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Need for immunoprophylaxis in infants born to HBsAg-positive carrier mothers who are HBeAg negative
Volume 105 Number 6
be an additive but not the main cause of the disease. Other undetected factor(s) might be involved. Because no further study was conducted, we do not have any evidence of impaired vitamin K absorption in these infants; such a possibility should be defined in the future. Komazawa a~ showed that orally administered vitamin K was less well absorbed in infants, with or without hepatic dysfunction, compared with healthy adults. The outcome in our infants was unfavorable (Table). Our observations support the concept that vitamin K prophylaxis is exclusively breast-fed infants is necessary.9.10 A recent study suggested that breast-fed babies who received vitamin K at birth did not have vitamin K deficiency at 1 month of age. 12 However, this study was criticized because the number of infants studied was small 13 and the report did not address the issue of vitamin K deficiency in breast-fed infants who do not receive prophylaxis. 9 In Japan, oral administration of vitamin K two or three times during the first month of life is being studied in an effort to prevent vitamin K deficiency, 1 but a final conclusion has not been reached.
REFERENCES 1. Nakayama K: Etiology of vitamin K deficiency in infants. Perinat Med (Japanese) 12:1029, 1982. 2. American Academy of Pediatrics: Vitamin K supplementation for infants receiving milk substitute infant formulas and for those with rate malabsorption. Pediatrics 137:601, 1983.
Clinical and laboratory observations
945
3. Malia RG, Preston FE, Mitchell VE: Evidence against vitamin K deficiency in normal neonates. Thromb Haemost 44:159, 1980. 4. Owren PA, Strandli OK: Normotest. Farmakoterapi 25:14, 1969. 5. Motohara K, Kuroki Y, Matsuda I, et al: Quantitative estimation of circulating PIVKA-II by enzyme-linked immunosorbent assay using monoclonal antibody. Acta Pediatr Jpn [Japanese] 88:1508, 1983. 6. Clarke HGM, Freemen TA: Quantitative immunoelectrophoresis method (Laurell electr0phoresis). Protides Biol Fluids 14:503, 1966. 7. Manes JD, Fluckiger HB, Schneider DL: Chromatographic analysis of vitamin K~: Application to infant formula products. J Agric Food Chem 20:1130, 1972. 8. Abe K, Hiroshima 'O, Ishibashi K, et al: Fluorometric determination of phylloguinone and menaquinone-4 in biological materials using high-performance liquid chromatography. J Jpn Pharmacol Assoc (Japanese) 99:192, 1979. 9. Lane PA, Hathaway WE, Githens JH, et al: Fetal intracranial hemorrhage in a normal infant secondary to vitamin K deficiency. Pediatrics 72:562, 1983. 10. O'Connor ME, Livingstone DS, Hannah J, Wilkins D: Vitamin K deficiency and breast-feeding. Am J Dis Child 137:601, 1983. 11. Komazawa M: TWO problems in neonatal hematology. J Obstet Gynecol Neonat Hematol (Japanese) 7:13, 1983. 12. Jiminez R, Navarette M, Jiminez E, et al: Vitamin Kdependent clotting factors in normal breast-fed infants. J PEDIATR 100:424, 1982. 13. Tay JSH, Tip WCL: Vitamin K-dependent clotting factors in normal breast-fed infant [letter]. J PEDIATR 101:795, I982.
Need for immunoprophylaxis in infants born to HB~Ag-positive carrier mothers who are HBeAg negative Myron J. Tong, M.D., Ph, D,, Frank R. Sinatra, M.D., Daniel W. Thomas, M.D., Prem V. Nair, M.D., Russell J. Merritt, M.D., Ph.D., and David W. Wang, M.D. Pasadena and L o s Angeles, California
From the Liver Center, Huntington Memorial Hospital; French Hospital; and the Gastroenterology Program, Children's Hospital of Los Angeles. Submitted for publication April 2, 1984; accepted June 8, 1984. Reprint requests: Myron or. Tong, Ph.D., M.D., Liver Center, Huntington Memorial Hospital, 100 Congress St., Pasadena, CA 91105.
