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Hepatitis

MedGen UID:
5515
Concept ID:
C0019158
Disease or Syndrome
Synonyms: Liver inflammation
SNOMED CT: Inflammatory disorder of liver (128241005); Inflammatory disease of liver (128241005); Hepatitis (128241005); Inflammatory liver disease (128241005)
 
HPO: HP:0012115

Definition

Your liver is the largest organ inside your body. It helps your body digest food, store energy, and remove poisons. Hepatitis is an inflammation of the liver. . Viruses cause most cases of hepatitis. The type of hepatitis is named for the virus that causes it; for example, hepatitis A, hepatitis B or hepatitis C. Drug or alcohol use can also cause hepatitis. In other cases, your body mistakenly attacks healthy cells in the liver. Some people who have hepatitis have no symptoms. Others may have. -Loss of appetite. -Nausea and vomiting. -Diarrhea. -Dark-colored urine and pale bowel movements. -Stomach pain. -Jaundice, yellowing of skin and eyes. Some forms of hepatitis are mild, and others can be serious. Some can lead to scarring, called cirrhosis, or to liver cancer. Sometimes hepatitis goes away by itself. If it does not, it can be treated with drugs. Sometimes hepatitis lasts a lifetime. Vaccines can help prevent some viral forms.  [from MedlinePlus]

