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PROLONGED EXPIRATORY APNOEA IN CHILDREN
953 HTLV ANTIBODIES DETECTED WITH ELISA IN AFRICAN SERA
’762 Lambarene climc attenders, 63 Afncan AIDS suspects. t257 Lambarene clinic attenders, 63 African AIDS suspects.
Nigerian leukaemia/lymphoma
patients, and
Nigerian leukaemia/lymphoma
patients, and 14
14
subjects and 57 from African patients showed positive immunoprecipitation for HTLV-1. None was positive for HTLVIII, except 2 sera from the only patients in the series with clinically diagnosed AIDS. Biggar and colleagues reported strong positive correlations between positive ELISA against HTLV-I, HTLV-II, and HTLVIII on the one hand and antibodies to Plasmodium falciparum and levels of immune complexes on the other. Northern Nigerians experience hyperendemic malaria’ with very high levels of transmission during the rainy season: they have high titres of antimalarial antibodies and high levels of immune complexes.2,3 The same is true of subjects from other parts of tropical Africa included in this series. Our low frequency of HTLV-I and HTLVIII positivity with the specific immunoprecipitation method applied to sera showing ELISA positivity suggests that African sera yield a high prevalence of false-positive reactions with the ELISA for HTLV-1 and HTLV-III. The three other possible explanations put forward by Biggar et al seem less likely-namely, fortuitous codistribution of malaria and retrovirus infections, similar mode of transmission, or virus activation or enhanced antibody production after malaria. Sub-Saharan Africa is an important area endemic for HTLV-I, with up to 6’5% of adults showing specific antibodies.4,5 On the other hand, the data suggest that HTLV-III was rare in Africa until recently, and still is rare in much of the continent. It would seem that the epidemic of AIDS in Africastarted at about the same time as, or even later than, the epidemics in America and Europe. Our results do not support the hypothesis that HTLV-III virus originated in Africa. G. HUNSMANN Deutsches Primatenzentrum, D-3400 Gottingen, West Germany; and Tropical Diseases Research Centre, Ndola, Zambia
J. SCHNEIDER I. WENDLER A. F. FLEMING
J, Bayer H, Bienzle U, Hunsmann G. A glycopolypeptide (gp100) is the antigen detected by HTLV-III antisera. Med Microbiol Immunol 1985; 174:
1. Schneider main
35-42. 2. Molineaux L, Gramiccia G. The Garki Project. Geneva: WHO, 1980. 3. Mohammed I. The role of immune complexes in human malaria and some of its complications. J Infect 1982; 4: 97-104. 4. Fleming AF, Yamamoto N, Bhusnurmath SR, Maharajan R, Schneider J, Hunsmann G Antibodies to ATLV (HTLV) in Nigerian blood donors and patients with chronic lymphatic leukaemia or lymphoma. Lancet 1983; ii: 334-35. 5. Hunsmann G, Bayer H, Schneider J, et al. Antibodies to ATLV/HTLV-I in Africa. Med Microbiol Immunol 1984; 173: 167-70. 6 Bayley AC, Cheingsong-Popov R, Dalgleish AG, Downing RG, Tedder RS, Weiss RA. HTLV-III serology distinguishes atypical and endemic Kaposi’s sarcoma in Africa. Lancet 1985; i: 359-61.
PROLONGED EXPIRATORY APNOEA IN CHILDREN
SIR,-If
I understand correctly, Dr Southall and colleagues’ p 571) is that what ordinary doctors call "blue attacks" are as serious as they look, deserve elaborate breath-holding investigation, and are an important potential cause of neurological damage or sudden death. Their studies have confirmed pure prolonged expiratory apnoea as a mechanism for reflex syncopes of early life unaccompanied by asystole. They have also shown that in early infancy some of these episodes may appear "white" rather than "blue", but they will not easily dislodge the term "breath-holding", which has survived despite the knowledge that such attacks often begin in the neonatal penod2 before the emergence of voluntary action in the usual sense.
message
(Sept 14,
What is disturbing is Southall and colleagues’ attitude to these children and the inferences they draw. "... during most of the observed episodes, it was considered essential to attempt resuscitation". What effect did this have on the parents? It is the opposite of the approach recommended in asystolic reflex anoxic seizures where, once an attack has been reproduced by ocular compression, "the doctor does not touch the child at all. If he does, the mother will continue to believe that her child may die in an attack, and cannot be blamed for continuing potentially dangerous practices". The published evidence on death after one of these reflex syncopes is confined to a single case in which vomit was blown into the child’s lungs.3Ihave been involved in one unpublished fatality, but in this instance the repeated severe breathholding attacks (prolonged expiratory apnoea) appeared at necropsy to have a neurological basis, with malformation of the brainstem and cerebellum and fourth ventricle outlet obstruction. Southall et al refer to ataxic cerebral palsy in 3 cases, with nerve deafness in 2 of them, but this suggests pre-existing neurological abnormality. Even in the non-handicapped, the frequent coexistence2 of "blue breathholding" and a tendency to asystole favours an aberrant brainstem reflex rather than a primary pulmonary lesion. Repeated acute cerebral hypoxia sufficient to flatten the EEG for many seconds does not appear to have any serious consequences: the epidemiological data could be improved, but follow-up information, not cited by Southall et al, fits in with the view that sequelae do not
occur.2 The mother of an affected child whom I saw earlier this month would not have understood the oxygen saturation curves. Fortunately she had not heard the message of Southall’s article on the radio-if she had it might have been much more difficult to convince her that her boy would not die or be brain-damaged, as she had silently feared. Fraser of Allander Unit and EEG Department, Royal Hospital for Sick Children,
J. B. P. STEPHENSON
Glasgow G3 85J
Stephenson JBP. Reflex anoxic seizures and ocular compression. Dev Med Child Neurol 1980; 22: 380-86 2. Laxdal T, Gomez MR, Reiher J. Cyanotic and pallid syncopal attacks in children (breath-holding spells). Dev Med Child Neurol 1969; 11: 755-63. 3 Paulson G Breath holding spells: a fatal case. Dev Med Child Neurol 1963; 5: 246-51. 1.
