Hepatitis C natural history: Difference between revisions
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==Natural History== | ==Natural History== | ||
Upon exposure, HCV causes an acute phase that is usually asymptomatic. Acute HVC is characterized by its persistence to a duration of less than 6 months. In 15-45% of cases, HCV is an isolated acute infection with no chronic sequelae, even if no treatment was administered whatsoever. Patients exposed to HCV will subsequently develop anti-HCV antibodies but undetectable viral levels and negative HCV RNA. | |||
In the majority of cases, however, HCV persists beyond 6 months and individuals thus become chronic carriers of HCV. Chronic HCV occurs in approximately 55-85% of patients. These patients will have positive anti-HCV antibodies and positive nucleic acid test (NAT) for HCV RNA, demonstrating the persistence of HCV and inability to appropriately clear the infection.(58,59) | |||
[[Image:HCV_NH.png|thumb|600px|center|Natural History of HCV [http://www.who.int/hiv/pub/hepatitis/hepatitis-c-guidelines/en/ Source]]] | [[Image:HCV_NH.png|thumb|600px|center|Natural History of HCV [http://www.who.int/hiv/pub/hepatitis/hepatitis-c-guidelines/en/ Source]]] | ||
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==Complications== | |||
* | One major complications of chronic HCV infection are cirrhosis, which ultimately lead to a decompensated state, or transform into a malignant hepatocellular carcinoma (HCC).<ref name=WHO>{{cite web |url=http://apps.who.int/iris/bitstream/10665/111747/1/9789241548755_eng.pdf?ua=1&ua=1 |title=Guidelines for the screening, care, and treatment of persons with HCV infection|date=April 2014 |website=WHO |publisher=WHO |accessdate=Jul 27 2014}}</ref> Not all patients develop cirrhosis at the same rate; exposure to other risk factors of cirrhosis, such as alcohol, HBV or HIV infection, or immunocompromised states may hasten fibrosis of the liver and development of HCC.<ref name="pmid12823595">{{cite journal| author=Freeman AJ, Law MG, Kaldor JM, Dore GJ| title=Predicting progression to cirrhosis in chronic hepatitis C virus infection. | journal=J Viral Hepat | year= 2003 | volume= 10 | issue= 4 | pages= 285-93 | pmid=12823595 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12823595 }} </ref> | ||
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Chronic HCV eventually progresses to cause hepatic cirrhosis due to persistence of tissue inflammation and necrosis, along with fibrogenesis and deposition of components in the extracellular matrix. When left untreated, '''15-30% of patients with chronic HCV develop cirrhosis within 20 years.'''<ref name=WHO>{{cite web |url=http://apps.who.int/iris/bitstream/10665/111747/1/9789241548755_eng.pdf?ua=1&ua=1 |title=Guidelines for the screening, care, and treatment of persons with HCV infection|date=April 2014 |website=WHO |publisher=WHO |accessdate=Jul 27 2014}}</ref> | |||
Similarly, HCC is a known complication of chronic HCV infection. Patients with HCV develop HCC when the liver reaches its cirrhotic stage. The annual risk of HCC in patients with cirrhosis is about 2-4%. | |||
Extrahepatic complications of HCV infection<ref name="pmid22497808">{{cite journal| author=Fletcher NF, McKeating JA| title=Hepatitis C virus and the brain. | journal=J Viral Hepat | year= 2012 | volume= 19 | issue= 5 | pages= 301-6 | pmid=22497808 | doi=10.1111/j.1365-2893.2012.01591.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22497808 }} </ref><ref name=WHO>{{cite web |url=http://apps.who.int/iris/bitstream/10665/111747/1/9789241548755_eng.pdf?ua=1&ua=1 |title=Guidelines for the screening, care, and treatment of persons with HCV infection|date=April 2014 |website=WHO |publisher=WHO |accessdate=Jul 27 2014}}</ref>: | |||
*Cryoglobulinemia | |||
*Glomerulonephritis | |||
*Thyroiditis | |||
*Sjogren syndrome | |||
*Insulin resistance and type-2 diabetes mellitus | |||
*Porphyria cutanea tarda | |||
*Lichen Planus | |||
*Cognitive dysfunction | |||
*Depression | |||
==Complications== | ==Complications== | ||
Revision as of 05:50, 28 July 2014
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Hepatitis C |
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Diagnosis |
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Treatment |
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Hepatitis C natural history On the Web |
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American Roentgen Ray Society Images of Hepatitis C natural history |
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Risk calculators and risk factors for Hepatitis C natural history |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Natural History
Upon exposure, HCV causes an acute phase that is usually asymptomatic. Acute HVC is characterized by its persistence to a duration of less than 6 months. In 15-45% of cases, HCV is an isolated acute infection with no chronic sequelae, even if no treatment was administered whatsoever. Patients exposed to HCV will subsequently develop anti-HCV antibodies but undetectable viral levels and negative HCV RNA.