Conditions with this feature

Halothane hepatitis
MedGen UID:
66842
Concept ID:
C0241913
Disease or Syndrome
Xerocytosis
MedGen UID:
124415
Concept ID:
C0272051
Disease or Syndrome
Dehydrated hereditary stomatocytosis (DHS), also known as hereditary xerocytosis, is an autosomal dominant hemolytic anemia characterized by primary erythrocyte dehydration. DHS erythrocytes exhibit decreased total cation and potassium content that are not accompanied by a proportional net gain of sodium and water. DHS patients typically exhibit mild to moderate compensated hemolytic anemia, with an increased erythrocyte mean corpuscular hemoglobin concentration and a decreased osmotic fragility, both of which reflect cellular dehydration (summary by Zarychanski et al., 2012). Patients may also show perinatal edema and pseudohyperkalemia due to loss of K+ from red cells stored at room temperature. A minor proportion of red cells appear as stomatocytes on blood films. Complications such as splenomegaly and cholelithiasis, resulting from increased red cell trapping in the spleen and elevated bilirubin levels, respectively, may occur. The course of DHS is frequently associated with iron overload, which may lead to hepatosiderosis (summary by Albuisson et al., 2013). The 'leaky red blood cells' in familial pseudohyperkalemia show a temperature-dependent loss of potassium when stored at room temperature, manifesting as apparent hyperkalemia. The red blood cells show a reduced life span in vivo, but there is no frank hemolysis. Studies of cation content and transport show a marginal increase in permeability at 37 degrees C and a degree of cellular dehydration, qualitatively similar to the changes seen in dehydrated hereditary stomatocytosis. Physiologic studies show that the passive leak of potassium has an abnormal temperature dependence, such that the leak is less sensitive to temperature than that in normal cells (summary by Iolascon et al., 1999). Carella et al. (2004) noted that 3 clinical forms of pseudohyperkalemia unassociated with hematologic manifestations, based predominantly on the leak-temperature dependence curve, had been reported: (1) pseudohyperkalemia Edinburgh, in which the curve has a shallow slope; (2) pseudohyperkalemia Chiswick or Falkirk (see 609153), in which the curve is shouldered; and (3) pseudohyperkalemia Cardiff (see 609153), in which the temperature dependence of the leak shows a 'U-shaped' profile with a minimum at 23 degrees C. Gore et al. (2004) stated that potassium-flux temperature profiles are consistent both from year to year in an individual as well as consistent within affected members of a pedigree. Genetic Heterogeneity of Hereditary Stomatocytosis Dehydrated hereditary stomatocytosis-2 (DHS2; 616689) is caused by mutation in the KCNN4 gene (602754) on chromosome 19q13. Another form of stomatocytosis, involving familial pseudohyperkalemia with minimal hematologic abnormalities (PSHK2; 609153), is caused by mutation in the ABCB6 gene (605452) on chromosome 2q35. Cryohydrocytosis (CHC; 185020) is caused by mutation in the SLC4A1 gene (109270) on chromosome 17q21, and stomatin-deficient cryohydrocytosis with neurologic defects (SDCHCN; 608885) is caused by mutation in the SLC2A1 gene (138140) on chromosome 1p34. An overhydrated form of hereditary stomatocytosis (OHST; 185000) is caused by mutation in the RHAG gene (180297) on chromosome 6p12. See 137280 for a discussion of the association of familial stomatocytosis and hypertrophic gastritis in the dog, an autosomal recessive syndrome. Reviews Delaunay (2004) reviewed genetic disorders of red cell membrane permeability to monovalent cations, noting 'inevitable' overlap between entities based on clinical phenotype. Bruce (2009) provided a review of hereditary stomatocytosis and cation-leaky red cells, stating that consistent features include hemolytic anemia, a monovalent cation leak, and changes in red cell morphology that appear to follow a continuum, from normal discocyte to stomatocyte to echinocyte in DHS, and from discocyte to stomatocyte to spherocyte to fragmentation in OHST. Bruce (2009) suggested that the underlying pathologic mechanism might involve misfolded mutant proteins that escape the quality control system of the cell and reach the red cell membrane, where they disrupt the red cell membrane structure and cause a cation leak that alters the hydration of the red cell, thereby changing the morphology and viability of the cell. King and Zanella (2013) provided an overview of 2 groups of nonimmune hereditary red cell membrane disorders caused by defects in membrane proteins located in distinct layers of the red cell membrane: red cell cytoskeleton disorders, including hereditary spherocytosis (see 182900), hereditary elliptocytosis (see 611804), and hereditary pyropoikilocytosis (266140); and cation permeability disorders of the red cell membrane, or hereditary stomatocytoses, including DHS, OHST, CHC, and PSHK. The authors noted that because there is no specific screening test for the hereditary stomatocytoses, a preliminary diagnosis is based on the presence of a compensated hemolytic anemia, macrocytosis, and a temperature- or time-dependent pseudohyperkalemia in some patients. King et al. (2015) reported the International Council for Standardization in Haematology (ICSH) guidelines for laboratory diagnosis of nonimmune hereditary red cell membrane disorders.
Hepatitis b vaccine, response to
MedGen UID:
333608
Concept ID:
C1840634
Finding
More than 2 billion people have been infected with the hepatitis B virus (HBV; see 610424), and more than 350 million of these people are chronic carriers. Each year more than half a million die as a result of acute or chronic HBV infection. Vaccination has been highly successful at preventing new HBV infections and has been implemented into the national immunization programs of more than 150 countries. However, the immune response to HBV vaccination varies greatly among individuals, with 5 to 10% of healthy adults failing to produce protective levels of antibodies. Several factors have been implicated in determining the response to HBV vaccination, including physical factors, such as age, gender, obesity, immunosuppression, and smoking, as well as variation in genes of the immune system (summary by Davila et al., 2010).
Lymphoproliferative syndrome 2, X-linked
MedGen UID:
336848
Concept ID:
C1845076
Disease or Syndrome
X-linked lymphoproliferative disease (XLP) has two recognizable subtypes, XLP1 and XLP2. XLP1 is characterized predominantly by one of three commonly recognized phenotypes: Inappropriate immune response to Epstein-Barr virus (EBV) infection leading to hemophagocytic lymphohistiocytosis (HLH) or severe mononucleosis. Dysgammaglobulinemia. Lymphoproliferative disease (malignant lymphoma). XLP2 is most often characterized by HLH (often associated with EBV), dysgammaglobulinemia, and inflammatory bowel disease. HLH resulting from EBV infection is associated with an unregulated and exaggerated immune response with widespread proliferation of cytotoxic T cells, EBV-infected B cells, and macrophages. Dysgammaglobulinemia is typically hypogammaglobulinemia of one or more immunoglobulin subclasses. The malignant lymphomas are typically B-cell lymphomas, non-Hodgkin type, often extranodal, and in particular involving the intestine.
Cyanosis and hepatic disease
MedGen UID:
387820
Concept ID:
C1857443
Disease or Syndrome
Complement component c1s deficiency
MedGen UID:
462428
Concept ID:
C3151078
Disease or Syndrome
Bile acid synthesis defect, congenital, 3
MedGen UID:
462497
Concept ID:
C3151147
Disease or Syndrome
Trichohepatoenteric syndrome 2
MedGen UID:
482919
Concept ID:
C3281289
Disease or Syndrome
Trichohepatoenteric syndrome (THES) is a rare and severe disease characterized by intrauterine growth retardation, facial dysmorphism, hair abnormalities, intractable diarrhea, and immunodeficiency (summary by Fabre et al., 2012). For a discussion of genetic heterogeneity of trichohepatoenteric syndrome, see THES1 (222470).

