Liver disease

Last updated

Liver disease
Other namesHepatic disease
Human liver with metastatic lesions from primary pancreas carcinoma (2).jpg
A gross pathology specimen of liver metastases caused by pancreatic cancer
Specialty Hepatology, gastroenterology
Types Fatty liver disease, Hepatitis (and several more) [1]
Diagnostic method Liver function tests [2]
TreatmentDepends on type (See types)

Liver disease, or hepatic disease, is any of many diseases of the liver. [1] If long-lasting it is termed chronic liver disease. [3] Although the diseases differ in detail, liver diseases often have features in common.

Contents

Liver diseases

There are more than a hundred different liver diseases. Some of the most common are: [4]

Signs and symptoms

Some of the signs and symptoms of a liver disease are the following:

Mechanisms

Liver diseases can develop through several mechanisms:

DNA damage

One general mechanism, increased DNA damage, is shared by some of the major liver diseases, including infection by hepatitis B virus or hepatitis C virus , heavy alcohol consumption, and obesity. [24]

Viral infection by hepatitis B virus, or hepatitis C virus causes an increase of reactive oxygen species. The increase in intracellular reactive oxygen species is about 10,000-fold with chronic hepatitis B virus infection and 100,000-fold following hepatitis C virus infection. [25] This increase in reactive oxygen species causes inflammation [25] and more than 20 types of DNA damage. [26] Oxidative DNA damage is mutagenic [27] and also causes epigenetic alterations at the sites of DNA repair. [28] Epigenetic alterations and mutations affect the cellular machinery that may cause the cell to replicate at a higher rate or result in the cell avoiding apoptosis, and thus contribute to liver disease. [29] By the time accumulating epigenetic and mutational changes eventually cause hepatocellular carcinoma, epigenetic alterations appear to have an even larger role in carcinogenesis than mutations. Only one gene, TP53, is mutated in more than 20% of liver cancers while 41 genes each have hypermethylated promoters (repressing gene expression) in more than 20% of liver cancers. [30]

Alcohol consumption in excess causes a build-up of acetaldehyde. Acetaldehyde and free radicals generated by metabolizing alcohol induce DNA damage and oxidative stress. [31] [32] [33] In addition, activation of neutrophils in alcoholic liver disease contributes to the pathogenesis of hepatocellular damage by releasing reactive oxygen species (which can damage DNA). [34] The level of oxidative stress and acetaldehyde-induced DNA adducts due to alcohol consumption does not appear sufficient to cause increased mutagenesis. [34] However, as reviewed by Nishida et al., [28] alcohol exposure, causing oxidative DNA damage (which is repairable), can result in epigenetic alterations at the sites of DNA repair. Alcohol-induced epigenetic alterations of gene expression appear to lead to liver injury and ultimately carcinoma. [35]

Obesity is associated with a higher risk of primary liver cancer. [36] As shown with mice, obese mice are prone to liver cancer, likely due to two factors. Obese mice have increased pro-inflammatory cytokines. Obese mice also have higher levels of deoxycholic acid, a product of bile acid alteration by certain gut microbes, and these microbes are increased with obesity. The excess deoxycholic acid causes DNA damage and inflammation in the liver, which, in turn, can lead to liver cancer. [37]

Other relevant aspects

Several liver diseases are due to viral infection. Viral hepatitides such as Hepatitis B virus and Hepatitis C virus can be vertically transmitted during birth via contact with infected blood. [38] [39] According to a 2012 NICE publication, "about 85% of hepatitis B infections in newborns become chronic". [40] In occult cases, Hepatitis B virus is present by hepatitis B virus DNA, but testing for HBsAg is negative. [41] High consumption of alcohol can lead to several forms of liver disease including alcoholic hepatitis, alcoholic fatty liver disease, cirrhosis, and liver cancer. [42] In the earlier stages of alcoholic liver disease, fat builds up in the liver's cells due to increased creation of triglycerides and fatty acids and a decreased ability to break down fatty acids. [43] Progression of the disease can lead to liver inflammation from the excess fat in the liver. Scarring in the liver often occurs as the body attempts to heal and extensive scarring can lead to the development of cirrhosis in more advanced stages of the disease. [43] Approximately 3–10% of individuals with cirrhosis develop a form of liver cancer known as hepatocellular carcinoma. [43] According to Tilg, et al., gut microbiome could very well have an effect, be involved in the pathophysiology, on the various types of liver disease which an individual may encounter. [44] Insight into the exact causes and mechanisms mediating pathophysiology of the liver is quickly progressing due to the introduction new technological approaches like Single cell sequencing and kinome profiling [45]

