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Hepatitis B antigens
My current age is 57 and when I was 23 years old I was involved in an auto accident and required numerous blood transfusions. Shortly after the accident I was informed by a blood bank that my deposit was positive for Hepatitis B surface antigens and was therefore not acceptable for whole blood except for the serum. I have been positive since that point. My doctor does not seem concerned. I recently have been diagnosed with hypothyroidism and was wondering is there any correlation between these two conditions. Also I was told that the Hepatitis B surface antigens would soon be disappear which it has not. I also have passed the said blood condition to my wife over the years. Should I be concerned about the Hepatitis B surface antigen status now?
In terms of the math of DNA lab counting, zellyf may be right.
In Hep B literature, "inactive carrier" refers not to zero HBV replication, but to patients who show such stable liver status that they are not different from non-HBVers, like the one below. I read somewhere too that about 75% of patients with HBeAg (-) HBeAb (+) fall into this category.
INACTIVE HBSAG CARRIERS: After seroconversion, most patients remain negative for HBeAg and positive for anti-HBe antibody. Seroconversion is usually accompanied by stabilization of hepatitis, characterized by normalization of ALT levels and decreases in HBV DNA to low (<1000 copies/mL) or undetectable levels, depending on the assays used. This condition is commonly referred to as the “inactive carrier state.”66 Histologically, minimal to mild hepatitis may be observed, although the degree of fibrosis may be variable.37 For example, inactive cirrhosis may be identified in patients who had severe liver injury before seroconversion.37 Most patients remain in this phase for many years, if not indefinitely.8 Their prognosis is generally favorable, particularly if this phase is reached early in the disease course. No difference in survival was observed between 296 healthy blood donors with positive HBsAg and 157 uninfected controls who were followed up over 30 years in a study from northern Italy.67 Similarly, in a study by Hsu et al68 of 283 inactive HBsAg carriers who seroconverted and remained HBeAg negative, 189 (67%) had persistently normal ALT levels over a 9-year follow-up period, and only 1 developed cirrhosis. Thus, unlike patients with continued active viral replication, most inactive carriers do not have progressive liver disease. The other 94 (33%) patients in the Hsu et al68 study had ALT levels that were more than twice the upper limit of normal; these elevated levels were attributed to HBeAg reversion (4%), HBeAg-negative chronic hepatitis (24%), and undetermined causes (5%). Hepatitis B e antigen reversion occurs in a minority of patients who have seroconversion. In a study by McMahon,69 432 of 541 seroconverters (80%) remained HBeAg negative and anti-HBe positive throughout the study, whereas the other 109 (20%) seroreverted after the initial seroconversion. Seroreverting patients tended to fluctuate between seroconversion and seroreversion, commonly having 2 to 3 reversions over the 6 to 7 years of this study. Seroreversion episodes are frequently accompanied by a flare of hepatitis activity.70 In the study by Hsu et al,68 12 patients reverted to HBeAg positivity, 5 of whom developed cirrhosis during follow-up. In addition to these spontaneous seroreversion episodes, HBV replication can reactivate in inactive HBV carriers as a result of immunosuppression or chemotherapy.46,48,52,71 Spontaneous clearance of HBsAg was delayed in a small number of inactive HBV carriers, at the estimated annual rate of 0.5% to 2% in Western countries and at a much lower rate of 0.1% to 0.8% in Asian countries.72,73 Patients with delayed spontaneous clearance of HBsAg are thought to have a favorable prognosis (ie, lack of progression to cirrhosis). However, patients with cirrhosis and HBsAg clearance should continue to be monitored because clearance of HBsAg may not necessarily preclude the development of complications of cirrhosis or HCC in these patients.74-76
In Hep B literature, "inactive carrier" refers not to zero HBV replication, but to patients who show such stable liver status that they are not different from non-HBVers, like the one below. I read somewhere too that about 75% of patients with HBeAg (-) HBeAb (+) fall into this category.
INACTIVE HBSAG CARRIERS: After seroconversion, most patients remain negative for HBeAg and positive for anti-HBe antibody. Seroconversion is usually accompanied by stabilization of hepatitis, characterized by normalization of ALT levels and decreases in HBV DNA to low (<1000 copies/mL) or undetectable levels, depending on the assays used. This condition is commonly referred to as the “inactive carrier state.”66 Histologically, minimal to mild hepatitis may be observed, although the degree of fibrosis may be variable.37 For example, inactive cirrhosis may be identified in patients who had severe liver injury before seroconversion.37 Most patients remain in this phase for many years, if not indefinitely.8 Their prognosis is generally favorable, particularly if this phase is reached early in the disease course. No difference in survival was observed between 296 healthy blood donors with positive HBsAg and 157 uninfected controls who were followed up over 30 years in a study from northern Italy.67 Similarly, in a study by Hsu et al68 of 283 inactive HBsAg carriers who seroconverted and remained HBeAg negative, 189 (67%) had persistently normal ALT levels over a 9-year follow-up period, and only 1 developed cirrhosis. Thus, unlike patients with continued active viral replication, most inactive carriers do not have progressive liver disease. The other 94 (33%) patients in the Hsu et al68 study had ALT levels that were more than twice the upper limit of normal; these elevated levels were attributed to HBeAg reversion (4%), HBeAg-negative chronic hepatitis (24%), and undetermined causes (5%). Hepatitis B e antigen reversion occurs in a minority of patients who have seroconversion. In a study by McMahon,69 432 of 541 seroconverters (80%) remained HBeAg negative and anti-HBe positive throughout the study, whereas the other 109 (20%) seroreverted after the initial seroconversion. Seroreverting patients tended to fluctuate between seroconversion and seroreversion, commonly having 2 to 3 reversions over the 6 to 7 years of this study. Seroreversion episodes are frequently accompanied by a flare of hepatitis activity.70 In the study by Hsu et al,68 12 patients reverted to HBeAg positivity, 5 of whom developed cirrhosis during follow-up. In addition to these spontaneous seroreversion episodes, HBV replication can reactivate in inactive HBV carriers as a result of immunosuppression or chemotherapy.46,48,52,71 Spontaneous clearance of HBsAg was delayed in a small number of inactive HBV carriers, at the estimated annual rate of 0.5% to 2% in Western countries and at a much lower rate of 0.1% to 0.8% in Asian countries.72,73 Patients with delayed spontaneous clearance of HBsAg are thought to have a favorable prognosis (ie, lack of progression to cirrhosis). However, patients with cirrhosis and HBsAg clearance should continue to be monitored because clearance of HBsAg may not necessarily preclude the development of complications of cirrhosis or HCC in these patients.74-76
Although, no disrespect to cajim, there is not really any such thing as inactive chronic HepB. The virus is always replicating even if it is at low levels.
Both you and your wife need to have your HBV followed by your doctor. Hopefully you are just inactive carriers.
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