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Liver Diseases

A reference to liver diseases, covering causes, symptoms, affected structures, diagnostic methods, treatment approaches and prognosis.

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A reference to liver diseases, covering causes, symptoms, affected structures, diagnostic methods, treatment approaches and prognosis.

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Sample rows from Liver Diseases. Field types are labelled in each column heading.
#	TextNo.	TextDisease Name	TextCategory	TextPrimary Cause / Etiology	TextPrevalence	TextAge of Onset	TextKey Symptoms	TextAffected Organ(s)	TextDiagnostic Method	TextTreatment Approach	TextPrognosis	TextICD-10 Code
01	1	Acute Hepatitis B	Viral Hepatitis	Hepatitis B virus (HBV) is a partially double-stranded DNA hepadnavirus that replicates through reverse transcription of a pregenomic RNA intermediate. Transmission occurs through percutaneous or mucosal exposure to infected blood and body fluids, including sexual contact, perinatal transmission, injection drug use, and occupational needlestick exposure. HBV enters hepatocytes via the sodium taurocholate cotransporting polypeptide (NTCP) receptor and establishes covalently closed circular DNA (cccDNA) in the hepatocyte nucleus, which serves as the template for viral transcription. Hepatocellular injury in acute HBV is predominantly immune-mediated through vigorous CD8+ cytotoxic T-cell and NK cell responses against HBV-expressing hepatocytes, with the strength of immune response determining both disease severity and likelihood of viral clearance.	Approximately 296 million people worldwide are living with chronic HBV infection (WHO 2022), with an estimated 1.5 million new infections annually. Prevalence is highest in the WHO Western Pacific and African regions, where 6-8% of the adult population is HBsAg-positive. In the United States and Western Europe, prevalence is 0.3-0.5%, with acute HBV incidence approximately 1-2 per 100,000 following widespread vaccination. Universal infant HBV vaccination programs have dramatically reduced new infections, with global childhood prevalence falling from 4.7% pre-vaccine to under 1%.	The risk of chronicity is inversely related to age at infection: perinatal transmission leads to chronic infection in 90% of cases, infection in children aged 1-5 years leads to chronicity in 25-50%, while adult-acquired infection becomes chronic in less than 5% of immunocompetent individuals. Acute symptomatic hepatitis B primarily affects adolescents and adults, with peak incidence in the 20-49 age group. In endemic areas, most infections occur perinatally or in early childhood and are typically asymptomatic.	The incubation period is 45-180 days (mean 75 days). Approximately 70% of adults with acute HBV have subclinical or anicteric hepatitis. Symptomatic patients develop a prodromal serum-sickness-like illness with fever, arthralgia, urticarial rash, and malaise, followed by anorexia, nausea, right upper quadrant pain, and jaundice. ALT levels typically rise to 1000-3000 IU/L. Fulminant hepatic failure develops in approximately 0.1-0.5% of acute cases, characterized by coagulopathy, encephalopathy, and multiorgan failure. Extrahepatic manifestations include polyarteritis nodosa, glomerulonephritis, and aplastic anemia.	Liver (hepatocytes); immune system; kidneys (membranous nephropathy, polyarteritis nodosa); joints (immune-complex arthritis); skin (urticaria, papular acrodermatitis of childhood/Gianotti-Crosti syndrome)	Serologic diagnosis follows a characteristic pattern: HBsAg appears first (1-10 weeks after exposure), followed by HBeAg and high HBV DNA levels indicating active viral replication. Anti-HBc IgM is the hallmark of acute infection and is critical for diagnosis during the window period when HBsAg has cleared but anti-HBs has not yet appeared. HBV DNA quantification by real-time PCR confirms viremia. Markedly elevated ALT/AST (typically 10-100 times ULN) with elevated bilirubin in icteric cases. Resolution is indicated by HBsAg clearance, appearance of anti-HBs, and normalization of ALT within 6 months.	