ALTHOUGH UNCOMMON, both acute and fulminant hepatitis have been described in infants born to HBsAg, positive carrier mothers. ',2 The majority of these HBsAgpositive carrier mothers have been either negative for both HBeAg and anti-HBo or anti-HBo positive? -5 In contrast, infants born to HB~Ag-positive carrier mothers who are HBoAg positive frequently become chronic H B V carriers
946
Clinical and laboratory observations
Anti-HBc Anti-HB~ HBoAg HBIG HB,Ag HBV
Antibody Antibody Hepatitis Hepatitis Hepatitis Hepatitis
to HBoAg to HB~Ag B e antigen B immune globulin B surface antigen B virus
and seldom develop acute icteric hepatitis during the initial viral infection. 6 Efforts to prevent H B V infection in the newborn infant by immunoprophylaxis have mainly been directed toward those b o r n to HBsAg-positive, HBoAg-positive carrier mothers, because perinatal transmission of the hepatitis B virus most frequently occurs under these circumstances. 7, 8 However, because acute hepatitiS or fatal fulminant hepatitis may develop in infants born to HB~Ag-positive carrier mothers who are HBoAg negative, immunoprophylaxis for these infants is just as essential. We describe an infant who developed fatal fulminant hepatitis B, whose mother was an HB~Ag-positive, HBoAg-negative carrier. CASE REPORTS Patient 1. This infant boy, the 3.07 kg product of a full-term pregnancy, was born to a 30-year-old primigravida Chinese mother from Vietnam. The pregnancy was uncomp!ieated and labor and delivery unremarkable, and the infant was discharged to home at 3 days of age. At 289 months of age he was referred to Children's Hospital of Los Angeles for evaluation of jaundice. His mother had noted increasingly dark urine, light stools, and yellow skin during the 2 days prior to admission. There was no history of travel, drug use, blood transfusions, or exposure to anyone with hepatitis: The mother had not received screening for hepatitis B during pregnancy. On admission, physical examination revealed a well-developed, well-n0urished but jaundiced infant in no acute distress. His height, weight, and head circumference were appropriate for age (50th percentile). The lungs and heart were normal. The abdomen was soft, flat, and without ascites. The liver Was palpable 3 cm below the right costal margin and had a Smooth, firm edge; the spleen was not felt, and there was no edema. The neurologic examination revealed mild lethargy but no clonus, asterixis, or other signs of encephalopathy. Results of laboratory studies on admission were as follows: aspartate and alanine aminotransferase 3540 and 2920 U/L, respectively, serum bilirubin 9.6 mg/dl with a direct fraction of 4.4 mg/dl, prothrombin time 52 seconds with a control of 11.4 seconds, and blood ammonia 125 ~tg/dl (normal <120 ~tg/dl). Results of the HBsAg test were positive. Serologic studies for other causes of hepatitis (i.e., hepatitis A virus infection, mononucleosis, syphilis, toxoplasmosis, CYtomegalovirus, and rubella) yielded negative findings. The patient's mother was positive for HBsAg and negative for both HBCAg and anti-HB,. The patient's father was positive for anti-HB, and negative for HB~Ag. Both parents had normal liver function test results and no clinical evidence of liver diseasel Despite supportive measures, the patient developed progressive
The Journal of Pediatrics December 1984
liver dysfunction manifested by ascites, increasing jaundice, and a marked decrease in liver size. The course was complicated by the development of hyponatremia, gastrointestinal hemorrhage, gram-negatiye sepsis, and hepatic coma. He died in hepatic failure on day 86 of hospitalization at 589 months of age. Permission for autopsy was denied. Patient 2. This second infant boy was born 12 months later after a normal gestation and uncomplicated delivery. At this time the mother was still HBsAg positive and both the HB~Ag and anti-HBo were negative. Based on the current immunoprophylaxis program at our Liver Center at the time, 8 this infant was given 0.16 ml/kg body weight hepatitis B immune globulin within 24 hours of birth and again every 5 weeks for a total of six injections. Soon after, he was given the first dose of the hepatitis B virus vaccine, followed by two additional doses at 1 and 5 months later. At the last follow-up, when the child was 189years of age, he had normal liver function test results, was strongly anti-HBs positive, and was considered to be immune to infection by the hepatitis B virus. DISCUSSION Although perinatal transmission of H B V is uncommon in infants born to carrier mothers who are either HBcAg negative