Disease Knowledge Centres

  • Hepatology - Disease Topic Overview

    Hepatology is the medical specialty detailing the study, diagnosis and treatment of diseases relating to the liver and biliary tree.

    The liver originates from endoderm and forms as an outgrowth of the duodenum. It is divided into right and left lobes; the former is approximately six times larger than the latter.1 The liver receives oxygenated blood from the hepatic artery; however, it also receives blood through the hepatic portal vein. The latter contains the products of digestion that have been absorbed from the intestines. The main role of the liver is to metabolise the products of digestion, drugs and alcohol. It also syntheses blood proteins.2

    The biliary tree consists of; the hepatic ducts, the common hepatic ducts, the gall bladder, the cystic duct, the common bile duct and the sphincter of Oddi.3 Its function is to transport bile, which is formed in the liver, to the duodenum to aid digestion. Bile is ejected from the gall bladder, a storage organ, in the presence of cholecystokinin (CCK) to ensure it is present in the duodenum at the optimum time. The common diseases of the biliary system are; gall stones, gall-bladder polyps, sphincter of Oddi dysfunction and cancer of the gall bladder and biliary tree.4

    Hepatic diseases consists of, but are not limited to; acute, chronic and drug induced hepatitis, alcoholic liver disease5, cirrhosis of the liver6, jaundice7, and hepatic cancer.7 Hepatic diseases can affect people of all ages. Jaundice is one such disease; resulting from the accumulation of billirubin, either due to overproduction, or failure of the liver to metabolise and excrete it through the bile ducts.7 Jaundice can be a symptom of many other liver diseases such as hepatitis and cancer. Hepatitis is a viral disease with five forms (A, B, C, D and E) that cause inflammation of the liver. Hepatitis B and hepatitis C can lead to cirrhosis (scaring) of the liver and hepatocellular carcinoma.5

    1. Kuntz E. et al. Hepatology: Textbook and Atlas. Springer. 2008 : 18.
    2. Cavendish M. Diseases and Disorders. Marshall Cavendish. 2007 : 521.
    3. Dooley J.S. Sherlock’s Diseases of the Liver and Biliary Tract. John Willey and Sons. 2011 : 5.
    4. Talley N.J. et al. Practical Gastroenterology and Hepatology: Liver and Biliary Disease. John Willey and Sons. 2010 : 349-381.
    5. Mushahwar I.K. Viral Hepatitis: Molecular Biology, Diagnosis, Epidemiology, and Control. Gulf Professional Publishing. 2007 : vii-1.
    6. Cavendish M. Diseases and Disorders. Marshall Cavendish. 2007 : 203.
    7. Gilmore I. et al. Investigation of Jaundice. Medicine. January 2007 ; 35 (1) : 13-16.

Latest Multi Media

An Animation of The Hepatitis C Virus and How it Affects the Body

Hepatology Drug Data - A-Z English

Drug Updates

Fenofibrate 267mg Capsules
Fenofibrate is indicated as an adjunct to diet and other non-pharmacological treatment (e.
Docefrez 20 mg powder and solvent for concentrate for solution for infusion
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Dovobet Ointment
Topical treatment of scalp psoriasis.

