Thursday, September 2, 2021

Jaundice Case File

Posted By: Medical Group - 9/02/2021 Post Author : Medical Group Post Date : Thursday, September 2, 2021 Post Time : 9/02/2021
Jaundice Case File
Eugene C. Toy MD, Donald Briscoe, MD, FA  AFP, Bruce Britton, MD, Joel J. Heidelbaugh, MD, FA  AFP, FACG

A 33-year-old African-American man presents to the office for an acute visit with nausea and diarrhea present for the past week. Along with these symptoms, he has had a low-grade fever, some right upper quadrant (RUQ) abdominal pain, and has noticed that the whites of his eyes appear yellow. He has no significant medical history and takes no medications regularly. He denies alcohol, tobacco, or IV drug use at any time in his life. He works as a pastor in a local church that went on a mission to build a medical clinic in a rural area of Central America about 5 weeks ago. He had a mild case of traveler's diarrhea while there, recovered within a week, and has otherwise felt well. On examination, he is a well-developed man who appears to be moderately ill. His temperature is 99.8°F (37.6°C), his blood pressure is 110/80 mm Hg, his pulse is 90 beats/min, and his respiratory rate is 14 breaths/min. He has a prominent yellow color to his sclera and under his tongue. His mucous membranes are moist. Lung and cardiac examinations are unremarkable. His abdomen examination reveals normal bowel sounds yet moderate tenderness in the RUQ. His liver edge is palpable just below the costal margin and his spleen is not palpable. There are no abdominal masses palpated, and no rebound tenderness or guarding. On rectal examination, he has clay-colored soft stool that is fecal occult blood test negative.

 What is the most likely diagnosis?
 When and how did he most probably contract this illness?
 How can you confirm the diagnosis?
 What is the treatment at this point?


Summary: A 33-year-old man with no significant medical history develops diarrhea, abdominal pain, and jaundice about a month after traveling to Central America. He is noted to have scleral icterus and tender hepatomegaly.
  • Most likely diagnosis: Acute infection with hepatitis A.
  • Most probable timing and source of infection: Ingestion of contaminated food or water while on his mission to Central America 5 weeks earlier.
  • Test to confirm the diagnosis: Anti-hepatitis A immunoglobulin (Ig) M.
  • Treatment of acute hepatitis A: Supportive care and symptomatic treatment for the patient; report infection to local health department; consider giving hepatitis A vaccine or Ig prophylaxis to close household or sexual contacts. Hepatitis A immunization will not be required for the patient.

  • Develop a differential diagnosis for adults with jaundice, with and without pain.
  • Know the symptoms, management, complications, and modes of transmission of hepatitis A, B, and C.
  • Be able to interpret the results of hepatitis viral serology tests.

This presentation of nonbloody diarrhea along with nonspecific, crampy abdominal pain is most often caused by viral gastroenteritis, and is self-limited. However, this patient has several signs and symptoms that serve as clues to point to other potential diagnoses. Of particular importance, the complaint of yellow eyes should prompt an evaluation for causes of jaundice.

Bilirubin is a breakdown product of red blood cells. During the breakdown of hemoglobin, bilirubin is formed and bound to albumin, which carries it to the liver. In the liver, a portion of the bilirubin is made water soluble by conjugation to a glucuronide. This "conjugated bilirubin'' is excreted in the bile and then largely excreted in the stool. Unconjugated bilirubin in the liver remains mostly bound to albumin and to a lesser degree high-density lipoproteins.

Most cases of jaundice can be characterized as having prehepatic, hepatic, or posthepatic causes. Prehepatic jaundice most often results from hemolysis of red blood cells, which overwhelms the liver's ability to conjugate and clear the bilirubin through its normal pathways. This results in a state of hyperbilirubinemia that is primarily unconjugated.

Hepatic causes of jaundice can lead to either unconjugated or conjugated hyperbilirubinemia. Viruses including hepatitis and alcohol reduce the liver's ability to transport bilirubin after it has been conjugated, resulting in a conjugated hyperbilirubinemia.

Posthepatic jaundice is usually caused by obstruction to the flow of bile through the bile ducts. This can be caused by bile duct stones, strictures, or tumors that narrow or block the ducts. Posthepatic jaundice is, therefore, a conjugated hyperbilirubinemia.

