Clinical Vignettes

Chapter 1—Swallowing Disorders and Dysphagia

A 28-year-old internal medicine resident presented to the emergency department with food impaction after eating a chicken sandwich at a noon conference. He was unable to swallow his own saliva and presented for medical attention after 2 hours. He reports no gastrointestinal symptoms until 5 years prior to this event, when he developed food impaction after eating a large piece of steak. At that time he underwent endoscopy and was treated with dilatation. He was started on a proton pump inhibitor at that time and was asymptomatic for approximately 1 year. Since that point, he has had mild dysphagia to solid food only, which has occurred approximately three times per week. His worst foods are meats and bread. He reports no heartburn or other gastrointestinal symptoms.

He was taken urgently to endoscopy where he underwent endoscopic disimpaction of the food bolus. A large piece of chicken was found in the distal esophagus with a superficial tear ( CV Figure 1-1 ). This piece of chicken was macerated with biopsy forceps and pushed beyond the gastroesophageal junction into the stomach. Biopsies were taken at the time, which showed dense esophageal eosinophilia, with greater than 70 eosinophils per high-power field. He was given a diagnosis of eosinophilic esophagitis and started on swallowed fluticasone (440 mcg twice daily). A follow-up endoscopy showed absence of esophageal eosinophils. He was noted to have a stricture at the gastroesophageal junction and dilatation was performed with a through-the-scope balloon. He did well for several years and had no symptoms while on swallowed fluticasone and a proton pump inhibitor. After 2 years, fluticasone was discontinued and a follow-up biopsy 6 months later showed no eosinophilia. He completed residency training and moved to a different part of the country. Unfortunately, he developed recurrent food impaction after he moved and was restarted on swallowed fluticasone, which he has remained on since that time.

Chapter 2—Gastroesophageal Reflux Disease

A 25-year-old man was referred for evaluation of severe loss of dental enamel. The patient had experienced severe progression of dental carries for the last 2 years. His dentist referred the patient for evaluation of “high” gastroesophageal reflux disease (GERD).

Past medical and surgical history was unremarkable.

The patient is not taking any medications.

Review of systems remarkable for significant job stress and weight gain of 30 pounds during the preceding 18 months. No history of heart burn, dysphagia, nausea, or vomiting. His wife related no history of snoring or bruxism during sleep.

Laboratory testing was unremarkable.

Physical examination revealed an obese man 5′9″ tall and 250 pounds. Pertinent physical findings were confined to the oral pharynx ( CV Figure 2-1 A and B ). CV Figure 2-1 A demonstrates loss of dental enamel on the lingual surface and an amalgam filling and CV Figure 2-1 B demonstrates profound loss or enamel on the lingual surface of several teeth.

This patient is likely to have high acid reflux causing damage to the dental enamel. An esophagogastroduodenoscopy should be performed and if gastroesophageal reflux disease (GERD) is identified, then he should be started on aggressive antireflux therapy with proton pump inhibitor, weight reduction, and dietary and lifestyle modification. If this patient continues to show signs of GERD and high acid reflux, surgical fundoplication should be considered.

Chapter 3—Esophageal CAUSES of Chest Pain

• A 28-year-old healthy man is referred by his primary care provider for the evaluation of chest pain. He has no cardiac risk factors and an electrocardiogram (ECG) was normal prior to referral. He describes a midsternal chest discomfort throughout the day, which is not exacerbated by strenuous activity. He also has intermittent heartburn, particularly after large meals. He denies dysphagia, odynophagia, weight loss, melena, early satiety, or constitutional symptoms. He reports only mild relief with a 8-week trial of high-dose omeprazole. He takes no other medications and has no significant family history. His examination is only notable for being slightly overweight. What is the next step in evaluating his chest pain?

  An esophageal manometry and ambulatory pH/impedance study are the next steps. This patient has no personal or family risk factors for a cardiac cause. Following a normal ECG, his primary care provider proceeded with a proton pump inhibitor trial. Because this patient had only mild relief with acid suppression, further evaluation is warranted. The next best diagnostic study is esophageal manometry followed by transnasal pH/impedance testing. The manometry screens for a motility disorder as a potential source of chest discomfort and allows for proper placement of the transnasal pH/impedance catheter. Using a combined pH/impedance catheter can provide valuable diagnostic information such as ensuring adequate acid suppression and diagnosing nonacid reflux.