and anti-HBo negative, or anti-HBo positive, fulminant hepatitis B has been described in successive infants born to such chronic HBsAg-positive carrier mothers. Dupuy et al.' reported two fatal cases from one family, Fawaz et al. 2 described a brother and a Sister who contracted fatal fulminant hepatitis B, and Mollica et al. 9 reported four siblings who died of neonatal hepatitis, all of whom were HBsAg positive and born to an asymptomatic carrier mother. These studies were published prior to the availability of HBoAg testing. In the case presented here, the carrier mother was HBoAg and anti-HB~ negative at the time of birth of her first and second infants. Inasmuch as perinatal transmission of the H B V did occur, it is possible that the amount of HBcAg in the mother's circulation was too low to be detected by the currently available radioimmunoassay test (Abbott HB~, Chicago) or that HBcAg was complexed with anti-HBo and neither was detected. In such instances a more sensitive test for infectivity, (i.e., detection of H B V - D N A by a molecular hybridization test) may ge more informative, l~ Prophylaxis against perinatal transmission of HBV has primarily been directed toward infants born to chronic H B V carrier mothers who are HB~Ag positive. The use of H B I G alone 'was found to be 70% effective in preventing perinatal transmission of HBV. 7,8 The combination of H B I G along with the H B V vaccine promises to be even more effective. "~ ~2 Based on our previous experience with three infants 'born to HBsAg-positive, HBoAg-negative carrier mothers who developed acute icteric hepatitis B, 4 and also because of the reports that fulminant hepatitis B may occur in successive infants born to HB~Ag-positive carrier mothers, we thought it essential to protect our
Volume 105 Number 6
Clinical and laboratory observations
patient's second infant against H B V infection. After immunoprophylaxis, this infant's serum was strongly antiHBs at 11/2 years of age and the infant is immune to H B V infection. Therefore, we strongly suggest that treatment with H B I G and the H B V vaccine be offered to all infants born to chronic HB~Ag carrier mothers, regardless of the HBcAg status of the mothers. Based on current recommendations, 0.5 ml H B I G should be administered within 24 hours of birth and the hepatitis B vaccine given within 7 days of birth and again at 1 and 6 months of age.
REFERENCES 1. Dupuy JM, Frommel D, Alagille D: Severe viral hepatitis type B in infancy. Lancet 1:191, 1975. 2. Fawaz KA, Grady GF, Kaplan MM, et al: Repetitive maternal-fetal transmission of fatal hepatitis B. N Engl J Med 293:1357, 1975. 3. Shiraki K, Yoshihara N, Sakurai M, et al: Acute hepatitis B in infants born to carrier mothers with the antibody to hepatitis e antigen. J PED1ATR97:768, 1980. 4. Sinatra FR, Shah P, Weissman JY, et al: Perinatal transmitted acute icteric hepatitis B in infants born to hepatitis B surface antigen-positive and anti-hepatitis Be-positive carrier mothers. Pediatrics 70:557, 1982. 5. Delaplane D, Yogev R, Crussi F, et al: Fatal hepatitis B in early infancy: The importance of identifying HB~Ag-positive pregnant women and providing immunoprophylaxis to their newborns. Pediatrics 72:176, 1983.
947
6. Stevens CE, Beasley RP, Tsui J, et al: Vertical transmission of hepatitis B antigen in Taiwan. N Engl J Med 292:771, 1975. 7. Beasley RP, Hwang LY, Stevens CE, et al: Efficacy of hepatitis B immune globulin for prevention of perinatal transmission of the hepatitis B virus carrier state: Final report of a randomized double-blind, placebo-controlled trial. Hepatology 3:135, 1983. 8. Nair PV, Weissman JY, Tong M J, et al: The efficacy of hepatitis B immune globulin in prevention of perinatal transmission of the hepatitis B virus. Gastroenterology 87:293, 1984. 9. Mollica F, Musumeci S, Fischer A: Neonatal hepatitis in five children of a hepatitis B surface antigen carrier woman. J P~D~ATR90:949, 1977. 10. Lieberman HM, Labrecque, DR, Kew MC, et al: Detection of hepatitis B virus DNA directly in human serum by a simplified molecular hybridization test: Comparison to HBeAg/anti-HB~ status in HBsAg carriers. Hepatology 3:285, 1983. 11. Beasley RP, Hwang LY, Lee GCY, et al: Prevention of perinatally transmitted hepatitis B virus infections with hepatitis B immune globulin and hepatitis B vaccine. Lancet 2:i099, 1983. 12. Wong VC, Ip HMH, Reesink HW, et al: Prevention of the HB~Ag carrier state in newborn infants of mothers who are chronic carriers of HBsAg and HBoAg by administration of hepatitis B vaccine and hepatitis B immunoglobulin. Lancet 1:921, 1983.