Recent clinical studies

Etiology

Albuquerque A, Rodrigues S, Macedo G
Scand J Gastroenterol 2016 Nov;51(11):1316-20. Epub 2016 Jul 7 doi: 10.1080/00365521.2016.1203017. PMID: 27387923
Wang X, Qian L, Jia L, Bellah R, Wang N, Xin Y, Liu Q
J Ultrasound Med 2016 Jul;35(7):1475-9. Epub 2016 May 26 doi: 10.7863/ultra.15.08031. PMID: 27229132
Nasta P, Salmon D, d'Arminio Monforte A, Pimenta JM, Cerini C, Giralda M, Winnock M, Cozzi-Lepri A
HIV Clin Trials 2016 May;17(3):96-108. Epub 2016 Mar 16 doi: 10.1080/15284336.2016.1150409. PMID: 27125364
Feng IC, Wang SJ, Sheu MJ, Koay LB, Lin CY, Ho CH, Sun CS, Kuo HT
World J Gastroenterol 2015 Nov 28;21(44):12620-7. doi: 10.3748/wjg.v21.i44.12620. PMID: 26640338Free PMC Article
Tapper EB, Sengupta N, Bonder A
Am J Med 2015 Dec;128(12):1314-21. Epub 2015 Aug 21 doi: 10.1016/j.amjmed.2015.07.033. PMID: 26299319

Diagnosis

Adiga A, Nugent K
Am J Med Sci 2017 Apr;353(4):329-335. Epub 2016 Nov 4 doi: 10.1016/j.amjms.2016.10.014. PMID: 28317620
Albuquerque A, Rodrigues S, Macedo G
Scand J Gastroenterol 2016 Nov;51(11):1316-20. Epub 2016 Jul 7 doi: 10.1080/00365521.2016.1203017. PMID: 27387923
Wang X, Qian L, Jia L, Bellah R, Wang N, Xin Y, Liu Q
J Ultrasound Med 2016 Jul;35(7):1475-9. Epub 2016 May 26 doi: 10.7863/ultra.15.08031. PMID: 27229132
Tagawa Y, Saito T, Takada K, Kawahata K, Kohsaka H
Lupus 2016 Apr;25(5):543-6. Epub 2016 Jan 12 doi: 10.1177/0961203315625118. PMID: 26762472
Bishara R, Braun-Moscovici Y, Dagan A, Toledano K, Saadi T, Sabo E, Balbir-Gurman A
Clin Rheumatol 2016 Mar;35(3):795-800. Epub 2014 Nov 22 doi: 10.1007/s10067-014-2829-2. PMID: 25413736

Therapy

Nasta P, Salmon D, d'Arminio Monforte A, Pimenta JM, Cerini C, Giralda M, Winnock M, Cozzi-Lepri A
HIV Clin Trials 2016 May;17(3):96-108. Epub 2016 Mar 16 doi: 10.1080/15284336.2016.1150409. PMID: 27125364
Tagawa Y, Saito T, Takada K, Kawahata K, Kohsaka H
Lupus 2016 Apr;25(5):543-6. Epub 2016 Jan 12 doi: 10.1177/0961203315625118. PMID: 26762472
Zou H, Jin L, Wang LR, Braddock M, Cai WW, Zheng MH
Oncotarget 2016 Jan 26;7(4):5088-91. doi: 10.18632/oncotarget.6144. PMID: 26498145Free PMC Article
Bishara R, Braun-Moscovici Y, Dagan A, Toledano K, Saadi T, Sabo E, Balbir-Gurman A
Clin Rheumatol 2016 Mar;35(3):795-800. Epub 2014 Nov 22 doi: 10.1007/s10067-014-2829-2. PMID: 25413736
Gupta N, Njei B
J Dig Dis 2015 Nov;16(11):683-8. doi: 10.1111/1751-2980.12273. PMID: 26147671Free PMC Article