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Latest Clinical Trials

Q-Trial in Patients With Hepatitis C
The goal of this study is to translate laboratory findings that Quercetin, a bioflavonoid, is safe and has antiviral activity in people with hepatitis C.
Viral Kinetics and Liver Gene Expression in Response to Ribavirin and Peginterferon Therapy of Chronic Hepatitis C
Up to 120 patients with chronic hepatitis C will be enrolled in a study of viral kinetics and liver gene expression before and during combination therapy with peginterferon and ribavirin. Adult patients with chronic hepatitis C virus (HCV) infection who have compensated liver disease and have not received interferon in the past will be randomized into one of four groups. Groups A and C will undergo liver biopsy before starting peginterferon therapy and Groups B and D will undergo biopsy 6 hours after the initial dose of peginterferon. Furthermore, Groups C and D will receive a run-in period of 4 weeks of ribavirin therapy before starting peginterferon. All patients will receive the standard recommended doses of peginterferon alfa 2a (180 mcg sc weekly) and ribavirin (1000 or 1200 mg daily for genotypes 1, 4-6 and 800 mg daily for genotype 2 and 3) for up to 48 weeks (24 weeks for genotype 2 and 3). All patients in Groups C and D, irrespective of genotype, will be pretreated with ribavirin at a dose of 1000 or 1200 mg, depending on patient body-weight. After the initial peginterferon injection, patients will have blood taken and symptoms recorded at 6, 24, 48, 72 hours and weekly thereafter for four weeks to assess viral kinetic response. Liver biopsy tissue taken before or 6 hours after the initial dose of peginterferon will be assessed by standard light microscopy and also subjected to RNA extraction and microarray analysis of mRNA expression. Patients will be monitored carefully during therapy and tested regularly for HCV RNA levels. Therapy will be given for 48 weeks, but will be discontinued early for patients with genotype 1 infection if HCV RNA levels do not decline by at least 2 log IU/ml by week 12 (lack of an early virological response) or do not decline to undetectable levels by week 24 (lack of HCV RNA clearance). Patients with other genotypes with be treated for a full course of therapy regardless of early responses. After completing therapy, patients will be followed at 4 to 8 week intervals and undergo repeat medical evaluation with liver biopsy 24 weeks after stopping therapy. The primary clinical criterion for success of therapy is a sustained virological response, as marked by the absence of HCV RNA from serum at least 24 weeks after stopping. The focus of this study, however, will be on viral kinetics comparing patients who were pretreated with ribavirin (Groups C and D) to those who were not (Groups A and B) as well as on gene expression studies assessing the effects of peginterferon on intrahepatic mRNA profiles by comparing Group A and B and the effects of ribavirin by comparing Group A to Group C and Group B to Group D. Results will also be compared between different HCV genotypes. These studies are aimed at assessing the mechanisms of action of peginterferon and ribavirin against HCV and evaluating the basis for the lack of virologic response to combination therapy.

Latest Journal Publications

Journal of Medical Virology
The incidence of acute hepatitis C has decreased in the world. However, new cases are still reported. The objective of this study was to obtain data of acute hepatitis C in Brazil and to identify risk factors of transmission, diagnostic criteria, clinical presentation, evolution, and treatment. A questionnaire was sent to all members of the Brazilian Society of Hepatology. Sixteen centers participated with a total of 170 cases between 2000 and 2008. Among them, 37 had chronic renal failure on hemodialysis and were evaluated separately. The main diagnostic criterion in non-uremic patients was ALT (alanine aminotransferase) elevation associated with risk factors. In patients with chronic renal failure, anti-hepatitis C virus (HCV) seroconversion was the most frequent criterion. Among the 133 non-uremic patients the main risk factors were hospital procedures, whereas in hemodialysis patients, dialysis was the single risk factor in 95% of the cases. Jaundice was more frequent in non-uremic patients (82% vs. 13%; P < 0.001) and ALT levels were higher in these individuals (P < 0.001). Spontaneous clearance was more frequent in non-uremic patients (51% vs. 3%; P < 0.001). Sixty-five patients were treated: 39 non-uremic patients and 26 on dialysis. Sustained virological response rates were 60% for non-uremic and 58% for uremic patients (P = 0.98). There was no association of these rates with the study variables. These findings show that cases of acute hepatitis C are still occurring and have been related predominantly to hospital procedures. Measures to prevent nosocomial transmission should be adopted rigorously and followed to minimize this important source of infection observed in this survey.
Cell Biochemistry and Biophysics
In this study, the investigation of the expression of HIWI and its protein in hepatocellular carcinoma (HCC) was performed, and the relationships between HIWI expression and the location of HCC metastases were analyzed. Sets of fresh HCC and matched adjacent normal hepatic tissue and paraffin-embedded tissue slides were provided by the hospital hepatology and pathology departments. RT-PCR, Western blot, and immunohistochemistry were performed to detect HIWI mRNA and protein. Correlations between HIWI expression and patient’s age, sex, type of tumor, and metastasis location were recorded. HIWI mRNA and protein levels were significantly higher in HCC tissues than in adjacent normal hepatic tissue (P < 0.05). Immunohistochemistry showed positive staining for HIWI in cell cytoplasm; however, the number of HIWI-positive cells in HCC tissue (65.2%; 60/92) was significantly higher than in adjacent normal hepatic tissue (27.2%; 25/92) (P < 0.05). HIWI expression was not correlated with patients’ age, gender, tumors’ size, and location but correlated with metastasis involving lymph nodes and other remote organs (P < 0.05). HIWI expression is significantly higher in HCC tissue than in adjacent normal hepatic tissue. The results of this study suggest that HIWI may have a crucial role in HCC carcinogenesis and could serve as a potential biomarker or treatment target for HCC.

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Hepatology