Chapter 4—Achalasia

A 62-year-old woman presents with a 2-year history of progressive dysphagia. It was first noted with solids, but now has progressed to liquids. Hang up occurs primarily in the cervical esophagus, usually with every meal. The patient eats slowly and is the last to leave the dinner table. Regurgitation of undigested food occurs several times a week, usually after the evening meal. The patient has an intermittent nighttime cough, and her husband notes “gurgling” while she sleeps. She sometimes has white phlegm on her pillowcase in the morning. There is no chest pain. She is experiencing worsening heartburn unrelated to meals, and is not responding to twice-daily proton pump inhibitors. A 10-pound weight loss has occurred. Otherwise, she is in excellent health.

Initial endoscopy found minimally dilated esophagus with 50 ml of retained saliva. The lower esophageal sphincter seemed “spastic” but opened easily with pressure from the endoscope. The patient was dilated with an 18-mm bougie with no symptom relief. Barium esophagram suggests bird’s beak, a mildly dilated esophagus with to and fro movement. In the upright position, the patient maintained a column of barium 20 cm high (just below the clavicle) 5 minutes after drinking 8 oz of barium. High-resolution manometry identified pattern of Type II achalasia.

Treatment options of pneumatic dilation and laparoscopic myotomy with partial fundoplication was discussed with the patient with appropriate risks and benefits. She chose pneumatic dilation, which was performed with a 30-mm Rigiflex balloon under fluoroscopic guidance at the time of endoscopy in the ambulatory surgery center. Follow up at 1 month found her free of symptoms. Timed barium swallow was repeated and now had a 3-cm column at 5 minutes. Follow-up 2 years later finds her doing well with excellent esophageal emptying. No dietary restrictions are necessary, and she has gained 20 pounds.

Chapter 6—Esophageal Anomalies, Infections, and Nonacid Injuries

A 46-year-old man, status post–renal transplantation, presents with chest pain and odynophagia for 2 weeks. Symptoms have been so severe that he has had difficulty maintaining adequate oral intake. He also reports intermittent fevers and chills. Vital signs include temperature 38.2 ° C, heart rate 110, blood pressure 115/90. On physical examination, he has oral ulcerations.

On upper endoscopy, there are multiple small ulcers with diffuse friability in the distal esophagus. Biopsies were obtained and histologic examination revealed Cowdry type A intranuclear inclusions and multinucleated cells, see Figure 6-8 . The diagnosis is Herpes simplex virus (HSV) esophagitis. He was treated with oral acyclovir 400 mg five times daily for 14 days with subsequent improvement in his symptoms.

Chapter 7—Barrett’s Esophagus

See http://www.youtube.com/watch?v=eLBSWlGgVgE .

Chapter 10—Gastric Cancer

A 37-year-old man presented to the emergency department with hematemesis. An emergent endoscopy revealed an ulcerated nodule in the proximal stomach. Biopsies revealed a carcinoid tumor.

Endoscopic ultrasound evaluation ( CV Video 10-1 ) showed the tumor to be approximately 15 mm in cross-section. The tumor infiltrated through the gastric wall. Further evaluation revealed an abnormal lymph node. The node underwent endoscopic ultrasound–guided fine-needle aspiration, which demonstrated nodal involvement by carcinoid tumor.

The patient’s gastrin level was normal. He was given the diagnosis of metastatic Type III carcinoid tumor and underwent partial gastrectomy with lymphadenectomy.

He continues to be without evidence of reoccurrence 3 years following surgery.

CV Video 10-1. Endoscopic ultrasound (EUS) evaluation of a patient with an ulcerated nodule in the proximal stomach. Previous biopsies revealed carcinoid tumor. EUS staging revealed a lesion that penetrated the gastric wall and had metastasized to a perigastric lymph node.

