Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (191 page)

Suggested Readings

Beinhardt S, Rutter K, Stättermayer AF, et al. Revisiting the predictors of a sustained virologic response in the era of direct-acting antiviral therapy for hepatitis C virus.
Clin Infect Dis.
2013;56:118–122.

Bräu N. Evaluation of the hepatitis C virus-infected patient: the initial encounter.
Clin Infect Dis.
2013;56(6):853–860.

Center for Disease Control and Prevention.
Viral Hepatitis.
www.cdc.gov/hepatitis/index.htm
. Accessed June 18, 2013.

Centers for Disease Control and Prevention. Vital Signs: Evaluation of Hepatitis C Virus Infection Testing and Reporting—Eight U.S. Sites, 2005–2011.
MMWR.
2013;62(No. 18):357–361.

Ferenci P. Response guided therapy in patients with chronic hepatitis C—yesterday, today and tomorrow.
Best Pract Res Clin Gastroenterol.
2012;26:463–469.

Hoofnagle JH, Nelson KE, Purcell RH. Hepatitis E.
N Engl J Med.
2012;367:1237–1244.

Niesters HGM, Zoulim F, Pichoud C, et al. Validation of the INNO-LiPA HBV DR assay (version 2) in monitoring hepatitis B virus-infected patients receiving nucleoside analog treatment.
Antimicrob Agents Chemother.
2010;54:1283–1289.

Rotman Y, Liang TJ. Hepatitis C virus. In: Richman DD, Whitley RJ, Hayden FG.
Clinical Virology
, 3rd ed. Washington, DC: ASM Press; 2009.

Sherman KE. Therapeutic approach to the treatment-naïve patient with hepatitis C virus genotype 1 infection: a step-by-step approach.
Clin Infect Dis.
2012;55:1236–1241.

Sonneveld MJ, Zoutendijk R, Flink HJ, et al. Close monitoring of hepatitis B surface antigen levels helps classify flares during peginterferon therapy and predicts treatment response.
Clin Infect Dis.
2013;56:100–105.

Strader DB, Wright T, Thomas DL, et al. Diagnosis, management, and treatment of hepatitis C.
Hepatology.
2004;39:1147–1171.

VASCULAR AND ISCHEMIC DISORDERS OF THE LIVER

BUDD-CHIARI SYNDROME

   Definition

Heterogeneous group of disorders due to obstruction of hepatic venous outflow

   Causes

   Thrombosis due to hypercoagulable states (e.g., polycythemia vera [10– 40% of cases], essential thrombocythemia, myelofibrosis; antiphospholipid syndrome; and deficiencies of protein C, protein S, and antithrombin III) (See Chapter
10
, Hematologic Disorders, Paroxysmal Nocturnal Hemoglobinuria)

   Membranes and webs

   Others (e.g., neoplasms, collagen vascular diseases, cirrhosis, and polycystic liver disease)

   Laboratory Findings

   
Core laboratory
: Due to parenchymal cell necrosis and malfunction (e.g., increased serum AST), ALT may be increased >5 times in acute and fulminant forms. ALP and bilirubin may be increased and serum albumin decreased. Ascitic fluid total protein is usually >2.5 g/dL.

   Radiologic visualization (e.g., ultrasound, CT scan, MRI, hepatic angiography).

   Liver biopsy.

Suggested Reading

Menon KVN, Shah N, Kamath PS, et al. The Budd-Chiari syndrome.
N Engl J Med.
2004;350:578.

CONGESTIVE HEART FAILURE

   Laboratory Findings Related to Altered Liver Function