Approach To:

CAPUT MEDUSAE: Dilated superficial paraumbilical veins that usually result from shunting associated with severe portal hypertension and liver failure.

SPIDER ANGIOMA/TELANGIECTASIAS: Dilated, small, superficial veins with the distribution of the superior vena cava that appear as red, blue, or purple web-like formations, most often seen on the face, neck, upper trunk and abdomen, and lower extremities. The persistent dilation of blood vessels is due to increased serum estrogen levels, which remain elevated due to the inability of the impaired liver to conjugate estrone.


History and Examination
The most important information in the diagnostic evaluation of the patient with jaundice is derived from the history and should include questions focused on identifying the most common etiologies. Specific information should include when the jaundice commenced and whether it is of acute or gradual onset. The presence of gastrointestinal symptoms including abdominal pain, nausea, vomiting, diarrhea, or changes in stool or urine color is significant. Skin pruritis is common in patients with jaundice and this symptom may precede the onset of jaundice.

Associated constitutional symptoms, including unintentional weight loss or the development of lymphadenopathy should prompt the clinician to consider an underlying malignancy. Fever, shaking chills, and right upper quadrant abdominal pain can be signs of acute cholangitis, cholecystitis, or choledocholithiasis. Anorexia, fatigue, myalgias, and flu-like symptoms commonly indicate viral hepatitis. Bruising or bleeding disorders may suggest severe hepatic dysfunction that is interfering with the production of clotting factors. Increasing abdominal girth may be caused by ascites and peripheral edema by obstruction of venous return from the lower extremities and hypoalbuminemia.

A complete review of the past medical history is mandatory. Any medications, whether prescription, nonprescription, or herbal supplements, should be reviewed.

Acetaminophen and aspirin are widely used over-the-counter agents that in toxic amounts can cause hepatocellular damage. Numerous herbal agents (eg,Jamaican bush tea, Kava Kava, and Ma Huang) have also been associated with liver damage.

The social history is of critical importance in a patient with jaundice. The abuse of alcohol is the most common cause of cirrhosis in the United States. Intravenous drug use, transfusions of blood or blood products, and unsafe sexual practices can lead to infection with hepatitis B or C. Viral hepatitis has also been linked to tattooing when unsterilized or shared equipment is used. Travel history, especially the location and timing of any international travel, and recent exposure to persons with jaundice or contaminated foods ( eg, raw oysters, contaminated produce) can lead to the consideration of hepatitis A.

A comprehensive physical examination is also paramount in the workup of the patient with jaundice. Along with a general physical examination, certain areas should be emphasized. Jaundice typically remains undetected on examination until the serum bilirubin level is at least greater than twice the normal upper limit, approaching 4 mg/ dL. The yellow pigmentation may initially be detected as a yellowing of the sclera, especially in persons with darker skin types. Yellow discoloration can also commonly be seen in oral mucosal membranes such as under the tongue and hard palate.

Examination of the skin should document the jaundice and also look for clues to its cause. The stigmata of alcohol abuse ( eg, caput medusae, spider angioma) or IV drug use (eg, needle track marks, ruptured veins, cellulitis) should be noted. Large hematomas, by themselves, could be a cause of jaundice as the blood reabsorbs. Evidence of easy bruising or bleeding should also be documented and quantified.

Abdominal examination must include the evaluation of the general contour of the abdomen, the presence of ascites or hepatosplenomegaly, and any rebound guarding or localized tenderness. A grossly enlarged liver with nodular contour may suggest malignancy, cirrhosis, or hepatitis. Hepatomegaly may occur due to underlying liver disease or hepatic congestion due to right-sided heart failure. Right upper quadrant tenderness can be associated with acute hepatitis but also with acute gallstone disease. Splenomegaly may suggest portal hypertension from cirrhosis, malignancy, or splenic sequestration of damaged red blood cells.

Laboratory Testing
The most important initial laboratory evaluation of jaundice is the serum bilirubin level, which is usually reported as a total bilirubin level. Direct and indirect concentrations can also be readily obtained. The degree of jaundice generally correlates with the level of serum bilirubin concentration. The reported direct bilirubin is a measurement of the conjugated bilirubin level. Unconjugated bilirubin can be determined by subtracting the direct bilirubin from the total bilirubin.