Chapter 11—Thickened Gastric Folds

A 54-year-old woman undergoes esophagogastroduodenoscopy to evaluate epigastric pain and has an incidental finding of a 2.5-cm subepithelial lesion in the gastric body. The overlying mucosa appears normal, and there is no “pillow sign.” Follow-up endoscopic ultrasound (EUS) reveals a hypoechoic, homogenous lesion in the fourth layer without calcifications or internal cystic spaces. What is the best option for diagnosis? What is in the differential diagnosis for this lesion? What additional testing can be done on the tissue to aid in diagnosis and determining its malignant potential?

Hypoechoic, fourth-layer gastric tumors smaller than 3 cm are best diagnosed with EUS and fine-needle aspiration with immunohistochemical analysis of the aspirated cells. The differential diagnosis for these lesions includes leiomyoma, leiomyosarcoma, neural origin tumors (schwannoma, neuroma, neurofibroma), gastrointestinal stromal tumor, lymphoma, and glomus tumors. Immunohistochemical stains including CD117, CD34, SMA, S100, and desmin can be used to distinguish these lesions.

Chapter 12—Gastroparesis

• A 31-year-old woman with a 15-year history of diabetes mellitus and gastroparesis since 2006 presents with persistent nausea and vomiting despite treatment with ondansetron, metoclopramide, and domperidone. Her gastric emptying scintigraphy test showed severe gastric retention of 65% 4 hours after ingestion of the test meal. She has already had a pyloroplasty and jejunostomy tube placement. What is the next available option for the patient?

The patient qualifies for a gastric electrical stimulator (GES) placement under the Food and Drug Administration’s Humanitarian Device Exemption rule. She has failed medical therapy as well as pyloroplasty. The patient has very severely delayed gastric emptying time based on the preferred 4-hour gastric emptying study. She has tried the only available prokinetic in the United States, metoclopramide, which was stopped because of unacceptable side effects after 1 month. Additionally, she has failed the best antiemetic prokinetic in the world, domperidone. However, dosing could be reinvestigated because dosing must be 20 mg four times a day and can be increased to 30 mg four times a day before being considered a failure. Ondansetron is one of the preferred antiemetics for gastroparesis, and it is available in oral dissolvable tablets for patients with severe nausea and vomiting. It is a 5-HT ₃ agonist that inhibits receptors in the area postrema of the brain. Granisetron is another 5-HT ₃ agonist, and is also available as a 7-day patch for sustained blood levels. Pyloroplasty has been noted to lead to symptom improvement, acceleration in gastric emptying, and reduced need for prokinetics in one report of gastroparesis patients, particularly with short follow-up. GES offers a pathway to control nausea and vomiting at the central nervous system level and also increase vagal activity (e.g., fundic relaxation). Combining pyloroplasty with GES placement is a new development ensuring accelerated gastric emptying. Jejunostomy tubes can be combined with the GES surgery to provide additional nutrition for 3-6 months. See Chapter 12, Figure 12-4 , Algorithm for gastroparesis management.

Overall, the patient has not improved after multiple interventions and she is now a candidate for GES device placement.

Chapter 13—Evaluation of Abnormal Liver Tests

A 30-year-old man with periodic midepigastric abdominal pain after eating was referred to a gastroenterologist for evaluation of possible gallbladder or liver disease. His primary care physician has obtained screening laboratory tests that showed the total bilirubin to be elevated to 3 (< 1.5 mg/dL upper limit of normal [ULN]) with normal aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase values. His complete blood count (CBC) is normal and an ultrasound of the liver and gallbladder are normal. The patient was an avid runner and had frequently taken over-the-counter nonsteroidal antiinflammatory drugs (NSAIDs) for ankle and knee pains. He had not passed black stools or vomited blood or vomit with the appearance of coffee grounds. His physical examination was only remarkable for slight yellow tinge to the sclera.

The gastroenterologist obtained fractionated bilirubin, lactate dehydrogenase (LDH), CBC, and liver tests after a 24-hour fast. All tests were normal, except total bilirubin was now 3.8 md/dL, all of which was unconjugated. The peripheral smear was normal and LDH enzyme was not elevated, making the diagnosis of hemolysis unlikely. The patient was given a prescription of omeprazole 20 mg, advised to substitute acetaminophen for NSAIDS, and try ice and topical analgesics for joint pain. His postprandial abdominal pain resolved completely.