Prognosis

Adiga A, Nugent K
Am J Med Sci 2017 Apr;353(4):329-335. Epub 2016 Nov 4 doi: 10.1016/j.amjms.2016.10.014. PMID: 28317620
Albuquerque A, Rodrigues S, Macedo G
Scand J Gastroenterol 2016 Nov;51(11):1316-20. Epub 2016 Jul 7 doi: 10.1080/00365521.2016.1203017. PMID: 27387923
Wang X, Qian L, Jia L, Bellah R, Wang N, Xin Y, Liu Q
J Ultrasound Med 2016 Jul;35(7):1475-9. Epub 2016 May 26 doi: 10.7863/ultra.15.08031. PMID: 27229132
Tagawa Y, Saito T, Takada K, Kawahata K, Kohsaka H
Lupus 2016 Apr;25(5):543-6. Epub 2016 Jan 12 doi: 10.1177/0961203315625118. PMID: 26762472
Tapper EB, Sengupta N, Bonder A
Am J Med 2015 Dec;128(12):1314-21. Epub 2015 Aug 21 doi: 10.1016/j.amjmed.2015.07.033. PMID: 26299319

Clinical prediction guides

Albuquerque A, Rodrigues S, Macedo G
Scand J Gastroenterol 2016 Nov;51(11):1316-20. Epub 2016 Jul 7 doi: 10.1080/00365521.2016.1203017. PMID: 27387923
Wang X, Qian L, Jia L, Bellah R, Wang N, Xin Y, Liu Q
J Ultrasound Med 2016 Jul;35(7):1475-9. Epub 2016 May 26 doi: 10.7863/ultra.15.08031. PMID: 27229132
Nasta P, Salmon D, d'Arminio Monforte A, Pimenta JM, Cerini C, Giralda M, Winnock M, Cozzi-Lepri A
HIV Clin Trials 2016 May;17(3):96-108. Epub 2016 Mar 16 doi: 10.1080/15284336.2016.1150409. PMID: 27125364
Tagawa Y, Saito T, Takada K, Kawahata K, Kohsaka H
Lupus 2016 Apr;25(5):543-6. Epub 2016 Jan 12 doi: 10.1177/0961203315625118. PMID: 26762472
Feng IC, Wang SJ, Sheu MJ, Koay LB, Lin CY, Ho CH, Sun CS, Kuo HT
World J Gastroenterol 2015 Nov 28;21(44):12620-7. doi: 10.3748/wjg.v21.i44.12620. PMID: 26640338Free PMC Article

Recent systematic reviews

Tapper EB, Sengupta N, Bonder A
Am J Med 2015 Dec;128(12):1314-21. Epub 2015 Aug 21 doi: 10.1016/j.amjmed.2015.07.033. PMID: 26299319
Head MG, Fitchett JR, Cooke GS, Foster GR, Atun R
J Viral Hepat 2015 Mar;22(3):230-7. Epub 2014 Aug 22 doi: 10.1111/jvh.12300. PMID: 25146854Free PMC Article
Zou X, Chow EP, Zhao P, Xu Y, Ling L, Zhang L
BMC Infect Dis 2014 Sep 8;14:490. doi: 10.1186/1471-2334-14-490. PMID: 25200651Free PMC Article
Zheng R, Zhao W, Dai D, Li C
Tumour Biol 2014 Feb;35(2):1313-8. Epub 2013 Oct 24 doi: 10.1007/s13277-013-1174-4. PMID: 24155211
Vajro P, Paolella G, Maggiore G, Giordano G
J Pediatr Gastroenterol Nutr 2013 Jun;56(6):663-70. doi: 10.1097/MPG.0b013e31828dc5c5. PMID: 23434875

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