Treatment of acute HBV is primarily supportive, as over 95% of immunocompetent adults achieve spontaneous clearance. Antiviral therapy with nucleos(t)ide analogues (entecavir 0.5 mg daily or tenofovir disoproxil 300 mg daily) is indicated for severe acute hepatitis with coagulopathy (INR >1.5), protracted course exceeding 4 weeks, or immunosuppressed patients per AASLD 2018 guidelines. Fulminant hepatic failure requires intensive care and urgent liver transplantation evaluation. Post-exposure prophylaxis with hepatitis B immunoglobulin (HBIG) and HBV vaccine should be administered within 24 hours of exposure. Prevention through universal HBV vaccination (3-dose series: 0, 1, 6 months) is the cornerstone strategy.	Good - Over 95% of immunocompetent adults achieve complete spontaneous recovery with clearance of HBsAg and development of protective anti-HBs antibodies within 6 months. Fulminant hepatic failure occurs in 0.1-0.5% and carries a mortality rate of 60-80% without liver transplantation. Progression to chronic hepatitis B occurs in less than 5% of adult-acquired infections. Recovery confers lifelong immunity, although trace cccDNA may persist in hepatocytes indefinitely (occult HBV infection). Patients who recover should still be monitored if undergoing immunosuppressive therapy, as reactivation can occur.	B16.9
02	2	Acute Hepatitis C	Viral Hepatitis	Hepatitis C virus (HCV) is an enveloped, single-stranded positive-sense RNA flavivirus transmitted primarily through percutaneous blood exposure. HCV displays remarkable genetic diversity with 8 genotypes and over 90 subtypes, which has complicated vaccine development. The virus enters hepatocytes through a multi-step process involving CD81, scavenger receptor class B type 1 (SR-BI), claudin-1, and occludin receptors. Acute HCV infection elicits both innate (interferon) and adaptive (CD4+ helper and CD8+ cytotoxic T-cell) immune responses; spontaneous viral clearance occurs in 15-45% of cases, primarily driven by vigorous, multi-specific T-cell responses, while viral escape mutations and T-cell exhaustion contribute to chronicity in the majority.	An estimated 58 million people worldwide have chronic HCV infection, with approximately 1.5 million new infections annually (WHO 2023). In the United States, the estimated incidence of acute HCV increased from 2010 to 2020 due to the opioid epidemic and injection drug use, with approximately 66,700 new infections in 2020 (CDC). HCV genotype 1 is the most prevalent worldwide (46% of all infections), followed by genotype 3 (30%). High-prevalence countries include Egypt (genotype 4), Pakistan (genotype 3), and China (genotype 1b).	Acute HCV can occur at any age. In the United States, the highest incidence is among young adults aged 20-39 years, driven by injection drug use related to the opioid epidemic. A second peak is observed in adults over 60 (baby boomer cohort) who were infected decades ago through medical procedures, blood transfusions (before 1992 screening), or other exposures. In endemic countries, new infections may occur at younger ages through healthcare-associated transmission.	Acute HCV is asymptomatic in 70-80% of cases, which contributes to underdiagnosis. When symptoms occur, they develop 2-12 weeks after exposure and include fatigue, malaise, anorexia, nausea, right upper quadrant pain, and jaundice (20-30% of symptomatic cases). ALT levels rise to 10-20 times ULN, typically peaking 8-12 weeks post-exposure. Fulminant hepatic failure is exceedingly rare (<0.1%) in acute HCV. Paradoxically, symptomatic acute HCV (particularly jaundice) is associated with higher rates of spontaneous clearance, likely reflecting a more vigorous immune response.	Liver (hepatocytes); immune system (cryoglobulinemia, lymphoproliferative disorders); kidneys (membranoproliferative glomerulonephritis); blood vessels (vasculitis)	Diagnosis of acute HCV requires demonstration of HCV RNA (by PCR) with or without anti-HCV antibodies, in the context of a compatible clinical presentation and recent exposure. Anti-HCV antibodies may be negative in early acute infection (seronegative window up to 8-12 weeks), making HCV RNA testing essential. Seroconversion (new-onset anti-HCV positivity in a previously seronegative individual) is the most definitive diagnostic criterion. ALT elevation precedes antibody development and may be the first laboratory abnormality detected. HCV genotyping guides treatment selection if therapy is initiated. Quantitative HCV RNA levels do not reliably predict spontaneous clearance or treatment response in acute infection.	