This patient has indirect hyper bilirubinemia with normal liver enzyme tests, referred to as Gilbert’s syndrome. It is found in 5% to 10% of the white population. Gilbert’s syndrome is a congenital disorder, characterized by a 70% to 80% reduction in the glucuronidation activity of the enzyme, uridine 5′diphosphate-glucuronosyltransferase. The principle differential diagnosis of indirect hyperbilirubinemia with normal liver enzyme tests and function is hemolysis, which can be excluded by a full blood count, haptoglobin, lactate dehydrogenase levels, and the absence of reticulocytosis. Gilbert’s syndrome is a benign disorder that requires no therapy. When Gilbert’s syndrome occurs in the background of elevated AST, ALT, or alkaline phosphatase, the clinical overlap can be confusing if the contributory diagnosis is not considered.

Chapter 14—General Concepts of Viral Hepatitis

• A 30-year-old Nigerian woman who immigrated to the United States 10 years ago is now pregnant. She is G1, P1, and 14 weeks’ pregnant. Prenatal blood tests showed normal complete blood count (CBC) and full chemistry panel, but the patient was hepatitis B surface antigen (HBsAg) positive. She has not previously been seen by a health care provider. She does not smoke tobacco or marijuana, or drink alcohol. She is a sales clerk at a department store, and is married and in a monogamous relationship. Physical examination is remarkable for a gravid uterus that is two to three fingerbreadths below the umbilicus. There are no stigmata of chronic liver disease on physical examination.

• The patient is concerned about risk of transmitting the hepatitis B virus (HBV) to her baby. What are the new guidelines for managing HBV infection during pregnancy?

All women are checked for HBV infection at the initial prenatal visit. Those women identified to be HBsAg positive should undergo thorough serologic testing: hepatitis Be antigen, hepatitis Be antibody, HBV-DNA, complete liver panel, CBC, international normalized ratio, and liver ultrasound.

• If testing reveals inactive HBV infection, then HBV-DNA should be rechecked at 26 to 28 weeks of gestation.

• If testing reveals active HBV hepatitis or cirrhosis, then oral antiviral treatment should be considered.

For maternal HBV-DNA results at 26 to 28 weeks of gestation:

• For mothers with HBV DNA of more than 10 ⁶ copies, oral antiviral therapy should be considered.

• For mothers with HBV DNA of less than 10 ⁶ copies, close monitoring during the later stages of pregnancy is necessary.

Oral HBV antiviral therapy during pregnancy requires the caregiver to have extensive hepatology and obstetrical experience. Obtaining informed consent is advisable.

At birth neonates should receive:

• Passive immunization

• Hepatitis B immune globulin less than 12 hours after birth

• Active immunization:

  • The first dose at birth (within 12 hours if the mother has hepatitis B infection)

  • A second dose at 1 through 3 months

  • A third dose at 6 through 18 months of age

Chapter 15—Antiviral Therapy for Hepatitis C

A 53-year-old white man is found to have elevated alanine aminotransferase (ALT) levels on routine examination for a life insurance physical. The patient denied risk factors for viral hepatitis, was taking no medications, and denied use of alcohol. A hepatitis C virus (HCV) antibody test was positive, and HCV infection was confirmed with an HCV-RNA test by polymerase chain reaction revealing a viral load of 3,450,000 IU/mL. Liver function was normal with an albumin of 4.2 g/dL and a total bilirubin of 0.4 mg/dL. Infection with hepatitis B and human immunodeficiency viruses were excluded, and the patient was not immune to hepatitis A or B infection. Baseline hemoglobin was 14.8 g/dL, absolute neutrophil count was 4700/mm ³ , and the platelet count was 235,000/mm ³ .

A careful history uncovered no depression or history of psychiatric illness. The patient was counseled on the natural history of hepatitis C infection and the available therapies; immunizations against hepatitis A and B were initiated. The patient expressed interest in therapy and tested positive for genotype 1b HCV infection. A sustained virologic response rate of 70% to 75% was quoted to the patient and he agreed to therapy.

