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.
|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|
|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-HBc (acute, persistently infected nonprotective)
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|
|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|
|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|