Current AASLD/IDSA guidelines recommend treatment of acute HCV with direct-acting antivirals (DAAs) using the same pan-genotypic regimens as chronic HCV. Monitoring for spontaneous clearance can be considered for 12-16 weeks before initiating treatment per some guidelines (EASL). Preferred regimens include sofosbuvir/velpatasvir (Epclusa) 400/100 mg daily for 8 weeks or glecaprevir/pibrentasvir (Mavyret) 300/120 mg daily for 8 weeks. Cure rates (SVR12: sustained virologic response 12 weeks post-treatment) exceed 95% with DAA therapy. Post-exposure prophylaxis with DAAs is under investigation but not yet standard practice. All persons with identified acute HCV should be tested for HIV and HBV co-infection.	Good - Spontaneous viral clearance occurs in 15-45% of acute HCV cases within 6 months, more commonly in symptomatic patients, women, younger individuals, those with IL28B CC genotype, and immunocompetent hosts. For the 55-85% who progress to chronic infection, DAA treatment achieves cure (SVR12) in over 95% of cases. Without treatment, chronic HCV develops insidiously, leading to cirrhosis in 15-30% over 20-30 years. Fulminant hepatic failure from acute HCV is extremely rare. Early DAA treatment during the acute phase prevents chronicity and long-term complications in essentially all treated patients.	B17.1
03	3	Adenovirus Hepatitis	Viral Hepatitis	Adenoviruses are non-enveloped double-stranded DNA viruses (family Adenoviridae) with over 100 types classified into 7 species (A-G). Adenovirus hepatitis is most commonly caused by species C (types 1, 2, 5) and species B (types 3, 7) and occurs primarily in immunocompromised patients, particularly pediatric hematopoietic stem cell transplant recipients and solid organ transplant recipients. The virus directly infects hepatocytes, causing coagulative necrosis with characteristic smudge cells (amphophilic intranuclear inclusions that fill and distort the nucleus). In immunocompetent hosts, adenovirus hepatitis is very rare and typically self-limiting, though severe cases and outbreaks of acute hepatitis of unknown etiology in children (2022) raised concern about potential adenovirus involvement.	Adenovirus is ubiquitous, with most children seropositive for multiple serotypes by age 10. Adenovirus hepatitis is rare in immunocompetent individuals but has an incidence of 6-12% in pediatric HSCT recipients, representing one of the most serious viral complications of transplantation. In solid organ transplant recipients, adenovirus hepatitis is less common (1-5%) but particularly affects liver transplant recipients through donor-derived infection. The 2022 global cluster of acute hepatitis of unknown etiology in children led to investigation of adenovirus type 41 as a potential cause, though definitive causality remains debated.	Adenovirus hepatitis predominantly affects immunocompromised children and young adults post-transplantation, with the highest incidence in the first 100 days after HSCT. Pediatric liver transplant recipients are particularly vulnerable due to donor-derived adenovirus infection. Neonates can develop severe disseminated adenovirus disease including hepatitis. In immunocompetent hosts, adenovirus hepatitis is extremely rare at any age, though the 2022 outbreak primarily affected otherwise healthy children aged 1-5 years.	In immunocompromised patients, adenovirus hepatitis presents with rapidly rising transaminases (often >10-20 times ULN), fever, and hepatomegaly. Progression to liver failure with coagulopathy and encephalopathy can occur over days. Concurrent adenovirus involvement of other organs (pneumonitis, hemorrhagic cystitis, colitis, nephritis) is common in disseminated disease. In HSCT recipients, adenovirus disease may present with viremia before organ-specific symptoms develop. In the 2022 pediatric cluster, affected children presented with acute hepatitis, jaundice, and liver failure requiring transplantation in some cases. Diarrhea, vomiting, and respiratory symptoms may precede hepatic involvement.	Liver (hepatocytes); gastrointestinal tract (gastroenteritis); respiratory tract (pneumonitis); urinary tract (hemorrhagic cystitis); kidneys (nephritis); bone marrow (graft failure in HSCT); eyes (keratoconjunctivitis)	Adenovirus DNA quantification by PCR in blood is the standard for diagnosing disseminated disease in immunocompromised patients, with regular monitoring (weekly) in high-risk transplant recipients. Liver biopsy shows coagulative necrosis with characteristic smudge cells and can confirm the diagnosis by immunohistochemistry or in situ hybridization. Adenovirus typing by PCR or sequencing identifies the specific serotype. In immunocompetent patients, nasopharyngeal or stool adenovirus PCR may be positive but does not necessarily confirm hepatotropism. Electron microscopy can visualize characteristic viral particles. ALT/AST elevation may be dramatic (>5000 IU/L) in severe cases.	