The relative relationship of conjugated and unconjugated bilirubin in a jaundiced person can be indirectly evaluated by performing a urinalysis. Conjugated bilirubin is excreted in the urine, whereas unconjugated bilirubin is bound to albumin and exempted from glomerular filtration. A high bilirubin level in the urinalysis in a jaundiced patient suggests a conjugated hyperbilirubinemia; absence of bilirubin on the urinalysis suggests an unconjugated hyperbilirubinemia. An overproduction or impaired conjugation or uptake of bilirubin generally results in unconjugated hyperbilirubinemia. Conversely, a decreased excretion or biliary obstruction typically leads to conjugated hyperbilirubinemia.

Unconjugated hyperbilirubinemia, usually identified as an incidental finding when liver enzymes are tested for some other reason, in a patient without jaundice or known underlying hepatic dysfunction, is often caused by Gilbert syndrome. Gilbert syndrome is a congenital reduction of conjugation of bilirubin in the liver due to an autosomal recessive gene involved in glucuronidation. It occurs in approximately 5% of the population and is of no health significance. Patients generally present with normal physical examination and routine laboratory tests, except for icterus and mild unconjugated (2-4 mg/dL) hyperbilirubinemia. It is also more commonly diagnosed in males due to higher daily bilirubin production. Occasionally, the bilirubin level will increase during times of stress, illness, fasting, and then recover to its baseline, slightly elevated level (usually <3 mg/mL), after the illness resolves. In a patient with mildly elevated unconjugated bilirubinemia, otherwise normal liver enzymes, thyroid-stimulating hormone (TSH), and complete blood count (CBC), and who is otherwise well, no further workup is indicated.

Hemolysis can cause an unconjugated hyperbilirubinemia in proportion to the amount of hemolysis that occurs. It is most often diagnosed by the identification of anemia along with the presence of red cell fragments on peripheral smear, and elevated serum lactate dehydrogenase and haptoglobin. The serum bilirubin level typically remains below 5 mg/dL in hemolytic conditions such as spherocytosis, thalassemias, sickle cell disease, glucose-6-phosphate dehydrogenase deficiency, malaria, thrombotic thrombocytopenic purpura (TTP), and hemolytic uremic syndrome (HUS). The treatment is to treat the underlying cause of the hemolysis.

Hepatitis A is an acute viral infection of the liver primarily transmitted via fecal-oral contamination and accounts for 30% of acute viral hepatitis in the United States. Contaminated food and water are the primary sources of infection, although risks also include drug use (both injection and noninjection), male-male sexual contact, household and sexual contact with another infected individual, and working in a daycare setting. Hepatitis A virus (HAV) is also more widespread among those who live in low socioeconomic areas likely due to inadequate sanitation and hygiene practices. Hepatitis A infection is widespread in Africa, Asia, Greenland, Middle East, Mexico, and Central and South America. Travelers to these areas are at risk for infection and should be immunized prior to travel with two separate immunizations 6 months apart.

Hepatitis A causes a self-limited illness characterized by jaundice, fever, fatigue, malaise, nausea, vomiting, anorexia, right upper quadrant abdominal discomfort, and clay-colored stools. Common physical findings include jaundice and hepatomegaly. HAV infection can lead to fulminant hepatic failure in those who have chronic hepatitis B or C infection. The average incubation period is 25 to 50 days and transmission is possible 2 weeks prior to the development of symptoms and for 1 week after jaundice appears. While the symptoms can resemble a mild flu-like illness, or even be asymptomatic in younger patients, there is an approximately 0.1% to 1% fatality rate which increases in those over age 40. The icteric phase commonly lasts for 6 to 8 weeks. Most persons will recover from the associated fatigue within 3 months, although some people have an illness that will last up to 6 months. While there is no specific treatment for hepatitis A, supportive care and symptomatic treatments are indicated. Patients who develop fulminant hepatitis should be hospitalized in a facility with liver transplant capability.

