Robert's HBV Page - Diagnosis


DIAGNOSIS Clinical Phases During Acute Infection Acute viral hepatitis infection can be broken into four stages: i) incubation period, which is the time between initial viral entry into the cell to first day of symptoms; ii) prodromal or pre-icteric period; iii) the icteric phase; and iv) recovery. Symptoms during the onset of acute hepatitis B viral infection vary, depending on the individual. Many children and some adults infected with the virus never show any discernible symptoms. However, most infected individuals experience a certain level of jaundice which tends to develop soon after the virus can be detected in the blood. Often, jaundice is preceded by mild fevers, fatigue, malaise, loss of appetite, and sometimes nausea and vomiting. During the icteric or blood-borne phase, an infected individual's urine tends to have a dark, golden-brown appearance. This is often followed by the lightening of the stool as well as the yellowing of the skin, typically seen in jaundice. Jaundice is considered clinically apparent once total bilirubin levels are greater than 2-4mg/dl Signs of Liver Trouble There are some common signs that suggest one may have a liver problem. However, not all liver problems are attributable to the Hepatitis B virus. Hepatitis A, C, D, E, G viruses, as well as alcohol, chemical, bacterial, and other conditions can damage one's liver. The following is a list of the common symptoms of liver problem: Yellow discoloration of skin and/or eyes, Abdominal swelling or severe abdominal pain, Prolonged itching of the skin, Very dark urine, Pale stools, Passage of bloody or tar-like stools, and Chronic fatigue, nausea, or loss of appetite. If one suspects one has a liver condition, it is highly recommended that one sees a doctor and be tested to determine whether one's concerns are well-founded. Early detection may help simplify treatment. Blood Tests for Diagnosing Hepatitis B A variety of serological assays may be employed to differentiate the type of viral infection as well as disciminate between chronic and acute hepatitis B virus (HBV) infection. The most sensitive and specific methods used commercially in diagnosis are radioimmunoassays (RIA) and enzyme-linked immunosorbent assays (ELISA). Both assays make use of specific antibodies against various HBV proteins and can detect HBsAg proteins as low as 0.25 ng/mL and anti-HBs antibodies at a level of 1 mIU/mL. PCR has also been used in detecting low levels of HBV DNA present in both blood and liver tissue samples.
Presence of HBsAg	Presence of Anti-HBs	Presence of Anti-HBc	Interpretation of Assay Results
Positive	Negative	Negative	These results are characteristic of early acute HBV infection.
Positive	Positive or Negative	Positive	These results suggest either acute or chronic HBV infection which may be differentiated with respect to IgM anti-HBc.
Negative	Positive	Positive	These results are characteristic of previous HBV infection and current immunity to the virus.
Negative	Negative	Positive	These results do not have a clear interpretation. They could be due to HBV infection in the remote past, low-level HBV infection, or false-positive/ non-specific reactions. If present, anti-HBs help validate anti-HBc reactivity.
Negative	Negative	Negative	These results suggest that liver toxicity is due to some other agent other than HBV.
Negative	Positive	Negative	These results are typical of a vaccinated individual.

Reference Ranges in Clinical Biochemistry Tests
These are average ranges and times I have managed to compile, but may not exactly match those used by all medical centres.

AST (Aspartate Aminotransferase) or SGOT (Serum Glutamic-Oxalocetic Transaminase): 5-54 U/L | This enzyme is found mainly in heart, kidney, liver, muscle, and pancreatic tissues. Tissue damage releases this enzyme and elevated levels can be detected in the blood. Vitamin B deficiency and pregnancy may actually decrease levels of this enzyme found in the blood.
ALT (Alanine Aminotransferase) or SGPT (Serum Glutamic-Pyruvic Transaminase): 0-36 U/L | This enzyme is found mainly in the liver, but can also be seen in lower amounts in heart, muscle, and other tissues. Increased levels of this enzyme in the blood can be attributed to liver damage, kidney infection, chemical toxins, or even a cardiac infarction (heart attack).
Alkaline Phosphatase (during growth and pregnancy): 40-120 U/L | This enzyme is primarily found in bone and liver tissue. Growing children typically have an increased level of this enzyme in their blood compared to adults.
(for children): 40-400 U/L
GGT (Gamma Glutamyltransferase): 3-59 U/L | This enzyme is primarily found in liver cells and is quite sensitive to alcohol consumption. Elevated levels of this enzyme are found in liver disease, bile-duct obstruction, and drug abuse, to name a few.
LDH (Lactose Dehydrogenase): 135-225 U/L | This enzyme is primarily found in brain, heart, kidney, liver, lung, and skeletal muscle tissues. Increased levels are associated with cell death. Decreased levels can be associated with malnutrition or low tissue/organ activity.
Albumin: 35-50 g/L | This protein is synthesized in the liver and is involved in maintaining blood protein base levels. Liver damage may result in low levels of albumin produced. When albumin levels drop to extremely low levels, fluid from the blood may leak into surrounding tissues, resulting in swelling known as edema.
Bilirubin (non-neonatal) - Total (conjugated and unconjugated): 1-17 µmol/L | Bilirubin is a byproduct of red blood cell breakdown. It is actually formed when the hemoglobin ring is opened through other enzyme activities. Bilirubin is typically excreted into the bile, giving bile its pigmentation. Increased levels are associated with liver disease, mononucleosis, toxicity due to some types of drugs, and hemolytic anemia.
Bilirubin (non-neonatal) - Direct (conjugated): 0-5 µmol/L
PT (Prothrombin Coagulation Time): 10-12s

Serological Patterns of Acute HBV Infection

References

Hollinger, F.B. and Dienstag, J.L. 1995. Hepatitis B and D Viruses. In: Murray, P.R., Baron, E.J., Pfaller, M.A., Tenover, F.C. and Yolken, R.H. (eds.) Manual of Clinical Microbiology, 6th ed. Washington, D.C.: ASM Press; pp. 1033-1049.