Lymphoid interstitial pneumonia in juvenile rheumatoid arthritis Daniel Lovell, M.D., Carol Lindsley, M.D., and Claire Langston, M.D. H o u s t o n , Texas, and K a n s a s City, K a n s a s
ALTHOUGH THE PREVALENCE of pulmonary parenchyreal involvement in adult rheumatoid arthritis is thought to be approximately 5%, ~clinically evident pulmonary paren-
From the Departments of Pediatrics and Pathology, Texas Children's Hospital and Baylor College of Medicine, and the Department of Pediatrics, University of Kansas Medical Center. Submitted for publication March 9, 4984; accepted June 8, 1984. Reprint requests: Daniel Lovell, M.D., Cincinnati Children's Hospital Medical Center, Special Treatment Center for Childhood Arthritis, Pavilion Building, Rm. 1-29, Elland and Bethesda Ave., Cincinnati, OH 45229.
chymal disease in juvenile rheumatoid arthritis is extremely uncommon. ~ Approximately 30% of the patients with J R A but without pulmonary symptoms show abnormal pulmonary function test results. The most frequent abnorJRA LIP
Juvenile rheumatoid arthritis Lymphoid interstitial pneumonia
mality is in carbon monoxide diffusing capacity, suggesting an abnormality of the alvdolar capillary interface compatible with either diffuse vascular or parenchymal lung disease? We, report a child in whom pulmonary parenchymal involvement preceded the more common manifestations of J R A .
be an additive but not the main cause of the disease. Other undetected factor(s) might be involved. Because no further study was conducted, we do not have any evidence of impaired vitamin K absorption in these infants; such a possibility should be defined in the future. Komazawa a~ showed that orally administered vitamin K was less well absorbed in infants, with or without hepatic dysfunction, compared with healthy adults. The outcome in our infants was unfavorable (Table). Our observations support the concept that vitamin K prophylaxis is exclusively breast-fed infants is necessary.9.10 A recent study suggested that breast-fed babies who received vitamin K at birth did not have vitamin K deficiency at 1 month of age. 12 However, this study was criticized because the number of infants studied was small 13 and the report did not address the issue of vitamin K deficiency in breast-fed infants who do not receive prophylaxis. 9 In Japan, oral administration of vitamin K two or three times during the first month of life is being studied in an effort to prevent vitamin K deficiency, 1 but a final conclusion has not been reached.
REFERENCES 1. Nakayama K: Etiology of vitamin K deficiency in infants. Perinat Med (Japanese) 12:1029, 1982. 2. American Academy of Pediatrics: Vitamin K supplementation for infants receiving milk substitute infant formulas and for those with rate malabsorption. Pediatrics 137:601, 1983.
Clinical and laboratory observations
945
3. Malia RG, Preston FE, Mitchell VE: Evidence against vitamin K deficiency in normal neonates. Thromb Haemost 44:159, 1980. 4. Owren PA, Strandli OK: Normotest. Farmakoterapi 25:14, 1969. 5. Motohara K, Kuroki Y, Matsuda I, et al: Quantitative estimation of circulating PIVKA-II by enzyme-linked immunosorbent assay using monoclonal antibody. Acta Pediatr Jpn [Japanese] 88:1508, 1983. 6. Clarke HGM, Freemen TA: Quantitative immunoelectrophoresis method (Laurell electr0phoresis). Protides Biol Fluids 14:503, 1966. 7. Manes JD, Fluckiger HB, Schneider DL: Chromatographic analysis of vitamin K~: Application to infant formula products. J Agric Food Chem 20:1130, 1972. 8. Abe K, Hiroshima 'O, Ishibashi K, et al: Fluorometric determination of phylloguinone and menaquinone-4 in biological materials using high-performance liquid chromatography. J Jpn Pharmacol Assoc (Japanese) 99:192, 1979. 9. Lane PA, Hathaway WE, Githens JH, et al: Fetal intracranial hemorrhage in a normal infant secondary to vitamin K deficiency. Pediatrics 72:562, 1983. 10. O'Connor ME, Livingstone DS, Hannah J, Wilkins D: Vitamin K deficiency and breast-feeding. Am J Dis Child 137:601, 1983. 11. Komazawa M: TWO problems in neonatal hematology. J Obstet Gynecol Neonat Hematol (Japanese) 7:13, 1983. 12. Jiminez R, Navarette M, Jiminez E, et al: Vitamin Kdependent clotting factors in normal breast-fed infants. J PEDIATR 100:424, 1982. 13. Tay JSH, Tip WCL: Vitamin K-dependent clotting factors in normal breast-fed infant [letter]. J PEDIATR 101:795, I982.
Need for immunoprophylaxis in infants born to HB~Ag-positive carrier mothers who are HBeAg negative Myron J. Tong, M.D., Ph, D,, Frank R. Sinatra, M.D., Daniel W. Thomas, M.D., Prem V. Nair, M.D., Russell J. Merritt, M.D., Ph.D., and David W. Wang, M.D. Pasadena and L o s Angeles, California
From the Liver Center, Huntington Memorial Hospital; French Hospital; and the Gastroenterology Program, Children's Hospital of Los Angeles. Submitted for publication April 2, 1984; accepted June 8, 1984. Reprint requests: Myron or. Tong, Ph.D., M.D., Liver Center, Huntington Memorial Hospital, 100 Congress St., Pasadena, CA 91105.
ALTHOUGH UNCOMMON, both acute and fulminant hepatitis have been described in infants born to HBsAg, positive carrier mothers. ',2 The majority of these HBsAgpositive carrier mothers have been either negative for both HBeAg and anti-HBo or anti-HBo positive? -5 In contrast, infants born to HB~Ag-positive carrier mothers who are HBoAg positive frequently become chronic H B V carriers
946
Clinical and laboratory observations
Anti-HBc Anti-HB~ HBoAg HBIG HB,Ag HBV
Antibody Antibody Hepatitis Hepatitis Hepatitis Hepatitis
to HBoAg to HB~Ag B e antigen B immune globulin B surface antigen B virus
and seldom develop acute icteric hepatitis during the initial viral infection. 6 Efforts to prevent H B V infection in the newborn infant by immunoprophylaxis have mainly been directed toward those b o r n to HBsAg-positive, HBoAg-positive carrier mothers, because perinatal transmission of the hepatitis B virus most frequently occurs under these circumstances. 7, 8 However, because acute hepatitiS or fatal fulminant hepatitis may develop in infants born to HB~Ag-positive carrier mothers who are HBoAg negative, immunoprophylaxis for these infants is just as essential. We describe an infant who developed fatal fulminant hepatitis B, whose mother was an HB~Ag-positive, HBoAg-negative carrier. CASE REPORTS Patient 1. This infant boy, the 3.07 kg product of a full-term pregnancy, was born to a 30-year-old primigravida Chinese mother from Vietnam. The pregnancy was uncomp!ieated and labor and delivery unremarkable, and the infant was discharged to home at 3 days of age. At 289 months of age he was referred to Children's Hospital of Los Angeles for evaluation of jaundice. His mother had noted increasingly dark urine, light stools, and yellow skin during the 2 days prior to admission. There was no history of travel, drug use, blood transfusions, or exposure to anyone with hepatitis: The mother had not received screening for hepatitis B during pregnancy. On admission, physical examination revealed a well-developed, well-n0urished but jaundiced infant in no acute distress. His height, weight, and head circumference were appropriate for age (50th percentile). The lungs and heart were normal. The abdomen was soft, flat, and without ascites. The liver Was palpable 3 cm below the right costal margin and had a Smooth, firm edge; the spleen was not felt, and there was no edema. The neurologic examination revealed mild lethargy but no clonus, asterixis, or other signs of encephalopathy. Results of laboratory studies on admission were as follows: aspartate and alanine aminotransferase 3540 and 2920 U/L, respectively, serum bilirubin 9.6 mg/dl with a direct fraction of 4.4 mg/dl, prothrombin time 52 seconds with a control of 11.4 seconds, and blood ammonia 125 ~tg/dl (normal <120 ~tg/dl). Results of the HBsAg test were positive. Serologic studies for other causes of hepatitis (i.e., hepatitis A virus infection, mononucleosis, syphilis, toxoplasmosis, CYtomegalovirus, and rubella) yielded negative findings. The patient's mother was positive for HBsAg and negative for both HBCAg and anti-HB,. The patient's father was positive for anti-HB, and negative for HB~Ag. Both parents had normal liver function test results and no clinical evidence of liver diseasel Despite supportive measures, the patient developed progressive
The Journal of Pediatrics December 1984
liver dysfunction manifested by ascites, increasing jaundice, and a marked decrease in liver size. The course was complicated by the development of hyponatremia, gastrointestinal hemorrhage, gram-negatiye sepsis, and hepatic coma. He died in hepatic failure on day 86 of hospitalization at 589 months of age. Permission for autopsy was denied. Patient 2. This second infant boy was born 12 months later after a normal gestation and uncomplicated delivery. At this time the mother was still HBsAg positive and both the HB~Ag and anti-HBo were negative. Based on the current immunoprophylaxis program at our Liver Center at the time, 8 this infant was given 0.16 ml/kg body weight hepatitis B immune globulin within 24 hours of birth and again every 5 weeks for a total of six injections. Soon after, he was given the first dose of the hepatitis B virus vaccine, followed by two additional doses at 1 and 5 months later. At the last follow-up, when the child was 189years of age, he had normal liver function test results, was strongly anti-HBs positive, and was considered to be immune to infection by the hepatitis B virus. DISCUSSION Although perinatal transmission of H B V is uncommon in infants born to carrier mothers who are either HBcAg negative and anti-HBo negative, or anti-HBo positive, fulminant hepatitis B has been described in successive infants born to such chronic HBsAg-positive carrier mothers. Dupuy et al.' reported two fatal cases from one family, Fawaz et al. 2 described a brother and a Sister who contracted fatal fulminant hepatitis B, and Mollica et al. 9 reported four siblings who died of neonatal hepatitis, all of whom were HBsAg positive and born to an asymptomatic carrier mother. These studies were published prior to the availability of HBoAg testing. In the case presented here, the carrier mother was HBoAg and anti-HB~ negative at the time of birth of her first and second infants. Inasmuch as perinatal transmission of the H B V did occur, it is possible that the amount of HBcAg in the mother's circulation was too low to be detected by the currently available radioimmunoassay test (Abbott HB~, Chicago) or that HBcAg was complexed with anti-HBo and neither was detected. In such instances a more sensitive test for infectivity, (i.e., detection of H B V - D N A by a molecular hybridization test) may ge more informative, l~ Prophylaxis against perinatal transmission of HBV has primarily been directed toward infants born to chronic H B V carrier mothers who are HB~Ag positive. The use of H B I G alone 'was found to be 70% effective in preventing perinatal transmission of HBV. 7,8 The combination of H B I G along with the H B V vaccine promises to be even more effective. "~ ~2 Based on our previous experience with three infants 'born to HBsAg-positive, HBoAg-negative carrier mothers who developed acute icteric hepatitis B, 4 and also because of the reports that fulminant hepatitis B may occur in successive infants born to HB~Ag-positive carrier mothers, we thought it essential to protect our
Volume 105 Number 6
Clinical and laboratory observations
patient's second infant against H B V infection. After immunoprophylaxis, this infant's serum was strongly antiHBs at 11/2 years of age and the infant is immune to H B V infection. Therefore, we strongly suggest that treatment with H B I G and the H B V vaccine be offered to all infants born to chronic HB~Ag carrier mothers, regardless of the HBcAg status of the mothers. Based on current recommendations, 0.5 ml H B I G should be administered within 24 hours of birth and the hepatitis B vaccine given within 7 days of birth and again at 1 and 6 months of age.