Four weeks after starting therapy with pegylated interferon alfa 2a 180 mcg/week, ribavirin 1200 mg/day and telaprevir 750 mg every 8 hours, the HCV was nondetectable. The patient complained of generalized pruritus and a macular rash was noted involving the trunk and proximal upper extremities. A topical steroid cream and systemic nonsedating antihistamines were prescribed and the patient was cautioned to avoid sun exposure.

At 6 weeks of therapy, the hemoglobin was 9.5 g/dL and the patient complained of fatigue. Ribavirin dose was reduced to 600 mg/day and therapy continued. By week 8 of therapy, the hemoglobin had stabilized at 10 g/dL and the rash had not progressed. Treatment with telaprevir was completed at week 12 and he continued pegylated interferon and ribavirin. The patient remained virus nondetectable at weeks 12 and 24 of therapy, and he stopped interferon and ribavirin at week 24. Twenty-four weeks after discontinuation of therapy, the patient continued to test negative for HCV and was declared cured of infection.

Chapter 16—Antiviral Therapy for Hepatitis B

A 45-year-old man was diagnosed with hepatitis B infection while trying to donate blood. Six years later he underwent evaluation for possible therapy. At presentation, the patient was asymptomatic. The alanine aminotransferase (ALT) level was normal at 23 IU/mL, hepatitis B viral load was elevated at 25,000 IU/mL. The patient was hepatitis Be antigen–negative, hepatitis Be antibody–positive, and tested negative for human immunodeficiency virus (HIV) antibody. Liver synthetic function was normal. The patient declined a liver biopsy.

Because the liver enzyme levels were normal and the patient declined a liver biopsy, serial testing of liver enzymes was done. Three months later, ALT level was 98, hepatitis B virus (HBV)–DNA was 75,000 IU/mL, and the patient remained asymptomatic; renal function was normal.

With evidence of liver inflammation and viremia (ALT 98, HBV-DNA > 2000 IU/mL), the patient was started on tenofovir 300 mg once a day. Because the patient is e-antigen negative, lifelong therapy was recommended. He was asked to return in 3 months for reevaluation.

Three month later, the ALT was normal at 20 IU/mL, and the HBV-DNA was nondetectable, indicating a good response to therapy. Continued therapy with tenofovir 300 mg daily and follow-up every 6 months was recommended. The patient remained virus negative and with normal ALT for the next 1.5 years.

Three years later he presents for follow up. Repeat laboratory data shows an ALT of 210 IU/mL and a HBV-DNA level of 110,000 IU/mL. The patient was carefully questioned and he admitted to not being compliant with tenofovir because of cost. Tenofovir was restarted at the same dose and 6 months later the ALT had normalized and HBV-DNA was less than 40 IU/mL but detectable. Therapy was continued and the patient was again cautioned about the risks of discontinuation of therapy.

Chapter 17—Autoimmune Hepatitis: Diagnosis

A 25-year-old woman presents with jaundice, fatigue, and arthralgia that developed during a 4-week period. Laboratory tests disclose serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels greater than tenfold the upper limit of normal (ULN) range; serum immunoglobulin G level greater than twofold ULN; antinuclear antibodies 1:640; smooth muscle antibodies 1:640; hepatitis A, B, and C markers negative; and ceruloplasmin level greater than ULN. Liver tissue examination discloses moderate to severe interface hepatitis with dense lymphoplasmacytic infiltrates and stage 2 fibrosis. Past history indicates that she took minocycline for 10 days for acne two weeks prior to the onset of symptoms and that she drinks two to three glasses of beer on weekends with friends. Treatment with prednisone and azathioprine induced clinical and laboratory resolution within 3 months and liver tissue examination at 6 months was normal. Gradual treatment withdrawal was followed by an increase in serum AST and ALT levels to fourfold ULN, and combination therapy was restarted.

Clinical clues to classical severe acute-onset autoimmune hepatitis are onset after discontinuation of minocycline, hepatic fibrosis, and relapse after corticosteroid withdrawal.

