Sarcopenia represents a prevalent complication in individuals with liver disease, with mounting evidence indicating its significant prognostic implications for cirrhosis patients. Ponziani and Gasbarrini (2018) reported that sarcopenia afflicts approximately 70% of individuals with end-stage liver disease. Compared to numerous chronic conditions, sarcopenia’s occurrence in cirrhosis patients is notably high. While its prevalence in patients with cardiovascular diseases stands at 29.7%, those with liver cirrhosis experience a strikingly elevated rate of 48.1% (Kim et al., 2017). Research by Ponziani and Gasbarrini (2018) found sarcopenia incidence among cirrhosis patients to fluctuate between 20% and 70%. Additionally, a study by Hanai et al. (2016) observed cirrhosis patients exhibiting over twice the muscle loss rate compared to healthy individuals, with a notable increase in mortality when muscle loss exceeded 3%. Presently, burgeoning research delves into cirrhosis and sarcopenia, with findings indicating potential pathogenic links to systemic inflammatory responses (Keller et al., 2011; Sinclair et al., 2016), heightened catabolic states (Plauth et al., 2019), liver-muscle interactions (Qiu et al., 2013; Welch et al., 2020), inadequate energy intake (Cheung et al., 2012), and disruptions in protein homeostasis (Periyalwar and Dasarathy, 2012; Tandon et al., 2021).

Hepatic encephalopathy stands as a prevalent complication of cirrhosis and ranks among the primary causes of mortality in affected patients. It manifests as a metabolic disorder stemming from central nervous system dysfunction in individuals with acute or chronic liver ailments. Nevertheless, its occurrence in cirrhosis patients signifies heightened mortality risk and a relatively grim prognosis (Shen et al., 2015). Presently, the precise pathogenesis of hepatic encephalopathy remains incompletely elucidated, with theories encompassing ammonia toxicity, neurotransmitter imbalances, and amino acid perturbations, among which ammonia toxicity serves as a focal point. Risk factors for hepatic encephalopathy in cirrhosis patients encompass infections, ascites, electrolyte imbalances, and upper gastrointestinal bleeding. Furthermore, Maqsood et al. (2006) identified prothrombin time as a prominent precipitating factor for hepatic encephalopathy. Additionally, hyponatremia-induced reduction in extracellular osmotic pressure and resultant cerebral edema are deemed significant contributors to hepatic encephalopathy development, with a reported 8% increase in hepatic encephalopathy risk for every 1 mmol/L reduction in serum sodium (Iwasa and Takei, 2015; Bossen et al., 2019). Addressing the substantial incidence of hepatic encephalopathy in cirrhosis patients warrants profound attention and contemplation for future interventions.

Ascites represent a prevalent complication of cirrhosis and stand as a common ailment encountered in clinical practice (Ginés et al., 1987; Runyon et al., 1992). Its emergence often signals an advanced stage of cirrhosis, with a prognosis characterized by complexity and variability. Particularly in refractory cirrhosis, ascites often accompany other cirrhosis-related complications, leading to a poor clinical outlook and a significant decline in patients’ quality of life. Cirrhotic ascites refers to the accumulation of free fluid within the abdominal cavity of cirrhosis patients. Substantial ascitic fluid can induce symptoms like reduced appetite and abdominal distension, profoundly impacting patients’ quality of life and heightening the risk of complications such as hepatic encephalopathy, hepatorenal syndrome, and spontaneous peritonitis (Tandon and Garcia-Tsao, 2008). The 1-year mortality rate among cirrhosis patients with ascites reaches 15%, while the 5-year mortality rate can soar as high as 44% (Biecker, 2011). The mechanism underlying ascite formation involves various factors, including portal hypertension, hypoalbuminemia, inadequate effective circulating blood volume, and heightened production of hepatic lymph fluid, all contributing to ascite development.

