteria, or who combine (2) and (3), may be diagnosed with acute hepatitis C.

2. Chronic Hepatitis C (1) Diagnostic Criteria: When HCV infection has persisted for more than 6 months, or when the onset date is unknown and there is no history of hepatitis, but liver tissue pathology reveals chronic hepatitis, or when clinical symptoms, signs, laboratory tests, and imaging findings are comprehensively analyzed, a diagnosis may also be made. (2) Assessment of Disease Severity: The severity of the lesion can be determined based on the diagnostic criteria revised jointly by the Infectious Diseases and Parasitology Branch and the Liver Disease Branch of the Chinese Medical Association in the “Viral Hepatitis Prevention and Treatment Guidelines” (2000, Xi’an). HCV alone rarely causes severe hepatitis; however, when HCV is co-infected with HIV, HBV, or other viruses, or when excessive alcohol consumption or the use of hepatotoxic drugs occurs, severe hepatitis may develop. The clinical manifestations of severe hepatitis caused by HCV are largely similar to those of severe hepatitis caused by other hepatotropic viruses, and may present as acute, subacute, or chronic conditions. (3) Extrahepatic Manifestations of Chronic Hepatitis C: Extrahepatic clinical manifestations or syndromes may result from abnormal immune responses in the body, including rheumatoid arthritis, dry conjunctivitis and keratitis, lichen planus, glomerulonephritis, mixed cryoglobulinemia, B-cell lymphoma, and late-onset cutaneous porphyria. (4) Liver Cirrhosis and HCC: The most severe outcome of chronic HCV infection is liver cirrhosis and HCC caused by progressive hepatic fibrosis. (5) Mixed Infections: When HCV is co-infected with other viruses, these combined infections are referred to as mixed infections. In China, HCV is often found in combination with HBV or HIV. (6) Recurrence of HCV Infection After Liver Transplantation: Hepatitis C often recurs after liver transplantation, and the progression of the disease is significantly faster than in patients with hepatitis C whose immune function is normal. Once liver cirrhosis develops in transplanted liver tissue, the risk of complications is higher than in patients with cirrhosis whose immune function is normal. Recurrence of hepatitis C after liver transplantation is related to HCV RNA levels at the time of transplantation and the degree of immunosuppression following transplantation. (7) Laboratory Examinations: ALT levels are often mildly or moderately elevated, with positive anti-HCV and HCV-RNA ≥1×10³. (3) Diagnosis of Other Types of Hepatitis In addition to epidemiological data, other types of hepatitis may present with common hepatitis symptoms such as fatigue, loss of appetite, and jaundice; however, pathogen detection remains the most reliable diagnostic tool. By analyzing hepatitis virus-specific antigens, antibodies, and viral nucleic acid test results, diagnoses for each type of hepatitis can be established. Anti-HAV IgM is positive in hepatitis A; in hepatitis D, in addition to HBV markers (HBV-M), serum HDAg, anti-HDV, anti-HDV IgM, and HDV RNA are also positive, while HDAg and HDV RNA are present in liver tissue. Anti-HEV IgM is positive in hepatitis E, anti-HEV IgM is positive in hepatitis G, and TTV infection is detected with anti-TTV antibodies. (4) Differential Diagnosis The main characteristics of hepatitis include jaundice, gastrointestinal symptoms, hepatosplenomegaly, and liver function abnormalities. However, besides liver and biliary diseases, many other infectious and systemic illnesses can present with similar clinical manifestations. Although we now have pathogen-based diagnostic methods for each type of hepatitis, due to the large number of asymptomatic carriers and the potential for overlapping or mixed infections, differential diagnosis remains quite challenging. Below are some key distinctions:

3. Liver Damage Caused by Other Infectious Diseases ① Infectious Mononucleosis: Fever, pharyngitis, swollen lymph nodes, with abnormal lymphocytes accounting for over 10% of white blood cell count, positive heterophile agglutination tests, and increasing serum EBV antibody titers. ② CMV Infection: Similar to EBV infection, CMV antibody titers rise while EBV antibody titers remain negative; viral isolation can be performed from blood, urine, sputum, and stool. ③ Salmonella infections, septicemia, tuberculosis, malaria, echinococcosis, amoebiasis, schistosomiasis, and other diseases share distinct etiological characteristics and supporting evidence.

4. Drug- and Alcohol-Induced Liver Damage This is the second most common liver disease after viral hepatitis. Antipyretic analgesics, tetracyclines, rifampicin, novocaine, sulfonamides, isoniazid, chloroquine, sodium aminosalicylate, erythromycin, 6-mercaptopurine, methyltestosterone, chlorpromazine, methyldopa, tranquilizers, oral contraceptives, cholecystography agents, and alcohol poisoning—all can cause drug-induced hepatitis, hepatocellular necrosis, and cirrhosis. This condition often has a clear history of drug use; initial symptoms may include fever, rash, itching, and other allergic reactions, with eosinophils in peripheral blood exceeding 6%. When the same medication is re-administered, liver damage may recur, yet viral hepatitis markers remain negative.