Air pollutants

Particulate matter or carbon black are common pollutants. They have a direct toxic effect on the liver; cause inflammation of liver caused by and thereby impact lipid metabolism and fatty liver disease; and can translocate from the lungs to the liver. [46]

Because particulate matter and carbon black are very diverse and each has different toxicodynamics, detailed mechanisms of translocation are not clear. Water-soluble fractions of particulate matter are the most important part of translocation to the liver, through extrapulmonary circulation. When particulate matter gets into the bloodstream, it combines with immune cells and stimulates innate immune responses. Pro-inflammatory cytokines are released and cause disease progression. [46]

Epidemiology

Liver diseases, including conditions such as non-alcoholic fatty liver disease (NAFLD), alcohol-related liver disease (ALD), and viral hepatitis, are significant public health concerns worldwide. In the United States, NAFLD is the most common chronic liver condition, affecting approximately 24% of the population, with the prevalence rising due to increasing rates of obesity and metabolic syndrome. [47] [48] Alcohol-related liver disease accounts for about 4.5% of liver-related deaths globally, underscoring the substantial burden of alcohol misuse. [49] Viral hepatitis, primarily hepatitis B and hepatitis C, remains a leading cause of liver cirrhosis and liver cancer worldwide, despite advances in antiviral therapies and vaccination efforts. [50] Additionally, recent studies have highlighted lean steatotic liver disease (SLD), a subset of NAFLD, affecting over 12% of U.S. adults even in the absence of obesity. [51] These data emphasize the importance of early detection and targeted interventions to manage liver disease and its associated complications effectively.

New research reports the prevalence of lean steatotic liver disease (SLD) in the United States using data from the National Health and Nutrition Examination Survey (2017-2023), researchers estimated the age-adjusted prevalence of lean SLD at 12.8%. [52] This includes 9.3% for lean metabolic dysfunction-associated steatotic liver disease, 1.3% for metabolic dysfunction and alcohol-related steatotic liver disease, and 1.0% for alcohol-related liver disease. [53]

Diagnosis

A number of liver function tests are available to test the proper function of the liver. These test for the presence of enzymes in blood that are normally most abundant in liver tissue, metabolites or products. serum proteins, serum albumin, serum globulin, alanine transaminase, aspartate transaminase, prothrombin time, partial thromboplastin time. [2]

Imaging tests such as transient elastography, ultrasound and magnetic resonance imaging can be used to show the liver tissue and the bile ducts. Liver biopsy can be performed to examine liver tissue to distinguish between various conditions; tests such as elastography may reduce the need for biopsy in some situations. [54]

In liver disease, prothrombin time is longer than usual. [22] In addition, the amounts of both coagulation factors and anticoagulation factors are reduced as a diseased liver cannot productively synthesize them as it did when healthy. [55] Nonetheless, there are two exceptions in this falling tendency: coagulation factor VIII and von Willebrand factor, a platelet adhesive protein. [55] Both inversely rise in the setting of hepatic insufficiency, thanks to the drop of hepatic clearance and compensatory productions from other sites of the body. [55] Fibrinolysis generally proceeds faster with acute liver failure and advanced stage liver disease, unlike chronic liver disease in which concentration of fibrinogen remains unchanged. [55]

A previously undiagnosed liver disease may become evident first after autopsy.[ citation needed ] Following are gross pathology images:

Treatment

Ursodeoxycholic acid Ursodeoxycholic acid acsv.svg
Ursodeoxycholic acid

Anti-viral medications are available to treat infections such as hepatitis B. [56] Other conditions may be managed by slowing down disease progression, for example:

See also

Related Research Articles

<span class="mw-page-title-main">Hepatitis</span> Inflammation of the liver

Hepatitis is inflammation of the liver tissue. Some people or animals with hepatitis have no symptoms, whereas others develop yellow discoloration of the skin and whites of the eyes (jaundice), poor appetite, vomiting, tiredness, abdominal pain, and diarrhea. Hepatitis is acute if it resolves within six months, and chronic if it lasts longer than six months. Acute hepatitis can resolve on its own, progress to chronic hepatitis, or (rarely) result in acute liver failure. Chronic hepatitis may progress to scarring of the liver (cirrhosis), liver failure, and liver cancer.

<span class="mw-page-title-main">Hepatitis C</span> Human viral infection

Hepatitis C is an infectious disease caused by the hepatitis C virus (HCV) that primarily affects the liver; it is a type of viral hepatitis. During the initial infection period, people often have mild or no symptoms. Early symptoms can include fever, dark urine, abdominal pain, and yellow tinged skin. The virus persists in the liver, becoming chronic, in about 70% of those initially infected. Early on, chronic infection typically has no symptoms. Over many years however, it often leads to liver disease and occasionally cirrhosis. In some cases, those with cirrhosis will develop serious complications such as liver failure, liver cancer, or dilated blood vessels in the esophagus and stomach.

Liver function tests, also referred to as a hepatic panel or liver panel, are groups of blood tests that provide information about the state of a patient's liver. These tests include prothrombin time (PT/INR), activated partial thromboplastin time (aPTT), albumin, bilirubin, and others. The liver transaminases aspartate transaminase and alanine transaminase are useful biomarkers of liver injury in a patient with some degree of intact liver function.

<span class="mw-page-title-main">Hepatocellular carcinoma</span> Medical condition

Hepatocellular carcinoma (HCC) is the most common type of primary liver cancer in adults and is currently the most common cause of death in people with cirrhosis. HCC is the third leading cause of cancer-related deaths worldwide.

<span class="mw-page-title-main">Alcoholic liver disease</span> Medical condition

Alcoholic liver disease (ALD), also called alcohol-related liver disease (ARLD), is a term that encompasses the liver manifestations of alcohol overconsumption, including fatty liver, alcoholic hepatitis, and chronic hepatitis with liver fibrosis or cirrhosis.

<span class="mw-page-title-main">Viral hepatitis</span> Liver inflammation from a viral infection

Viral hepatitis is liver inflammation due to a viral infection. It may present in acute form as a recent infection with relatively rapid onset, or in chronic form, typically progressing from a long-lasting asymptomatic condition up to a decompensated hepatic disease and hepatocellular carcinoma (HCC).

<span class="mw-page-title-main">Alcoholic hepatitis</span> Medical condition

Alcoholic hepatitis is hepatitis due to excessive intake of alcohol. Patients typically have a history of at least 10 years of heavy alcohol intake, typically 8–10 drinks per day. It is usually found in association with fatty liver, an early stage of alcoholic liver disease, and may contribute to the progression of fibrosis, leading to cirrhosis. Symptoms may present acutely after a large amount of alcoholic intake in a short time period, or after years of excess alcohol intake. Signs and symptoms of alcoholic hepatitis include jaundice, ascites, fatigue and hepatic encephalopathy. Mild cases are self-limiting, but severe cases have a high risk of death. Severity in alcoholic hepatitis is determined several clinical prediction models such as the Maddrey's Discriminant Function and the MELD score.

<span class="mw-page-title-main">Fatty liver disease</span> Medical condition related to obesity

Fatty liver disease (FLD), also known as hepatic steatosis and steatotic liver disease (SLD), is a condition where excess fat builds up in the liver. Often there are no or few symptoms. Occasionally there may be tiredness or pain in the upper right side of the abdomen. Complications may include cirrhosis, liver cancer, and esophageal varices.

