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HBsAg in placements
Correspondence
Volume 162 !';umber 5
paedia Medicine Chirurgie vol 10. Paris: Gynecologie, 1982:155.
Reply To the Editors: We thank Professeurs Ritter and Philipe for their letter. We obtained a computer search going back 30 years, but I'm afraid we did not adequately search the French literature. We are comforted that similar cases have been reported previously, and because of the suspicion of this possible preexistence, we did not make any claims that this was the first case report of this phenomenon. In fact, we did have a previous case of primary amenorrhea with apparent regular ovulation in which the patient conceived and then spontaneously aborted. Unfortunately, she never returned for more investigative procedures so we never submitted a case report. Jerome H. Check, MD Suite 1020 1015 Chestnut St. Philadelphia, PA 19107
HBsAg in placentas To the Editors: I read with great interest the article by Lucifora et al. (Lucifora G, Calabro S, Carroccio G, Brigandi A. Immunocytochemical HBsAg evidence in placentas of asymptomatic carrier mothers. AM J OBSTET GYNECOL 1988; 159:839-42). On review of the literature, this was the first description that HBsAg was detected in the placentas of HBsAg-positive asymptomatic carrier mothers. However, there were two mistakes in the manuscript. The first was in the right column of page 840, lines 4 to 7 from the top; the correct sentence should be "Positive controls were obtained by submitting to the same procedure sections obtained by biopsy of chronic active hepatitis B patients or acute exacerbation of hepatitis in HBsAg carriers. "1 The second mistake was in the left column of page 842, lines 18 to 19 from the top; the correct sentence should be "Babies born to HBsAg carrier mothers did not always have IgM anti-HBc."2 Moreover, we have pointed out that the cases infected in utero by hepatitis B virus (HBV) were most likely caused by transplacental leakage of HBeAg-positive maternal blood during pregnancy, which was clinically expressed by uterine contractions. This resulted in disruption of part of the placental barriers to let maternal blood leak into fetal circulation, such as in threatened abortion or threatened preterm labor. Moreover, the duration between the occurrence of the episode and delivery must be >6 weeks. Therefore, I point out the following: 1. The three carrier mothers must not be selected at random because the rate of HBV intrauterine infection is about 3% to 5% of perinatal transmission. 2. The three carrier mothers should not only be
1361
HBsAg-positive, but also HBeAg- and HBV-DNApositive, because the high infectivity of the carrier mother is the sole condition to possibly allow HBV intrauterine infection to occur. 3. The duration between the delivery and occurrence of threatened preterm labor in each case must be >6 weeks, which may be enough incubation time to let infection occur. 4. The three newborns should become HBV carriers because the placentas were infected by HBV with the evidence of HBsAg in them. H o-Hsiung Lin, MD Department of Obstetrics and Gynecology College of Medicine National Taiwan University Taipei, Taiwan, Republic of China REFERENCES 1. Su IJ, Kuo TT, Liaw YF. Hepatocyte hepatitis B surface antigen. Arch Pathol Lab Med 1985; 109:400-2. 2. Lin HH, Lee TY, Chen DS, et al. Transplacental leakage of HBeAg-positive maternal blood as the most likely route in causing intrauterine infection with hepatitis B virus. J Pediatr 1987;111:877-81.
Reply To the Editors: With reference to your letter and your comments on my article, I would like to point out the following: We carried out positive controls on the sections obtained by liver biopsies of persons affected with acute viral hepatitis B, surely positive to the antigen. We regret that we omitted this detail from the material and methods section. In the Comment section we wanted to point out the presence of IgM in the babies born to HBsAg carrier mothers. This is also mentioned in the literatllre hilt we did not intend to consider it as a general rule. In the meantime we have enlarged our field of research to other cases of carrier mothers. Echographic data give no evidence of retroplacental hematoma (i.e., that maternal blood mixes with fetal blood). We focused our attention on the presence of viral antigen in definite placental cytotypes that belong to the fetal compartment. Among these cytotypes that appear especially involved are the elements of the phagocytarian system (MPs). In our opinion this shows an active response of placental defence structures to the extraneous agent and suggests that the neonatal hepatitis depends on the immunoreply of placental structures and of the baby itself. I hope that my reply has been exhaustive enough. With great interest I read the results you were able to obtain from your researches and, if possible, I would like to be kept informed of your new findings. Giovanna Lucifora, MD Via San Corrado Complesso INCAM Palazzina A Messina, Italy 98100
Volume 162 !';umber 5
paedia Medicine Chirurgie vol 10. Paris: Gynecologie, 1982:155.
Reply To the Editors: We thank Professeurs Ritter and Philipe for their letter. We obtained a computer search going back 30 years, but I'm afraid we did not adequately search the French literature. We are comforted that similar cases have been reported previously, and because of the suspicion of this possible preexistence, we did not make any claims that this was the first case report of this phenomenon. In fact, we did have a previous case of primary amenorrhea with apparent regular ovulation in which the patient conceived and then spontaneously aborted. Unfortunately, she never returned for more investigative procedures so we never submitted a case report. Jerome H. Check, MD Suite 1020 1015 Chestnut St. Philadelphia, PA 19107
HBsAg in placentas To the Editors: I read with great interest the article by Lucifora et al. (Lucifora G, Calabro S, Carroccio G, Brigandi A. Immunocytochemical HBsAg evidence in placentas of asymptomatic carrier mothers. AM J OBSTET GYNECOL 1988; 159:839-42). On review of the literature, this was the first description that HBsAg was detected in the placentas of HBsAg-positive asymptomatic carrier mothers. However, there were two mistakes in the manuscript. The first was in the right column of page 840, lines 4 to 7 from the top; the correct sentence should be "Positive controls were obtained by submitting to the same procedure sections obtained by biopsy of chronic active hepatitis B patients or acute exacerbation of hepatitis in HBsAg carriers. "1 The second mistake was in the left column of page 842, lines 18 to 19 from the top; the correct sentence should be "Babies born to HBsAg carrier mothers did not always have IgM anti-HBc."2 Moreover, we have pointed out that the cases infected in utero by hepatitis B virus (HBV) were most likely caused by transplacental leakage of HBeAg-positive maternal blood during pregnancy, which was clinically expressed by uterine contractions. This resulted in disruption of part of the placental barriers to let maternal blood leak into fetal circulation, such as in threatened abortion or threatened preterm labor. Moreover, the duration between the occurrence of the episode and delivery must be >6 weeks. Therefore, I point out the following: 1. The three carrier mothers must not be selected at random because the rate of HBV intrauterine infection is about 3% to 5% of perinatal transmission. 2. The three carrier mothers should not only be
1361
HBsAg-positive, but also HBeAg- and HBV-DNApositive, because the high infectivity of the carrier mother is the sole condition to possibly allow HBV intrauterine infection to occur. 3. The duration between the delivery and occurrence of threatened preterm labor in each case must be >6 weeks, which may be enough incubation time to let infection occur. 4. The three newborns should become HBV carriers because the placentas were infected by HBV with the evidence of HBsAg in them. H o-Hsiung Lin, MD Department of Obstetrics and Gynecology College of Medicine National Taiwan University Taipei, Taiwan, Republic of China REFERENCES 1. Su IJ, Kuo TT, Liaw YF. Hepatocyte hepatitis B surface antigen. Arch Pathol Lab Med 1985; 109:400-2. 2. Lin HH, Lee TY, Chen DS, et al. Transplacental leakage of HBeAg-positive maternal blood as the most likely route in causing intrauterine infection with hepatitis B virus. J Pediatr 1987;111:877-81.
Reply To the Editors: With reference to your letter and your comments on my article, I would like to point out the following: We carried out positive controls on the sections obtained by liver biopsies of persons affected with acute viral hepatitis B, surely positive to the antigen. We regret that we omitted this detail from the material and methods section. In the Comment section we wanted to point out the presence of IgM in the babies born to HBsAg carrier mothers. This is also mentioned in the literatllre hilt we did not intend to consider it as a general rule. In the meantime we have enlarged our field of research to other cases of carrier mothers. Echographic data give no evidence of retroplacental hematoma (i.e., that maternal blood mixes with fetal blood). We focused our attention on the presence of viral antigen in definite placental cytotypes that belong to the fetal compartment. Among these cytotypes that appear especially involved are the elements of the phagocytarian system (MPs). In our opinion this shows an active response of placental defence structures to the extraneous agent and suggests that the neonatal hepatitis depends on the immunoreply of placental structures and of the baby itself. I hope that my reply has been exhaustive enough. With great interest I read the results you were able to obtain from your researches and, if possible, I would like to be kept informed of your new findings. Giovanna Lucifora, MD Via San Corrado Complesso INCAM Palazzina A Messina, Italy 98100