In the majority of cases, however, HCV persists beyond 6 months and individuals thus become chronic carriers of HCV. Chronic HCV occurs in approximately 55-85% of patients. These patients will have positive anti-HCV antibodies and positive nucleic acid test (NAT) for HCV RNA, demonstrating the persistence of HCV and inability to appropriately clear the infection.(58,59)
Complications
One major complications of chronic HCV infection are cirrhosis, which ultimately lead to a decompensated state, or transform into a malignant hepatocellular carcinoma (HCC).[1] Not all patients develop cirrhosis at the same rate; exposure to other risk factors of cirrhosis, such as alcohol, HBV or HIV infection, or immunocompromised states may hasten fibrosis of the liver and development of HCC.[2]
Chronic HCV eventually progresses to cause hepatic cirrhosis due to persistence of tissue inflammation and necrosis, along with fibrogenesis and deposition of components in the extracellular matrix. When left untreated, 15-30% of patients with chronic HCV develop cirrhosis within 20 years.[1]
Similarly, HCC is a known complication of chronic HCV infection. Patients with HCV develop HCC when the liver reaches its cirrhotic stage. The annual risk of HCC in patients with cirrhosis is about 2-4%.
Extrahepatic complications of HCV infection[3][1]:
- Cryoglobulinemia
- Glomerulonephritis
- Thyroiditis
- Sjogren syndrome
- Insulin resistance and type-2 diabetes mellitus
- Porphyria cutanea tarda
- Lichen Planus
- Cognitive dysfunction
- Depression
Complications
- Hepatitis C infection can continue over many years leading to chronic hepatitis
- Over years, liver may undergo extensive damage and scarring resulting in cirrhosis
- Liver failure
- Hepatocellular carcinoma may occur in patients with chronic hepatitis C infection.[4]
In diagnosis of cirrhosis (Ishak scores, 5-6) in patients with hepatitis C, the aspartate aminotransferase to platelet ratio index (APRI) ratio > 1 suggests cirrhosis with accuracy of:[5]
- Sensitivity = 79%
- Specificity = 78%
Prognosis
- Acute Infection
- 20% recover
- 80% have persistent infection
- 30% of these patients develop cirrhosis
- Genotype
- Predicts response to treatment
- Genotype 1 less responsive than types 2 & 3
References
- ↑ 1.0 1.1 1.2 "Guidelines for the screening, care, and treatment of persons with HCV infection" (PDF). WHO. WHO. April 2014. Retrieved Jul 27 2014. Check date values in:
|accessdate=(help) - ↑ Freeman AJ, Law MG, Kaldor JM, Dore GJ (2003). "Predicting progression to cirrhosis in chronic hepatitis C virus infection". J Viral Hepat. 10 (4): 285–93. PMID 12823595.
- ↑ Fletcher NF, McKeating JA (2012). "Hepatitis C virus and the brain". J Viral Hepat. 19 (5): 301–6. doi:10.1111/j.1365-2893.2012.01591.x. PMID 22497808.
- ↑ Nash KL, Woodall T, Brown AS, Davies SE, Alexander GJ (2010). "Hepatocellular carcinoma in patients with chronic hepatitis C virus infection without cirrhosis". World Journal of Gastroenterology : WJG. 16 (32): 4061–5. PMC 2928460. PMID 20731020. Retrieved 2012-02-26. Unknown parameter
|month=ignored (help) - ↑ Gara N, Zhao X, Kleiner DE, Liang TJ, Hoofnagle JH, Ghany MG (2013). "Discordance among transient elastography, aspartate aminotransferase to platelet ratio index, and histologic assessments of liver fibrosis in patients with chronic hepatitis C." Clin Gastroenterol Hepatol. 11 (3): 303–308.e1. doi:10.1016/j.cgh.2012.10.044. PMID 23142332.