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Immunization Dialogue Indian Pediatrics 2000;37: 1388-1389 |
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Jaundice in Hepatitis B Immunized |
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Ashish Jain, Dr. Ashish Jain has presented some very interesting observations and raised important questions. After answering the specific questions, I shall make some additional points about the observations presented by him
The HB vaccine consists of purified HBsAg, which is injected into the child’s tissues. Therefore, the child’s body now contains HBsAg. However, since the injected dose is minute, in the range of 10 micrograms, the antigen will not be picked up in an HBsAg ELISA (or another test) of the peripheral blood specimen.
The antigen is handled in the tissues two ways. The antigen presenting cells pick up as much antigen as they find, and process it by dis-assembly and presentation of the relevant epitopes on their surfaces for inducing the immune responses. The antigen not picked up in this manner gets diluted in body fluids and get catabolised by proteolysis, which is a normal process in physiology. Within days, small amounts of antibody (anti-HBs) are secreted by the immunostimulated B cells (now called plasma cells). If the amount of antibody is sufficient to be detected by laboratory test, then the subject is proven to have seroconverted. If any antigen (HBsAg) is left over at the time of antibody circulation in body fluids, then antigen-antibody com-plexes will form and they will be removed and destroyed by normal physiological process.
If a fully vaccinated person is subse-quently found to be HBsAg positive, there are two possibilities. One, he/she was already a chronic HB virus carrier prior to vaccination. HB vaccination of a carrier does not result in seroconversion (of anti-HBs), which is nece-ssary for elimination of the carrier state. Alternatively, the 3 doses did not induce any immunity (that is, vaccine failure); subse-quently the person got infected and is now HBsAg positive. In this case, we do not know if the infection is recent and the person is in the acute infection stage, or in a chronic carrier stage. Since the person is having hepatitis, the chances are that this is a symptomatic acute infection, but this must be proved with further evidence, for which further testing is necessary. Let us examine the 3 children reported with jaundice, cited in the question by Dr. Jain. Usually, children respond well to HB vaccination; so the finding of HBsAg so soon after (6 to 18 months) the third dose is most likely due to prior carrier state. Such carrier children do not respond to HB vaccination; they continue to be carriers. If this is the case, then the jaundice was most likely not due to HB virus, but more likely to be due to Hepatitis A virus. Anti-HAV IgM test would have settled this issue. If anti-HAV IgM is positive, the jaundice is due to acute HAV infection. If IgM antibody is negative, but IgG is positive then the cause is not HAV, but may be another infection such as HEV. Tests are now available for checking anti-HEV antibodies.. When children are seen with jaundice, we must consider all possibilties, namely acute viral hepatitis as well as other causes, including metabolic/genetic disorders. While most medical teachers emphasize that medical persons should learn common diseases, I emphasize that we must also know the uncommon diseases as well. Not that we should investigate for uncommon conditions, but the onus is on us to collect evidence that the disease belongs to the common or uncommon variety. In short, we do not have a definitive diagnosis given to us on these children and the one thing I can be reasonably confident about is that none of them had acute viral hepatitis due to hepatitis B virus. What else did they have? That can range from viral hepatitis due to virus A or E, to a variety of uncommon causes, to be diagnosed by clinical clues and investigations. T. Jacob John, |