Cidofovir (5 mg/kg IV weekly with probenecid and saline hydration to prevent nephrotoxicity) is the standard antiviral for severe adenovirus disease, though evidence is limited to case series. Brincidofovir (oral lipid conjugate of cidofovir) was developed for adenovirus and shows improved oral bioavailability with less nephrotoxicity but has not achieved FDA approval for this indication. Reduction of immunosuppressive therapy is essential when possible. Adoptive transfer of adenovirus-specific cytotoxic T lymphocytes (viral-specific T cells) is an emerging and promising therapy in HSCT recipients, achieving viral clearance in 70-80% of cases. Intravenous immunoglobulin (IVIG) may provide passive antibody protection. Liver transplantation may be necessary for fulminant hepatic failure.	Poor - In immunocompromised patients, disseminated adenovirus hepatitis carries a mortality rate of 50-80% in HSCT recipients without effective treatment. Early detection through surveillance monitoring and prompt treatment with cidofovir improves outcomes. Adoptive T-cell therapy has shown encouraging results, reducing mortality to 20-30% in treated patients. In immunocompetent children with severe adenovirus hepatitis (as in the 2022 cluster), most recover but some required liver transplantation. Risk factors for mortality include high viral load (>10^6 copies/mL), disseminated disease, lack of immune reconstitution, and delay in treatment initiation.	B34.0
04	4	Chronic Hepatitis B	Viral Hepatitis	Chronic hepatitis B (CHB) is defined by the persistence of HBsAg for more than 6 months, resulting from failure of the immune system to clear HBV infection. The virus maintains a stable nuclear reservoir of covalently closed circular DNA (cccDNA) within hepatocyte nuclei, which is resistant to current antiviral therapies and serves as the template for ongoing viral transcription. CHB progresses through four immunologic phases: immune-tolerant (HBeAg-positive chronic infection with high viral load and normal ALT), immune-active (HBeAg-positive chronic hepatitis with elevated ALT and liver inflammation), inactive carrier (HBeAg-negative chronic infection with low viral load and normal ALT after HBeAg seroconversion), and HBeAg-negative chronic hepatitis (reactivation phase with precore/basal core promoter mutants). Persistent hepatic necroinflammation drives progressive fibrosis, cirrhosis, and hepatocarcinogenesis through both direct viral oncogenic mechanisms (HBV DNA integration into host genome) and indirect mechanisms (chronic inflammation, oxidative stress, regenerative hyperplasia).	Approximately 296 million people worldwide have chronic HBV infection, with 820,000-880,000 deaths annually from HBV-related cirrhosis and hepatocellular carcinoma. The highest prevalence is in the WHO Western Pacific Region (6.2%) and African Region (6.1%), with intermediate prevalence in the Eastern Mediterranean and Southeast Asia regions. In the United States, an estimated 2.2 million persons have chronic HBV, predominantly among foreign-born individuals from endemic countries. HBV is the leading cause of hepatocellular carcinoma globally, accounting for approximately 50% of HCC cases worldwide.	The age at infection is the primary determinant of chronicity risk: perinatal infection leads to chronicity in approximately 90%, early childhood infection in 25-50%, and adult infection in less than 5%. In highly endemic areas, most chronic HBV carriers acquired the infection perinatally or in early childhood. The immune-tolerant phase may persist for decades in perinatally-infected individuals, with active hepatitis typically developing in the third to fourth decade of life. HBeAg seroconversion occurs at a rate of approximately 5-15% per year in the immune-active phase.	Many patients with CHB are asymptomatic for years to decades, identified incidentally through screening. When symptoms develop, they include fatigue, malaise, right upper quadrant discomfort, and occasionally nausea. Acute flares of hepatitis (ALT elevation >5 times ULN) can occur during immune-active phases or during HBeAg seroconversion, mimicking acute hepatitis. Extrahepatic manifestations include polyarteritis nodosa, membranous nephropathy, cryoglobulinemia, and aplastic anemia. Patients with advancing fibrosis develop signs of portal hypertension including splenomegaly, thrombocytopenia, and eventually ascites, variceal bleeding, and hepatic encephalopathy. HCC may develop even in the absence of cirrhosis, particularly in African and Asian patients with longstanding high viral loads.	Liver (hepatocytes, stellate cells in fibrosis); kidneys (membranous nephropathy, polyarteritis nodosa); immune system; blood vessels (polyarteritis nodosa); bone marrow (aplastic anemia)	Diagnosis requires HBsAg positivity for more than 6 months. Complete serologic profiling includes HBeAg/anti-HBe status, quantitative HBV DNA by PCR, and anti-HDV screening. ALT levels guide treatment decisions but may be normal despite significant fibrosis. Liver fibrosis assessment is essential: non-invasive methods include transient elastography (FibroScan), FIB-4 index, APRI score, and serum fibrosis biomarkers. Liver biopsy remains the gold standard for grading necroinflammation (Knodell/Ishak score) and staging fibrosis. HCC surveillance with abdominal ultrasound with or without alpha-fetoprotein every 6 months is recommended for at-risk patients per AASLD guidelines.	First-line antiviral therapy per AASLD 2018 and EASL 2017 guidelines includes nucleos(t)ide analogues with high barrier to resistance: entecavir (0.5 mg daily for treatment-naive, 1 mg for lamivudine-experienced) or tenofovir disoproxil fumarate (300 mg daily) or tenofovir alafenamide (25 mg daily, preferred in patients with renal or bone disease risk). Treatment is indicated for immune-active disease (elevated ALT plus HBV DNA >20,000 IU/mL if HBeAg-positive or >2,000 IU/mL if HBeAg-negative), significant fibrosis (F2 or greater), cirrhosis regardless of ALT/DNA level, and selected special populations. Pegylated interferon alfa-2a (180 mcg weekly for 48 weeks) offers a finite treatment course with higher rates of HBsAg loss (3-7% at 1 year) but significant side effects. Functional cure (HBsAg loss with or without anti-HBs seroconversion) is achieved in less than 1% per year with NUC therapy. Novel therapies targeting cccDNA silencing, capsid assembly, and HBsAg secretion are in clinical trials.	Variable - The natural history varies widely depending on the phase of infection, host immune response, HBV genotype, and presence of cofactors. Without treatment, 15-40% of patients with chronic HBV develop cirrhosis, hepatocellular carcinoma, or end-stage liver disease. Annual incidence of cirrhosis is 2-6% in HBeAg-positive patients and 8-10% in those with active HBeAg-negative disease. HCC develops at a rate of 0.5-1% per year in non-cirrhotic CHB patients and 2-5% per year in those with established cirrhosis. Long-term nucleos(t)ide analogue therapy can halt or reverse fibrosis progression, reduce HCC risk by 50-70%, and improve overall survival. Functional cure (HBsAg loss) is associated with the best long-term outcomes but is achieved in only 1-3% of treated patients over 5 years.	B18.1
05	5	Chronic Hepatitis C	Viral Hepatitis	Chronic hepatitis C (CHC) is defined by persistence of HCV RNA for more than 6 months after initial infection, resulting from the failure of host immune responses to clear the virus. HCV replicates with high mutation rates (lacking proofreading polymerase activity), generating quasispecies diversity that enables viral escape from neutralizing antibodies and T-cell recognition. Chronic hepatic inflammation is driven by ongoing immune responses to persistent virus, with activation of hepatic stellate cells leading to progressive fibrosis through TGF-beta, PDGF, and connective tissue growth factor signaling. HCV also promotes hepatocarcinogenesis through both indirect mechanisms (chronic inflammation, fibrosis, oxidative stress) and direct viral protein effects (NS5A and core protein interactions with cell growth and apoptosis pathways), with HCC developing even in the absence of cirrhosis in rare cases.	