(129:1402-1405, 1975), may I note that there has been described1 a simple physical sign that might expedite the diagnosis in cases of complete unilateral diaphragmatic paralysis, the usual situation encountered, before intermittent positive pressure breathing is instituted. It consists of a respiratory shift visualized on the epigastric abdominal wall, which reflects the paradoxical movement of the diaphragm within. This is seen in infants and young children but not in adults, and may not be present in older children. J. S. LIGHT, MD 465 N Roxbury Dr Beverly Hills, CA 90210 1. Light JS: Respiratory shift in epigastric abdominal wall: Physical sign seen with complete unilateral paralysis of the diaphragm in infants and children. J Pediatr 24:627-634, 1944.
Mother-Infant Transmission of Hepatitis B Antigen
Sir.\p=m-\Anderson et al, in a recent article in the Journal (129:1389,1975), stated that the high hepatitis B infection rates in their study were most probably related to (1) maternal-fetal transfusion at the time of delivery, (2) fetal ingestion of maternal blood during the passage through the birth canal, or (3) fetal exposure to maternal blood during delivery through dermatological lesions. Stevens et al,1 in a very similar article, reported a high transmission rate of hepatitis B infection to infants from mothers who were asymptomatic carriers. This article prompted Smith and Hindman,2 in a letter to the editor, to question whether breast feeding was a causative factor in this transmission. Beasley3 replied that the frequency of antigenemia was similar among breast- and formula\x=req-\ fed infants. I have the following questions concerning the study of Anderson and co-workers: 1. What was the incidence of antigenemia in infants who were breast\x=req-\ and bottle-fed? 2. Was the onset of antigenemia different in these two groups of infants? 3. Was the antigenemia persistent, transient, or intermittent more fre¬ quently in breast- or formula-fed infants? 4. Was the occurrence of liver
enzyme abnormalities
in
one
more
frequent
of the groups? ARTHUR R. EULER, MD Department of Pediatrics University of California School of Medicine Los Angeles, CA 90024
1. Stevens CE, Beasley RP, Tsuei JR, et al: Vertical transmission of hepatitis B antigen in Taiwan. N Engl J Med 292:771-774, 1975. 2. Smith JL, Hindman SH: Transmission of hepatitis by breast feeding. N Engl J Med 292:1354, 1975. 3. Beasley RP: Transmission of hepatitis by breast feeding. N Engl J Med 292:1354, 1975.
Reply.\p=m-\Ourarticle in the Journal, preliminary report of a study of 43
In a
infants in Taiwan, as well as an expanded study of an additional 158 infants,1 presented evidence that the hepatitis B virus was commonly transmitted from chronic hepatitis B antigen (HBsAg) carrier mothers to their offspring. Among the latter group of infants,2 we found no relationship between breast feeding and the development of antigenemia in the babies. In further response to Dr Euler's questions, there was no relationship in antigen-positive babies between breast feeding and either (1) age when first found to be HBsAg positive (mean, four months in both breast\x=req-\ and bottle-fed babies) or (2) persistence of HBsAg (antigen persisted in 29 of 33 breast-fed infants, or 88%, and in 15 of 18 bottle-fed infants, or 83%). Because the blood samples taken from infants were small, we were unable to test all of the samples for serum glutamic oxaloacetic transaminase (SGOT) values. Keeping this limitation in mind, an elevated SGOT level (> 55 Karmen units) was found more often among HB,Ag-positive babies (nine of 27 tested, or 33.3%) than among HBsAg-negative babies (only three of 38 tested, or 7.9%), and elevation of SGOT level was unrelated to breast or bottle feeding. KARL E. ANDERSON, MD Rockefeller University Hospital 1230 York Ave New York, NY 10021 CLADD E. STEVENS, MD R. PALMER BEASLEY, MD Department of Epidemiology and International Health School of Public Health and Community Medicine University of Washington Seattle, WA 98105 1. Stevens CE, Beasley RP, Tsuei JR, et al: Vertical transmission of hepatitis B antigen in Taiwan. N Engl J Med 292:771-774, 1975.
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 05/23/2015
2. Beasley RP, Stevens CE, Shiao I-S, et al: Evidence against breast feeding as a mechanism for vertical transmission of hepatitis B. Lancet
2:740-741, 1975.
Dental Anomalies in the
Morquio
Syndrome Sir.\p=m-\Whilewe generally agree with the comments in Dr Gardner's article that appeared in the December issue of the Journal (129:1445-1448, 1975), we feel he has understated the case for considering dental anomalies to be a constant feature of the Morquio syndrome. We would like to emphasize that dental anomalies are consistently found in the Morquio syndrome, and are a necessary component of the clinical diagnosis. In March 1975, an article by us was published that described the oral findings in 12 unrelated patients with the Morquio syndrome.1 These 12 patients
diagnosed on biochemical, roentgenographic, and clinical grounds. Dental examinations were performed were
after the diagnoses had been established. Therefore, no ascertainment bias influenced the results of our study. Each of the 12 patients had dental anomalies similar to those described in Dr Gardner's article. In April 1975, the oral findings of two siblings with Morquio syndrome were described in another article.2 The described anomalies were the same as those in Dr Gardner's report and in ours.
