Non-Alcoholic Fatty Liver Disease or
Non-alcoholic steatohepatitis
From Wikipedia, the free encyclopedia
Non-alcoholic fatty liver disease
Non-alcoholic steatohepatitis
Classification and external resources
ICD-10
K76.0
ICD-9
571.8
DiseasesDB
29786
eMedicine
med/775
Non-alcoholic fatty liver disease (NAFLD) is fatty inflammation of the liver when this is not due to excessive alcohol use. It is related to insulin resistance and the metabolic syndrome, and may respond to treatments originally developed for other insulin resistant states (e.g. diabetes mellitus type 2), such as weight loss, metformin and thiazolidinediones.[1] Non-alcoholic steatohepatitis (NASH) is the most extreme form of NAFLD, which is regarded as a major cause of cirrhosis of the liver of unknown cause.[2]
NASH was first described in 1980 in a series of patients of the Mayo Clinic.[3] Its relevance and high prevalence were recognized mainly in the 1990s. Some feel that NASH is a diagnosis of exclusion, and that many cases may be in fact be due to other causes.[4]
Contents[hide]
1 Signs and symptoms
1.1 Symptoms and associations
1.2 Secondary causes
2 Diagnosis
3 Pathophysiology
4 Treatment
5 See also
6 References
7 External links
//
[edit] Signs and symptoms
[edit] Symptoms and associations
Most patients with NAFLD have no or few symptoms. Infrequently, patients may complain of fatigue, malaise and dull right upper quadrant abdominal discomfort. Mild jaundice may, rarely, be noticed. More commonly NAFLD is diagnosed following abnormal liver function tests during routine blood tests. By definition, alcohol consumption of over 20 g/day (about 25ml/day) excludes the condition.[1]
NAFLD is associated with insulin resistance and the metabolic syndrome (obesity, combined hyperlipidemia, diabetes mellitus (type II) and high blood pressure).[2][1]
[edit] Secondary causes
NAFLD can also be caused by the following medications (termed secondary NAFLD):[citation needed]
Amiodarone
Antiviral drugs (nucleoside analogues)
Aspirin / NSAIDs
Corticosteroids
Methotrexate
Nifedipine
Perhexiline
Tamoxifen
Tetracycline
Valproic acid
[edit] Diagnosis
Disturbed liver enzymes are common, and liver ultrasound may show steatosis; it may also be used to exclude gallstone problems (cholelithiasis). A biopsy (tissue examination) of the liver is the only test which is widely accepted as definitively distinguishing NASH from other forms of liver disease, and can be used to assess the severity of the inflammation and resultant fibrosis.[1]
Other tests are often carried out. Relevant blood tests include erythrocyte sedimentation rate, glucose, albumin, and renal function etc. As the liver is important in coagulation, some coagulation studies are often carried out, especially the INR (international normalized ratio). Blood tests (serology) are usually carried out to rule out viral hepatitis (hepatitis A, B, C, EBV, CMV and herpes viruses), rubella, and autoimmune causes. Hypothyroidism is more prevalent in NASH patients, which would be detected by determining the TSH.[5]
Some suggest that in overweight patients whose blood tests do not improve on losing weight and exercising, a further search of underlying causes of fatty liver must be sought, as well as those with fatty liver who are very young or not overweight or insulin resistant, those whose physical appearance indicates the possibility of a congenital syndrome, have a family history of liver disease, have abnormalities in other organs, and those who present with moderate to advanced fibrosis or cirrhosis.[4]
[edit] Pathophysiology
NAFLD is considered to cover a spectrum of disease activity. This spectrum begins as fatty accumulation in the liver (hepatic steatosis). A liver can remain fatty without disturbing liver function, but by varying mechanisms and possible insults to the liver may also progress to outright inflammation of the liver. When inflammation occurs in this setting, the condition is then called NASH. Over time up to 20 percent of patients with NASH may develop cirrhosis.[citation needed] Cigarette smoking is not associated with an increased risk of developing NASH.
The exact cause of NAFLD is still unknown. However, both obesity and insulin resistance probably play a strong role in the disease process. The exact reasons and mechanisms by which the disease progresses from one stage to the next are the subject of much research and debate.
One debated mechanism proposes a "second hit", or further injury, enough to cause change that leads from hepatic steatosis to hepatic inflammation. Oxidative stress, hormonal imbalances and mitochondrial abnormalities are potential causes for this "second hit" phenomenon.[1]
[edit] Treatment
Trials to optimise treatment of NASH are being conducted (2007), and no treatment has yet emerged as the "gold standard". General recommendations include improving metabolic risk factors and reducing alcohol intake.[1]
A large number of treatments for NAFLD have been studied. While many appear to improve biochemical markers such as alanine transaminase levels, most have not been shown to reverse histological abnormalities or reduce clinical endpoints:[1].
Treatment of nutrition and excessive body weight:
Nutritional counseling: Diet changes have shown significant histological improvement.[6]
Weight loss: gradual weight loss may improve the process in obese patients; rapid loss may worsen NAFLD. The bad effect of rapid weight loss is controversial: the results of a meta-analysis showed that the risk of progression is very low.[1]
A recent meta-analysis presented at the Annual Meeting of American Association for Study of Liver Diseases(AASLD) reported that weight-loss surgery leads to improvement and or resolution of NASH in around 80 % of patients.[2]
Insulin sensitisers (metformin[7] and thiazolidinediones[8]) have shown efficacy in some studies.
Antioxidants and ursodeoxycholic acid, as well as lipid-lowering drugs, have little benefit.[citation needed]
In a study using the NHANES III dataset, it has been shown that mild alcohol consumption (one glass of wine a day) reduces the risk of NAFLD by half.[9]
[edit] See also
Fatty liver includes both non-alcoholic and alcoholic liver disease
Alcoholic liver disease
[edit] References
^ a b c d e f g Adams LA, Angulo P (2006). "Treatment of non-alcoholic fatty liver disease". Postgrad Med J 82: 315–22. doi:10.1136/pgmj.2005.042200. PMID 16679470. http://pmj.bmj.com/cgi/content/full/82/967/315.
