II. Clinical Manifestations and Complications of Hepatitis B

II. Clinical Manifestations and Complications of Hepatitis B

I will share my personal experiences, though some of my views may differ from current textbooks. Hepatitis B is generally categorized into three types: chronic persistent type, chronic active type, and acute type. My experience shows that Type I often presents without symptoms, with normal liver function; laboratory tests may reveal either big three positives or small three positives. Type II is characterized by discomfort in the liver area, irritability, bitter taste in the mouth, and abnormal liver function—most notably, an imbalance in the albumin-to-globulin ratio, with globulins exceeding normal levels, along with mild enlargement of the spleen and liver. Type III represents acute episodes or primary hepatitis B that arise suddenly, with significant liver damage manifested primarily by elevated ALT and AST levels. Hepatitis B viral testing often shows big three positives (E antigen positive), though some patients develop jaundice. Some patients experience more pronounced symptoms, including discomfort in the liver area, fever, loss of appetite, and abdominal distension.

Among these three types, chronic persistent hepatitis is the mildest, with the best prognosis; with appropriate treatment, it can quickly turn into small three positives. However, once patients transition to small three positives, some may become long-term carriers, remaining asymptomatic for extended periods. Chronic active hepatitis is more severe than chronic persistent hepatitis; in addition to obvious symptoms and significant liver damage, the main difference between the two lies in changes to the albumin-to-globulin ratio and mild splenic enlargement. The pathological changes in the liver of patients with this type are often difficult to distinguish from early-stage cirrhosis, as the two conditions overlap; clinical symptoms can also be challenging to differentiate. Chronic active hepatitis is sometimes misdiagnosed as early-stage cirrhosis, which is not entirely incorrect. Treatment is crucial: with proper, long-term therapy, symptoms often disappear, test results return to normal, and the spleen may shrink. Ultrasound imaging is helpful in distinguishing between chronic persistent hepatitis and chronic active hepatitis: the portal vein diameter is smaller in the former (<12 mm), while in the latter, the portal vein diameter is larger (>12 mm, <14 mm). The spleen thickness in the former is usually below 40 mm, whereas in the latter, the spleen thickness often exceeds 40 mm. The clinical presentation of acute hepatitis B is mostly insidious; a small portion of cases present with symptomatic episodes, but most are transient, with mild symptoms. Patients often unknowingly recover from the illness, with normal liver function, HBsAg turning negative, HBeAb positive, and some patients maintaining HBcAb positivity for several years. Acute hepatitis B secondary to chronic persistent hepatitis or chronic active hepatitis can be relieved with active treatment, and liver function can return to normal—but viral testing remains difficult to restore. Recurrent acute episodes in chronic persistent hepatitis can progress to chronic active hepatitis; recurrent acute episodes in chronic active hepatitis can lead to cirrhosis. Therefore, timely treatment of acute hepatitis B is essential.

The primary complications of hepatitis B include cirrhosis and liver cancer. Through a rough follow-up and statistical analysis of over 60,000 outpatient cases of hepatitis B, approximately 10% of patients develop cirrhosis—a figure broadly consistent with domestic and international data ranging from 3% to 13%. As previously mentioned, chronic hepatitis B often flares up repeatedly; if treatment is not timely, the condition can persist for a long time and eventually lead to cirrhosis. Patients with hepatitis B should practice self-regulation and maintain a cheerful lifestyle, approaching treatment with composure. Excessive stress or low mood can actually hinder treatment and promote recurrence; such patients are more likely to develop cirrhosis. Diet and lifestyle habits are also important factors influencing the progression of hepatitis B—especially avoiding alcohol consumption and eating foods containing alcohol, such as rice wine and sweet fermented foods. It is advisable to eat light, low-fat meals. A regular daily routine, balanced work and rest, and adequate sleep are essential prerequisites for treating liver disease. In the later stages of cirrhosis, symptoms such as splenomegaly, ascites, esophageal varices, and hardening of liver tissue are common, with a prominent shift in the albumin-to-globulin ratio in liver function tests. Diagnosis is often straightforward with physical examinations and laboratory tests. The distinction between early-stage cirrhosis and chronic active hepatitis has been discussed earlier; additionally, it’s worth noting that recent clinical studies have used four indicators of liver fibrosis—mucin, hyaluronic acid, collagen III, and collagen IV—to assess liver tissue. Changes in these four indicators can reveal the degree of fibrous tissue proliferation in the liver, providing a rough estimate and assessment of the progression of cirrhosis. However, due to significant individual variations in the body’s response, some patients with cirrhosis show normal results in these tests, while others with less advanced cirrhosis may exhibit abnormal findings. Therefore, I believe these tests should be used as a reference for clinical diagnosis and treatment, but not as the sole basis for diagnosis—and certainly not as a major criterion for determining treatment outcomes.

Liver cancer is another major complication of hepatitis B. According to domestic and international data, the incidence of liver cancer among hepatitis B patients is 10 times higher than that of the general population. Consequently, some scholars have suggested that hepatitis B plays a significant role in the development of liver cancer. Recent domestic reports indicate that approximately 0.8%–1.2% of hepatitis B patients develop liver cancer. These figures align with my experience over the years. The reasons behind the association between hepatitis B and liver cancer remain unclear, but most studies suggest that it may be related to changes in the immune system of hepatitis B patients. While liver cancer associated with hepatitis B is considered primary liver cancer, the earliest signs of this condition often include a sustained increase in alpha-fetoprotein levels. Alpha-fetoprotein levels may slightly rise in cases of cirrhosis, but remain below 400. If these levels persist at high levels (>400), it is advisable to consider liver cancer and undergo further examination. CT scans are generally the most valuable diagnostic tools, and enhanced CT scans can aid in definitive diagnosis. For patients with liver cancer, ultrasound examinations at lower-level hospitals can still provide accurate diagnoses at relatively low costs.

Liver cancer typically develops on the basis of cirrhosis, but some patients develop liver cancer directly from chronic persistent hepatitis B. Once liver cancer occurs, patients often first experience pain in the liver area or worsening liver discomfort. Some patients develop jaundice; if the ascites caused by cirrhosis initially responds well to diuretics like furosemide, but then suddenly fails to resolve, it’s important to consider whether liver cancer has developed concurrently. Of course, infections, hypoproteinemia, electrolyte imbalances, and kidney dysfunction can all contribute to the persistence of ascites—and liver cancer is one of the many factors contributing to the difficulty in resolving ascites. Such cases must be taken seriously, otherwise misdiagnosis and inappropriate treatment may occur.