Liver cirrhosis is often accompanied by multiple system involvement, and complications such as upper gastrointestinal bleeding and secondary infection often occur in the late stage. Upper gastrointestinal bleeding is the most common fatal complication, and the overall mortality rate of upper gastrointestinal bleeding can reach 30 percent (de Franchis and Baveno VI Faculty, 2015; Dango et al., 2017). The risk of portal hypertension and upper gastrointestinal bleeding can be determined by detecting the pressure gradient of hepatic veins. It is worth noting that this examination is a traumatic examination, so electronic endoscopy, a non-traumatic examination, is often used clinically to evaluate the degree of esophageal varices in patients with cirrhosis, so as to prevent the occurrence of upper gastrointestinal bleeding (Song and Kim, 2019). Related studies have confirmed that patients with advanced cirrhosis are more likely to develop esophageal varices. The severity of liver disease is correlated with the grade of esophageal varices. About 45% of patients with Child-PughA cirrhosis have varicose veins (Elsebaey et al., 2019), while 85% of patients with Child-PughC cirrhosis have varicose veins (Sousa et al., 2017). Patients with cirrhosis of the liver have a higher incidence of upper gastrointestinal bleeding if they have bad lifestyle habits such as smoking and drinking.

Patients with cirrhosis are prone to co-infection, which is one of the common causes of death in patients with cirrhosis. Related studies have confirmed that 39.7% of patients with cirrhosis can be complicated by various infections (Fernández et al., 2019). Piano et al. (2021) found through their research that the infection rate of hospitalized patients with cirrhosis was high, which was 4–5 times that of normal population, and the infection rate of patients with decompensated cirrhosis was up to 67%. Liver cirrhosis complicated with infection is also prone to septic shock, which can lead to multiple organ failure, leading to liver dysfunction, liver cell damage, and eventually liver failure and death (Hsu et al., 2021). Multiple mechanisms are involved in the co-infection of cirrhosis. First of all, the liver is closely related to the body’s immunity. Patients with cirrhosis have low liver reserve function, and their innate and acquired immune defense capabilities as well as the ability to remove microorganisms and toxins are severely impaired. Clinically, cirrhosis may be characterized by increased susceptibility to infection and poor prognosis after complicated with sepsis (Lebossé et al., 2019; Basho et al., 2021). Secondly, the characteristic clinical manifestation of decompensation in cirrhosis is portal hypertension. Anatomically, blood flow from the internal organs and intestines is connected to the portal vein, which enables bacteria in the intestine to enter the systemic circulation blood system through the collateral branches of the portal vein circulation and cause systemic infection (Tripathi et al., 2018; Solé et al., 2021). Another possibility is that portal hypertension in cirrhosis may show the characteristics of spleen enlargement in the early stage, and the occurrence of spleen enlargement may be accompanied by hypersplenism, which will further affect the immune function of the body, thus aggravating the development of liver cirrhosis (Asanoma et al., 2014).

Hepatopulsyndrome (HPS), first proposed by Knudson and Kennedy in 1977 (Kennedy and Knudson, 1977), is a clinical syndrome characterized by arterial oxygenation dysfunction due to dilation of blood vessels in the lung, characterized by dyspnea in upright position and dyspnea after movement (Weinfurtner and Forde, 2020). HPS is most common in patients with cirrhosis, and can also be seen in acute and chronic hepatitis, acute liver failure, etc., which is one of the common complications of chronic liver disease (Machicao et al., 2014). One study (Fallon et al., 2008) found that non-HPS patients with a similar degree of cirrhosis were only half as likely to die as those with HPS. Epidemiological studies have also shown that the incidence of HPS in adults with end-stage liver diseases such as cirrhosis ranges from 4% to 47% (Varghese et al., 2007), while the prevalence of HPS in all patients with cirrhosis is 20% (Møller et al., 2009). The prevalence of HPS in patients with cirrhosis requiring liver transplantation is about 5%–30% of the population (Rodríguez-Roisin and Krowka, 2008). Modern medicine has also found that the pathogenesis of HPS may be related to the release of various cytokines in the body resulting in angiogenesis and pulmonary vasodilation caused by cirrhosis. As a serious pulmonary complication of end-stage liver disease, HPS seriously affects the quality of life and prognosis of patients. When dyspnea and hypoxemia occur in patients with chronic liver disease or portal hypertension, attention should be paid to screening whether HPS is combined, so as to achieve early detection, diagnosis and treatment to prevent deterioration of the condition.