<span class="mw-page-title-main">Gastrointestinal disease</span> Illnesses of the digestive system

Gastrointestinal diseases refer to diseases involving the gastrointestinal tract, namely the esophagus, stomach, small intestine, large intestine and rectum; and the accessory organs of digestion, the liver, gallbladder, and pancreas.

Chronic liver disease in the clinical context is a disease process of the liver that involves a process of progressive destruction and regeneration of the liver parenchyma leading to fibrosis and cirrhosis. "Chronic liver disease" refers to disease of the liver which lasts over a period of six months. It consists of a wide range of liver pathologies which include inflammation, liver cirrhosis, and hepatocellular carcinoma. The entire spectrum need not be experienced.

<span class="mw-page-title-main">Steatohepatitis</span> Medical condition

Steatohepatitis is a type of fatty liver disease, characterized by inflammation of the liver with concurrent fat accumulation in liver. Mere deposition of fat in the liver is termed steatosis, and together these constitute fatty liver changes.

<span class="mw-page-title-main">Metabolic dysfunction–associated steatotic liver disease</span> Excessive fat buildup in the liver with other metabolic disease

Metabolic dysfunction–associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease (NAFLD), is a type of chronic liver disease. This condition is diagnosed when there is excessive fat build-up in the liver, and at least one metabolic risk factor. When there is also increased alcohol intake, the term MetALD, or metabolic dysfunction and alcohol associated/related liver disease is used, and differentiated from alcohol-related liver disease (ALD) where alcohol is the predominant cause of the steatotic liver disease. The terms non-alcoholic fatty liver (NAFL) and non-alcoholic steatohepatitis have been used to describe different severities, the latter indicating the presence of further liver inflammation. NAFL is less dangerous than NASH and usually does not progress to it, but this progression may eventually lead to complications, such as cirrhosis, liver cancer, liver failure, and cardiovascular disease.

<span class="mw-page-title-main">Liver cancer</span> Medical condition

Liver cancer, also known as hepatic cancer, primary hepatic cancer, or primary hepatic malignancy, is cancer that starts in the liver. Liver cancer can be primary in which the cancer starts in the liver, or it can be liver metastasis, or secondary, in which the cancer spreads from elsewhere in the body to the liver. Liver metastasis is the more common of the two liver cancers. Instances of liver cancer are increasing globally.

In medicine, the presence of elevated transaminases, commonly the transaminases alanine transaminase (ALT) and aspartate transaminase (AST), may be an indicator of liver dysfunction. Other terms include transaminasemia, and elevatedliver enzymes. Normal ranges for both ALT and AST vary by gender, age, and geography and are roughly 8-40 U/L. Mild transaminesemia refers to levels up to 250 U/L. Drug-induced increases such as that found with the use of anti-tuberculosis agents such as isoniazid are limited typically to below 100 U/L for either ALT or AST. Muscle sources of the enzymes, such as intense exercise, are unrelated to liver function and can markedly increase AST and ALT. Cirrhosis of the liver or fulminant liver failure secondary to hepatitis commonly reach values for both ALT and AST in the >1000 U/L range; however, many people with liver disease have normal transaminases. Elevated transaminases that persist less than six months are termed "acute" in nature, and those values that persist for six months or more are termed "chronic" in nature.

<span class="mw-page-title-main">Hepatitis B</span> Human viral infection

Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that affects the liver; it is a type of viral hepatitis. It can cause both acute and chronic infection.

<span class="mw-page-title-main">Cirrhosis</span> Chronic disease of the liver, characterized by fibrosis

Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, chronic liver failure or chronic hepatic failure and end-stage liver disease, is an acute condition of the liver in which the normal functioning tissue, or parenchyma, is replaced with scar tissue (fibrosis) and regenerative nodules as a result of chronic liver disease. Damage to the liver leads to repair of liver tissue and subsequent formation of scar tissue. Over time, scar tissue and nodules of regenerating hepatocytes can replace the parenchyma, causing increased resistance to blood flow in the liver's capillaries—the hepatic sinusoids—and consequently portal hypertension, as well as impairment in other aspects of liver function. The disease typically develops slowly over months or years.

<i>Hepatitis B virus</i> Species of the genus Orthohepadnavirus

Hepatitis B virus (HBV) is a partially double-stranded DNA virus, a species of the genus Orthohepadnavirus and a member of the Hepadnaviridae family of viruses. This virus causes the disease hepatitis B.

<span class="mw-page-title-main">Infectious causes of cancer</span> Pathogens as a cause of cancer

Estimates place the worldwide risk of cancers from infectious causes at 16.1%. Viral infections are risk factors for cervical cancer, 80% of liver cancers, and 15–20% of the other cancers. This proportion varies in different regions of the world from a high of 32.7% in Sub-Saharan Africa to 3.3% in Australia and New Zealand.

Hyperbilirubinemia is a clinical condition describing an elevation of blood bilirubin level due to the inability to properly metabolise or excrete bilirubin, a product of erythrocytes breakdown. In severe cases, it is manifested as jaundice, the yellowing of tissues like skin and the sclera when excess bilirubin deposits in them. The US records 52,500 jaundice patients annually. By definition, bilirubin concentration of greater than 3 mg/dL is considered hyperbilirubinemia, following which jaundice progressively develops and becomes apparent when plasma levels reach 20 mg/dL. Rather than a disease itself, hyperbilirubinemia is indicative of multifactorial underlying disorders that trace back to deviations from regular bilirubin metabolism. Diagnosis of hyperbilirubinemia depends on physical examination, urinalysis, serum tests, medical history and imaging to identify the cause. Genetic diseases, alcohol, pregnancy and hepatitis viruses affect the likelihood of hyperbilirubinemia. Causes of hyperbilirubinemia mainly arise from the liver. These include haemolytic anaemias, enzymatic disorders, liver damage and gallstones. Hyperbilirubinemia itself is often benign. Only in extreme cases does kernicterus, a type of brain injury, occur. Therapy for adult hyperbilirubinemia targets the underlying diseases but patients with jaundice often have poor outcomes.

References

  1. 1 2 "Liver Diseases". MedlinePlus.
  2. 1 2 MedlinePlus Encyclopedia : Liver function tests
  3. ↑ "NHS Choices". Cirrhosis. Retrieved 6 October 2015.
  4. ↑ "Liver disease – NHS Choices". www.nhs.uk. Retrieved 2015-06-20.
  5. ↑ "CDC – Fasciola". www.cdc.gov. Retrieved 2015-06-20.
  6. ↑ "Hepatitis". MedlinePlus.
  7. ↑ MedlinePlus Encyclopedia : Alcoholic liver disease
  8. ↑ "Hepatic steatosis" . Retrieved 2015-06-20.
  9. ↑ "Non-alcoholic fatty liver disease – NHS Choices". www.nhs.uk. Retrieved 2015-06-20.
  10. ↑ "Hemochromatosis". MedlinePlus.
  11. ↑ "Alpha-1 Antitrypsin Deficiency". MedlinePlus.
  12. ↑ Leslie N, Tinkle BT (1993). "Pompe Disease". In Pagon RA, Adam MP, Ardinger HH, Wallace SE, Amemiya A, Bean LJ, Bird TD, Dolan CR, Fong CT (eds.). Glycogen Storage Disease Type II (Pompe Disease). Seattle (WA): University of Washington, Seattle. PMID   20301438.
  13. ↑ "Transthyretin amyloidosis". Genetics Home Reference. Retrieved 2015-06-20.
  14. ↑ "Gilbert syndrome". Genetics Home Reference. Retrieved 2015-06-20.
  15. ↑ "Cirrhosis: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  16. ↑ "Liver cancer – Hepatocellular carcinoma: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  17. ↑ "Primary biliary cirrhosis: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  18. ↑ "Sclerosing cholangitis: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  19. ↑ "Hepatic vein obstruction (Budd-Chiari): MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-06-20.
  20. ↑ "Liver Disease | NIDDK". National Institute of Diabetes and Digestive and Kidney Diseases. Retrieved 2021-11-30.
  21. ↑ "Alcoholic Liver Disease". The Lecturio Medical Concept Library. Retrieved 27 June 2021.
  22. 1 2 Blonski W, Siropaides T, Reddy KR (2007). "Coagulopathy in liver disease". Current Treatment Options in Gastroenterology. 10 (6): 464–73. doi:10.1007/s11938-007-0046-7. ISSN   1092-8472. PMID   18221607. S2CID   23396752.
  23. ↑ Tripodi A, Mannucci PM (2011-07-14). "The Coagulopathy of Chronic Liver Disease". New England Journal of Medicine. 365 (2). Massachusetts Medical Society: 147–156. doi:10.1056/nejmra1011170. ISSN   0028-4793. PMID   21751907. S2CID   198152.
  24. ↑ "Chronic Liver Disease/Cirrhosis | Johns Hopkins Medicine Health Library". 12 April 2022.
  25. 1 2 Iida-Ueno A, Enomoto M, Tamori A, Kawada N (21 April 2017). "Hepatitis B virus infection and alcohol consumption". World Journal of Gastroenterology. 23 (15): 2651–2659. doi: 10.3748/wjg.v23.i15.2651 . PMC   5403744 . PMID   28487602.
  26. ↑ Yu Y, Cui Y, Niedernhofer LJ, Wang Y (December 2016). "Occurrence, Biological Consequences, and Human Health Relevance of Oxidative Stress-Induced DNA Damage". Chemical Research in Toxicology. 29 (12): 2008–2039. doi:10.1021/acs.chemrestox.6b00265. PMC   5614522 . PMID   27989142.
  27. ↑ Dizdaroglu M (December 2012). "Oxidatively induced DNA damage: mechanisms, repair and disease". Cancer Letters. 327 (1–2): 26–47. doi:10.1016/j.canlet.2012.01.016. PMID   22293091.
  28. 1 2 Nishida N, Kudo M (2013). "Oxidative stress and epigenetic instability in human hepatocarcinogenesis". Digestive Diseases. 31 (5–6): 447–53. doi: 10.1159/000355243 . PMID   24281019.
  29. ↑ Shibata T, Aburatani H (June 2014). "Exploration of liver cancer genomes". Nature Reviews. Gastroenterology & Hepatology. 11 (6): 340–9. doi:10.1038/nrgastro.2014.6. PMID   24473361. S2CID   8611393.