The 15 patients described in the articles cited above, and 25 others from the literature represent a total of 40 cases in which the reported dental anomalies are present. While it is true, as Dr Gardner states, that susceptibility to caries in the Morquio syndrome remains to be
adequately documented,
our
experi¬
suggests that the caries rate is no higher than average and may be lower. Finally, it is not difficult to explain on a developmental basis why the Morquio syndrome is the only type of mucopolysaccharidosis in which dental anomalies have been found. It is the only member of this group of disor¬ ders in which keratan sulfate is excreted in excessive amounts, and the only one for which chondroitin sulfate sulfatase deficiency has been suggested as the primary defect. Its clinical manifestations should differ from those with other primary de¬ fects. Even though we do not know the ence
Mother-Infant Transmission of Hepatitis B Antigen
Sir.\p=m-\Anderson et al, in a recent article in the Journal (129:1389,1975), stated that the high hepatitis B infection rates in their study were most probably related to (1) maternal-fetal transfusion at the time of delivery, (2) fetal ingestion of maternal blood during the passage through the birth canal, or (3) fetal exposure to maternal blood during delivery through dermatological lesions. Stevens et al,1 in a very similar article, reported a high transmission rate of hepatitis B infection to infants from mothers who were asymptomatic carriers. This article prompted Smith and Hindman,2 in a letter to the editor, to question whether breast feeding was a causative factor in this transmission. Beasley3 replied that the frequency of antigenemia was similar among breast- and formula\x=req-\ fed infants. I have the following questions concerning the study of Anderson and co-workers: 1. What was the incidence of antigenemia in infants who were breast\x=req-\ and bottle-fed? 2. Was the onset of antigenemia different in these two groups of infants? 3. Was the antigenemia persistent, transient, or intermittent more fre¬ quently in breast- or formula-fed infants? 4. Was the occurrence of liver
enzyme abnormalities
in
one
more
frequent
of the groups? ARTHUR R. EULER, MD Department of Pediatrics University of California School of Medicine Los Angeles, CA 90024
1. Stevens CE, Beasley RP, Tsuei JR, et al: Vertical transmission of hepatitis B antigen in Taiwan. N Engl J Med 292:771-774, 1975. 2. Smith JL, Hindman SH: Transmission of hepatitis by breast feeding. N Engl J Med 292:1354, 1975. 3. Beasley RP: Transmission of hepatitis by breast feeding. N Engl J Med 292:1354, 1975.
Reply.\p=m-\Ourarticle in the Journal, preliminary report of a study of 43
In a
infants in Taiwan, as well as an expanded study of an additional 158 infants,1 presented evidence that the hepatitis B virus was commonly transmitted from chronic hepatitis B antigen (HBsAg) carrier mothers to their offspring. Among the latter group of infants,2 we found no relationship between breast feeding and the development of antigenemia in the babies. In further response to Dr Euler's questions, there was no relationship in antigen-positive babies between breast feeding and either (1) age when first found to be HBsAg positive (mean, four months in both breast\x=req-\ and bottle-fed babies) or (2) persistence of HBsAg (antigen persisted in 29 of 33 breast-fed infants, or 88%, and in 15 of 18 bottle-fed infants, or 83%). Because the blood samples taken from infants were small, we were unable to test all of the samples for serum glutamic oxaloacetic transaminase (SGOT) values. Keeping this limitation in mind, an elevated SGOT level (> 55 Karmen units) was found more often among HB,Ag-positive babies (nine of 27 tested, or 33.3%) than among HBsAg-negative babies (only three of 38 tested, or 7.9%), and elevation of SGOT level was unrelated to breast or bottle feeding. KARL E. ANDERSON, MD Rockefeller University Hospital 1230 York Ave New York, NY 10021 CLADD E. STEVENS, MD R. PALMER BEASLEY, MD Department of Epidemiology and International Health School of Public Health and Community Medicine University of Washington Seattle, WA 98105 1. Stevens CE, Beasley RP, Tsuei JR, et al: Vertical transmission of hepatitis B antigen in Taiwan. N Engl J Med 292:771-774, 1975.
Downloaded From: http://archpedi.jamanetwork.com/ by a New York University User on 05/23/2015
2. Beasley RP, Stevens CE, Shiao I-S, et al: Evidence against breast feeding as a mechanism for vertical transmission of hepatitis B. Lancet
2:740-741, 1975.
Dental Anomalies in the
Morquio
Syndrome Sir.\p=m-\Whilewe generally agree with the comments in Dr Gardner's article that appeared in the December issue of the Journal (129:1445-1448, 1975), we feel he has understated the case for considering dental anomalies to be a constant feature of the Morquio syndrome. We would like to emphasize that dental anomalies are consistently found in the Morquio syndrome, and are a necessary component of the clinical diagnosis. In March 1975, an article by us was published that described the oral findings in 12 unrelated patients with the Morquio syndrome.1 These 12 patients
diagnosed on biochemical, roentgenographic, and clinical grounds. Dental examinations were performed were
after the diagnoses had been established. Therefore, no ascertainment bias influenced the results of our study. Each of the 12 patients had dental anomalies similar to those described in Dr Gardner's article. In April 1975, the oral findings of two siblings with Morquio syndrome were described in another article.2 The described anomalies were the same as those in Dr Gardner's report and in ours.
The 15 patients described in the articles cited above, and 25 others from the literature represent a total of 40 cases in which the reported dental anomalies are present. While it is true, as Dr Gardner states, that susceptibility to caries in the Morquio syndrome remains to be
adequately documented,
our
experi¬
suggests that the caries rate is no higher than average and may be lower. Finally, it is not difficult to explain on a developmental basis why the Morquio syndrome is the only type of mucopolysaccharidosis in which dental anomalies have been found. It is the only member of this group of disor¬ ders in which keratan sulfate is excreted in excessive amounts, and the only one for which chondroitin sulfate sulfatase deficiency has been suggested as the primary defect. Its clinical manifestations should differ from those with other primary de¬ fects. Even though we do not know the ence