Hepatorenal syndrome (HRS) is a serious complication mainly manifested by renal injury in patients with severe liver diseases such as cirrhosis combined with ascites (Meola et al., 2016). Nowadays, with the deepening of HRS research, great progress has been made in pathogenesis and treatment. The International Club of Ascites (ICA) proposed the concept of acute kidney injury (AKI). On this basis, the diagnostic criteria and treatment guidelines of the HRS were revised (Angeli et al., 2015). Nowadays, with the deepening of HRS research, great progress has been made in pathogenesis and treatment. Studies (Al-Khafaji et al., 2015) have shown that 35%–40% of patients with cirrhosis combined with ascites may develop HRS. The main risk factors of HRS include portal hypertension, sepsis caused by spontaneous peritonitis, and cardiac insufficiency is also a high risk factor for HRS (Lenz et al., 2014). At present, global scholars have not fully understood the pathogenesis of HRS. Existing studies have found that due to the influence of end-stage liver diseases such as cirrhosis, the inactivation of vasodilator factors in vivo is reduced, which leads to the dilation of visceral and peripheral arteries, the contraction of renal vessels, the reduction of glomerular filtration rate and the decrease of renal blood flow, and finally the occurrence of HRS (Sobhonslidsuk, 2015; Simonetto et al., 2020; Wu et al., 2024). At the same time, liver inflammation, intestinal flora displacement and concurrent infection caused by cirrhosis lead to the release of a large number of inflammatory factors and endotoxemia, causing renal microcirculation dysfunction, which can induce renal function injury (Rad et al., 2024).

Primary liver cancer, as a high incidence of human malignant tumor, lacks typical clinical symptoms in the early stage, but the disease progresses rapidly, has a high risk of death, and the prognosis of patients is generally poor. Liver cirrhosis is a major risk factor for liver cancer and hepatology-related death. Therefore, accurate evaluation of the severity of cirrhosis is of great significance for clinical monitoring efficacy and prognosis assessment (Ren et al., 2017). Modern medical research has found that patients with cirrhosis with a genetic history of primary liver cancer have a significantly increased risk of developing primary liver cancer. Previous studies have found that the incidence of cirrhosis complicated with liver cancer is 1.5–6 percent per year (Bruix et al., 2011), and this figure may be increasing. Therefore, the prevention of primary liver cancer is urgent. More studies have found that long-term excessive drinking can increase the risk of liver cirrhosis complicated with primary liver cancer, especially after hepatitis B virus attacks the human liver, alcohol will cause increased liver burden, resulting in liver damage, and ultimately accelerate the occurrence and development of liver cancer. While avoiding excessive drinking for a long time, all countries should also strengthen health education about liver cirrhosis and primary liver cancer, improve patients’ further understanding of liver cirrhosis and primary liver cancer, enhance patients’ awareness of prevention and treatment, and reduce the incidence of liver cirrhosis complicated with primary liver cancer.

Research on liver cirrhosis and its complications underscores the significant impact of these conditions on patient prognosis and quality of life. While there are advancements in understanding risk factors and pathogenesis, challenges remain in the form of high variability in incidence rates, limited understanding of mechanisms, and the need for more effective management and preventive strategies. Further research is essential to address these gaps and improve patient outcomes.

Yinchenhao decoction (YCHD) is a Chinese medicine widely used in clinics to treat cirrhosis. Jiang et al. (2015) found that YCHD could significantly reverse changes in the expression of immunoregulatory genes in liver tissue, increase serum albumin level, effectively reduce the activity of serum alanine amino transportase, and reduce the degree of liver inflammation and necrosis. These changes were related to the regulation of the expression of genes related to immune/inflammatory response. Additionally, YCHD did not cause spleen weight loss or hepatocyte degeneration in mice. Cai et al. (2019) identified 45 key active ingredients and 296 potential therapeutic targets for YCHD anti-liver fibrosis through transcriptomic and network pharmacological analysis, indicating that YCHD mainly acts on apoptosation-related signaling pathways. In vivo experiments confirmed that YCHD treatment reduced the apoptosis of liver parenchymal cells and alleviated the symptoms of liver fibrosis. Further research by Cai et al. (2018) demonstrated that YCHD inhibits the activation and proliferation of HSCs through the TGF-β1/Smad/ERK signaling pathway. Liu et al. (2008) conducted a controlled experimental study on a variety of traditional prescriptions for cirrhosis and found that YCHD most significantly inhibited α-SMA activation and regulated rat cirrhosis. A systematic review and meta-analysis by Shi et al. (2021) provided high evidence that YCHD has a favorable modulatory effect on cholestasis, delaying the onset and progression of cirrhosis.

