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In recent years, specialized formulas have been widely used to treat acute bacillary dysentery. Wu Lishu introduced a formula for treating 117 cases: 6g of Areca Nut, 12g of Angelica Sinensis, 9g each of Atractylodes Rhizome, Agarwood, Poria, Scutellaria Root, and White Peony, 15g of Dioscorea Rhizome, 3g of Raw Rhubarb, adding Dry Ginger and Burnt Ginger to spleen-yang deficiency cases, while also combining with SMZco (for those allergic to this drug, switch to Littler, Gentamicin), with remarkable efficacy compared to either Western medicine alone or traditional Chinese medicine groups. Wang Jianzhou reported treating 140 cases (115 cured, 25 improved), using formulas containing 30g of Poria and Agarwood, 20g of Arctium, 12g of Citrus Aurantium, 12g of Atractylodes Rhizome, 8g of Aconit, 9g of Red Peony, 6g of Burnt Ginger, 5g of Scutellaria Root, brewed in water and taken. Xu Yaoheng treated 65 cases using formulas containing 20g of Cinnamon and Arctium, 18g of Hawthorn and Honeysuckle, 24g of Clams and Golden Pearls, brewed in water and taken. Some used the Two White Kǔ Shen Ai Decoction (White Peony, White Headed Herb, Kǔ Shen, Mugwort Leaves), the Moss Medication Tablets (each tablet contains 0.3g, with 2g of Kǔ Shen, White Headed Herb, and raw herbs, 6 tablets per dose), the Xian Di Decoction (Xian Hua Cao 20g, Arctium 15g, White Headed Herb 12g, Artemisia 12g, Agarwood 10g, Portulaca 60g, Huang Lian 5g, brewed in water and taken), the Huang Lian-Fu Ling Decoction (Huang Lian 60g, Fu Ling 12g, White Peony 15g, Scutellaria Root, A Jiao (dissolved), 9g of Prepared Pinellia, 6g of Licorice added to spleen deficiency cases, 6g of Thick Ginger to abdominal fullness, 9g of Half-Seasoned Ginger to relieve thirst, 9g of Cucumber Root added to reduce the need for Half-Seasoned Ginger), the Jie Gu Peony Decoction (Peony, Scutellaria Root, Agarwood, Areca Nut, each 10g, 3g of Huang Lian, 3g of Angelica Sinensis, 5g of Raw Rhubarb, 2g of Cinnamon), the Modified Shengmaa-Gu Ling Decoction (Gu Ling 12g, Shengmaa, Red Peony 9g, Licorice 5g, brewed in water and taken). (Sichuan Chinese Medicine, 1987.6)

In treating toxic dysentery, complications such as urinary retention were addressed by pressing the urination points (the midpoint between the navel and the pubic symphysis); for abdominal distension caused by damp-heat toxins or due to qi stagnation and food obstruction, use methods to remove stagnation and regulate qi to open the six organs and balance qi and blood. For iatrogenic abdominal distension, use 60g of Dried Soybean, 30g each of Scallions and Ginger, crush them, heat them, and drip 5ml of 95% alcohol onto the abdomen; for severe cases, first place 0.9–0.5g of Musk inside the navel, secure with adhesive tape, then apply heat therapy and perform anal gas drainage. For prolonged diarrhea that does not stop, use Codonopsis, Atractylodes Rhizome, Poria, Fried Broad Beans, Roasted Hawthorn, Lotus Seeds, Huang Lian, Agarwood, Khoe, Dried Ginger, Nutmeg, and Licorice, brewed in water and taken. For cases of cerebral palsy involving “blindness or deafness,” in the early stages: ① use Rehmannia Root, Codonopsis, Dioscorea Rhizome, Peach Kernel, Red Flower, Dragon Bone, Grass of the Valley, and Green Box, brewed in water and taken; ② use 654-2 (1–2mg/kg) combined with Vitamin B₁₂ (100–200μg) for acupoint injections, focusing on Main Acupoints I and II, along with Hegu and Sanyinjiao as auxiliary points, administering injections alternately once daily, completing 7 sessions as one course. For malnutrition, treatment should be tailored according to the individual’s condition. Treat with Atropine, administering Huang Lian, Huang Qin, Kudzu Root, White Peony, Huang Lian, Cinnabar, Plantago Seed, and other herbal decoctions. (Yunnan College of Traditional Chinese Medicine Journal, 1987.10)

Professor Zhou Zhongying achieved good therapeutic results using a combination of cooling and warming therapies for bacterial dysentery. Chen Siqing and others summarized his experience as follows: bacterial dysentery primarily presents clinically with abdominal pain, bloody diarrhea that is red and white, and tenesmus; in TCM, this condition is referred to as “Dysentery,” “Intestinal Obstruction,” “Chiro,” or “Zhu.”

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Task output rules: Translate this markdown block from Chinese to English. Preserve markdown markers, links, and formatting. Keep headings and list structure unchanged. Return only the translated block.

Input: It is a new virus that was first discovered internationally in the second half of 1995. HGV is a positive-sense single-stranded RNA virus measuring 50–100 nm in size, transmitted through blood and causing chronic infection in the population with a relatively high prevalence rate. Currently, our understanding of HGV’s biological characteristics remains limited, particularly regarding its relationship with liver diseases, which are still subject to considerable debate.

7. TT Virus (TTV) – Hepatitis: In 1987, Japanese scholars first discovered that TTV could cause hepatitis. In June 1998, the Academy of Military Medical Sciences in China successfully isolated the Chinese strain of TTV for the first time. In September of the same year, Hunan Medical University identified the first case of TTV infection, followed by the cloning of partial gene sequences of TTV. TTV is a 3.7 kb, non-enveloped, single-stranded DNA virus, potentially belonging to the Parvoviridae family. TTV infections are widespread; according to epidemiological surveys conducted across various countries among different populations, the positive rate of TTV DNA in the general population often exceeds 10%. TTV is primarily transmitted through blood, and the positive rate of TTV DNA among individuals exposed to blood—such as professional blood donors, intravenous drug users, patients undergoing hemodialysis or receiving blood transfusions—is significantly higher than in the general population. TTV can also be transmitted vertically from mother to child; domestic reports have confirmed that TTV can be transmitted from mother to child during pregnancy. While sexual transmission may not play a major role, TTV infection rates are not high, but its pathogenicity is relatively low. The vast majority of TTV-infected individuals remain asymptomatic carriers without obvious hepatic biochemical abnormalities. Some reports suggest that TTV infection may be associated with acute hepatitis, post-hepatitis liver cirrhosis, and chronic hepatitis characterized by prolonged ALT fluctuations. However, there is still considerable debate regarding whether TTV infection can trigger inflammatory responses in the liver.

(2) Pathology

The pathological characteristics of chronic hepatitis B include prominent intrahepatic bile duct inflammation, with infiltrating inflammatory cells predominantly consisting of lymphocytes, along with a small number of plasma cells and macrophages. The aggregation of inflammatory cells often leads to dilation of the bile ducts and can disrupt the bile duct walls, resulting in interface hepatitis, also known as piecemeal necrosis. Intrahepatic bile duct inflammation and interface hepatitis are hallmark features of active disease progression and the progression of chronic hepatitis B. Hepatocellular degeneration and necrosis within the lobules—including fusion necrosis and bridge necrosis—become increasingly pronounced as the disease progresses. Hepatocellular inflammation and necrosis, along with intrahepatic bile duct inflammation and interface hepatitis, can lead to excessive collagen deposition within the liver, resulting in liver fibrosis and the formation of fibrous septa. If the condition continues to worsen, it may cause disruption of the lobular architecture, leading to the formation of pseudo-lobules and ultimately progressing to liver cirrhosis.

Immunohistochemical staining can reveal whether hepatocytes express HBsAg and HBcAg. Diffuse cytoplasmic expression of HBsAg and cytoplasmic expression of HBcAg, as well as nuclear expression of HBcAg, indicate active HBV replication; however, inclusion bodies and peripheral expression of HBsAg, as well as nuclear expression of HBcAg, suggest that HBV is present within hepatocytes.

Hepatitis C pathology is crucial for diagnosis, assessing the degree of inflammation and fibrosis, evaluating drug efficacy, and determining prognosis. Acute hepatitis C may exhibit intrahepatic inflammation and various lesions in the bile ducts, similar to those seen in hepatitis A and B. However, other histological features may also be observed, such as: ① mononuclear cell infiltration, where mononuclear cells invade the hepatic sinus and form string-like structures; ② hepatocellular ballooning degeneration; ③ bile duct damage accompanied by extensive lymphocytic infiltration in the bile ducts, even forming lymphoid follicles. Bile duct cells are damaged, the number of interlobular bile ducts decreases, resembling autoimmune hepatitis; ④ frequent interface inflammation. In chronic hepatitis C, intrahepatic bile duct inflammation, bile duct damage, hepatocellular fatty degeneration within the lobules, and clusters of Kupffer cells or lymphocytes are often observed—these characteristic histological findings provide valuable reference points for the diagnosis of chronic hepatitis C.

(3) Symptoms and Signs The incubation period for hepatitis ranges from 1 to 3 months. The primary symptoms and signs include fatigue, loss of appetite, pain in the liver region, hepatosplenomegaly, or jaundice. Each type—acute, chronic, severe, or cholestatic—has its own distinct characteristics. Types A, B, C, D, and E all exhibit acute and severe cases; types B, C, and D can become chronic and may progress to liver cirrhosis or liver cancer. Acute jaundice hepatitis often presents with chills, fever, fatigue, loss of appetite, aversion to oily foods, diarrhea or constipation, pain in the liver region, and darkened urine; during the jaundice phase, the fever subsides, digestive symptoms may be mild or severe, jaundice becomes more pronounced, liver enlargement is accompanied by tenderness upon palpation, or mild splenomegaly may occur. During the recovery phase, jaundice and symptoms subside, liver and spleen return to normal, and the course of the disease lasts 2–4 months. Acute non-jaundice hepatitis is more common than jaundice-type hepatitis, with milder illness, no jaundice, and some patients may experience no obvious symptoms or signs. After six months of chronic liver disease, most patients do not develop jaundice, instead experiencing recurrent fatigue, dizziness, gastrointestinal symptoms, and discomfort in the liver region, sometimes with mild hepatosplenomegaly. Chronic liver disease typically lasts for more than six months, with noticeable fatigue and gastrointestinal symptoms, progressive hepatosplenomegaly, with liver tissue ranging from moderate to severe, and possibly accompanied by spider angiomas and a “liver face.” A small number of patients may also exhibit extrahepatic manifestations such as arthritis, nephritis, vasculitis, or Sjögren’s syndrome. Severe hepatitis is classified into three types: acute, subacute, and chronic. Acute severe hepatitis involves rapid worsening of jaundice within 10 days after the onset of acute hepatitis, with liver shrinkage, bleeding, ascites, toxic bowel obstruction, renal failure, and varying degrees of hepatic encephalopathy. Subacute severe hepatitis occurs more than 10 days after the onset of acute hepatitis but within 8 weeks, and shares the above-mentioned severe symptoms. Chronic severe hepatitis refers to cases where patients have developed chronic liver disease or post-hepatitis cirrhosis with the aforementioned severe symptoms. Cholestatic hepatitis begins similarly to acute jaundice hepatitis, with milder symptoms, but marked hepatosplenomegaly, skin itching, and intrahepatic obstructive jaundice lasting for more than 3 weeks.