REFERENCES 1. Dupuy JM, Frommel D, Alagille D: Severe viral hepatitis type B in infancy. Lancet 1:191, 1975. 2. Fawaz KA, Grady GF, Kaplan MM, et al: Repetitive maternal-fetal transmission of fatal hepatitis B. N Engl J Med 293:1357, 1975. 3. Shiraki K, Yoshihara N, Sakurai M, et al: Acute hepatitis B in infants born to carrier mothers with the antibody to hepatitis e antigen. J PED1ATR97:768, 1980. 4. Sinatra FR, Shah P, Weissman JY, et al: Perinatal transmitted acute icteric hepatitis B in infants born to hepatitis B surface antigen-positive and anti-hepatitis Be-positive carrier mothers. Pediatrics 70:557, 1982. 5. Delaplane D, Yogev R, Crussi F, et al: Fatal hepatitis B in early infancy: The importance of identifying HB~Ag-positive pregnant women and providing immunoprophylaxis to their newborns. Pediatrics 72:176, 1983.
947
6. Stevens CE, Beasley RP, Tsui J, et al: Vertical transmission of hepatitis B antigen in Taiwan. N Engl J Med 292:771, 1975. 7. Beasley RP, Hwang LY, Stevens CE, et al: Efficacy of hepatitis B immune globulin for prevention of perinatal transmission of the hepatitis B virus carrier state: Final report of a randomized double-blind, placebo-controlled trial. Hepatology 3:135, 1983. 8. Nair PV, Weissman JY, Tong M J, et al: The efficacy of hepatitis B immune globulin in prevention of perinatal transmission of the hepatitis B virus. Gastroenterology 87:293, 1984. 9. Mollica F, Musumeci S, Fischer A: Neonatal hepatitis in five children of a hepatitis B surface antigen carrier woman. J P~D~ATR90:949, 1977. 10. Lieberman HM, Labrecque, DR, Kew MC, et al: Detection of hepatitis B virus DNA directly in human serum by a simplified molecular hybridization test: Comparison to HBeAg/anti-HB~ status in HBsAg carriers. Hepatology 3:285, 1983. 11. Beasley RP, Hwang LY, Lee GCY, et al: Prevention of perinatally transmitted hepatitis B virus infections with hepatitis B immune globulin and hepatitis B vaccine. Lancet 2:i099, 1983. 12. Wong VC, Ip HMH, Reesink HW, et al: Prevention of the HB~Ag carrier state in newborn infants of mothers who are chronic carriers of HBsAg and HBoAg by administration of hepatitis B vaccine and hepatitis B immunoglobulin. Lancet 1:921, 1983.
Lymphoid interstitial pneumonia in juvenile rheumatoid arthritis Daniel Lovell, M.D., Carol Lindsley, M.D., and Claire Langston, M.D. H o u s t o n , Texas, and K a n s a s City, K a n s a s
ALTHOUGH THE PREVALENCE of pulmonary parenchyreal involvement in adult rheumatoid arthritis is thought to be approximately 5%, ~clinically evident pulmonary paren-
From the Departments of Pediatrics and Pathology, Texas Children's Hospital and Baylor College of Medicine, and the Department of Pediatrics, University of Kansas Medical Center. Submitted for publication March 9, 4984; accepted June 8, 1984. Reprint requests: Daniel Lovell, M.D., Cincinnati Children's Hospital Medical Center, Special Treatment Center for Childhood Arthritis, Pavilion Building, Rm. 1-29, Elland and Bethesda Ave., Cincinnati, OH 45229.
chymal disease in juvenile rheumatoid arthritis is extremely uncommon. ~ Approximately 30% of the patients with J R A but without pulmonary symptoms show abnormal pulmonary function test results. The most frequent abnorJRA LIP
Juvenile rheumatoid arthritis Lymphoid interstitial pneumonia
mality is in carbon monoxide diffusing capacity, suggesting an abnormality of the alvdolar capillary interface compatible with either diffuse vascular or parenchymal lung disease? We, report a child in whom pulmonary parenchymal involvement preceded the more common manifestations of J R A .