^ a b Clark JM, Diehl AM (2003). "Nonalcoholic fatty liver disease: an underrecognized cause of cryptogenic cirrhosis". JAMA 289: 3000–4. doi:10.1001/jama.289.22.3000. PMID 12799409.
^ Ludwig J, Viggiano TR, McGill DB, Oh BJ (1980). "Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease". Mayo Clin Proc 55. PMID 7382552.
^ a b Cassiman D, Jaeken J (2008). "NASH may be trash". Gut 57 (2): 141–4. doi:10.1136/gut.2007.123240. PMID 18192446.
^ Liangpunsakul S, Chalasani N (2003). "Is hypothyroidism a risk factor for non-alcoholic steatohepatitis?". J Clin Gastroenterol 37: 340–3. doi:10.1097/00004836-200310000-00014. PMID 14506393.
^ Huang MA, Greenson JK, Chao C, et al (2005). "One-year intense nutritional counseling results in histological improvement in patients with non-alcoholic steatohepatitis: a pilot study". Am. J. Gastroenterol. 100 (5): 1072–81. doi:10.1111/j.1572-0241.2005.41334.x. PMID 15842581.
^ Bugianesi E, Gentilcore E, Manini R, et al (2005). "A randomized controlled trial of metformin versus vitamin E or prescriptive diet in nonalcoholic fatty liver disease". Am. J. Gastroenterol. 100 (5): 1082–90. doi:10.1111/j.1572-0241.2005.41583.x. PMID 15842582.
^ Belfort R, Harrison SA, Brown K, et al (2006). "A placebo-controlled trial of pioglitazone in subjects with nonalcoholic steatohepatitis". N. Engl. J. Med. 355 (22): 2297–307. doi:10.1056/NEJMoa060326. PMID 17135584.
^ Dunn W, Xu R, Schwimmer JB (February 2008). "Modest wine drinking and decreased prevalence of suspected nonalcoholic fatty liver disease". Hepatology 47 (6): 1947–1954. doi:10.1002/hep.22292. PMID 18454505.
[edit] External links
Medscape article on NASH.
MEDICINENET article on Steatosis.
NIH page on Nonalcoholic Steatohepatitis
[hide]
v • d • eDigestive system · Digestive disease · Gastroenterology (primarily K20-K93, 530-579)
Upper GI tract
Esophagus
Esophagitis (Candidal) · rupture (Boerhaave syndrome, Mallory-Weiss syndrome) · UES (Zenker's diverticulum) · LES (Barrett's esophagus) · Esophageal motility disorder (Nutcracker esophagus, Achalasia, Diffuse esophageal spasm, GERD) · Esophageal stricture · Megaesophagus
Stomach
Gastritis (Atrophic, Ménétrier's disease, Gastroenteritis) · Peptic (gastric) ulcer (Cushing ulcer, Dieulafoy's lesion) · Dyspepsia · Pyloric stenosis · Achlorhydria · Gastroparesis · Gastroptosis · Portal hypertensive gastropathy · Gastric antral vascular ectasia · Gastric dumping syndrome · Gastric volvulus
Intestinal/enteropathy
Small intestine/(duodenum/jejunum/ileum)
Enteritis (Duodenitis, Jejunitis, Ileitis) — Peptic (duodenal) ulcer (Curling's ulcer) — Malabsorption: Coeliac · Tropical sprue · Blind loop syndrome · Whipple's · Short bowel syndrome · Steatorrhea · Milroy disease
Large intestine(appendix/colon)
Appendicitis · Colitis (Pseudomembranous, Ulcerative, Ischemic, Microscopic, Collagenous, Lymphocytic) · Functional colonic disease (IBS, Intestinal pseudoobstruction/Ogilvie syndrome) — Megacolon/Toxic megacolon · Diverticulitis/Diverticulosis
Large and/or small
Enterocolitis (Necrotizing) · IBD (Crohn's disease) — vascular: Abdominal angina · Mesenteric ischemia · Angiodysplasia — Bowel obstruction: Ileus · Intussusception · Volvulus · Fecal impaction — Constipation · Diarrhea (Infectious)
Rectum
Proctitis (Radiation proctitis) · Proctalgia fugax · Rectal prolapse
Anus
Anal fissure/Anal fistula · Anal abscess · Anal dysplasia · Pruritus ani
Accessory
Liver
Hepatitis (Viral hepatitis, Autoimmune hepatitis, Alcoholic hepatitis) · Cirrhosis (PBC) · Fatty liver (NASH) · vascular (Hepatic veno-occlusive disease, Portal hypertension, Nutmeg liver) · Alcoholic liver disease · Liver failure (Hepatic encephalopathy, Acute liver failure) · Liver abscess (Pyogenic, Amoebic) · Hepatorenal syndrome · Peliosis hepatis
Gallbladder
Cholecystitis · Gallstones/Cholecystolithiasis · Cholesterolosis · Rokitansky-Aschoff sinuses · Postcholecystectomy syndrome
Bile duct/other biliary tree
Cholangitis (PSC, Secondary sclerosing cholangitis, Ascending) · Cholestasis/Mirizzi's syndrome · Biliary fistula · Haemobilia · Gallstones/Cholelithiasiscommon bile duct (Choledocholithiasis, Biliary dyskinesia)
Pancreatic
Pancreatitis (Acute, Chronic, Hereditary) · Pancreatic pseudocyst · Exocrine pancreatic insufficiency · Pancreatic fistula
Hernia
Diaphragmatic: Congenital diaphragmatic · Hiatus — Abdominal hernia: Inguinal (Indirect, Direct) · Umbilical · Incisional · Femoral — Obturator hernia · Spigelian hernia · Internal hernia
Peritoneal
Peritonitis (Spontaneous bacterial peritonitis) · Hemoperitoneum · Pneumoperitoneum
GI bleeding/BIS
Upper (Hematemesis, Melena) · Lower (Hematochezia)
See also: congenital and neoplasia
Retrieved from "http://en.wikipedia.org/wiki/Non-alcoholic_fatty_liver_disease"
Categories: Gastroenterology Hepatitis
Hidden categories: All articles with unsourced statements Articles with unsourced statements since February 2007 Articles with unsourced statements since March 2008 Articles with unsourced statements since May 2008
From Wikipedia, the free encyclopedia
Non-alcoholic steatohepatitis
Classification and external resources
ICD-10
K76.0
ICD-9
571.8
DiseasesDB
29786
eMedicine
med/775
Non-alcoholic fatty liver disease (NAFLD) is fatty inflammation of the liver when this is not due to excessive alcohol use. It is related to insulin resistance and the metabolic syndrome, and may respond to treatments originally developed for other insulin resistant states (e.g. diabetes mellitus type 2), such as weight loss, metformin and thiazolidinediones.[1] Non-alcoholic steatohepatitis (NASH) is the most extreme form of NAFLD, which is regarded as a major cause of cirrhosis of the liver of unknown cause.[2]
NASH was first described in 1980 in a series of patients of the Mayo Clinic.[3] Its relevance and high prevalence were recognized mainly in the 1990s. Some feel that NASH is a diagnosis of exclusion, and that many cases may be in fact be due to other causes.[4]
Contents[hide]
1 Signs and symptoms
1.1 Symptoms and associations
1.2 Secondary causes
2 Diagnosis
3 Pathophysiology
4 Treatment
5 See also
6 References
7 External links
//
[edit] Signs and symptoms
[edit] Symptoms and associations
Most patients with NAFLD have no or few symptoms. Infrequently, patients may complain of fatigue, malaise and dull right upper quadrant abdominal discomfort. Mild jaundice may, rarely, be noticed. More commonly NAFLD is diagnosed following abnormal liver function tests during routine blood tests. By definition, alcohol consumption of over 20 g/day (about 25ml/day) excludes the condition.[1]
NAFLD is associated with insulin resistance and the metabolic syndrome (obesity, combined hyperlipidemia, diabetes mellitus (type II) and high blood pressure).[2][1]
[edit] Secondary causes
NAFLD can also be caused by the following medications (termed secondary NAFLD):[citation needed]
Amiodarone
Antiviral drugs (nucleoside analogues)
Aspirin / NSAIDs
Corticosteroids
Methotrexate
Nifedipine
Perhexiline
Tamoxifen
Tetracycline
Valproic acid
[edit] Diagnosis
Disturbed liver enzymes are common, and liver ultrasound may show steatosis; it may also be used to exclude gallstone problems (cholelithiasis). A biopsy (tissue examination) of the liver is the only test which is widely accepted as definitively distinguishing NASH from other forms of liver disease, and can be used to assess the severity of the inflammation and resultant fibrosis.[1]
Other tests are often carried out. Relevant blood tests include erythrocyte sedimentation rate, glucose, albumin, and renal function etc. As the liver is important in coagulation, some coagulation studies are often carried out, especially the INR (international normalized ratio). Blood tests (serology) are usually carried out to rule out viral hepatitis (hepatitis A, B, C, EBV, CMV and herpes viruses), rubella, and autoimmune causes. Hypothyroidism is more prevalent in NASH patients, which would be detected by determining the TSH.[5]
Some suggest that in overweight patients whose blood tests do not improve on losing weight and exercising, a further search of underlying causes of fatty liver must be sought, as well as those with fatty liver who are very young or not overweight or insulin resistant, those whose physical appearance indicates the possibility of a congenital syndrome, have a family history of liver disease, have abnormalities in other organs, and those who present with moderate to advanced fibrosis or cirrhosis.[4]
[edit] Pathophysiology
NAFLD is considered to cover a spectrum of disease activity. This spectrum begins as fatty accumulation in the liver (hepatic steatosis). A liver can remain fatty without disturbing liver function, but by varying mechanisms and possible insults to the liver may also progress to outright inflammation of the liver. When inflammation occurs in this setting, the condition is then called NASH. Over time up to 20 percent of patients with NASH may develop cirrhosis.[citation needed] Cigarette smoking is not associated with an increased risk of developing NASH.
The exact cause of NAFLD is still unknown. However, both obesity and insulin resistance probably play a strong role in the disease process. The exact reasons and mechanisms by which the disease progresses from one stage to the next are the subject of much research and debate.
One debated mechanism proposes a "second hit", or further injury, enough to cause change that leads from hepatic steatosis to hepatic inflammation. Oxidative stress, hormonal imbalances and mitochondrial abnormalities are potential causes for this "second hit" phenomenon.[1]
[edit] Treatment
Trials to optimise treatment of NASH are being conducted (2007), and no treatment has yet emerged as the "gold standard". General recommendations include improving metabolic risk factors and reducing alcohol intake.[1]
A large number of treatments for NAFLD have been studied. While many appear to improve biochemical markers such as alanine transaminase levels, most have not been shown to reverse histological abnormalities or reduce clinical endpoints:[1].
Treatment of nutrition and excessive body weight:
Nutritional counseling: Diet changes have shown significant histological improvement.[6]
Weight loss: gradual weight loss may improve the process in obese patients; rapid loss may worsen NAFLD. The bad effect of rapid weight loss is controversial: the results of a meta-analysis showed that the risk of progression is very low.[1]
A recent meta-analysis presented at the Annual Meeting of American Association for Study of Liver Diseases(AASLD) reported that weight-loss surgery leads to improvement and or resolution of NASH in around 80 % of patients.[2]
Insulin sensitisers (metformin[7] and thiazolidinediones[8]) have shown efficacy in some studies.
Antioxidants and ursodeoxycholic acid, as well as lipid-lowering drugs, have little benefit.[citation needed]
In a study using the NHANES III dataset, it has been shown that mild alcohol consumption (one glass of wine a day) reduces the risk of NAFLD by half.[9]
[edit] See also
Fatty liver includes both non-alcoholic and alcoholic liver disease
Alcoholic liver disease
[edit] References
^ a b c d e f g Adams LA, Angulo P (2006). "Treatment of non-alcoholic fatty liver disease". Postgrad Med J 82: 315–22. doi:10.1136/pgmj.2005.042200. PMID 16679470. http://pmj.bmj.com/cgi/content/full/82/967/315.
^ a b Clark JM, Diehl AM (2003). "Nonalcoholic fatty liver disease: an underrecognized cause of cryptogenic cirrhosis". JAMA 289: 3000–4. doi:10.1001/jama.289.22.3000. PMID 12799409.
^ Ludwig J, Viggiano TR, McGill DB, Oh BJ (1980). "Nonalcoholic steatohepatitis: Mayo Clinic experiences with a hitherto unnamed disease". Mayo Clin Proc 55. PMID 7382552.
^ a b Cassiman D, Jaeken J (2008). "NASH may be trash". Gut 57 (2): 141–4. doi:10.1136/gut.2007.123240. PMID 18192446.
^ Liangpunsakul S, Chalasani N (2003). "Is hypothyroidism a risk factor for non-alcoholic steatohepatitis?". J Clin Gastroenterol 37: 340–3. doi:10.1097/00004836-200310000-00014. PMID 14506393.
^ Huang MA, Greenson JK, Chao C, et al (2005). "One-year intense nutritional counseling results in histological improvement in patients with non-alcoholic steatohepatitis: a pilot study". Am. J. Gastroenterol. 100 (5): 1072–81. doi:10.1111/j.1572-0241.2005.41334.x. PMID 15842581.
^ Bugianesi E, Gentilcore E, Manini R, et al (2005). "A randomized controlled trial of metformin versus vitamin E or prescriptive diet in nonalcoholic fatty liver disease". Am. J. Gastroenterol. 100 (5): 1082–90. doi:10.1111/j.1572-0241.2005.41583.x. PMID 15842582.
^ Belfort R, Harrison SA, Brown K, et al (2006). "A placebo-controlled trial of pioglitazone in subjects with nonalcoholic steatohepatitis". N. Engl. J. Med. 355 (22): 2297–307. doi:10.1056/NEJMoa060326. PMID 17135584.
^ Dunn W, Xu R, Schwimmer JB (February 2008). "Modest wine drinking and decreased prevalence of suspected nonalcoholic fatty liver disease". Hepatology 47 (6): 1947–1954. doi:10.1002/hep.22292. PMID 18454505.
[edit] External links
Medscape article on NASH.
MEDICINENET article on Steatosis.
NIH page on Nonalcoholic Steatohepatitis
[hide]
v • d • eDigestive system · Digestive disease · Gastroenterology (primarily K20-K93, 530-579)
Upper GI tract
Esophagus
Esophagitis (Candidal) · rupture (Boerhaave syndrome, Mallory-Weiss syndrome) · UES (Zenker's diverticulum) · LES (Barrett's esophagus) · Esophageal motility disorder (Nutcracker esophagus, Achalasia, Diffuse esophageal spasm, GERD) · Esophageal stricture · Megaesophagus
Stomach
Gastritis (Atrophic, Ménétrier's disease, Gastroenteritis) · Peptic (gastric) ulcer (Cushing ulcer, Dieulafoy's lesion) · Dyspepsia · Pyloric stenosis · Achlorhydria · Gastroparesis · Gastroptosis · Portal hypertensive gastropathy · Gastric antral vascular ectasia · Gastric dumping syndrome · Gastric volvulus
Intestinal/enteropathy
Small intestine/(duodenum/jejunum/ileum)
Enteritis (Duodenitis, Jejunitis, Ileitis) — Peptic (duodenal) ulcer (Curling's ulcer) — Malabsorption: Coeliac · Tropical sprue · Blind loop syndrome · Whipple's · Short bowel syndrome · Steatorrhea · Milroy disease
Large intestine(appendix/colon)
Appendicitis · Colitis (Pseudomembranous, Ulcerative, Ischemic, Microscopic, Collagenous, Lymphocytic) · Functional colonic disease (IBS, Intestinal pseudoobstruction/Ogilvie syndrome) — Megacolon/Toxic megacolon · Diverticulitis/Diverticulosis
Large and/or small
Enterocolitis (Necrotizing) · IBD (Crohn's disease) — vascular: Abdominal angina · Mesenteric ischemia · Angiodysplasia — Bowel obstruction: Ileus · Intussusception · Volvulus · Fecal impaction — Constipation · Diarrhea (Infectious)
Rectum
Proctitis (Radiation proctitis) · Proctalgia fugax · Rectal prolapse
Anus
Anal fissure/Anal fistula · Anal abscess · Anal dysplasia · Pruritus ani
Accessory
Liver
Hepatitis (Viral hepatitis, Autoimmune hepatitis, Alcoholic hepatitis) · Cirrhosis (PBC) · Fatty liver (NASH) · vascular (Hepatic veno-occlusive disease, Portal hypertension, Nutmeg liver) · Alcoholic liver disease · Liver failure (Hepatic encephalopathy, Acute liver failure) · Liver abscess (Pyogenic, Amoebic) · Hepatorenal syndrome · Peliosis hepatis
Gallbladder
Cholecystitis · Gallstones/Cholecystolithiasis · Cholesterolosis · Rokitansky-Aschoff sinuses · Postcholecystectomy syndrome
Bile duct/other biliary tree
Cholangitis (PSC, Secondary sclerosing cholangitis, Ascending) · Cholestasis/Mirizzi's syndrome · Biliary fistula · Haemobilia · Gallstones/Cholelithiasiscommon bile duct (Choledocholithiasis, Biliary dyskinesia)
Pancreatic
Pancreatitis (Acute, Chronic, Hereditary) · Pancreatic pseudocyst · Exocrine pancreatic insufficiency · Pancreatic fistula
Hernia
Diaphragmatic: Congenital diaphragmatic · Hiatus — Abdominal hernia: Inguinal (Indirect, Direct) · Umbilical · Incisional · Femoral — Obturator hernia · Spigelian hernia · Internal hernia
Peritoneal
Peritonitis (Spontaneous bacterial peritonitis) · Hemoperitoneum · Pneumoperitoneum
GI bleeding/BIS
Upper (Hematemesis, Melena) · Lower (Hematochezia)
See also: congenital and neoplasia
Retrieved from "http://en.wikipedia.org/wiki/Non-alcoholic_fatty_liver_disease"
Categories: Gastroenterology Hepatitis
Hidden categories: All articles with unsourced statements Articles with unsourced statements since February 2007 Articles with unsourced statements since March 2008 Articles with unsourced statements since May 2008
Monday, May 04, 2009
Wednesday, November 12, 2008
Liver
Liver
From Wikipedia, the free encyclopedia
Anterior view of the position of the liver (red) in the human abdomen.
Latin
jecur
Gray's
subject #250 1188
Vein
hepatic vein, hepatic portal vein
Nerve
celiac ganglia, vagus[1]
Precursor
foregut
MeSH
Liver
The liver is a vital organ present in vertebrates and some other animals; it has a wide range of functions, a few of which are detoxification, protein synthesis, and production of biochemicals necessary for Digestion. The liver is necessary for survival; a human can only last up to 24 hours without liver function.
The liver plays a major role in metabolism and has a number of functions in the body, including glycogen storage, decomposition of red blood cells, plasma protein synthesis, and detoxification. The liver is also the largest gland in the human body. It lies below the diaphragm in the thoracic region of the abdomen. It produces bile, an alkaline compound which aids in digestion, via the emulsification of lipids (fats). It also performs and regulates a wide variety of high-volume biochemical reactions requiring very specialized tissues.[2]
Medical terms related to the liver often start in hepato- or hepatic from the Greek word for liver, hēpar (ήπαρ).[3]
Anatomy
The adult human liver normally weighs between 1.4 - 1.6 kilograms (3.1 - 3.5 pounds),[4] and it is a soft, pinkish-brown, triangular organ. Averaging about the size of an American football in adults, it is both the largest internal organ and the largest gland in the human body.
It is located on the right side of the upper abdomen below the diaphragm anatomy. The liver lies to the right of the stomach and overlies the Gallbladder .
Flow of blood
The splenic vein joins the inferior mesenteric vein, which then together join the superior mesenteric vein to form the hepatic portal vein, bringing venous blood from the spleen, The Pancreas, Stomach, small intestine, and large intestine, so that the liver can process the nutrients and by-products of food digestion.
The hepatic veins of the blood can be from other branches such as the superior mesenteric artery.
Both the portal venules & the hepatic arterioles enter approximately one million identical lobules acini, likened to and changes in the size of chylomicrons lipoproteins of dietary origin brought about by the quantity & types of food fats.
Approximately 60% to 80% of the blood flow to the liver is from the portal venous system, and 1/5th of blood flow is from the hepatic artery.
Flow of bile
The bile produced in the liver is collected in bile canaliculi, which merge to form bile ducts.
These eventually drain into the right and left hepatic ducts, which in turn merge to form the common hepatic duct. The cystic duct (from the gallbladder) joins with the common hepatic duct to form the common bile duct.
Bile can either drain directly into the duodenum via the common bile duct or be temporarily stored in the gallbladder via the cystic duct. The common bile duct and the pancreatic duct enter the duodenum together at the Ampulla of Vater.
The branchings of the bile ducts resemble those of a tree, and indeed the term "Biliary Tree", is commonly used in this setting.
The Biliary Tree.
Regeneration
The liver is among the few internal human organs capable of natural regeneration of lost tissue; as little as 25% of a liver can regenerate into a whole liver.
This is predominantly due to the hepatocytes re-entering the cell cycle (i.e. the hepatocytes go from the quiescent G0 phase to the G1 phase and undergo mitosis). There is also some evidence of bipotential stem cells, called ovalocyte (o´və-lo-sīt), which exist in the Canals of Hering. These cells can differentiate into either hepatocytes or cholangiocytes (cells that line the bile ducts).
Traditional (Surface) anatomy
Peritoneal ligaments
Apart from a patch where it connects to the diaphragm, the liver is covered entirely by visceral peritoneum, a thin, double-layered membrane that reduces friction against other organs. The peritoneum folds back on itself to form the falciform ligament and the right and left triangular ligaments.
These "ligaments" are in no way related to the true anatomic ligaments in joints, and have essentially no functional importance, but they are easily recognizable surface landmarks.
Lobes
Traditional gross anatomy divided the liver into four lobes based on surface features. The falciform ligament is visible on the front (anterior side) of the liver. This divides the liver into a left anatomical lobe, and a right anatomical lobe.
If the liver flipped over, to look at it from behind (the visceral surface), there are two additional lobes between the right and left. These are the caudate lobe (the more superior), and below this the quadrate lobe.
From behind, the lobes are divided up by the ligamentum venosum and ligamentum teres (anything left of these is the left lobe), the transverse fissure (or porta hepatis) divides the caudate from the quadrate lobe, and the right sagittal fossa, which the inferior vena cava runs over, separates these two lobes from the right lobe.
Each of the lobes is made up of lobules, a vein goes from the centre of each lobule which then joins to the hepatic vein to carry blood out from the liver.
On the surface of the lobules there are ducts, veins and arteries that carry fluids to and from them.
Modern (Functional) anatomy
The central area where the common bile duct, hepatic portal vein, and hepatic artery enter is the hilum or "porta hepatis". The duct, vein, and artery divide into left and right branches, and the portions of the liver supplied by these branches constitute the functional left and right lobes.
The liver performs over 500 jobs, and produces over 1,000 essential enzymes.
The functional lobes are separated by a plane joining the gallbladder fossa to the inferior vena cava. This separates the liver into the true right and left lobes. The middle hepatic vein also demarcates the true right and left lobes. The right lobe is further divided into an anterior and posterior segment by the right hepatic vein. The left lobe is divided into the medial and lateral segments by the left hepatic vein. The fissure for the ligamentum teres (the ligamentum teres becomes the falciform ligament) also separates the medial and lateral segments. The medial segment is what used to be called the quadrate lobe. In the widely used Couinaud or "French" system, the functional lobes are further divided into a total of eight subsegments based on a transverse plane through the bifurcation of the main portal vein. The caudate lobe is a separate structure which receives blood flow from both the right- and left-sided vascular branches.[5][6] The subsegments corresponding to the anatomical lobes are as follows:
Segment*
Couinaud segments
Caudate...1
Lateral.....2, 3
Medial.....4a, 4b
Right.......5, 6, 7, 8
or lobe in the Caudate's case.
Each number in the list corresponds to one in the table.
- Caudate
- Superior subsegment of the lateral segment
- Inferior subsegment of the lateral segment
- a
- b
- Inferior subsegment of the medial segment
- Inferior subsegment of the anterior segment
- Superior subsegment of the posterior segment
- Superior subsegment of the anterior segment
Physiology
The various functions of the liver are carried out by the liver cells or hepatocytes.
The liver produces and excretes bile (a greenish liquid) required for emulsifying fats. Some of the bile drains directly into the duodenum, and some is stored in the gallbladder.
- The liver performs several roles in carbohydrate metabolism:
- Gluconeogenesis (the synthesis of glucose from certain amino acids, lactate or
glycerol) - Glycogenolysis (the breakdown of glycogen into glucose) (muscle
tissues can also do this) - Glycogenesis (the formation of glycogen from
glucose) - The breakdown of insulin and other hormones
- The liver is responsible for the mainstay of protein metabolism. For instance, the liver can convert lactic acid to alanine.
- The liver also performs several roles in lipid (fat) metabolism:
- Cholesterol synthesis
- Lipogenesis, the production
of triglycerides (fats). - The liver produces coagulation factors I (fibrinogen), II
(prothrombin), V, VII, IX, X and XI, as well as protein C, protein S
and antithrombin. - The liver breaks down hemoglobin, creating metabolites that are added to bile as pigment (bilirubin and biliverdin).
- The liver breaks down toxic substances and most medicinal products in a process called drug metabolism. This sometimes results in toxication, when the metabolite is more toxic than its precursor.
- The liver converts ammonia to urea.
- The liver stores a multitude of substances, including glucose (in the form of glycogen), vitamin A (1-2 years' supply), vitamin D (1-4 months' supply), vitamin B12, iron, and copper.
- In the first trimester fetus, the liver is the main site of red blood cell production. By the 32nd week of gestation, the bone marrow has almost completely taken over that task.
- The liver is responsible for immunological effects- the reticuloendothelial system of the liver contains many immunologically active cells, acting as a 'sieve' for antigens carried to it via the portal system.
- The liver produces albumin, the major osmolar component of blood serum.
Currently, there is no artificial organ or device capable of emulating all the functions of the liver. Some functions can be emulated by liver dialysis, an experimental treatment for liver failure.
Diseases of the liver
Main article: Liver disease
Many diseases of the liver are accompanied by jaundice caused by increased levels of bilirubin in the system. The bilirubin results from the breakup of the hemoglobin of dead red blood cells; normally, the liver removes bilirubin from the blood and excretes it through bile.
There are also many pediatric liver diseases, including biliary atresia, alpha-1 antitrypsin deficiency, alagille syndrome, progressive familial intrahepatic cholestasis, and Langerhans cell histiocytosis to name but a few.
Liver transplantation
Main article: Liver transplantation
Human liver transplant was first performed by Thomas Starzl in USA and Roy Calne in Cambridge, England in 1963 and 1965 respectively.
Liver transplantation is the only option for those with irreversible liver failure. Most transplants are done for chronic liver diseases leading to cirrhosis, such as chronic hepatitis C, alcoholism, autoimmune hepatitis, and many others. Less commonly, liver transplantation is done for fulminate hepatic failure, in which liver failure occurs over days to weeks.
Liver allografts for transplant usually come from non-living donors who have died from fatal brain injury. Living donor liver transplantation is a technique in which a portion of a living person's liver is removed and used to replace the entire liver of the recipient. This was first performed in 1989 for pediatric liver transplantation. Only 20% of an adult's liver (Couperin segments 2 and 3) is needed to serve as a liver allograft for an infant or small child.
More recently, adult-to-adult liver transplantation has been done using the donor's right hepatic lobe which amounts to 60% of the liver. Due to the ability of the liver to regenerate, both the donor and recipient end up with normal liver function if all goes well. This procedure is more controversial as it entails performing a much larger operation on the donor, and indeed there have been at least 2 donor deaths out of the first several hundred cases. A recent publication has addressed the problem of donor mortality, and at least 14 cases have been found.[7] The risk of postoperative complications (and death) is far greater in right sided hepatectomy than left sided operations.
With the recent advances of non-invasive imaging, living liver donors usually have to undergo imaging examinations for liver anatomy to decide if the anatomy is feasible for donation. The evaluation is usually performed by multi-detector row computed tomography (MDCT) and magnetic resonance imaging (MRI). MDCT is good in vascular anatomy and volumetry. MRI is used for biliary tree anatomy. Donors with very unusual vascular anatomy, which makes them unsuitable for donation, could be screened out to avoid unnecessary operation.
Development
Fetal blood supply
In the growing fetus, a major source of blood to the liver is the umbilical vein which supplies nutrients to the growing fetus. The umbilical vein enters the abdomen at the umbilicus, and passes upward along the free margin of the falciform ligament of the liver to the inferior surface of the liver. There it joins with the left branch of the portal vein. The ductus venosus carries blood from the left portal vein to the left hepatic vein and then to the inferior vena cava, allowing placental blood to bypass the liver.
In the fetus, the liver develops throughout normal gestation, and does not perform the normal filtration of the infant liver. The liver does not perform digestive processes because the fetus does not consume meals directly, but receives nourishment from the mother via the placenta. The fetal liver releases some blood stem cells that migrate to the fetal thymus, so initially the lymphocyte, called T-cells, are created from fetal liver stem cells. Once the fetus is delivered, the formation of blood stem cells in infants shifts to the red bone marrow.
After birth, the umbilical vein and ductus venosus are completely obliterated two to five days postpartum; the former becomes the ligamentum teres and the latter becomes the ligamentum venosum. In the disease state of cirrhosis and portal hypertension, the umbilical vein can open up again.
Cultural allusions
In Greek mythology, Prometheus was punished by the gods for revealing fire to humans, by being chained to a rock where a vulture (or an eagle) would peck out his liver, which would regenerate overnight. (The liver is the only human internal organ that actually can regenerate itself to a significant extent.)
Many ancient peoples of the Near East and Mediterranean areas practised a type of divination called haruspicy, whereby they tried to obtain information from examining the livers of sheep and other animals.
The Talmud (tractate Berakhot 61b) refers to the liver as the seat of anger, with the gallbladder counteracting this.
In Arabic, Persian and Urdu languages, the liver is used in figurative speech to refer to courage and strong feelings, or "their best," e.g. "This Mecca has thrown to you the pieces of its liver!" [10]. The term jan e jigar literally "the strength (power) of my liver" is a term of endearment in Urdu.
In Persian Slang, Liver (Persian: جگر)Is Used as An Adjective for Any Object Which Is So Desirable (esp Women)
The legend of Liver-Eating Johnson says that he would cut out and eat the liver of each man killed after dinner.
In the motion picture The Message, Hind bint Utbah is implied or portrayed eating the liver of Hamza ibn ‘Abd al-Muttalib during the Battle of Uhud.
Inuit will not eat the liver of polar bears (a polar bear's liver contains so much Vitamin A as to be poisonous to humans), or seals [11]
See also
Look up liver in Wiktionary, the free dictionary.
Artificial liver
Bile
Bile canaliculus
Hepatocyte
Liver function tests
Further reading
The following are standard medical textbooks:
Eugene R. Schiff, Michael F. Sorrell, Willis C. Maddrey, eds. Schiff's diseases of the liver, 9th ed. Philadelphia : Lippincott, Williams & Wilkins, 2003. ISBN 0-7817-3007-4
Sheila Sherlock, James Dooley. Diseases of the liver and biliary system, 11th ed. Oxford, UK ; Malden, MA : Blackwell Science. 2002. ISBN 0-632-05582-0
David Zakim, Thomas D. Boyer. eds. Hepatology: a textbook of liver disease, 4th ed. Philadelphia: Saunders. 2003. ISBN 0-7216-9051-3
These are for the lay reader or patient:
Sanjiv Chopra. The Liver Book: A Comprehensive Guide to Diagnosis, Treatment, and Recovery, Atria, 2002, ISBN 0-7434-0585-4
Melissa Palmer. Dr. Melissa Palmer's Guide to Hepatitis and Liver Disease: What You Need to Know, Avery Publishing Group; Revised edition May 24, 2004, ISBN 1-58333-188-3. her webpage.
Howard J. Worman. The Liver Disorders Sourcebook, McGraw-Hill, 1999, ISBN 0-7373-0090-6. his Columbia University web site, "Diseases of the liver"
References
^ Physiology at MCG 6/6ch2/s6ch2_30
^ Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1. OCLC 32308337.
^ The Greek word "ήπαρ" was derived from hēpaomai (ηπάομαι): to mend, to repair, hence hēpar actually means "repairable", indicating that this organ can regenerate itself spontaneously in the case of lesion.
^ Robbins and Cotran Pathologic Basis of Disease, 7th Edition, p. 878
^ Three-dimensional Anatomy of the Couinaud Liver Segments - University of Iowa
^ Limitations and Pitfalls of Couinaud`s Segmentation of the Liver in Transaxial Imaging - Prof. Dr. Holger Strunk
^ Bramstedt K (2006). "Living liver donor mortality: where do we stand?". Am J Gastrointestinal 101 (4): 755–9. doi:10.1111/j.1572-0241.2006.00421.x. PMID 16494593.
^ A. Aggrawal, Death by Vitamin A
^ Myhre et al., "Water-miscible, emulsified, and solid forms of retinol supplements are more toxic than oil-based preparations", Am. J. Clinical Nutrition, 78, 1152 (2003)
^ THE GREAT BATTLE OF BADAR (Yaum-e-Furqan)
^ Man's best friend? - Student BMJ
Diseases of the liver
Main article: Liver disease
Many diseases of the liver are accompanied by jaundice caused by increased levels of bilirubin in the system. The bilirubin results from the breakup of the hemoglobin of dead red blood cells; normally, the liver removes bilirubin from the blood and excretes it through bile.
There are also many pediatric liver diseases, including biliary atresia, alpha-1 antitrypsin deficiency, alagille syndrome, progressive familial intrahepatic cholestasis, and Langerhans cell histiocytosis to name but a few.
Liver transplantation
Main article: Liver transplantation
Human liver transplant was first performed by Thomas Starzl in USA and Roy Calne in Cambridge, England in 1963 and 1965 respectively.
Liver transplantation is the only option for those with irreversible liver failure. Most transplants are done for chronic liver diseases leading to cirrhosis, such as chronic hepatitis C, alcoholism, autoimmune hepatitis, and many others. Less commonly, liver transplantation is done for fulminate hepatic failure, in which liver failure occurs over days to weeks.
Liver allografts for transplant usually come from non-living donors who have died from fatal brain injury. Living donor liver transplantation is a technique in which a portion of a living person's liver is removed and used to replace the entire liver of the recipient. This was first performed in 1989 for pediatric liver transplantation. Only 20% of an adult's liver (Couperin segments 2 and 3) is needed to serve as a liver allograft for an infant or small child.
More recently, adult-to-adult liver transplantation has been done using the donor's right hepatic lobe which amounts to 60% of the liver. Due to the ability of the liver to regenerate, both the donor and recipient end up with normal liver function if all goes well. This procedure is more controversial as it entails performing a much larger operation on the donor, and indeed there have been at least 2 donor deaths out of the first several hundred cases. A recent publication has addressed the problem of donor mortality, and at least 14 cases have been found.[7] The risk of postoperative complications (and death) is far greater in right sided hepatectomy than left sided operations.
With the recent advances of non-invasive imaging, living liver donors usually have to undergo imaging examinations for liver anatomy to decide if the anatomy is feasible for donation. The evaluation is usually performed by multi-detector row computed tomography (MDCT) and magnetic resonance imaging (MRI). MDCT is good in vascular anatomy and volumetry. MRI is used for biliary tree anatomy. Donors with very unusual vascular anatomy, which makes them unsuitable for donation, could be screened out to avoid unnecessary operation.
Development
Fetal blood supply
In the growing fetus, a major source of blood to the liver is the umbilical vein which supplies nutrients to the growing fetus. The umbilical vein enters the abdomen at the umbilicus, and passes upward along the free margin of the falciform ligament of the liver to the inferior surface of the liver. There it joins with the left branch of the portal vein. The ductus venosus carries blood from the left portal vein to the left hepatic vein and then to the inferior vena cava, allowing placental blood to bypass the liver.
In the fetus, the liver develops throughout normal gestation, and does not perform the normal filtration of the infant liver. The liver does not perform digestive processes because the fetus does not consume meals directly, but receives nourishment from the mother via the placenta. The fetal liver releases some blood stem cells that migrate to the fetal thymus, so initially the lymphocyte, called T-cells, are created from fetal liver stem cells. Once the fetus is delivered, the formation of blood stem cells in infants shifts to the red bone marrow.
After birth, the umbilical vein and ductus venosus are completely obliterated two to five days postpartum; the former becomes the ligamentum teres and the latter becomes the ligamentum venosum. In the disease state of cirrhosis and portal hypertension, the umbilical vein can open up again.
Cultural allusions
In Greek mythology, Prometheus was punished by the gods for revealing fire to humans, by being chained to a rock where a vulture (or an eagle) would peck out his liver, which would regenerate overnight. (The liver is the only human internal organ that actually can regenerate itself to a significant extent.)
Many ancient peoples of the Near East and Mediterranean areas practised a type of divination called haruspicy, whereby they tried to obtain information from examining the livers of sheep and other animals.
The Talmud (tractate Berakhot 61b) refers to the liver as the seat of anger, with the gallbladder counteracting this.
In Arabic, Persian and Urdu languages, the liver is used in figurative speech to refer to courage and strong feelings, or "their best," e.g. "This Mecca has thrown to you the pieces of its liver!" [10]. The term jan e jigar literally "the strength (power) of my liver" is a term of endearment in Urdu.
In Persian Slang, Liver (Persian: جگر)Is Used as An Adjective for Any Object Which Is So Desirable (esp Women)
The legend of Liver-Eating Johnson says that he would cut out and eat the liver of each man killed after dinner.
In the motion picture The Message, Hind bint Utbah is implied or portrayed eating the liver of Hamza ibn ‘Abd al-Muttalib during the Battle of Uhud.
Inuit will not eat the liver of polar bears (a polar bear's liver contains so much Vitamin A as to be poisonous to humans), or seals [11]
See also
Look up liver in Wiktionary, the free dictionary.
Artificial liver
Bile
Bile canaliculus
Hepatocyte
Liver function tests
Further reading
The following are standard medical textbooks:
Eugene R. Schiff, Michael F. Sorrell, Willis C. Maddrey, eds. Schiff's diseases of the liver, 9th ed. Philadelphia : Lippincott, Williams & Wilkins, 2003. ISBN 0-7817-3007-4
Sheila Sherlock, James Dooley. Diseases of the liver and biliary system, 11th ed. Oxford, UK ; Malden, MA : Blackwell Science. 2002. ISBN 0-632-05582-0
David Zakim, Thomas D. Boyer. eds. Hepatology: a textbook of liver disease, 4th ed. Philadelphia: Saunders. 2003. ISBN 0-7216-9051-3
These are for the lay reader or patient:
Sanjiv Chopra. The Liver Book: A Comprehensive Guide to Diagnosis, Treatment, and Recovery, Atria, 2002, ISBN 0-7434-0585-4
Melissa Palmer. Dr. Melissa Palmer's Guide to Hepatitis and Liver Disease: What You Need to Know, Avery Publishing Group; Revised edition May 24, 2004, ISBN 1-58333-188-3. her webpage.
Howard J. Worman. The Liver Disorders Sourcebook, McGraw-Hill, 1999, ISBN 0-7373-0090-6. his Columbia University web site, "Diseases of the liver"
References
^ Physiology at MCG 6/6ch2/s6ch2_30
^ Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1. OCLC 32308337.
^ The Greek word "ήπαρ" was derived from hēpaomai (ηπάομαι): to mend, to repair, hence hēpar actually means "repairable", indicating that this organ can regenerate itself spontaneously in the case of lesion.
^ Robbins and Cotran Pathologic Basis of Disease, 7th Edition, p. 878
^ Three-dimensional Anatomy of the Couinaud Liver Segments - University of Iowa
^ Limitations and Pitfalls of Couinaud`s Segmentation of the Liver in Transaxial Imaging - Prof. Dr. Holger Strunk
^ Bramstedt K (2006). "Living liver donor mortality: where do we stand?". Am J Gastrointestinal 101 (4): 755–9. doi:10.1111/j.1572-0241.2006.00421.x. PMID 16494593.
^ A. Aggrawal, Death by Vitamin A
^ Myhre et al., "Water-miscible, emulsified, and solid forms of retinol supplements are more toxic than oil-based preparations", Am. J. Clinical Nutrition, 78, 1152 (2003)
^ THE GREAT BATTLE OF BADAR (Yaum-e-Furqan)
^ Man's best friend? - Student BMJ
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