Hepatitis A is diagnosed based on the presence of a conjugated hyperbilirubinemia, elevated serum transaminases, and positive antibody titers. An acute infection causes an elevation of anti-HVA IgM. In the absence of HAV symptoms, an elevated IgM anti-HAV may indicate a false-positive result, asymptomatic infection, or prolonged presence of the immunoglobulin after the initial infection. An elevated anti-HAV IgG but negative IgM indicates a history of a previous hepatitis A infection but not an acute illness. Additional laboratory findings may include nonspecific elevations of acute-phase reactants including serum alkaline phosphatase, platelets, and erythrocyte sedimentation rate (ESR).

Effective measures in preventing HAV transmission include adequate hand washing, avoidance of contaminated foods and water, and proper food handling and preparation. Hepatitis A vaccination is recommended for children aged 12 to 18 in identified high-risk counties, travelers to endemic areas, persons with chronic liver disease or chronic clotting-factor disorders, men who have sex with men, IV drug users, HIV-infected individuals, and workers with a high risk of exposure including food handlers, in addition to anyone who desires immunity to hepatitis A. Household or sexual contacts of persons infected with hepatitis A and previously unvaccinated can be offered postexposure prophylaxis with hepatitis A vaccination or lg. lg is preferred in patients for whom vaccine is contraindicated, adults greater than 40 years, immunocompromised individuals, and those who have been diagnosed with chronic liver disease.

Hepatitis B has infected over 2 billion people worldwide and there are currently 350 million chronic carriers, of whom a million will die from hepatitis B virus (HBV)-associated liver disease each year. Areas of the world with intermediate-tohigh rates of infections are Eastern Europe, Asia, sub-Saharan Africa, Middle East, and the Pacific islands. Hepatitis B is a viral infection transmitted via contact with contaminated blood or body fluids. Sexual contact ( eg, men having sex with men, multiple partners, and sexual contact with an infected person) and needle sharing are common mechanisms of infection in the United States. Hepatitis B may also be vertically transmitted from mother to baby. The incubation period from exposure to clinical symptoms is 6 to 24 weeks. Only 50% of infections with hepatitis B are symptomatic. Up to 5% of the world's population is affected with chronic HBV infection and approximately 1% of infections result in hepatic failure and death. Along with the acute-phase symptoms, which are similar to hepatitis A, hepatitis B can cause a chronic infection. The risk of developing chronic hepatitis B is inversely related to the age at infection-90% of infected infants, 20% to 50% of children younger than age 5, and less than 5% infected adults-develop chronic hepatitis B, which can lead to cirrhosis and hepatocellular carcinoma. Hepatitis B causes up to 80% of cases of hepatocellular carcinoma worldwide.

Serologic evaluation is necessary to determine the presence and type of hepatitis B infection. Hepatitis B surface antigen (HBsAg) is present in both acute and chronic infections and viral load is associated with risk of transmission to others. HBsAg typically becomes detectable in 1 to 10 weeks following HBV exposure and disappears in 4 to 6 months in those who subsequently recover and clear the virus spontaneously. Persistent detection of HBsAg after 6 months postexposure generally indicates chronic HBV infection. Hepatitis e antigen (HBeAg) is accepted as a marker for HBV replication and degree of infectivity. Patients with the HBeAg are 100 times more infectious than those lacking this antigen. Antibody to the surface antigen (anti-HBs) in the absence of HBsAg is seen in resolved infections and is the serologic marker produced after hepatitis B vaccination. An IgM antibody to the hepatitis B core antigen (anti-HBcAg IgM) is diagnostic of an acute HBV infection. Anti-HBcAg IgM is the only serologic marker detectable during the window period of seroconversion. A measurable level of HBsAg with a negative anti-HBcAg IgM is diagnostic of chronic hepatitis B. Figures 46-1 and 46-2 show the serologic studies associated with acute hepatitis B infection and chronic hepatitis B infection, respectively.

Acute hepatitis B infection is treated supportively. Persons with chronic hepatitis B may be candidates for antiviral therapy and should be referred to a hepatologist, both to evaluate the appropriateness of therapy and to monitor for the development of hepatocellular carcinoma, cirrhosis, and other potential complications of antiviral therapy.

