Liver Disease

The liver has a number of key functions, including metabolism of the byproducts of food, detoxification of drugs, conversion of nitrogenous substances to be excreted by the kidneys, formation of blood clotting factors, metabolism of bilirubin, processing of lipids from the intestines, and storage of glycogen. Obviously then, clinical consequences of liver dysfunction manifest in loss of hepatocellular function, including diminished detoxification, metabolic, elimination, and coagulation problems. Liver dysfunction may be attributed to a number of causes, including acquired infections and other pathologic conditions, as well as drug use. A patient with liver disease presents a significant management challenge for the dentist because the liver plays a vital role in metabolic functions, including the secretion of bile needed for fat absorption; conversion of sugar to glycogen; and excretion of bilirubin, a waste product of hemoglobin metabolism. Impairment of liver function can lead to abnormalities in many biochemical functions performed by the liver, such as synthesis of coagulation factors and drug metabolism, and dental patients with acute or chronic liver disease may be adversely affected. Therefore, significant bleeding may be a problem. In many cases, the liver dysfunction will continue to progress over time. Ultimately, serious end-stage liver dysfunction or cirrhosis may result.

Cirrhosis is the consequence of long-term damage to the liver tissues. This condition is irreversible and leads to fibrosis, resulting in jaundice, ascites, and portal hypertension, as well as significant liver dysfunction. The potential causes of viral hepatitis–related cirrhosis are listed in Table 10.1 . Obviously, liver disorders in persons presenting for treatment are of significant clinical interest to dentists in the context of the proper management of such patients. In this chapter, the two most common liver disorders and main causes of cirrhosis, hepatitis and alcoholic liver disease, are presented.

TABLE 10.1
Most Common Agents of Acute Viral Hepatitis, With Associated Characteristics
Hepatitis Virus Size (nm) Genome Spread * Incubation Period (Days) Fatality Rate (%) Chronicity Rate (%) Antibody Diagnosis Chronic Carrier State Complications § of the Liver Associated Clinical Syndromes IMMUNIZATION
Passive Active
A (HAV) 27 RNA Fecal–oral 15–45; mean, 25 1 None Anti-HAV Anti-HAV IgG No Rare Immune globulin (0.02 mg/kg) Harivax, Vaqta, Twinrix
B (HBV) 45 DNA Parenteral 30–180; mean, 75 1 2–7 Anti-HBs HBsAg (infectious)
Anti-HBsAg (recovery)
Anti-HBc (acute, persistently infected nonprotective)
HBeAg (infectious)
Anti-HBeAg (clearing/cleared infection)
Yes—90% risk of becoming carrier if infected as neonate; 25%–50% risk if infected as infant; 5%–10% risk if infected as adult Yes—increased risk of cirrhosis and HCC after 25–30 years of infection Yes Hepatitis B immune globulin (HBIg) (0.06 mg/kg) Recombivax, Engerix, Twinrix
Sexual Anti-HBc
C (HCV) 60 RNA Parenteral 15–150; mean, 50 <0.1 50–85 Anti-HCV Anti-HCV (previous infection)
HCV RNA (infectivity)
Yes—risk of becoming carrier is 80%–90% Yes—10-fold increased risk of liver cirrhosis within 20 years; 1%–5% of carriers develop HCC by 20 years, risk of HCC with chronic HCV infection exceeds risk with chronic HBV infection Yes Not available None (difficult development because of the many genotypes)
D (delta) (HDV) 40 RNA Parenteral 30–150 2–10 2–7 Anti-HDV Anti-HDV
Yes—carrier state in 20%–70% Yes Not available Yes—protected with Recombivax, Engerix , and Twinrix
Sexual 50
E (HEV) 32 RNA Fecal–oral 30–60 1 None Anti-HEV Anti-HEV No Rare morbidity and mortality except in pregnant women Not available Genentech has applied for vaccine patent

HBc, Hepatitis B core; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; HCC, hepatocellular carcinoma; IgG, immunoglobulin G.
The U.S. Food and Drug Administration requires that all donated whole blood, transfusable components, and plasma for human blood use in the United States be subjected to serologic testing for syphilis, HBsAg, anti-HBc, anti-HCV, and anti-HIV. The current incidence of posttransfusion hepatitis B is approximately 0.002% per transfusion recipient.
Only gold members can continue reading. Log In or Register to continue

Sep 3, 2018 | Posted by in General Dentistry | Comments Off on Liver Disease
Premium Wordpress Themes by UFO Themes