  30. ↑ Ozen C, Yildiz G, Dagcan AT, Cevik D, Ors A, Keles U, Topel H, Ozturk M (May 2013). "Genetics and epigenetics of liver cancer". New Biotechnology. 30 (4): 381–4. doi:10.1016/j.nbt.2013.01.007. hdl: 11693/20956 . PMID   23392071.
  31. ↑ Yu HS, Oyama T, Isse T, Kitagawa K, Pham TT, Tanaka M, Kawamoto T (December 2010). "Formation of acetaldehyde-derived DNA adducts due to alcohol exposure". Chemico-Biological Interactions. 188 (3): 367–75. Bibcode:2010CBI...188..367Y. doi:10.1016/j.cbi.2010.08.005. PMID   20813101.
  32. ↑ Lee SM, Kim-Ha J, Choi WY, Lee J, Kim D, Lee J, Choi E, Kim YJ (July 2016). "Interplay of genetic and epigenetic alterations in hepatocellular carcinoma". Epigenomics. 8 (7): 993–1005. doi: 10.2217/epi-2016-0027 . PMID   27411963.
  33. ↑ "Drinking alcohol causes cancer by 'damaging DNA' - Independent.ie". 5 January 2018.
  34. 1 2 Wang HJ, Gao B, Zakhari S, Nagy LE (August 2012). "Inflammation in alcoholic liver disease". Annual Review of Nutrition. 32: 343–68. doi:10.1146/annurev-nutr-072610-145138. PMC   3670145 . PMID   22524187.
  35. ↑ Shukla SD, Lim RW (2013). "Epigenetic effects of ethanol on the liver and gastrointestinal system". Alcohol Research. 35 (1): 47–55. PMC   3860425 . PMID   24313164.
  36. ↑ Aleksandrova K, Stelmach-Mardas M, Schlesinger S (2016). "Obesity and Liver Cancer". Obesity and Cancer. Recent Results in Cancer Research. Vol. 208. pp. 177–198. doi:10.1007/978-3-319-42542-9_10. ISBN   978-3-319-42540-5. PMID   27909908.{{cite book}}: |journal= ignored (help)
  37. ↑ Benova L, Mohamoud YA, Calvert C, Abu-Raddad LJ (September 2014). "Vertical transmission of hepatitis C virus: systematic review and meta-analysis". Clinical Infectious Diseases. 59 (6): 765–73. doi:10.1093/cid/ciu447. PMC   4144266 . PMID   24928290.
  38. ↑ Komatsu H (July 2014). "Hepatitis B virus: where do we stand and what is the next step for eradication?". World Journal of Gastroenterology. 20 (27): 8998–9016. doi: 10.3748/wjg.v20.i27.8998 (inactive 1 November 2024). PMC   4112872 . PMID   25083074.{{cite journal}}: CS1 maint: DOI inactive as of November 2024 (link)
  39. ↑ "Hepatitis B and C: ways to promote and offer testing to people at increased risk of infection | Guidance and guidelines | NICE". www.nice.org.uk. 12 December 2012. Retrieved 2015-06-24.
  40. ↑ Samal J, Kandpal M, Vivekanandan P (January 2012). "Molecular mechanisms underlying occult hepatitis B virus infection". Clinical Microbiology Reviews. 25 (1): 142–63. doi:10.1128/CMR.00018-11. PMC   3255968 . PMID   22232374.
  41. ↑ Suk KT, Kim MY, Baik SK (September 2014). "Alcoholic liver disease: treatment". World Journal of Gastroenterology. 20 (36): 12934–44. doi: 10.3748/wjg.v20.i36.12934 . PMC   4177474 . PMID   25278689.
  42. 1 2 3 Williams JA, Manley S, Ding WX (September 2014). "New advances in molecular mechanisms and emerging therapeutic targets in alcoholic liver diseases". World Journal of Gastroenterology. 20 (36): 12908–33. doi: 10.3748/wjg.v20.i36.12908 . PMC   4177473 . PMID   25278688.
  43. ↑ Tilg H, Cani PD, Mayer EA (December 2016). "Gut microbiome and liver diseases". Gut. 65 (12): 2035–2044. doi: 10.1136/gutjnl-2016-312729 . PMID   27802157.
  44. ↑ Yu B, Mamedov R, Fuhler GM, Peppelenbosch MP (March 2021). "Drug Discovery in Liver Disease Using Kinome Profiling". International Journal of Molecular Sciences. 22 (5): 2623. doi: 10.3390/ijms22052623 . PMC   7961955 . PMID   33807722.
  45. 1 2 Kim JW, Park S, Lim CW, Lee K, Kim B (June 2014). "The role of air pollutants in initiating liver disease". Toxicological Research. 30 (2): 65–70. Bibcode:2014ToxRe..30...65K. doi:10.5487/TR.2014.30.2.065. PMC   4112066 . PMID   25071914.