Xiaochaihu Decoction (XCHD), derived from Shanghan Zabing Lun, is a multi-functional classic decoction for treating a variety of diseases. Qiang et al. (2022) identified 164 key compounds of XCHD and 95 core targets of regulating liver fibrosis. They found that XCHD prevents liver cirrhosis by regulating several key pathways such as the TNF, IL-17, and PI3K-Akt signaling pathway. Huang et al. (2020) found that XCHD significantly inhibits the upregulation of Hsp47, TGF-β1, Col1A1, α-SMA, etc., mediating the HSP47/TGF-β axis to protect the liver. Wang et al. (2023a) found that XCHD significantly alleviated liver fibrosis in a mouse model, improving liver function, reduction liver collagen accumulation, and inhibition of HSC activation. Besides chronic liver diseases, XCHD is also widely used in clinical practice for its regulatory effects on common mental disorders such as depression (Sun et al., 2023).

Huangqi decoction (HQD) has been used for the preventing and treating hepatic fibrosis and cirrhosis since ancient times. Zhang et al. (2015) found that HQD significantly downregulated the expression of PDGFrb, PDGFra, PDGFd, PDGFb, THBS1, COL1A1, COL1A2, and COL5A2 in rat liver fibrosis, and downregulated PDGF and TGF-β signaling pathways, thus treating cirrhosis. Liu et al. (2012) found that HQD promotes CD68 expression in liver fibrosis development and protects against liver cell apoptosis. Wang et al. (2021) identified various active components in HQD for liver fibrosis using a pharmacokinetics-based strategy, which was validated in the CCl4-induced mouse liver fibrosis model. Dong et al. (2023) found that HQD adjusted the LCC-C18ORF26-1/miR-663a/TGF-b1/TGF-bRI/p-Smad2 axis to inhibited HSCs activation and proliferation, preventing liver cirrhosis. HQD also alleviates biliary fibrosis and chronic cholestatic liver injury by inhibiting the NF-κB pathway and inducing the Nrf2 pathway in a chronic cholestatic mouse model, preventing liver cirrhosis onset and exacerbation (Li et al., 2019).

The traditional prescription Dahuang Zhechong pill (DHZCP), consisting of rhubarb, native turtle worm, leech, tabanus worm, scutellaria baicalensis, and peach kernel, promotes blood circulation, Gong et al. (2018) found that DHZCP inhibits p-Erk and regulates other factors to inhibit p-p38 by increasing the expression of growth arrest specific 5 (GAS5), alleviating liver fibrosis and preventing cirrhosis. Another study by Gong et al. (2020) found that DHZCP prevents cirrhosis in animal models by inactivating the PI3K/Akt pathway, protecting the liver from damage. Fu et al. (2023) found that DHZCP improves hepatic sinusoids’ capillaries by inhibiting the MK/Itgα signaling pathway, delaying disease progression. Key active molecules affecting this pathway include Liquiritin, Naringenin, Rhein, and PMEG. A systematic review and meta-analysis found that DHZCP reduces the serum biomarkers of liver fibrosis in chronic hepatitis B patients (Wei et al., 2015). Combining Entecavir and DHZCP is an effective intervention for cirrhosis, with an optimal treatment course of about 6 months (Ye et al., 2022). He et al. (2024) recently found that DHZCP effectively regulates the enterohepatic axis, improving intestinal barrier integrity by regulating metabolites and intestinal flora, ultimately inhibiting liver fibrosis progression.

Xiayuxue decoction (XYXD) came from Jingui Yaolue. Zhang et al. (2020) prepared different fractions including ethyl acetate fraction (EF) from XYXD. It was found that the potential mechanism of EF prevention of liver cirrhosis may be related to the induction of apoptosis of HSCs. Ma et al. (2017) believe that enterogenic endotoxin plays an important role in the further development of liver fibrosis, and experimental studies have confirmed that XYXD treatment can significantly improve CCl4-induced cell death and intestinal inflammation, indicating that XYXD can inhibit the further development of liver fibrosis by improving intestinal epithelial damage. In addition to interfering with the progression of liver cirrhosis, another study (Liu et al., 2015) found that XYXD can also promote the apoptosis of macrophages in rats with renal histopathological damage caused by liver cirrhosis, thus reducing kidney damage in rats. A recent pharmacological study (Deng et al., 2024) also found that XYXD was able to exert significant anti-HCC effects by modulating the interaction between bile acids and intestinal flora, ultimately triggering the immune action of NKT cells against HCC.

As a more commonly used classical prescription, Yiguanjian (YGJ) decoction is widely used clinically to treat liver disease, which mainly consists of rehmannia, Radix saphora, Angelica, ophiopogon, and wolfberry. Related studies (Tian et al., 2016) found that YGJ was able to increase the expression of MTH1 and Bax, decrease the expression of TNF-α, and significantly improve the degree of hepatic inflammation and fibrosis in mice with chronic hepatitis in a mouse model of hepatic injury, and ultimately was able to inhibit DNA damage in mice with immune liver damage. Relevant researchers (Zhou et al., 2015) found that YGJ and its main component iYGJ can inhibit liver angiogenesis in cirrhotic mice by inhibiting the HIF-1α/VEGF signaling pathway, and finally confirmed that its anti-angiogenesis effect is closely related to improving the liver hypoxic microenvironment. Xu et al. (2018) also established a liver cirrhosis rat model and treated the liver cirrhosis rats with YGJ, and found that YGJ can enhance the liver cirrhosis repair of FLSPC-mediated by regulating the activation state of macrophages, and finally confirmed that YGJ combined with stem cell transplantation is one of the main methods for the treatment of end-stage liver cirrhosis. Through more in-depth studies, Wang et al. (2012) confirmed that YGJ can also inhibit the transfer of bone marrow cells to the liver, further inhibit the differentiation of bone marrow cells, inhibit the proliferation of hepatocytes and progenitor cells in the injured liver, and ultimately play a role in the treatment of liver fibrosis and fundamentally prevent the formation of cirrhosis. Some scholars (Xu et al., 2021) also believe that YGJ can regulate the state of macrophages, and the main anti-cirrhosis effect of YGJ is related to its ability to inhibit the polarization of macrophages M1.

Kangxian ruangan (KXRG) capsule is a classic homemade prescription. It is composed of seven Chinese medicines, including salvia miltiorrhiza, red peony root, bupleurum, and turtle shell. It has the key role of supplementing the spleen and warming Yang. Clinically, it can significantly reduce or even reverse liver fibrosis and prevent the development of liver cirrhosis. Relevant scholars (Liu et al., 2018) have conducted experimental studies on KXRG and found that it can effectively alleviate liver fibrosis, histopathological changes, and inflammation in rats, and further relieve liver inflammation by maintaining the balance of TNF-α/IL-10, positively regulate the balance of Bcl-XL/Bax or Bcl-2/Bax, and activate damaged liver cells. It can alleviate the progression of nonalcoholic fatty liver disease from liver fibrosis to cirrhosis. As one of the clinical experience prescriptions for the treatment of cirrhosis, KXRG has a remarkable effect, which lays a foundation and provides a direction for the treatment of cirrhosis by modern Chinese medicine in the future.

Chinese medicine decoctions show promise in treating liver cirrhosis by reducing inflammation, improving liver function, and preventing fibrosis. However, studies often have small sample sizes, lack standardized protocols, and offer limited long-term data. Most research is regionally confined to China, requiring broader validation to confirm efficacy and safety globally.

An-Luo-Hua-Xian pill (ALHX) is one of the commonly used Chinese patent medicine for the treatment of liver cirrhosis. As a patented medicine, it has been used in China for more than 15 years. It has the effects of invigorating spleen and nourishing liver, nourishing blood and promoting blood circulation, and softening and dispersing masses. In clinical practice, it is mainly used for chronic hepatitis B and early and middle stage cirrhosis after hepatitis B, and has achieved good curative effect. A clinical study (Liu et al., 2023) of 780 patients found that ALHX combined with Entecal can significantly improve liver fibrosis in patients with chronic hepatitis B and prevent further progression to cirrhosis, so the clinical study to some extent confirmed the positive effect of ALHX in the treatment of liver disease. Xiao and many other researchers (Xiao et al., 2022) conducted a randomized controlled trial that confirmed that chronic hepatitis B patients with F ≤ 2 and alanine aminotransferase (ALT) < 2ULN treated with ALHX could improve the degree of liver fibrosis after 48 weeks. The results of related meta-analysis also confirmed that ALHX and Entecavir had a significant effect on liver fibrosis or cirrhosis (Song et al., 2019). An earlier study (Huang et al., 2009) also found that ALHX was also effective in alleviating liver fibrosis caused by schistosomiasis and further confirmed its excellent hepatoprotective and antifibrotic effects.

Fuzhenghuayu (FZHY) Decoction is also one of the Chinese patent medicines used to treat cirrhosis clinically, many important components of which are compounds extracted from natural plants. Now, the effect of Fuzhenghuayu (FZHY) decoction has been further proved in clinical studies and experiments. Liu et al. (2019) found that FZHY not only alleviates liver fibrosis and impedes its further progression to cirrhosis, but also improves vascular remodeling in mouse models. Song et al. (2018) recruited 113 subjects, including 63 cirrhosis patients and 50 healthy controls, and applied FZHY to their intervention. The curative effect evaluation showed that the liver stagnation syndrome (LSS) and liver-kidney Yin deficiency syndrome (LKYDS) were effective. The metabolic mechanism may be related to the improvement of the LSS energy supply and the enhancement of the LKYDS detoxification function. Another multi-center clinical study (Liu et al., 2005) found that FZHY can significantly reduce inflammation score and mean inflammatory activity, and has a very good therapeutic effect on chronic hepatitis B-induced liver fibrosis, and the efficacy is better than the Heluoshugan capsule. In addition, Hu et al. (2019) confirmed through animal experiments that FZHY can rapidly upregulate the expression of metabolic enzymes such as Gpt, Adh1, and Hk2, downregulate the expression of Acss2 and Gs, and can also improve rat liver fibrosis and prevent the occurrence of cirrhosis by changing metabolic pathways. Chen et al. (2016) also identified major biomarkers for evaluating the efficacy of FZHY in the treatment of cirrhosis caused by chronic hepatitis B based on transcriptional profiling and miRNA-target network analysis. A miRNA panel with -326, -1182, hsa-miR-18a-5p and -193b-5p were established.

In recent years, Biejia-Ruangan (BR) has been approved as an anti-fibrotic Chinese medicine for the treatment of chronic liver disease and has good efficacy in the prevention and treatment of cirrhosis. A double-blind randomized controlled trial (Ji et al., 2022) has shown that BR combined with entecavir significantly reduces the risk of hepatogenic death and liver cancer in patients with chronic viral hepatitis B and cirrhosis. Another similar study (Rong et al., 2022) also found that in chronic hepatitis B patients with cirrhosis, adding BR to the current standard treatment can help better improve liver fibrosis and alleviate clinical symptoms. Yang et al. (2013) also found in relevant experimental studies that BR can significantly inhibit the progression of liver fibrosis in vitro and in vivo, and its main mechanism of action may be closely related to the downregulation of fibrosis signal transduction in the TGF-β-Smad pathway. A meta-analysis (Meng et al., 2022) of 26 studies involving 2,717 patients showed that BR significantly improved liver function alleviated the degree of liver fibrosis, and prevented the occurrence of cirrhosis. Interestingly, one study (Luo et al., 2023) also explored the relationship between BR compound and incidence of HCC, but the exact effect and mechanism of action are not fully understood, and more work or scientific studies are still needed to elucidate the clinical effects of BR in the future. To summarize, the efficacy of using Chinese medicine therapies in the treatment of liver cirrhosis is remarkable and has a wide range of application prospects, which is worthy of our further in-depth excavation and exploration.

Chinese patent medicines such as ALHX, FZHY and BR have shown promise in treating liver cirrhosis by improving liver fibrosis, reducing inflammation, and preventing disease progression. However, limitations include small sample sizes, variability in protocols, and a need for larger, rigorous trials to understand their mechanisms and long-term effects. Most studies are limited to China, requiring broader validation. Studies related to the treatment of cirrhosis by Chinese medicine are shown in Table 1. Comparison of drug/medicine selection and efficacy in the treatment of liver cirrhosis between Western or Chinese medicine is shown in Table 2.