Chapter 18—Autoimmune Hepatitis: Treatment

A 32-year-old woman is discovered to have fourfold elevations of the serum aspartate and alanine aminotransferase levels above the upper limit of the normal (ULN) range during a routine medical examination. She is asymptomatic, taking no medication, has no other illnesses, has no alcohol or toxin exposures, maintains a body mass index of 24, and has a negative family history of liver disease. Antinuclear antibodies (1:320) and smooth muscle (1:160) are present; serum immunoglobulin G level is more than twofold the ULN. Liver tissue examination discloses mild to moderate interface hepatitis, lymphoplasmacytic infiltrate, and stage 1 fibrosis. Therapy was started with budesonide (3 mg thrice daily) and azathioprine (50 mg daily), and laboratory resolution was achieved in 3 months. Treatment was continued to ensure histologic resolution.

Justifications for treatment of asymptomatic mild autoimmune hepatitis the following: disease activity fluctuates unpredictably, indolent progression is possible, 26% to 70% of patients become symptomatic, mild hepatic fibrosis is already present, spontaneous resolution is uncertain, and budesonide has few side effects in noncirrhotic patients.

Chapter 19—Primary Biliary Cirrhosis and Primary Sclerosing Cholangitis

A 46-year-old man is referred to a hepatologist after his primary care doctor incidentally noted elevated liver tests that have persisted during the preceding 6 months. He occasionally has three to four loose, nonbloody bowel movements, but otherwise has no complaints. He is otherwise healthy and does not have a family history of medical problems.

His physical examination is normal. His liver tests include an alkaline phosphatase 290 U/L, aspartate aminotransferase 45 U/L, alanine aminotransferase 75 U/L, total bilirubin 1.5 mg/dL, and direct bilirubin 1.0 mg/dL. The remainder of the laboratory tests, including albumin and international normalized ratio, are normal. Prior to the referral, the primary care doctor obtained a liver ultrasound, which was normal.

A magnetic resonance cholangiography is obtained (see Chapter 19, Figure 19-1 ) and shows stricturing and dilation of the intrahepatic bile ducts. A colonoscopy reveals pancolitis with a decreased vascular pattern and very mild friability. Surveillance biopsies demonstrated mild active chronic colitis without evidence of neoplasia.

This case is consistent with primary sclerosing cholangitis–chronic ulcerative colitis. Mesalamine is initiated and the patient is enrolled in a surveillance program that includes an annual ultrasound of the gallbladder and an annual colonoscopy with surveillance biopsies.

Chapter 20—Vaccinations and Immunoprophylaxis in Gastrointestinal and Liver Disorders

• 1.

  A 25-year-old female medical student comes to your clinic after a high-risk exposure to hepatitis A. What should be done? What vaccines should she have already received, and what other vaccines should be considered in this young woman?

  She should receive a single-dose antigen hepatitis A vaccine for postexposure prophylaxis.

  She should have already received the measles-mumps-rubella, varicella, and tetanus-diphtheria-pertussis (Tdap) vaccines. If not, she should have these administered.

  Furthermore, she should receive the hepatitis B virus (HBV) vaccine as well because she is a health care worker.

  Because she is younger than 26, she should receive the human papillomavirus (HPV) vaccine as well.

  She should also receive the influenza vaccine yearly.

• 2.

  A 67-year-old man with cirrhosis comes to your office for a checkup. What vaccinations should be considered?

  He’s eligible for live vaccines unless he has received a liver transplantation. Given worsening immune system function with the progression of cirrhosis, he should be brought up to date and administered hepatitis A virus (HAV), HBV, Tdap, and varicella zoster vaccines.

  Given this chronic illness as well as his age older than 65, he should also receive the pneumococcus vaccine and the influenza vaccine yearly.

• 3.

  An 18-year-old woman with Crohn’s disease, controlled on infliximab as monotherapy, lives in a college dormitory. What vaccinations should be considered?

  She’s living in a college dormitory. She should undergo vaccination against influenza (killed injection formulation, not live intranasal), HAV, HBV, meningococcus, and pneumococcus.