(4) Laboratory Tests

1. Pathogen Detection With the rapid advancement of virology, various types of hepatitis now have specific diagnostic methods for identifying pathogens. Typically, enzyme-linked immunosorbent assays (ELISA) are used to detect hepatitis virus markers in patient serum, such as anti-HAV IgM and HAV RNA for hepatitis A; qualitative or quantitative detection of the three hepatitis virus systems—HBsAg, anti-HBs, HBeAg, anti-HBe, and anti-HBc—for hepatitis B; anti-HCV and HCV RNA for hepatitis C; anti-HDV IgM, HDV Ag, and HDV RNA for hepatitis D; and anti-HEV IgM for hepatitis E. TTV infection can also be diagnosed using anti-TTV antibodies. The most sensitive method is polymerase chain reaction (PCR), an in vitro genetic amplification technique used to detect hepatitis virus DNA or RNA; in some cases, immunoelectron microscopy can be employed to examine hepatitis virus particles or markers in feces or liver tissue.

For hepatitis B, HBV-DNA genotyping and mutation detection are also available. Methods include: (1) Qualitative and quantitative HBV-DNA testing to assess viral replication levels, primarily used for diagnosing chronic HBV infection, monitoring serum HBV-DNA levels, and evaluating antiviral treatment efficacy. (2) HBV genotyping: Common methods include: ① gene-specific primer PCR; ② restriction fragment length polymorphism analysis (RFLP); ③ linear probe reverse hybridization (INNO-LiPA); ④ PCR microplate nucleic acid hybridization enzyme-linked immunosorbent assay; ⑤ gene sequencing, among others. However, currently, no HBV genotyping kits have been officially approved by the State Food and Drug Administration (SFDA). (3) HBV drug resistance mutation detection: Common methods include: ① HBV polymerase gene sequence analysis; ② restriction fragment length polymorphism analysis (RFLP); ③ real-time fluorescent PCR; ④ linear probe reverse hybridization, among others.

2. Biochemical Testing (1) Serum ALT and AST levels generally reflect the extent of hepatocellular injury and are the most commonly used indicators. (2) Serum bilirubin levels correlate with the degree of hepatocellular necrosis; elevated levels often occur in severe hepatitis, but it is important to differentiate these elevations from those caused by intrahepatic and extrahepatic bile duct obstruction. Patients with liver failure often exhibit elevated serum bilirubin levels, which increase progressively, with daily increases reaching ≥10 µmol/L; bilirubin levels may also show a separation from ALT and AST, indicating severe liver disease.

(3) Prothrombin time (PT) and prothrombin activity (PTA): PT is an important indicator of liver synthetic function, while PTA is a common way to express PT values, offering significant value for assessing disease progression and prognosis. A recent decline in PTA below 40% is one of the key diagnostic criteria for liver failure; values below 20% indicate a poor prognosis.

(4) Cholinesterase levels can reflect liver synthetic function and provide valuable insights into the severity of the disease and the monitoring of liver disease progression.

(5) Serum albumin reflects liver synthetic function; in patients with chronic hepatitis B, liver cirrhosis, or liver failure, serum albumin levels may decrease or globulin levels may increase, resulting in a reduced albumin-to-globulin ratio.

(6) Elevated alpha-fetoprotein (AFP) levels often indicate HCC, making it useful for monitoring the development of HCC; elevated AFP levels may also suggest hepatocellular regeneration following extensive hepatocellular necrosis, potentially aiding in prognosis assessment. However, it is important to consider the magnitude of AFP elevation, its duration, dynamic changes, and its relationship with ALT and AST, while combining these findings with the patient’s clinical presentation and imaging results such as ultrasound to arrive at a comprehensive analysis. Liver biopsy is of great importance for distinguishing chronic hepatitis and evaluating treatment efficacy, and is considered a gold standard.

(5) Pathological Examination The grading of hepatocellular 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 like Ishak, Scheuer, and Chevallier, as well as semi-quantitative scoring schemes, can also be employed to assess the degree of hepatocellular inflammation and fibrosis, and to 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 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 occasional sporadic cases. 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 respectively formulated the “Hepatitis C Prevention and Treatment Guidelines” and the “Chronic Hepatitis B Prevention and Treatment Guidelines” in 2004 and 2005, respectively, outlining the following diagnostic criteria:

(1) Classification and Diagnosis of Hepatitis B