Approximately 58 million people worldwide have chronic HCV infection, making it a leading cause of chronic liver disease, cirrhosis, HCC, and liver transplantation globally. In the United States, an estimated 2.4 million people have chronic HCV, with the highest prevalence among the baby boomer cohort (born 1945-1965) and increasing prevalence among young adults who inject drugs. HCV genotype 1 accounts for 75% of US infections. Chronic HCV accounts for approximately 25% of HCC cases globally and is the leading indication for liver transplantation in many Western countries.	Chronic HCV affects all age groups, reflecting the diverse modes and timing of acquisition. In the United States, a bimodal age distribution exists: the largest cohort comprises individuals born 1945-1965 who were infected through blood transfusion, healthcare exposure, or drug use decades ago; a second growing cohort comprises young adults aged 20-39 with injection drug use. In endemic countries, infections may occur at any age through healthcare-associated or household transmission. Disease progression to significant fibrosis typically takes 20-30 years from initial infection.	Most patients with chronic HCV are asymptomatic or have nonspecific symptoms such as fatigue, malaise, mild cognitive impairment (brain fog), myalgia, and arthralgia. Extrahepatic manifestations affect 40-74% of patients and include mixed cryoglobulinemia (type II/III) causing vasculitis, palpable purpura, membranoproliferative glomerulonephritis, peripheral neuropathy, and non-Hodgkin B-cell lymphoma. Other extrahepatic associations include type 2 diabetes mellitus, lichen planus, porphyria cutanea tarda, sicca syndrome, and insulin resistance. As fibrosis progresses to cirrhosis, symptoms of portal hypertension develop: ascites, variceal bleeding, hepatic encephalopathy, jaundice, spider angiomata, palmar erythema, and muscle wasting.	Liver (hepatocytes, stellate cells, Kupffer cells); kidneys (membranoproliferative GN, cryoglobulinemic nephropathy); blood vessels (cryoglobulinemic vasculitis); hematologic/lymphatic system (B-cell NHL, mixed cryoglobulinemia); endocrine system (type 2 diabetes, thyroid disorders); skin (porphyria cutanea tarda, lichen planus); nervous system (peripheral neuropathy)	Diagnosis requires anti-HCV antibody screening (by enzyme immunoassay) followed by confirmatory HCV RNA testing by quantitative PCR. Reflex testing (automatic HCV RNA if antibody positive) is recommended to streamline diagnosis. HCV genotyping is performed to guide treatment selection, though pan-genotypic regimens have reduced its importance. Liver fibrosis staging is essential and uses non-invasive methods: FibroScan (transient elastography) with thresholds of <7.1 kPa for F0-F1 and >12.5 kPa for F4, FIB-4 index, and APRI score. Liver biopsy is reserved for discordant non-invasive results or suspected concomitant liver disease. HCC surveillance (ultrasound every 6 months) is recommended for patients with cirrhosis or advanced fibrosis (F3) per AASLD guidelines.	Direct-acting antiviral (DAA) therapy has revolutionized HCV treatment, achieving cure rates (SVR12) exceeding 95% across all genotypes. Pan-genotypic regimens include: sofosbuvir/velpatasvir (Epclusa) 400/100 mg daily for 12 weeks; glecaprevir/pibrentasvir (Mavyret) 300/120 mg daily for 8 weeks (treatment-naive without cirrhosis) or 12 weeks (with compensated cirrhosis). For decompensated cirrhosis (Child-Pugh B/C), sofosbuvir/velpatasvir or sofosbuvir/velpatasvir/voxilaprevir is used (protease inhibitors are contraindicated in decompensated disease). Treatment is recommended for all patients with chronic HCV regardless of fibrosis stage per AASLD/IDSA and EASL guidelines. Post-SVR follow-up includes continued HCC surveillance for patients with advanced fibrosis/cirrhosis, as HCC risk persists despite cure (reduced by 71% but not eliminated).	Good - SVR12 (virologic cure) is achieved in over 95% of treated patients with current DAA regimens. Achieving SVR significantly improves all-cause mortality, liver-related mortality, HCC risk (71% reduction), and extrahepatic manifestations. Fibrosis regression occurs in 40-80% of patients post-SVR, including reversal of cirrhosis in some cases. However, patients with established cirrhosis at the time of cure retain a residual HCC risk of 1-3% per year, necessitating ongoing surveillance. Reinfection can occur (1-5% per year in high-risk populations) as SVR does not confer sterilizing immunity. Without treatment, 15-30% of CHC patients develop cirrhosis over 20-30 years, with annual HCC rates of 1-4% once cirrhosis is established.	B18.2

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