Hepatitis B vaccination is universally recommended for children. Vaccination is also recommended for adults at high risk of disease, including health-care and public safety workers, household contacts of patients with HBV, IV drug users, persons with chronic liver disease, individuals requiring periodic blood or blood

Acute hepatitis B with recovery

Figure 46-1. Serologic Markers in Acute Hepatitis B Infection With Recovery.

Chronic hepatitis B infection

Figure 46-2. Serologic Markers in Chronic Hepatitis B Infection.

product transfusions, and patients receiving dialysis. Postexposure prophylaxis with hepatitis B lg and/or vaccination is recommended for all unvaccinated persons who are exposed to infected bodily fluids or secretions.

Hepatitis C (HCV ) is the most common cause of chronic liver disease in the United States, with more than 3 million infected persons. Infection is most prevalent in persons born between 1945 and 1965, the majority of whom were likely infected during the 1970s and 1980s. Approximately 2% to 3% (130-170 million) of the world population has been infected with the HCV. Transmission occurs via exposure to infected blood or body fluids via sexual contact and use of illicit drugs, sharing of needles and other drug paraphernalia, tattooing, accidental exposure of health-care workers, or by vertical transmission. Blood or blood-product transfusion and organ transplantation from infected donors were common sources of exposure prior to 1992.

HCV can be detected in the blood within 1 to 3 weeks of exposure, followed by an acute hepatitis C infection between 2 and 12 weeks of postexposure, with liver cell injury detectable in 4 to 12 weeks. Most infections are asymptomatic, yet hepatitis C can also cause an acute illness with jaundice, abdominal pain, malaise, and anorexia. Of those infected with hepatitis C, 60% to 80% will develop a chronic infection, with measurable levels of hepatitis C virus RNA (HCV RNA) for more than 6 months.

Chronic hepatitis C can lead to cirrhosis, hepatic decompensation, and hepatocellular carcinoma. Up to 30% of those with chronic HCV infection will develop cirrhosis during a 20- to 30-year time frame, making hepatitis C the current leading cause for liver transplantation in the United States. Patients with HCV infection should avoid alcohol consumption, acetaminophen, and nonsteroidal anti-inflammatory drugs (NSAIDs), and should receive hepatitis A and B vaccinations to prevent rapid disease progression and risk of coinfection. The progression of chronic HCV infection can be assessed by the amount of inflammation and cirrhosis seen on liver biopsy, which is commonly performed to evaluate extent of fibrosis and to determine candidacy for antiviral treatment with ribavirin and/or interferon. Treatment and cure results are highly variable depending on virus genotype, patient risk factors, and chronic health conditions. Treatment goals are to reduce long-term complications of chronic infection by inducing a sustained remission of HCV. There is currently no vaccination available for hepatitis C.

Hepatitis D is a rare cause of viral hepatitis in the United States that uses the viral envelope of hepatitis B to infect its host and thus requires coinfection of hepatitis B and D. It is commonly encountered in patients infected with HIV. Approximately 5% of HBV carriers may be coinfected with hepatitis D worldwide. It is endemic in the Mediterranean, Middle East, the Pacific islands, and South America. The clinical manifestations of HBV and hepatitis D virus (HDV) coinfection typically resemble that of an HBV infection. In coinfection, 10% or less will become chronically infected. Interferon is the only approved drug for treating chronic hepatitis D. Hepatitis B vaccine is the mainstay in HDV prevention. There is currently no vaccination available for hepatitis D.

Hepatitis E is transmitted via the fecal-oral route and while it is rare in the United States, it has a high prevalence in Asia, Africa, Middle East, and Central America. The incubation period is 4 to 5 weeks. The clinical signs and symptoms of hepatitis E virus (HEV) infection are generally more severe compared to those seen in HAV with a greater likelihood of prolonged cholestasis. It has a very high mortality rate, mostly in the third trimester for pregnant women. Malnourished individuals or those with underlying liver disease are also more likely to develop fulminant hepatitis. Diagnosis of acute HEV infection can be confirmed by detection of HEV in serum or stool or IgM anti-HEV. Treatment is supportive. lg prophylaxis is available in countries where HEV is endemic, but its efficacy remains unproven. There is currently no vaccination available for hepatitis E.