  She’s on biologic therapy, so vaccination against varicella is generally contraindicated.

  The HPV vaccine is indicated given her age.

Chapter 21—Pregnancy and Liver Disease

• A 28-year-old woman, G4 P0 AB3, is now pregnant at 12 weeks of gestation. Her first prenatal checkup showed that she was hepatitis C virus (HCV) antibody–positive. The remainder of her prenatal blood tests were normal and she is hepatitis B surface antigen–negative and human immunodeficiency virus (HIV)–negative. She has not previously been seen by a health care provider. She does not smoke tobacco or marijuana or drink alcohol. She relates promiscuous sexual behavior and cocaine use in college, and now works as an accountant for a trucking firm. She is married in a monogamous relationship. Physical examination is remarkable for a gravid uterus that is two to three fingerbreadths below the umbilicus. There are no stigmata of chronic liver disease on physical examination. Additional blood tests showed alanine aminotransferase elevation to 68 (upper limit of normal < 40 IU/L) and HCV with polymerase chain reaction at 500,000 copies and HCV genotype 1. Ultrasound of the liver, serum total protein, albumin, international normalized ratio, and complete blood cell count were all normal.

• The patient is concerned about risk of transmitting HCV to her baby. What are the new guidelines for managing HCV infection during pregnancy?

The risk for perinatal transmission of HCV is low when the viral load is less than 1 million copies, and not associated with HIV coinfection. Maternal-fetal HCV transmission rates are not decreased by elective cesarean section. Breast feeding does not appreciably increase the risk of transmitting HCV to the neonate.

Chapter 22—Rheumatologic Manifestations of Hepatobiliary Diseases

• A 35-year-old woman with Crohn’s disease is referred to your office. She has failed mesalamine and azathioprine. She requires 20 mg of prednisone to control her symptoms and you decide to start infliximab. She has a normal chest radiograph and negative QuantiFERON gold test for tuberculosis. For what additional infectious disease should she be tested?

She should be tested for hepatitis B. Guidelines recommend that all patients who will receive an anti–tumor necrosis factor (TNF) agent should be screened for hepatitis B and C infection. Although the use of TNF inhibitors have not been shown to exacerbate hepatitis C infection, several reports of hepatitis B virus (HBV) reactivation and fatalities have been reported particularly with infliximab therapy. Despite these recommendations, only 25% of patients are screened in clinical practice. At a minimum, patients should be tested for hepatitis B surface antigen (HBsAg) and hepatitis B core antibody (HBcAb). Patients with chronic HBV or inactive HBV are both HBsAg +. These HBsAg + patients are most at risk for developing liver inflammation and necrosis caused by HBV if treated with anti-TNF therapy. Therefore these patients should not receive biologic therapy. If biologic therapy is absolutely needed, they should receive antiviral prophylaxis while on therapy.

Patients with normal liver-associated enzymes, HBsAg–, and HBcAb + have resolved HBV. Patients with resolved HBV will have undetectable HBV DNA viral loads and may or may not have antibodies to HBsAg. Patients with resolved hepatitis (HBsAg–, HBcAb +) can receive anti-TNF therapy without antiviral prophylaxis because the HBV reactivation rate in these patients is less than 2% to 3%. However, because HBV reactivation has occurred in these patients, they should be monitored prospectively for symptoms, increased hepatic enzymes, and viral DNA quantification. Prior to starting an anti-TNF agent, the algorithm can be followed ( CV Figure 22-1 ).

Chapter 24—Drug-Induced Liver Disease

A 20-year-old man presents to his college dispensary with a complaint of yellow eyes, dark urine, and claylike stools. He is a college student athlete who competes in lacrosse. He does not drink alcohol, smoke marijuana or tobacco, or do illicit drugs. Medical and surgical history is remarkable for appendectomy at 5 years old. Physical examination shows a healthy but jaundiced man with scleral icterus. No cervical or axillary adenopathy is present. The liver is 11 cm to percussion in the mid clavicular line, and there is no splenomegaly or stigmata of chronic liver disease. Laboratory test results are as follows: