Medical liver disease

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This article deals with medical liver disease. An introduction to the liver and approach is found in the liver article.

Every differential in liver pathology has "drugs"[1] -- if it isn't clearly malignancy.

Liver neoplasms are dealt with in the liver neoplasms article.

Viral hepatitis

These are common. The diagnoses are based on serology. The serology is covered in the viral hepatitis section in the liver pathology article.

Hepatitis A

  • Infection is self-limited, i.e. not persistent.
  • Usually asymptomatic in children.[2]
  • Serology is diagnostic.

Hepatitis B

General

Microscopic

Features:

  • Lobular inflammation - this is non-specific finding.
    • Hepatocyte necrosis:
      • Necrotic hepatocytes look a lot like neutrophils - however:
        • Cytoplasm is more pink.
        • Round apoptotic bodies.
  • Ground glass hepatocytes - see liver pathology article.

Image: GGH - high mag. (WC).

DDx:

Notes:

Hepatitis C

General

  • Leads to hepatocellular carcinoma in the setting of cirrhosis.
  • Tends to be chronic; the "C" in "hepatitis C" stands for chronic.
  • Diagnosis is by serology.

Microscopic

Features:

  • Lobular inflammation - this is non-specific finding.
    • Usually Grade 1, rarely Grade 2 and almost never Grade 3 or Grade 4.[3]
  • Periportal steatosis in genotype 3.[4]
    • Steatosis in hepatitis C is usually a secondary pathology, i.e. a separate pathologic process.[5]

DDx:

Other infections

  • Hydatid disease (Hydatid cyst).
  • Ascaris.
  • Fasciola

Hydatid disease

  • AKA hydatid cyst.

General

Microscopic

Features:

Images:

Metabolic and toxic

Alcoholic liver disease

  • Acute and/or chronic liver changes due to alcohol use.
  • Includes ASH (alcoholic steatohepatitis).
  • Alcoholic hepatitis can be with minimal steatosis.[7]

Classic lab findings in EtOH abusers

  • AST & ALT elevated with AST:ALT=2:1.
  • GGT elevated.
  • MCV increased.

Gross pathology/radiologic findings

  • Classically micronodular pattern.
    • May be macronodular.

Microscopic

See:

Features:

  • Often zone III damage.
  • Cholestatsis common, i.e. yellow staining.
    • NASH (non-alcoholic steatohepatitis) usu. does not have cholestasis.[8]
  • Fibrosis starts at central veins.
  • Neutrophils (often helpful) -- few other things have PMNs. (???)
    • Neutrophils cluster around cells with Mallory hyaline.

Notes:

  • If portal inflammatory infiltrates more than mild, r/o other causes i.e. viral hepatitis.
  • Mallory bodies once thought to be characteristic; now considered non-specific and generally poorly understood.[9]
  • Some consider alcoholic liver disease a clinical diagnosis, i.e. as a pathologist one does not diagnose it.[10]

Non-alcoholic fatty liver disease

  • Abbreviated NAFLD.
  • Fatty liver that is not due to alcohol; includes obesity-related fatty liver, metabolic disease/diabetes-related fatty liver.

NASH

  • Non-alcoholic steatohepatitis - see steatohepatitis section.
  • Histologically indistinguishable from ASH.
  • NASH is a clinical diagnosis based on exclusion of alcohol.

Steatohepatitis

General

  • Steatohepatitis is a label for a set of histopathologic findings.
  • Fat accumulation in hepatocytes.
    • It may be a pattern seen in drug toxicity, e.g. methotrexate toxicity.[11]

Etiology:

  1. Alcohol = alcoholic steatohepatitis (ASH).
  2. Not alcohol = non-alcoholic steatohepatitis (NASH).
  3. Other.

Notes:

  • Pathologists can comment on the etiology; however, the histomorphology is not distinctive. In other words, ASH and NASH are clinical diagnoses.

Microscopic

Features:

  • Steatosis (usually macrovesicular) - key feature.
    • If less than 10% ... consider alt. diagnosis/disease process.
  • Hepatocyte injury:
    • Ballooning degeneration - key feature (see introduction to liver).
    • Mallory bodies.
      • Mallory body wannabes: "occasional cytoplasmic clumping".
  • +/-Chicken-wire perisinusoidal fibrosis +/- zone III (centrilobular) fibrosis (early).
    • Late-stage disease - portal bridging.[12]

Important note:

  • Steatohepatitis is a misnomer. It is not an -itis, i.e. inflammation is not the (predominant) pathologic process.

Image: Steatohepatitis (WC).

Grading steatohepatitis

Grading inflammation:[13]

  • Grade 1 - steatosis, occasional ballooning degeneration, PMNs.
  • Grade 2 - obvious ballooning, obvious PMNs, chronic inflammation.
  • Grade 3 - panacinar steatosis.

Autoimmune

Autoimmune hepatitis

  • Abbreviated AIH.

General

  • Several criteria exist to diagnose and histology (alone) is not sufficient.

Diagnosis

Simplifed diagnostic criteria (2008):[14]

  1. Antibody titer.
  2. Elevated IgG.
  3. Liver pathology.
  4. Exclusion of viral hepatitis.

Details (scoring):[14]

  • ANA or SMA 1:40 1 point.
  • ANA or SMA 1:80 2 points.
  • LKM 1:40 2 points.
  • IgG upper normal 1 point.
  • IgG 1.1x upper limit 2 points.
  • Histology compatible 1 point.
  • Typical AIH histo. 2 points.
  • No viral hepatsis 2 points.

Interpretation: Definite >= 7. Probable = 6.

Notes:

  • Autoantibodies may be seen in HCV.[14]
  • A normal IgG is very unusual in AIH - but may be seen in atypical variants with zone III involvment.

Abbreviations:

  • ANA = anti-nuclear antibody.
  • SMA = smooth muscle antibody.
  • LKM-1 = liver kidney microsomal type 1 antibody.

Microscopic

Classification:[14]

  • Typical:
    • Interface hepatitis (zone 1).
      • Lymphoplasmacytic infiltration of portal tracts / lobule.
        • Periportal Plasma cells - key feature.[15]
    • Emperipolesis - one cell penetrates into another one (uncommon finding).
    • Hepatic rosette - inflammatory cells around reactive hepatocytes.[16]
  • Compatible:
    • Chronic hepatitis - lymphocytic dominant.
  • Atypical:
    • Signs of an other disease.

Notes:

  • PAS stain may be useful - find plasma cells.[17]
    • Lots of plasma cells should prompt consideration of AIH.
  • Atypical Autoimmune hepatitis may have zone III involvment (lymphoplasmacytic infiltrate)[18] and a normal IgG.[19]

Images:

Treatment

  • Immunosuppresants (prednisone, azathioprine).[18]

Primary biliary cirrhosis

  • Abbreviated PBC.

General

Epidemiology

Etiology

  • Autoimmune.

Serology

  • AMA+.

Classic presentation

  • Pruritis.

Pathophysiology

  • Septal bile duct attacked.

Treatment

  • Ursodeoxycholic acid.
  • May be indication for transplant.

Microscopic

Features:

  • Intraepithelial lymphocytes - in bile duct key feature.
  • Bile duct epithelial cells with eosinophilic cytoplasm.[21]
  • Plasma cells.
  • Granulomas - close to bile duct.
    • Seen in classic presentation -- often not present or poorly formed.
  • Focal damage (may be missed on biopsy -- due to sampling).
  • "Garland" cirrhosis -- has irregular border (unlike in EtOH).
    • Garland originally "wreath of flowers" (in French).[22]

Images:

DDx:[23]

Notes:

  • PAS stain useful for examining basement membrane... which is lost in PBC.
  • Lobular inflammation should be minimal.

Staging PBC

PBC is staged according to Ludwig:[25]

  • Stage 1: Portal - inflammation or bile duct abnormalities.
  • Stage 2: Periportal - periportal fibrosis (enlargement of portal tracts) +/- inflammation.
  • Stage 3: Septal - septal fibrosis +/-inflammation in septa.
  • Stage 4: Cirrhosis - nodules of hepatocytes +/- inflammation.

Notes:

  • There can be significant variation in staging on biopsy - due to variability of fibrosis in a PBC liver.[26]
    • "Worst area" in biopsy specimen is used to determine stage.

Autoimmune hepatitis-primary biliary cirrhosis overlap syndrome (AIH-PBC OS)

Epidemiology

  • Rare.

Serology

  • AMA+, anti-dsDNA+.[27]


Primary sclerosing cholangitis

  • Abbreviated PSC.

General

Diagnosis

  • Diagnosed radiologically.
  • Liver biopsy is rarely useful diagnostically[30] - as the disease may be patchy.
    • The utility of the biopsy is staging.

Treatment

  • None very good.
  • May be indication for transplant.

Microscopic

Features:

  • Classic: "onion-skinning" - cells layer around the bile ducts; "onion skin" present in approx. 40% of cases.[31]
    • Not pathognomonic for PSC[31] - but not too much else looks like this on microscopy (ergo good fellowship exam question).
  • +/-Ductopenia.
  • +/-Ductal proliferation.

DDx:

  • Big.

Images:

Notes:

  • PSC often has minimal inflammation.[34]

Staging

Features:[35]

  • Stage I - focal portal inflammation, +/- duct abnormalities, no fibrosis.
  • Stage II - portal enlargement (fibrosis), +/- inflammation.
  • Stage III - bridging fibrosis + necrosis.
  • Stage IV - cirrhosis.

Notes:

  • Similar to PBC staging.

Hereditary

Caroli disease

General

Clinical:[38]

Gross

  • Dilated bile ducts.[36]

Microscopic

Features:[38]

  • Dilated bile ducts.
  • Periductal fibrosis. (???)
  • +/-Fibrosis.

Image:

Hereditary hemochromatosis

Epidemiology/General

  • Genetic defect.
    • One mutation (C282Y mutation) in up to 12.5% of people in populations of northern and central European origin.[42]
  • Onset in males earlier than females (due to menses).
  • Mutation thought to confer survival advantage - several theories (increased resistance to TB, S. typhi vs. decr. iron def./incr. iron absorption)[42]
  • May lead to restrictive cardiomyopathy.

Pathophysiology

  • Iron overload --> cirrhosis.

Microscopic

  • Periportal changes (early), i.e. no iron centrilobular.
    • Late stage disease has diffuse iron deposition.
  • Brown granular -- may vaguely look like lipofuscin on H&E.

Diagnosis suggested by positive iron stain.

  • Light blue haze is not enough.
    • NOT siderosis -- in Kupffer cells.

Notes:

  • Iron in the bile ducts and endothelium used to be though specific of hereditary hemochromatosis.[43]
    • It is now thought to just reflect the severity of iron deposition, i.e. if the bile ducts and endothelium have iron - it is severe.

Images:

DDx

Wilson's disease

General

Epidemiology

  • Rare autosomal recessive - mutation in copper-transporting adenosine triphosphatase (ATPase) gene (ATP7B).[44]
    • Heterozygote carrier rate approximately 1/100 persons.[44]
  • Young individuals - usually 12-23 years old.

Clinical

  • Kayser-Fleischer rings --> on slit-lamp examination (green eyes).
  • May present to psychiatry or appear to be abusing EtOH.
  • Serum ceruloplasmin - lower than normal.

Etiology

  • Excess copper -- due to genetic defect.

Microscopic

Features:

  • Nothing specific.
  • Steatosis.
  • Portal fibrosis.

Staining:

  • Copper staining positive in ONLY 15%.
    • Other stains: rhodinine, orecin.

Notes:

  • Copper staining is a non-specific finding seen in many liver diseases; it is associated with impaired bile secretion.[45]

Alpha-1 antitrypsin deficiency

  • AKA alpha1-antiprotease inhibitor deficiency.

General

Etiology:

  • Genetic defect.
    • Prevalence 1 in 2000-5000.[46]

Causes:

  • Lung and liver injury.

Microscopic

Features:

  • Pink globules in zone 1 (periportal).
    • Globules not seen in children.
    • May not be present in late stage (cirrhotic).
    • Best seen on PASD stain.
    • Can be seen on H&E -- if one looks carefully.

Note:

  • The pink globules may be seen in the context of cirrhosis; cases should be confirmation with IHC.

Images:

IHC

  • A1-AT +ve globules.[47]

Other

Budd-Chiari syndrome

  • AKA hepatic vein obstruction.

General

  • Hepatic outflow obstruction.

Clinical triad:[48]

  • Ascites.
  • Abdominal pain.
  • Hepatomegaly.

Etiology:

Clinical DDx:

Microscopic

Features:[50]

  • Sinusoidal dilation in zone III (congestion).
  • +/-Hepatocyte drop-out.
  • +/-Centrilobular fibrosis.

DDx congestion:

Vanishing bile duct syndrome

General

  • Fatal.

DDx:[52]

Microscopic

Features:[52]

  • Loss of intrahepatitic bile ducts - key feature.
  • Cholestasis.

Note:

  • May occur without fibrosis and inflammation; thus, can be easy to miss.

IHC

  • CK7 -ve.
    • Marks bile ducts.

Congestive hepatopathy

General

  • Liver failure due to (right) heart failure.
  • AKA cardiac cirrhosis - a term used by clinicians.
    • Generally, it does not satisfy pathologic criteria for cirrhosis.[55]

Gross

  • "Nutmeg" liver - yellow spotted appearance.

Microscopic

Features:[56]

  • Zone III atrophy.
  • Portal venule (central vein) distension.
  • Perisinusoidal fibrosis - progresses to centrilobular fibrosis and then diffuse fibrosis.
  • Dilation of sinusoids in all zone III areas - key feature.[57]

Image: Congestive hepatopathy (WC).

Drug toxicity

  • Can do almost anything; may include: granulomata, bile duct loss, cholestasis, ischemic type injury.
  • Effects can be delayed -- temporal relationship not always obvious.

Microscopic:

Common

Acute hepatits:

  • Related to Rx - most often antibiotics.

Acetaminophen:

  • Zone 3 necrosis.
    • Tx: N-acetylcysteine (NAC).[59]
      • NAC is an endogenous precursor to glutathione.[60]
    • Hepatotoxicity from N-acetyl-p-benzoquinoneimine (NAPQI) due to depletion of glutathione.[59]

Methotrexate - chronic use:

  • Histology:[61]
    • Features of steatohepatitis.
      • Zone III steatosis.
      • Ballooning degeneration.
    • Portal inflammation with mixed population (lymphocytes, macrophages, PMNs).
    • Nuclear atypia (hyperchromasia, pleomorphism, vacuolation).
      • Described as just nuclear size variation by some.[62]

Others:

  • Tamoxifen.

Focal nodular hyperplasia

  • Abbreviated FNH.

General

  • Not commonly seen by pathologists, as these are usually distinctive on medical imaging.[63]
  • Benign lesions.
  • Associated with oral contraceptive pill (OCP) use.
  • May be seen in the context of hereditary hemorrhagic telangiectasia.[64]

Imaging

  • FNH enhances on the arterial phase in triphasic imaging, i.e. triphasic CT or MRI.[65][63]

Gross

Features:[66]

  • Well circumscribed, but no capsule.
  • Lighter than surrounding parenchyma, may be yellow.
  • +/-Stellate central scar with thick vessels.
    • Can be identified on medial imaging.

Note: Usually a solitary lesion.[65]

Microscopic

Features:[66]

  • Stellate scar has large arteries with fibromuscular hyperplasia.
    • Thin fibrous septa radiate from the central scar - surrounded by lymphocytes & bile ductules.
      • Normal hepatocytes between fibrous septae.

DDx:

  • Hepatic adenoma - may be difficult to distinguish, if no scar and no ductal proliferation.[67]
  • Cirrhosis - complete nodules
    • FNH has incomplete nodules.

Images:

Nodular regenerative hyperplasia

General

Etiology

  • Arterial hypervascularity secondary to loss of hepatic vein radicles (loss of central venule in hepatic lobule).[68]

ASIDE: radicle = ramulus - smallest branch or vessel or nerve.[69]

Gross

  • Diffuse nodularity - whole liver.

Microscopic

Features:[66]

  • "Plump" hepatocytes surrounded by atrophic ones.
  • No fibrosis.

Sinuosoidal obstruction syndrome

  • May be referred to as Hepatic veno-occlusive disease.[70]

General

  • Term for obstruction due to toxicity from a chemotherapeutic agent.[71][50]

Clinical DDx:

Microscopic

Features:[50]

  • Subendothelial swelling in hepatic venules.

Negatives:

  • No thrombosis.

Polycystic kidney disease and the liver

Main article: Cystic kidney disease

General

Complications of PKD in the liver:[72]

  1. Infected cyst.
  2. Cholangiocarcinoma.
  3. Cholestasis/obstruction due to duct compression.[73]

Cysts:

  • Cysts in the liver, like the kidney, are thought to enlarge with age.

Microscopic

Features:[74]

  • Von Meyenburg complexes (bile duct hamartoma):
    • Cluster of dilated ducts with "altered" bile.
    • Surrounded by collagenous stroma.
    • Separate from the portal areas.[75]

Images:

Notes:

  • Appearance on ultrasound[76] and CT (hypodense)[77] - similar to metastases.

Peliosis hepatis

General

  • Associated with:
    • Infections.
    • Malignancy.
    • Other stuff.
  • Rarely biopsied.

Microscopic

Features:

  • Cyst lined by endothelium.
    • Usu. incomplete.
  • Blood.

Total parenteral nutrition

  • Abbreviated TPN.

General

  • Indication: short gut syndrome, others.

Microscopic

Variable - may range from: steatosis, steatohepatitis, cholestasis, fibrosis and cirrhosis.[78]

Features (classic):[79][80]

  • Steatosis (periportal) - early.
  • Cholestasis - late.

Giant cell hepatitis

  • AKA neonatal giant cell hepatitis.
See: Giant cell hepatitis.

Hepatic amyloidosis

Main article: Amyloidosis

General

  • Diffuse abundant amyloid within the space of Disse is associated with portal hypertension.[81]

Microscopic

Features:

  • Amorphous extracellular pink stuff on H&E - see amyloid article.

Images:

Stains

See also

References

  1. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 448. ISBN 978-1416054542.
  2. ↑ Jeong SH, Lee HS (2010). "Hepatitis A: clinical manifestations and management". Intervirology 53 (1): 15–9. doi:10.1159/000252779. PMID 20068336.
  3. ↑ STC. 6 December 2010.
  4. ↑ Yoon EJ, Hu KQ. Hepatitis C virus (HCV) infection and hepatic steatosis. Int J Med Sci. 2006;3(2):53-6. Epub 2006 Apr 1. PMID 16614743. Avialable at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1415843. Accessed on: September 9, 2009.
  5. ↑ OA. September 2009.
  6. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 448. ISBN 978-1416054542.
  7. ↑ STC. 6 December 2010.
  8. ↑ STC. 6 December 2010.
  9. ↑ Jensen K, Gluud C (November 1994). "The Mallory body: theories on development and pathological significance (Part 2 of a literature survey)". Hepatology 20 (5): 1330-42. PMID 7927269.
  10. ↑ MG. September 2009.
  11. ↑ MG. 22 September 2009.
  12. ↑ Gramlich, T.; Kleiner, DE.; McCullough, AJ.; Matteoni, CA.; Boparai, N.; Younossi, ZM. (Feb 2004). "Pathologic features associated with fibrosis in nonalcoholic fatty liver disease.". Hum Pathol 35 (2): 196-9. PMID 14991537.
  13. ↑ Nonalcoholic steatohepatitis: a proposal for grading and staging the histological lesions. Brunt EM, Janney CG, Di Bisceglie AM, Neuschwander-Tetri BA, Bacon BR. Am J Gastroenterol. 1999 Sep;94(9):2467-74. PMID 10484010.
  14. ↑ 14.0 14.1 14.2 14.3 Scoring systems for the diagnosis of autoimmune hepatitis: past, present, and future. Wiegard C, Schramm C, Lohse AW. Semin Liver Dis. 2009 Aug;29(3):254-61. Epub 2009 Aug 12. PMID 19675998
  15. ↑ Mitchell, Richard; Kumar, Vinay; Fausto, Nelson; Abbas, Abul K.; Aster, Jon (2011). Pocket Companion to Robbins & Cotran Pathologic Basis of Disease (8th ed.). Elsevier Saunders. pp. 448. ISBN 978-1416054542.
  16. ↑ 16.0 16.1 Malik, TA.; Saeed, S. (May 2010). "Autoimmune hepatitis: a review.". J Pak Med Assoc 60 (5): 381-7. PMID 20527613. http://www.jpma.org.pk/full_article_text.php?article_id=2051.
  17. ↑ URL: http://iv.iiarjournals.org/content/19/6/1097.abstract. Accessed on: 9 December 2010.
  18. ↑ 18.0 18.1 Non-classical phenotypes of autoimmune hepatitis and advances in diagnosis and treatment. Czaja AJ, Bayraktar Y. World J Gastroenterol. 2009 May 21;15(19):2314-28. Review. PMID 19452572.
  19. ↑ FW. 21 September 2009.
  20. ↑ Tadrous, Paul.J. Diagnostic Criteria Handbook in Histopathology: A Surgical Pathology Vade Mecum (1st ed.). Wiley. pp. 162. ISBN 978-0470519035.
  21. ↑ OA. 11 September 2009.
  22. ↑ http://dictionary.reference.com/browse/garland
  23. ↑ Tadrous, Paul.J. Diagnostic Criteria Handbook in Histopathology: A Surgical Pathology Vade Mecum (1st ed.). Wiley. pp. 163. ISBN 978-0470519035.
  24. ↑ Vanishing bile duct syndrome and Hodgkin disease: a case series and review of the literature. Pass AK, McLin VA, Rushton JR, Kearney DL, Hastings CA, Margolin JF. J Pediatr Hematol Oncol. 2008 Dec;30(12):976-80. PMID 19131796.
  25. ↑ PBC. eMedicine.com. URL: http://emedicine.medscape.com/article/171117-diagnosis. Accessed on: 22 September 2009.
  26. ↑ J Clin Pathol. 1996 July; 49(7): 556-559. Available at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=500569. Accessed on: September 22, 2009.
  27. ↑ The serological profile of the autoimmune hepatitis/primary biliary cirrhosis overlap syndrome. Muratori P, Granito A, Pappas G, Pendino GM, Quarneti C, Cicola R, Menichella R, Ferri S, Cassani F, Bianchi FB, Lenzi M, Muratori L. Am J Gastroenterol. 2009 Jun;104(6):1420-5. Epub 2009 Apr 28. PMID 19491855.
  28. ↑ Khurana V, Singh T. Primary sclerosing cholangitis. eMedicine.com. URL: http://emedicine.medscape.com/article/187724-overview. Accessed on: 29 November 2009.
  29. ↑ Jesudian, AB.; Jacobson, IM. (2009). "Screening and diagnosis of cholangiocarcinoma in patients with primary sclerosing cholangitis.". Rev Gastroenterol Disord 9 (2): E41-7. PMID 19668124.
  30. ↑ Khurana V, Singh T. Primary sclerosing cholangitis. eMedicine.com. URL: http://emedicine.medscape.com/article/187724-diagnosis. Accessed on: 29 November 2009.
  31. ↑ 31.0 31.1 Steele et al. URL: http://www.medscape.com/viewarticle/552500_6. Accessed on: 29 November 2009.
  32. ↑ URL: http://trialx.com/curebyte/2011/07/08/clinical-trials-and-images-of-primary-sclerosing-cholangitis/. Accessed on: 1 January 2012.
  33. ↑ URL: http://www.onmedica.com/NewsArticle.aspx?id=d7f992b5-6dee-46c6-8383-bbdfb4528ccc. Accessed on: 1 January 2011.
  34. ↑ STC. 9 December 2010.
  35. ↑ Steele et al. URL: http://www.medscape.com/viewarticle/552500_6. Accessed on: 29 November 2009.
  36. ↑ 36.0 36.1 Online 'Mendelian Inheritance in Man' (OMIM) 263200
  37. ↑ Online 'Mendelian Inheritance in Man' (OMIM) 600643
  38. ↑ 38.0 38.1 Yonem, O.; Bayraktar, Y. (Apr 2007). "Clinical characteristics of Caroli's syndrome.". World J Gastroenterol 13 (13): 1934-7. PMID 17461493.
  39. ↑ Yonem, O.; Bayraktar, Y. (Apr 2007). "Clinical characteristics of Caroli's disease.". World J Gastroenterol 13 (13): 1930-3. PMID 17461492.
  40. ↑ Karim, AS. (Aug 2004). "Caroli's disease.". Indian Pediatr 41 (8): 848-50. PMID 15347876.
  41. ↑ URL: http://www.meddean.luc.edu/lumen/MedEd/orfpath/develop.htm. Accessed on: 1 December 2011.
  42. ↑ 42.0 42.1 Weinberg ED (2008). "Survival advantage of the hemochromatosis C282Y mutation". Perspect. Biol. Med. 51 (1): 98-102. doi:10.1353/pbm.2008.0001. PMID 18192769.
  43. ↑ MG. 17 September 2009.
  44. ↑ 44.0 44.1 http://emedicine.medscape.com/article/183456-overview
  45. ↑ Miyamura H, Nakanuma Y, Kono N (December 1988). "Survey of copper granules in liver biopsy specimens from various liver abnormalities other than Wilson's disease and biliary diseases". Gastroenterol. Jpn. 23 (6): 633–8. PMID 2464523.
  46. ↑ Stoller, JK.; Aboussouan, LS. (Sep 2011). "A Review of Alpha-1 Antitrypsin Deficiency.". Am J Respir Crit Care Med. doi:10.1164/rccm.201108-1428CI. PMID 21960536.
  47. ↑ Theaker, JM.; Fleming, KA. (Jan 1986). "Alpha-1-antitrypsin and the liver: a routine immunohistological screen.". J Clin Pathol 39 (1): 58-62. PMID 3512609.
  48. ↑ Fox, MA.; Fox, JA.; Davies, MH. (2011). "Budd-Chiari syndrome--a review of the diagnosis and management.". Acute Med 10 (1): 5-9. PMID 21573256.
  49. ↑ Plessier, A.; Valla, DC. (Aug 2008). "Budd-Chiari syndrome.". Semin Liver Dis 28 (3): 259-69. doi:10.1055/s-0028-1085094. PMID 18814079.
  50. ↑ 50.0 50.1 50.2 Aydinli, M.; Bayraktar, Y. (May 2007). "Budd-Chiari syndrome: etiology, pathogenesis and diagnosis.". World J Gastroenterol 13 (19): 2693-6. PMID 17569137. http://www.wjgnet.com/1007-9327/full/v13/i19/2693.htm.
  51. ↑ 51.0 51.1 Inomata, Y.; Tanaka, K. (2001). "Pathogenesis and treatment of bile duct loss after liver transplantation.". J Hepatobiliary Pancreat Surg 8 (4): 316-22. doi:10.1007/s0053410080316. PMID 11521176.
  52. ↑ 52.0 52.1 Reau, NS.; Jensen, DM. (Feb 2008). "Vanishing bile duct syndrome.". Clin Liver Dis 12 (1): 203-17, x. doi:10.1016/j.cld.2007.11.007. PMID 18242505.
  53. ↑ Yeh, KH.; Hsieh, HC.; Tang, JL.; Lin, MT.; Yang, CH.; Chen, YC. (Aug 1994). "Severe isolated acute hepatic graft-versus-host disease with vanishing bile duct syndrome.". Bone Marrow Transplant 14 (2): 319-21. PMID 7994249.
  54. ↑ Chitturi, S.; Farrell, GC. (Apr 2001). "Drug-induced cholestasis.". Semin Gastrointest Dis 12 (2): 113-24. PMID 11352118.
  55. ↑ URL: http://emedicine.medscape.com/article/151792-overview. Accessed on: 17 June 2010.
  56. ↑ URL: http://emedicine.medscape.com/article/151792-diagnosis. Accessed on: 17 June 2010.
  57. ↑ Suggested by OA. September 2009.
  58. ↑ Tadrous, Paul.J. Diagnostic Criteria Handbook in Histopathology: A Surgical Pathology Vade Mecum (1st ed.). Wiley. pp. 166. ISBN 978-0470519035.
  59. ↑ 59.0 59.1 Millea PJ (August 2009). "N-acetylcysteine: multiple clinical applications". Am Fam Physician 80 (3): 265–9. PMID 19621836.
  60. ↑ URL: http://www.mskcc.org/mskcc/html/69310.cfm. Accessed on: 19 October 2010.
  61. ↑ Burt, Alastair D.;Portmann, Bernard C.;Ferrell, Linda D. (2006). MacSween's Pathology of the Liver (5th ed.). Churchill Livingstone. pp. 715. ISBN 978-0-443-10012-3.
  62. ↑ MG. 23 September 2009.
  63. ↑ 63.0 63.1 Brancatelli, G.; Federle, MP.; Grazioli, L.; Blachar, A.; Peterson, MS.; Thaete, L. (Apr 2001). "Focal nodular hyperplasia: CT findings with emphasis on multiphasic helical CT in 78 patients.". Radiology 219 (1): 61-8. PMID 11274535.
  64. ↑ Khalid SK, Garcia-Tsao G (August 2008). "Hepatic vascular malformations in hereditary hemorrhagic telangiectasia". Semin. Liver Dis. 28 (3): 247–58. doi:10.1055/s-0028-1085093. PMID 18814078.
  65. ↑ 65.0 65.1 http://emedicine.medscape.com/article/368377-overview
  66. ↑ 66.0 66.1 66.2 66.3 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 922. ISBN 0-7216-0187-1.
  67. ↑ STC. 19 Jan 2009.
  68. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 922. ISBN 0-7216-0187-1.
  69. ↑ Dorland's Medical Dictionary. 30th Ed.
  70. ↑ DeLeve, LD.; Shulman, HM.; McDonald, GB. (Feb 2002). "Toxic injury to hepatic sinusoids: sinusoidal obstruction syndrome (veno-occlusive disease).". Semin Liver Dis 22 (1): 27-42. doi:10.1055/s-2002-23204. PMID 11928077..
  71. ↑ Helmy, A. (Jan 2006). "Review article: updates in the pathogenesis and therapy of hepatic sinusoidal obstruction syndrome.". Aliment Pharmacol Ther 23 (1): 11-25. doi:10.1111/j.1365-2036.2006.02742.x. PMID 16393276.
  72. ↑ Burt, Alastair D.;Portmann, Bernard C.;Ferrell, Linda D. (2006). MacSween's Pathology of the Liver (5th ed.). Churchill Livingstone. pp. 174-5. ISBN 978-0-443-10012-3.
  73. ↑ URL: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=9184868. Accessed on: 23 September 2009.
  74. ↑ Burt, Alastair D.;Portmann, Bernard C.;Ferrell, Linda D. (2006). MacSween's Pathology of the Liver (5th ed.). Churchill Livingstone. pp. 176. ISBN 978-0-443-10012-3.
  75. ↑ Meyenburg complex. Stedman's Medical Dictionary. 27th Ed.
  76. ↑ Bile duct hamartomas--the von Meyenburg complex. Salles VJ, Marotta A, Netto JM, Speranzini MB, Martins MR. Hepatobiliary Pancreat Dis Int. 2007 Feb;6(1):108-9. PMID 17287178.
  77. ↑ [The von Meyenburg complex] Schwab SA, Bautz W, Uder M, Kuefner MA. Rontgenpraxis. 2008;56(6):241-4. German. PMID 19294869.
  78. ↑ Guglielmi FW, Boggio-Bertinet D, Federico A, et al. (September 2006). "Total parenteral nutrition-related gastroenterological complications". Dig Liver Dis 38 (9): 623–42. doi:10.1016/j.dld.2006.04.002. PMID 16766237.
  79. ↑ Li, SJ.; Nussbaum, MS.; McFadden, DW.; Gapen, CL.; Dayal, R.; Fischer, JE. (Aug 1988). "Addition of glucagon to total parenteral nutrition (TPN) prevents hepatic steatosis in rats.". Surgery 104 (2): 350-7. PMID 3135627.
  80. ↑ Stanko, RT.; Nathan, G.; Mendelow, H.; Adibi, SA. (Jan 1987). "Development of hepatic cholestasis and fibrosis in patients with massive loss of intestine supported by prolonged parenteral nutrition.". Gastroenterology 92 (1): 197-202. PMID 3096806.
  81. ↑ Bion, E.; Brenard, R.; Pariente, EA.; Lebrec, D.; Degott, C.; Maitre, F.; Benhamou, JP. (Feb 1991). "Sinusoidal portal hypertension in hepatic amyloidosis.". Gut 32 (2): 227-30. PMC 1378815. PMID 1864548. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1378815/.
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