  46. ↑ Younossi ZM, Koenig AB, Abdelatif D, Fazel Y, Henry L, Wymer M (2016). "Global epidemiology of nonalcoholic fatty liver disease—Meta-analytic assessment of prevalence, incidence, and outcomes". Hepatology. 64 (1): 73–84. doi:10.1002/hep.28431. ISSN   0270-9139. PMID   26707365.
  47. ↑ Younossi ZM, Golabi P, Paik JM, Henry A, Van Dongen C, Henry L (2023). "The global epidemiology of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH): a systematic review". Hepatology. 77 (4): 1335–1347. doi:10.1097/HEP.0000000000000004. ISSN   0270-9139. PMC   10026948 . PMID   36626630.
  48. ↑ Rehm J, Shield KD (2019-12-13). "Global Burden of Alcohol Use Disorders and Alcohol Liver Disease". Biomedicines. 7 (4): 99. doi: 10.3390/biomedicines7040099 . ISSN   2227-9059. PMC   6966598 . PMID   31847084.
  49. ↑ Olaru ID, Beliz Meier M, Mirzayev F, Prodanovic N, Kitchen PJ, Schumacher SG, Denkinger CM (2023). "Global prevalence of hepatitis B or hepatitis C infection among patients with tuberculosis disease: systematic review and meta-analysis". eClinicalMedicine. 58: 101938. doi:10.1016/j.eclinm.2023.101938. ISSN   2589-5370. PMC   10113747 . PMID   37090436.
  50. ↑ Kim D, Danpanichkul P, Wijarnpreecha K, Cholankeril G, Loomba R, Ahmed A (2025-01-11). "Current Burden of Lean Metabolic Dysfunction-Associated Steatotic Liver Disease Among US Adults, 2017–2023". Alimentary Pharmacology & Therapeutics. doi:10.1111/apt.18501. ISSN   0269-2813.
  51. ↑ Kim D, Danpanichkul P, Wijarnpreecha K, Cholankeril G, Loomba R, Ahmed A (2025). "Current Burden of Lean Metabolic Dysfunction-Associated Steatotic Liver Disease Among US Adults, 2017–2023". Alimentary Pharmacology & Therapeutics. n/a (n/a). doi:10.1111/apt.18501. ISSN   1365-2036. PMID   39797575.
  52. ↑ "Lean Steatotic Liver Disease Affects 12% of US Adults, Study Finds". HCP Live. 2025-01-16. Retrieved 2025-01-18.
  53. ↑ Tapper EB, Lok AS (August 2017). "Use of Liver Imaging and Biopsy in Clinical Practice". The New England Journal of Medicine. 377 (8): 756–768. doi:10.1056/NEJMra1610570. PMID   28834467. S2CID   205117722.
  54. 1 2 3 4 Barton CA (2016). "Treatment of Coagulopathy Related to Hepatic Insufficiency". Critical Care Medicine. 44 (10). Ovid Technologies (Wolters Kluwer Health): 1927–1933. doi:10.1097/ccm.0000000000001998. ISSN   0090-3493. PMID   27635482. S2CID   11457839.
  55. ↑ De Clercq E, Férir G, Kaptein S, Neyts J (June 2010). "Antiviral treatment of chronic hepatitis B virus infections". Viruses. 2 (6): 1279–305. doi: 10.3390/v2061279 . PMC   3185710 . PMID   21994680.
  56. ↑ Hirschfield GM, Heathcote EJ (2011-12-02). Autoimmune Hepatitis: A Guide for Practicing Clinicians. Springer Science & Business Media. ISBN   978-1-60761-569-9.
  57. ↑ "Phlebotomy Treatment | Treatment and Management | Training & Education | Hemochromatosis (Iron Storage Disease) | NCBDDD | CDC". www.cdc.gov. Retrieved 2015-06-20.
  58. ↑ "Wilson Disease". www.niddk.nih.gov. Archived from the original on 2015-06-21. Retrieved 2015-06-20.
  59. ↑ Suchy FJ, Sokol RJ, Balistreri WF (2014-02-20). Liver Disease in Children. Cambridge University Press. ISBN   978-1-107-72909-4.
  60. ↑ Cheng K, Ashby D, Smyth RL (2017). "Ursodeoxycholic acid for liver disease related to cystic fibrosis". Cochrane Database of Systematic Reviews. 9 (9): CD000222. doi:10.1002/14651858.CD000222.pub4. PMC   6483662 . PMID   28891588 . Retrieved 2015-06-20.

Further reading

This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.