5. Biliary Infections and Stones Chronic biliary infections and stones often accompany liver damage, while chronic hepatitis and cirrhosis frequently co-infect with biliary infections and stones. This condition often presents with fever, upper abdominal pain accompanied by muscle tension, increased neutrophil counts, elevated direct bilirubin, alkaline phosphatase, and cholesterol levels; ALT levels may rise slightly. X-rays, ultrasounds, and CT scans can help identify stones and intrahepatic bile duct dilation.

6. Malignant Tumors

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Diagnosis of AIDS: Important Clues. The typical stage of AIDS is the final phase of HIV infection. This stage is characterized by three fundamental features: ① Severe cellular immune deficiency; ② Occurrence of various fatal opportunistic infections; ③ Development of various malignant tumors.

At room temperature, HIV in liquid environments can survive for up to 15 days. Items contaminated with HIV remain infectious for at least 3 days. However, HIV is extremely fragile; heating HIV in liquids to 56°C for 10 minutes is sufficient to inactivate it; boiling also leads to rapid inactivation. Treatment with disinfectants such as 70% alcohol, 10% bleach, 2% glutaraldehyde, 4% formalin, 35% isopropyl alcohol, 0.5% Lysol solution, and 0.3% hydrogen peroxide for 10 minutes can effectively inactivate HIV. HIV cannot be transmitted through air, ordinary social contact, or public facilities; daily life and work interactions with individuals infected with HIV or those with HIV infection will not result in HIV transmission.

II. Diagnosis (1) Diagnostic Criteria

1. Clinical Manifestations Main clinical manifestations include: ① Weight loss exceeding 10%; ② Persistent fever lasting more than one month; ③ Chronic diarrhea lasting more than one month. Secondary clinical manifestations include: ① Cough lasting more than one month; ② Generalized pruritic dermatitis; ③ Recurrent herpes simplex; ④ White candidiasis in the oral cavity; ⑤ Chronic progressive disseminated herpes simplex virus infection; ⑥ Generalized lymphadenopathy or adenopathy; ⑦ Kaposi's sarcoma affecting extensive areas of the body, as well as cryptococcal meningitis. Individuals who test positive for HIV antibodies through laboratory testing, and who exhibit two major clinical manifestations listed above along with one secondary clinical manifestation, may be diagnosed with AIDS.

2. Laboratory Tests (1) Peripheral Blood Examination: The total number of white blood cells and lymphocytes in peripheral blood decreases, while the number of mononuclear cells increases.

(2) Anti-HIV Antibody Testing: Using ELISA or other methods to detect HIV antibodies serves as an initial screening test for HIV infection. A positive result can be retested or further confirmed via immunoblotting.

(3) HIV RNA Detection: Positive results for HIV RNA or HIV culture are indicative of HIV infection.

(4) Immune Cell Analysis: The CD₄/CD₈ ratio—the ratio of helper T cells to suppressor T cells—is less than 1, or the CD₄ lymphocyte count is less than 0.2 x 10⁹/L.

3. Diagnostic Key Points for Each Stage: (1) Acute Phase: Patients often have a recent epidemiological history and acute infection symptoms. A diagnosis can be made when HIV antibody levels shift from negative to positive through laboratory testing.

(2) Asymptomatic Phase: Individuals with an epidemiological history but few clinical symptoms; if HIV antibody levels are positive through laboratory testing, or if only HIV antibodies are detected, a diagnosis can be made.

(3) AIDS Phase: Individuals with an epidemiological history, positive HIV antibody levels, and one of the following clinical manifestations may be diagnosed with AIDS: persistent fever of unknown origin lasting more than one month at a temperature above 38°C; chronic diarrhea occurring more than three times a day over a period of six months, resulting in a weight loss of over 10% within six months; recurrent white candidiasis in the oral cavity; recurrent herpes simplex virus or varicella-zoster virus infections; Pneumocystis jirovecii pneumonia; recurrent bacterial pneumonia; active tuberculosis or other mycobacterial infections; deep-seated fungal infections; space-occupying lesions in the central nervous system; dementia in young and middle-aged adults; active cytomegalovirus infection; toxoplasmosis encephalitis; penicillin infections; recurrent sepsis; Kaposi's sarcoma and lymphoma affecting the skin, mucous membranes, or internal organs. Additionally, if HIV antibody levels are positive and CD₄ T cell counts are below 2 x 10⁹/L, a diagnosis of AIDS should also be made.

(2) Differential Diagnosis (1) Primary Immunodeficiency Disorders. (2) Secondary Immunodeficiency Disorders: These may arise after corticosteroid therapy or radiation treatment, or due to secondary immune diseases such as malignancies. (3) Idiopathic CD₄ T lymphocytopenia, which closely resembles AIDS but does not involve HIV infection. (4) Autoimmune Diseases: Connective tissue disorders, hematological diseases, etc.; when AIDS presents with fever and weight loss, these conditions must be differentiated from the aforementioned diseases. (5) Lymphadenopathy-related diseases: Such as KS, Hodgkin's disease, lymphoma, or hematological disorders. (6) PseudAIDS Syndrome: AIDS phobia, where some individuals among British homosexuals experience neurological symptoms similar to early AIDS symptoms. (7) Central Nervous System Disorders: Brain damage may be caused by AIDS or other factors, requiring careful differentiation.