205 immunisation was not more readily obtained, despite greater interval (six months) between the two injections. Centre Edouard Rist,
a
S. DELONS D. KLEINKNECHT A. M. COUROUCE
Hôpital de Montreuil, 93105 Montreuil, and Centre National de Transfusion Sanguine, Pans, France.
LABORATORY-ACQUIRED HEPATITIS B SiR,—Dr Seder and his colleagues have recorded their significant and objective confirmation that splashes and aerosols from handling blood-samples can contaminate the working area with HBsAg and therefore potentially with hepatitis-B virus (Dec. 27, p. 1316). It is less clear how they relate this to "non-parenteral" exposure of workers to infection since there are many possibilities of inapparent parenteral infection as well as of enteral infection in these circumstances. My objections to the confusing and ambiguous neologism "non-parenteral" are on record.’ In discussions at the 15th European Symposium on Poliomyelitis and Other Virus Diseases, in Vienna in September, 1975, it was agreed that this term was unsatisfactory and should not be used. Can
a
Departments of Hæmatology, Obstetrics, and Gynæcology,
University Hospital, Wilhelmina Gasthuis, Amsterdam, The Netherlands.
contrary view be defended?
NORMAN R. GRIST
COAGULATION DISORDERS AFTER HYPERTONIC-SALINE ABORTION
StR,—We were interested in the article by Dr MacKenzie and others (Nov. 29, p. 1066) describing a significant rise in fibrin degradation products (F.D.P.) and factor-vm clotting activity during second-trimester abortion by intra-amniotic prostaglandin E2 alone or in combination with hypertonic glucose or urea.
As we described before,2 thrombin formation may be detected (by the generation of fibrinopeptide A and a positive ETHANOL-GELATION TEST BEFORE AND AFTER INSTILLATION OF
HYPERTONIC SALINE
*loading dose 20 mg followed by 6 mg/h continuously. t Loading dose 20 mg followed by 12 mg/h continuously.
ethanol-gelation test [E.G.T.]) as early as 2 hours after instillation of hypertonic saline. These findings precede the formation Of F.D.P. We also found a consistent decrease in factor-vm clotting activity, with a maximum 6-8 hours after the injection. We believe that the major coagulation events may be detected within 6-8 hours of intra-amniotic instillation of hypertonic solutions, and that these findings are missed in studies starting later. To prevent complications of hypertonic-saline-induced abortion due to disseminated intravascular coagulation, we decided to heparinise our patients. Heparin administration started imGrist, N. R. Lancet, 1974, i, 935. Royen, E. A. van, Treffers, P. E., Cate, J. 13, 166.
TEN CATE ERIC A. VAN ROYEN PIETER E. TREFFERS
JAN W.
DENTAL CARIES AND SUGAR INTAKE
SIR,-Dr McKendrick and others’
University Department of Infectious Diseases, Ruchill Hospital, Glasgow G20 9NB.
1 2
the intervention and was continued for 6 hours. The results were recorded by the E.G.T. (see table). Surprisingly high concentrations of heparin were needed to obtain a negative E.G.T. Concentrations of 0.3 to 0.9 u/ml plasma were measured when heparin was administered in a dose of 12 mg/h. 2 positive E.G.T.s were recorded 4 hours after hypertonic-saline instillation with heparin concentrations of 0-3and 035u respectively. 5 patients were also studied after 24 hr, and at that time no signs of intravascular coagulation could be demonstrated. Platelet function (bleeding-time, platelet-count, platelet-retention in a glass-bead column, platelet aggregation) were also studied in all patients in order to exclude haemorrhage. So far no bleeding problems have been encountered.
mediately before
aver that in our letter the that is not critical factor in dental maintaining sugar caries2 we gave only evidence favourable to our view. This is incorrect. A letter allows of few references, but virtually all points raised by these workers have been discussed elsewhere. Certainly some, but not all, studies on animals indicate sugar to be more cariogenic than other carbohydrate foods. Again, many, but not all, short-term in-vivo and in-vitro observations on oral biochemistry and microbiology in man have yielded the same conclusion. Assuredly too, the Vipeholm and Turku sugar studies have demonstrated that under acute and particular experimental conditions sugar is strongly cariogenic, and that total replacement of sugar inhibits dental decay. Additionally, the study on dentists’ young children at Bristol showed that restriction of soft foods, and regular dental care, led to better teeth. This investigation, however, undertaken 15 years ago, requires confirmation by others, with the provision of more dietary information and D.M.F. (decayed/missing/filled) scores on dentists’ much older children. In gross contrast, however, as indicated in our letter2 are the numerous observations on groups of children under everyday circumstances, with and without access to school tuck-shops, with and without snacks between meals, with and without soft foods at bedtime, &c., which have revealed D.M.F. scores differing by only about 1-2 units. Our own studies on four ethnic groups of adolescents revealed no significant differences in D.M.F. scores between segments accustomed to high and low consumptions of sugar. Added to this information are the results of epidemiological studies such as that made in 1946 at Lewis where children had excellent teeth despite a high intake of sugar. Not least to be considered are the disappointing results of the dental campaigns in which enormous curtailment of sugar and sugar-containing foods has been urged. Inexplicably, scarcely any of the foregoing items of information are mentioned or critically examined in recent reviews on diet and dental caries.4 J. A. Ryle stressed that the study of the unfit should be matched in endeavour by the study of the fit.’ Would it not be highly profitable to divert part of the tremendous effort now being expended on experimental caries studies in order to try to learn more of the dietary and other characteristics of moieties of adult populations who still possess good teeth? This task should be possible even though in Scotland half the population 1. 2. 3.
McKendrick, A. J. W., Roberts, G. S., Duguit, R. Lancet, 1975, ii, 1086. Walker, A. R. P., Cleaton-Jones, P. E. ibid. 1975, ii, 765. Retief, D. P., Cleaton-Jones, P. E., Walker, A. R. P. Br. dent. J. 1975, 138,
4. 5.
Hartles, R. L., Leach, S. A. Br. med. Bull. 1975, 31, 137. Ryle, J. A. Br. med. J. 1943, ii, 633.
463. W.
ten
Scand.
J.
Hœmat.
1974,
206 16 years is edentulous.6 Were this and other information secured it should be possible to arrive at the true risk factors for dental caries, as has been done, for example, in respect of coronary heart-disease. The overwhelming obsession that sugar is the sole or principal cause of dental caries is seriously obstructing caries research. In many ways the situation regarding sugar intake and caries is analogous to that of sugar intake and diabetes. The huge majority of diabetic clinics in the United Kingdom urge total or partial exclusion of sugar for the control of the disease.’ Yet authoritative opinion maintains that the most suitable diet remains to be elucidated.s9 over
South African Medical Research Council, Human Biochemistry Research Unit, South African Institute for Medical Research, Johannesburg, South Africa.
A. R. P. WALKER
Dental Research Unit of the University of the Witwatersrand and South African Medical Research Council,
P. E.
Johannesburg.
CLEATON-JONES
RABIES
SIR,-From experience of clinical rabies in Nigeria I would confirm the points made by Wilson et ail. 10 that the early symptoms can easily be mistaken for-hysteria. The overbreathing is frequently similar to that seen in a child who has been crying, with a two-stage ("sniff-sniff") inspiration, and a slow full expiration. When that type of "sobbing respiration" is seen, suspect rabies--even if the patient and relatives initially deny any bite by a rabid dog. They might not connect a bite two or three months before with the present illness, or, more likely, they are afraid to admit it to themselves or to the doctor because they are aware of the fatal consequences. I am not familiar with the "fan-test", but will certainly try it on the next case I see. Rural Health Centre,
Igbo-Ora,
c/o Ibarapa Project Office, University College Hospital, Ibadan, Nigeria
C. ANDREW PEARSON
AMNIOCENTESIS FOR PRENATAL DIAGNOSIS
SIR,-Dr Laxova and others (Nov. 15, p. 964) reported the results of prenatal diagnosis in 174 patients. We think several points deserve comment. We do not agree that a family history of Down syndrome is not an adequate reason for amniocentesis. One must first obtain a detailed pedigree with the age of the mother at the time of the birth of each affected child. Cytogenetic studies on all possible family members should be done to rule out any translocations and/or mosaicism involving chromosome 21. If trisomy 21 is diagnosed in a child even though normal chromosome constitutions have been demonstrated in its relatives, one cannot be certain that their chances of having a trisomic child is not greater than that of other women of the same age, Gonadal mosaicism and/or a gene predisposing to non-disjunction have been suggested as the cause of familial cases of Down syndrome.’ We feel that the patient should be informed about the possibility of increased risk of her having a trisomic child and the small risk of fetal mortality from amniocentesis. The decision as to whether amniocentesis is to be done in a future pregnancy should be made by the patient. With regard to young mothers with a previous child with Down syndrome, the risk of recurrence is about 1%, which is not much lower than that in women aged 35-39. Dr Laxova and her colleagues say that because 3 patients aborted after two amniocenteses, they decided not to repeat amniocentesis in other patients when the first amniocentesis was unsuccessful. Are they certain that the abortions were directly caused by amniocentesis? In one case, the abortion may have been caused by a large subperitoneal fibroid on the left side of the uterus. Unfortunately, no mention was made of the post-mortem examination of these 3 abortuses. In any event, the authors must be aware that a recent study by the National Institutes of Health of the U.S.A. of about 1000 pregnancies with amniocentesis and about 1000 age-matched control pregnancies without amniocentesis demonstrated that the overall fetal loss with amniocentesis is not significantly different from that without amniocentesis.2 With the assistance of sonography, our obstetricians have never hesitated to do a second or third tap. Our and others’ experience has not evidenced increased fetal mortality in cases where repeated taps were done. The authors also say that the average I.Q. of 9 XXX children was
THALASSÆMIA TRAIT, ABNORMAL HÆMOGLOBINS, AND RAISED FETAL HÆMOGLOBIN IN KARACHI
SIR,-Because of the absence of screening facilities little is known about the prevalence of thalassaemia trait and abnormal haemoglobins in Pakistan. We have investigated 1224 adults in Karachi (1066 males and 158 females) who were hospital employees, professional blood-donors, or naval recruits. 11 (0.9%) carried an abnormal haemoglobin (8 HbD, 2 HbC, and 1 for HbS). Thalassaemia trait was detected in 18 (1.4%). 28.8% of the subjects had a raised fetal Hb (above 1%). 75% of the raised values were between 1.1% and 2%, and 19% were between 2.1% and 3%; only 2 values of more than 5% were recorded. Further analysis revealed raised HbF in 21.4% of adults whose Hb was above 10 g/dl. This finding cannot be explained on the basis of acquired pathological conditions associated with activation of HbF synthesis, and would appear to be a racial characteristic. Similar studies conducted in other parts of Pakistan are needed to confirm these observations. Pakistan Medical Research Council, Jinnah Postgraduate Medical Centre, Karachi, Pakistan.
JAVID A. HASHMI FARIDA FARZANA
6. Todd, J. E., Whitworth, A. Adult Dental Health in Scotland. H. M. Stationery Office, 1974. 7. Truswell, A. S., Thomas, B. J. Proc. Nutr. Soc. 1975, 34, 22A. 8. Bierman, E. L., Albrink, M. J., Arky, R. A., Connor, W. E., Dayton, S., Spritz, N., Steinburg, D. Diabetes, 1971, 20, 633. 9. Lancet, 1974, i, 398. 10. Wilson, J. M., Hettiarachchi, J., Wijesuriya, L. M. ibid. 1975, ii, 1139.
80, and none was above average. They note, in addition, that "most had
problems and some physical abnormalities". According to Tennes et al.,3 in a comparable group of XXX children the majority were in the normal range of intelligence, with i.Q.s between 80 and 120. 6 XXX children had a Wechsler score 16 points lower than that of their normal sibs. This by no means indicates that the I.Q. of XXX females is under 80. Only 2 of 9 XXX children required psychiatric help. Twothirds were considered normal and adequately adjusted. Barr et aI,1 reviewed 155females with XXX chromosomal constitutions and found two-thirds were phenotypically normal with no distinctive physical traits.
behaviour
With regard to culture failure, we do not understand why amniotic fluid was taken from a patient at 33 weeks of gestation. Even if prenatal diagnosis had been made in this case, the baby would have been near term by the time the results were available. This work was supported by grants (GM-19443 and HD-02! from the U.S. Public Health Service and the National Foundation (r.-1)))
of Pediatrics, Division of Medical Genetics, Mount Sinai School of Medicine, New York, New York, 10029, U.S.A.
Department
LILLIAN Y. F. Hsu FELICE YAHR LYNN GODMILOW
KURT HIRSCHHORN
1. Mikkelson, M. Ann. hum. Genet. 1966, 30, 125. 2. Results of Amniocentesis Registry Project of the National Institute of child Health and Human Development, presented at the American Academy of
Pediatrics meeting, Washington, D.C., Oct. 20, 1975. 3. Tennes, K., Puck, M., Bryant, K., Frankenburg, W., Robinson, A. Am.J. hum. Genet. 1975, 27, 71. 4. Barr, M. L., Sergovich, F. R., Carr, D. H., Shaver, E. L. Can. med. Ass. J. 1969, 101, 247.
a
S. DELONS D. KLEINKNECHT A. M. COUROUCE
Hôpital de Montreuil, 93105 Montreuil, and Centre National de Transfusion Sanguine, Pans, France.
LABORATORY-ACQUIRED HEPATITIS B SiR,—Dr Seder and his colleagues have recorded their significant and objective confirmation that splashes and aerosols from handling blood-samples can contaminate the working area with HBsAg and therefore potentially with hepatitis-B virus (Dec. 27, p. 1316). It is less clear how they relate this to "non-parenteral" exposure of workers to infection since there are many possibilities of inapparent parenteral infection as well as of enteral infection in these circumstances. My objections to the confusing and ambiguous neologism "non-parenteral" are on record.’ In discussions at the 15th European Symposium on Poliomyelitis and Other Virus Diseases, in Vienna in September, 1975, it was agreed that this term was unsatisfactory and should not be used. Can
a
Departments of Hæmatology, Obstetrics, and Gynæcology,
University Hospital, Wilhelmina Gasthuis, Amsterdam, The Netherlands.
contrary view be defended?
NORMAN R. GRIST
COAGULATION DISORDERS AFTER HYPERTONIC-SALINE ABORTION
StR,—We were interested in the article by Dr MacKenzie and others (Nov. 29, p. 1066) describing a significant rise in fibrin degradation products (F.D.P.) and factor-vm clotting activity during second-trimester abortion by intra-amniotic prostaglandin E2 alone or in combination with hypertonic glucose or urea.
As we described before,2 thrombin formation may be detected (by the generation of fibrinopeptide A and a positive ETHANOL-GELATION TEST BEFORE AND AFTER INSTILLATION OF
HYPERTONIC SALINE
*loading dose 20 mg followed by 6 mg/h continuously. t Loading dose 20 mg followed by 12 mg/h continuously.
ethanol-gelation test [E.G.T.]) as early as 2 hours after instillation of hypertonic saline. These findings precede the formation Of F.D.P. We also found a consistent decrease in factor-vm clotting activity, with a maximum 6-8 hours after the injection. We believe that the major coagulation events may be detected within 6-8 hours of intra-amniotic instillation of hypertonic solutions, and that these findings are missed in studies starting later. To prevent complications of hypertonic-saline-induced abortion due to disseminated intravascular coagulation, we decided to heparinise our patients. Heparin administration started imGrist, N. R. Lancet, 1974, i, 935. Royen, E. A. van, Treffers, P. E., Cate, J. 13, 166.
TEN CATE ERIC A. VAN ROYEN PIETER E. TREFFERS
JAN W.
DENTAL CARIES AND SUGAR INTAKE
SIR,-Dr McKendrick and others’
University Department of Infectious Diseases, Ruchill Hospital, Glasgow G20 9NB.
1 2
the intervention and was continued for 6 hours. The results were recorded by the E.G.T. (see table). Surprisingly high concentrations of heparin were needed to obtain a negative E.G.T. Concentrations of 0.3 to 0.9 u/ml plasma were measured when heparin was administered in a dose of 12 mg/h. 2 positive E.G.T.s were recorded 4 hours after hypertonic-saline instillation with heparin concentrations of 0-3and 035u respectively. 5 patients were also studied after 24 hr, and at that time no signs of intravascular coagulation could be demonstrated. Platelet function (bleeding-time, platelet-count, platelet-retention in a glass-bead column, platelet aggregation) were also studied in all patients in order to exclude haemorrhage. So far no bleeding problems have been encountered.
mediately before
aver that in our letter the that is not critical factor in dental maintaining sugar caries2 we gave only evidence favourable to our view. This is incorrect. A letter allows of few references, but virtually all points raised by these workers have been discussed elsewhere. Certainly some, but not all, studies on animals indicate sugar to be more cariogenic than other carbohydrate foods. Again, many, but not all, short-term in-vivo and in-vitro observations on oral biochemistry and microbiology in man have yielded the same conclusion. Assuredly too, the Vipeholm and Turku sugar studies have demonstrated that under acute and particular experimental conditions sugar is strongly cariogenic, and that total replacement of sugar inhibits dental decay. Additionally, the study on dentists’ young children at Bristol showed that restriction of soft foods, and regular dental care, led to better teeth. This investigation, however, undertaken 15 years ago, requires confirmation by others, with the provision of more dietary information and D.M.F. (decayed/missing/filled) scores on dentists’ much older children. In gross contrast, however, as indicated in our letter2 are the numerous observations on groups of children under everyday circumstances, with and without access to school tuck-shops, with and without snacks between meals, with and without soft foods at bedtime, &c., which have revealed D.M.F. scores differing by only about 1-2 units. Our own studies on four ethnic groups of adolescents revealed no significant differences in D.M.F. scores between segments accustomed to high and low consumptions of sugar. Added to this information are the results of epidemiological studies such as that made in 1946 at Lewis where children had excellent teeth despite a high intake of sugar. Not least to be considered are the disappointing results of the dental campaigns in which enormous curtailment of sugar and sugar-containing foods has been urged. Inexplicably, scarcely any of the foregoing items of information are mentioned or critically examined in recent reviews on diet and dental caries.4 J. A. Ryle stressed that the study of the unfit should be matched in endeavour by the study of the fit.’ Would it not be highly profitable to divert part of the tremendous effort now being expended on experimental caries studies in order to try to learn more of the dietary and other characteristics of moieties of adult populations who still possess good teeth? This task should be possible even though in Scotland half the population 1. 2. 3.
McKendrick, A. J. W., Roberts, G. S., Duguit, R. Lancet, 1975, ii, 1086. Walker, A. R. P., Cleaton-Jones, P. E. ibid. 1975, ii, 765. Retief, D. P., Cleaton-Jones, P. E., Walker, A. R. P. Br. dent. J. 1975, 138,
4. 5.
Hartles, R. L., Leach, S. A. Br. med. Bull. 1975, 31, 137. Ryle, J. A. Br. med. J. 1943, ii, 633.
463. W.
ten
Scand.
J.
Hœmat.
1974,
206 16 years is edentulous.6 Were this and other information secured it should be possible to arrive at the true risk factors for dental caries, as has been done, for example, in respect of coronary heart-disease. The overwhelming obsession that sugar is the sole or principal cause of dental caries is seriously obstructing caries research. In many ways the situation regarding sugar intake and caries is analogous to that of sugar intake and diabetes. The huge majority of diabetic clinics in the United Kingdom urge total or partial exclusion of sugar for the control of the disease.’ Yet authoritative opinion maintains that the most suitable diet remains to be elucidated.s9 over
South African Medical Research Council, Human Biochemistry Research Unit, South African Institute for Medical Research, Johannesburg, South Africa.
A. R. P. WALKER
Dental Research Unit of the University of the Witwatersrand and South African Medical Research Council,
P. E.
Johannesburg.
CLEATON-JONES
RABIES
SIR,-From experience of clinical rabies in Nigeria I would confirm the points made by Wilson et ail. 10 that the early symptoms can easily be mistaken for-hysteria. The overbreathing is frequently similar to that seen in a child who has been crying, with a two-stage ("sniff-sniff") inspiration, and a slow full expiration. When that type of "sobbing respiration" is seen, suspect rabies--even if the patient and relatives initially deny any bite by a rabid dog. They might not connect a bite two or three months before with the present illness, or, more likely, they are afraid to admit it to themselves or to the doctor because they are aware of the fatal consequences. I am not familiar with the "fan-test", but will certainly try it on the next case I see. Rural Health Centre,
Igbo-Ora,
c/o Ibarapa Project Office, University College Hospital, Ibadan, Nigeria
C. ANDREW PEARSON
AMNIOCENTESIS FOR PRENATAL DIAGNOSIS
SIR,-Dr Laxova and others (Nov. 15, p. 964) reported the results of prenatal diagnosis in 174 patients. We think several points deserve comment. We do not agree that a family history of Down syndrome is not an adequate reason for amniocentesis. One must first obtain a detailed pedigree with the age of the mother at the time of the birth of each affected child. Cytogenetic studies on all possible family members should be done to rule out any translocations and/or mosaicism involving chromosome 21. If trisomy 21 is diagnosed in a child even though normal chromosome constitutions have been demonstrated in its relatives, one cannot be certain that their chances of having a trisomic child is not greater than that of other women of the same age, Gonadal mosaicism and/or a gene predisposing to non-disjunction have been suggested as the cause of familial cases of Down syndrome.’ We feel that the patient should be informed about the possibility of increased risk of her having a trisomic child and the small risk of fetal mortality from amniocentesis. The decision as to whether amniocentesis is to be done in a future pregnancy should be made by the patient. With regard to young mothers with a previous child with Down syndrome, the risk of recurrence is about 1%, which is not much lower than that in women aged 35-39. Dr Laxova and her colleagues say that because 3 patients aborted after two amniocenteses, they decided not to repeat amniocentesis in other patients when the first amniocentesis was unsuccessful. Are they certain that the abortions were directly caused by amniocentesis? In one case, the abortion may have been caused by a large subperitoneal fibroid on the left side of the uterus. Unfortunately, no mention was made of the post-mortem examination of these 3 abortuses. In any event, the authors must be aware that a recent study by the National Institutes of Health of the U.S.A. of about 1000 pregnancies with amniocentesis and about 1000 age-matched control pregnancies without amniocentesis demonstrated that the overall fetal loss with amniocentesis is not significantly different from that without amniocentesis.2 With the assistance of sonography, our obstetricians have never hesitated to do a second or third tap. Our and others’ experience has not evidenced increased fetal mortality in cases where repeated taps were done. The authors also say that the average I.Q. of 9 XXX children was
THALASSÆMIA TRAIT, ABNORMAL HÆMOGLOBINS, AND RAISED FETAL HÆMOGLOBIN IN KARACHI
SIR,-Because of the absence of screening facilities little is known about the prevalence of thalassaemia trait and abnormal haemoglobins in Pakistan. We have investigated 1224 adults in Karachi (1066 males and 158 females) who were hospital employees, professional blood-donors, or naval recruits. 11 (0.9%) carried an abnormal haemoglobin (8 HbD, 2 HbC, and 1 for HbS). Thalassaemia trait was detected in 18 (1.4%). 28.8% of the subjects had a raised fetal Hb (above 1%). 75% of the raised values were between 1.1% and 2%, and 19% were between 2.1% and 3%; only 2 values of more than 5% were recorded. Further analysis revealed raised HbF in 21.4% of adults whose Hb was above 10 g/dl. This finding cannot be explained on the basis of acquired pathological conditions associated with activation of HbF synthesis, and would appear to be a racial characteristic. Similar studies conducted in other parts of Pakistan are needed to confirm these observations. Pakistan Medical Research Council, Jinnah Postgraduate Medical Centre, Karachi, Pakistan.
JAVID A. HASHMI FARIDA FARZANA
6. Todd, J. E., Whitworth, A. Adult Dental Health in Scotland. H. M. Stationery Office, 1974. 7. Truswell, A. S., Thomas, B. J. Proc. Nutr. Soc. 1975, 34, 22A. 8. Bierman, E. L., Albrink, M. J., Arky, R. A., Connor, W. E., Dayton, S., Spritz, N., Steinburg, D. Diabetes, 1971, 20, 633. 9. Lancet, 1974, i, 398. 10. Wilson, J. M., Hettiarachchi, J., Wijesuriya, L. M. ibid. 1975, ii, 1139.
80, and none was above average. They note, in addition, that "most had
problems and some physical abnormalities". According to Tennes et al.,3 in a comparable group of XXX children the majority were in the normal range of intelligence, with i.Q.s between 80 and 120. 6 XXX children had a Wechsler score 16 points lower than that of their normal sibs. This by no means indicates that the I.Q. of XXX females is under 80. Only 2 of 9 XXX children required psychiatric help. Twothirds were considered normal and adequately adjusted. Barr et aI,1 reviewed 155females with XXX chromosomal constitutions and found two-thirds were phenotypically normal with no distinctive physical traits.
behaviour
With regard to culture failure, we do not understand why amniotic fluid was taken from a patient at 33 weeks of gestation. Even if prenatal diagnosis had been made in this case, the baby would have been near term by the time the results were available. This work was supported by grants (GM-19443 and HD-02! from the U.S. Public Health Service and the National Foundation (r.-1)))
of Pediatrics, Division of Medical Genetics, Mount Sinai School of Medicine, New York, New York, 10029, U.S.A.
Department
LILLIAN Y. F. Hsu FELICE YAHR LYNN GODMILOW
KURT HIRSCHHORN
1. Mikkelson, M. Ann. hum. Genet. 1966, 30, 125. 2. Results of Amniocentesis Registry Project of the National Institute of child Health and Human Development, presented at the American Academy of
Pediatrics meeting, Washington, D.C., Oct. 20, 1975. 3. Tennes, K., Puck, M., Bryant, K., Frankenburg, W., Robinson, A. Am.J. hum. Genet. 1975, 27, 71. 4. Barr, M. L., Sergovich, F. R., Carr, D. H., Shaver, E. L. Can. med. Ass. J. 1969, 101, 247.