Alcohol abuse can cause an acute severe hepatitis, chronic fatty liver disease, hepatitis, cirrhosis, and fibrosis. Alcohol leads to a conjugated hyperbilirubinemia by impairing bile acid secretion and uptake. Common physical findings include ascites, jaundice, cutaneous telangiectasias, palmer erythema, testicular atrophy, gynecomastia, and malnutrition. Transaminase levels from alcohol abuse typically show an aspartate aminotransferase (AST) out of proportion to the alanine aminotransferase (ALT), commonly with a ratio of 2 or greater; γ-glutamyl transferase (GGT) levels are often abnormal in alcohol hepatitis; viral hepatitis usually causes greater elevations of the ALT (see Case 41 for a more thorough discussion of alcohol abuse).

Physical obstructions of bile drainage can also cause conjugated hyperbilirubinemia. Common etiologies of obstruction include gallstones that become impacted in the bile ducts, postoperative biliary strictures, or extrinsic compression of the bile ducts by tumors, such as pancreatic cancer. Pancreatic cancer is the most common cause of painless jaundice in a patient with biliary obstruction. Imaging of the bile system with ultrasound, computed tomography (CT) scan, or magnetic resonance imaging (MRI) or magnetic resonance cholangiopancreatography (MRCP) is usually diagnostic. Endoscopic retrograde cholangiopancreatography (ERCP) can be diagnostic and, in some cases, therapeutic.

Nonalcoholic fatty liver disease (NAFLD) results from deposition of fat within the hepatocytes, commonly from obesity, diabetes mellitus, hyperlipidemia, and hypertriglyceridemia. Rapid weight loss and protein-calorie malnutrition may also lead to NAFLD. One of the leading causes of liver disease, up to 25% of persons with NAFLD may have underlying cirrhosis. While most cases are asymptomatic and detectable only via elevated serum transaminases, symptoms may mimic those of acute viral hepatitis. There are currently no acceptable treatments for NAFLD, yet appropriate nutrition, weight management, and avoidance of alcohol are recommended.


46.1 A 32-year-old man with asthma and hypertension comes in for evaluation of an elevated bilirubin level that was detected on blood work required for a preemployment physical. The bilirubin level was 2.5 mg/dL (normal up to 1.0 mg/dL) with an elevated unconjugated component. He feels well and generally drinks one beer per night. He is monogamous with his wife and has no history of IV drug abuse and has one tattoo. His sclerae are anicteric and there are no signs of jaundice. His liver enzymes, electrolytes, TSH, and CBC are normal. Which of the following is the next step in the evaluation of
this patient?
A. Reassurance
B. Counsel on alcohol abstinence
C. Abdominal ultrasound
D. Hepatitis serologies
E. Referral to a hepatologist

46.2 A 45-year-old woman was diagnosed 6 months ago with acute hepatitis B infection. She is unaware of how she contracted the virus. She takes no medications and since the diagnosis, she has started taking a multivitamin and has started exercising. She now has the following serologies: HBsAg negative; anti-HBsAg positive; HBeAg negative; anti-HBcAg positive. Which of the following is the correct diagnosis?
A. Chronic active infection with low infectivity
B. Chronic active infection with high infectivity
C. Resolved acute infection
D. Resolved acute infection but contagious to sexual contacts
E. Resolved infection but at risk for reinfection in the future

46.3 A 60-year-old retired Navy captain comes to the doctor after a 15-lb unintentional weight gain over the past 4 months. His medical history is significant for osteoarthritis and his only complaint is fatigue. He has smoked a pack of cigarettes daily since his early 20s and consumes two to three alcoholic beverages several times per week. On examination, he is slightly jaundiced, with no hepatomegaly or RUQ tenderness to palpation. He has mild shifting dullness in his abdomen, and significant lower extremity edema. His skin is noted to have several faded tattoos. Which of the following antibodies would most likely be present in this patient?
A. Anti-HAV IgG
B. Anti-HBc IgM
C. Anti-HBs IgG
D. Anti-HBe IgM
E. Anti-HCV IgG

46.4 A 21-year-old college student plans to take a trip to Thailand with his friends in a couple of months. He confesses that he has experimented with illicit drugs including smoking marijuana as well as intranasal and intravenous cocaine and heroin. He is excited about the upcoming trip and wants to find out which immunizations he will need prior to his departure. Which of the following vaccinations and serologic tests will you recommend?
A. Hepatitis A vaccination, hepatitis A and B serologies
B. Hepatitis A and B vaccination, hepatitis A and B serologies
C. Hepatitis B vaccination, hepatitis B and C serologies
D. Hepatitis A and B vaccination, hepatitis B and C serologies


46.1 A. This is a classic case of Gilbert disease, a benign mild elevation of unconjugated bilirubin. In the face of otherwise normal history, examination, and liver enzymes, no further workup is indicated. People with Gilbert syndrome can have icteric sclera and jaundice that worsens with stress or illness.

46.2 C. These serologies are consistent with resolved hepatitis B infection and ongoing immunity; the HBsAg antibodies indicate immunity. This patient has both negative surface and e antigens, so is not at risk to spread the disease to others.

46.3 E. The patient has chronic hepatitis C that has progressed to cirrhosis causing the edema, weight gain, and ascites. Hepatitis A does not proceed to cirrhosis. Anti-HBs is present in people immunized to hepatitis B. Anti-HBe IgM reflects viral infectivity of hepatitis B. Anti-HBc IgM reflects exposure to hepatitis B 4 to 36 weeks after exposure.

46.4 D. Both hepatitis A and B vaccination are recommended with travel to Asia. This patient has a high likelihood of hepatitis B and C infection given his history of intranasal and intravenous drug use. Vaccination recommendations can change and it is best to review travel recommendations at travel. An appointment with a primary care physician or travel clinic should be made 4 to 6 weeks prior to taking any international trips to determine the appropriate vaccinations needed and general health information. However, if a patient has not been immunized against hepatitis A, two separate vaccines 6 months apart are required to confer immunity.


 The acute onset of painless jaundice in a patient older than age 50 should prompt an examination for pancreatic cancer (malignancy in the head of the pancreas causing compression of the bile ducts) .

 All pregnant women should be screened for the presence of HBsAg. If positive, treating the newborns with hepatitis B immunoglobulin (HBlg) and vaccination can reduce the risk of vertical transmission.

 One of the greatest risks for the development of cirrhosis in those with chronic hepatitis C is alcohol use. Anyone with chronic hepatitis C should be counseled to avoid all alcohol intake .

⯈ All persons born between 1945 and 1965 should be screened for hepatitis C.

 Nonalcoholic fatty liver disease is a leading cause of cirrhosis in patients with obesity, diabetes mellitus, and hyperlipidemia.


Centers for Disease Control and Prevention. Diagnosis and management of food-borne illnesses. MMWR Morb Mortal Wkly Rep. 2004; 53(RR-04):1-33. 

Centers for Disease Control and Prevention. Traveler's health. Available at: travel. Accessed March 26, 2015. 

DienstagJL. Acute viral hepatitis. In: Kasper D, Fauci A, Hauser S, et al., eds. Harrison's Principles of Internal Medicine. 19th ed. New York, NY : McGraw-Hill Education; 2015. Available at: http:// Accessed May 25, 2015. 

Roche SP, Kobos R.Jaundice in tbe adult patient. Am Fam Physician. 2004; 69:299-304. 

United States Preventive Services Task Force. Hepatitis C: screening. June 2013. Available at: http:// recommendation-summary/hepatitisc- screening. Accessed March 26,2015. 

Ward RP, Kugelmas M, Libsch KO. Management of hepatitis C: evaluating suitability for drug therapy. Am Fam Physician. 2004; 69(6):1429-1436. 

Wilkins T, Malcolm JK, Raina D, Schade R. Hepatits C: diagnosis and treatment. Am Fam Physician. 2010; 81(11):1351-1357. 

Wilkins T, Tadkod A, Hepburn I, Schade RR. Nonalcoholic fatty liver disease: diagnosis and management. Am Fam Physician. 2013:88(1):35-42. 

Workowski KA, Levine WC. Sexually transmitted diseases treatment guidelines, 2002. MMWR Morb Mortal Wkly Rep. 2002; 51(RR-06):1-80. 

World Health Organization. Hepatitis. Available at: http://www.who/int/csr/disease/hepatitis/ whocdscslryo20022/en/index3.html. Accessed March 26, 2015.


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