MANAGEMENT OF INTUSSUSCEPTION IN CHILDHOOD
Singh (Aug 24, p 444) question the management in your Aug 3 editorial on acute intussusception in childhood (AIC). They suggest that the higher success rate of hydrostatic reduction reported from the USA and Scandinavia, compared with UK series,I.4 may be explained by earlier referral of children with bellyache to the radiologist, with SIR,-Mr Poston and
conclusions
Mr
on
consequent increased, sometimes unnecessary, use of barium insertion per rectum. Many such intussusceptions might, they think, have reduced spontaneously. Even so, is that not preferable to a late referral, which may lead to (equally unnecessary) surgery? In Malmö county in Sweden we found an incidence of AIC of 2 -55 per 1000 live births during a period of twelve years.The table shows further data on AIC, together with those from nine other surveys published during the past twelve years. The surveys, totalling 1230 patients, were comparable with respect to age and sex distribution, frequency of cardinal features, and the 24 h availability of a trained radiologist. As suggested by several workers 1,2,9,10 the remarkably different figures for attempt rates and success rates with hydrostatic reduction may reflect the considerable variation in duration of symptoms. In the studies listed in the table, in which various methods of recording symptom duration were used, about half the cases presented within 24 h. But, as pointed out in your editorial and by others,5-8 a strict threshold of duration of illness should not by itself be used as an indicator for primary surgical treatment, provided there is no associated peritonitis or profound hypovolaemic shock, which, with perforation and frank intestinal obstruction, are the only absolute contraindications to barium enema. Others who have correlated the site of the intussusception
’762 Lambarene climc attenders, 63 Afncan AIDS suspects. t257 Lambarene clinic attenders, 63 African AIDS suspects.
Nigerian leukaemia/lymphoma
patients, and
Nigerian leukaemia/lymphoma
patients, and 14
14
subjects and 57 from African patients showed positive immunoprecipitation for HTLV-1. None was positive for HTLVIII, except 2 sera from the only patients in the series with clinically diagnosed AIDS. Biggar and colleagues reported strong positive correlations between positive ELISA against HTLV-I, HTLV-II, and HTLVIII on the one hand and antibodies to Plasmodium falciparum and levels of immune complexes on the other. Northern Nigerians experience hyperendemic malaria’ with very high levels of transmission during the rainy season: they have high titres of antimalarial antibodies and high levels of immune complexes.2,3 The same is true of subjects from other parts of tropical Africa included in this series. Our low frequency of HTLV-I and HTLVIII positivity with the specific immunoprecipitation method applied to sera showing ELISA positivity suggests that African sera yield a high prevalence of false-positive reactions with the ELISA for HTLV-1 and HTLV-III. The three other possible explanations put forward by Biggar et al seem less likely-namely, fortuitous codistribution of malaria and retrovirus infections, similar mode of transmission, or virus activation or enhanced antibody production after malaria. Sub-Saharan Africa is an important area endemic for HTLV-I, with up to 6’5% of adults showing specific antibodies.4,5 On the other hand, the data suggest that HTLV-III was rare in Africa until recently, and still is rare in much of the continent. It would seem that the epidemic of AIDS in Africastarted at about the same time as, or even later than, the epidemics in America and Europe. Our results do not support the hypothesis that HTLV-III virus originated in Africa. G. HUNSMANN Deutsches Primatenzentrum, D-3400 Gottingen, West Germany; and Tropical Diseases Research Centre, Ndola, Zambia
J. SCHNEIDER I. WENDLER A. F. FLEMING
J, Bayer H, Bienzle U, Hunsmann G. A glycopolypeptide (gp100) is the antigen detected by HTLV-III antisera. Med Microbiol Immunol 1985; 174:
1. Schneider main
35-42. 2. Molineaux L, Gramiccia G. The Garki Project. Geneva: WHO, 1980. 3. Mohammed I. The role of immune complexes in human malaria and some of its complications. J Infect 1982; 4: 97-104. 4. Fleming AF, Yamamoto N, Bhusnurmath SR, Maharajan R, Schneider J, Hunsmann G Antibodies to ATLV (HTLV) in Nigerian blood donors and patients with chronic lymphatic leukaemia or lymphoma. Lancet 1983; ii: 334-35. 5. Hunsmann G, Bayer H, Schneider J, et al. Antibodies to ATLV/HTLV-I in Africa. Med Microbiol Immunol 1984; 173: 167-70. 6 Bayley AC, Cheingsong-Popov R, Dalgleish AG, Downing RG, Tedder RS, Weiss RA. HTLV-III serology distinguishes atypical and endemic Kaposi’s sarcoma in Africa. Lancet 1985; i: 359-61.
PROLONGED EXPIRATORY APNOEA IN CHILDREN
SIR,-If
I understand correctly, Dr Southall and colleagues’ p 571) is that what ordinary doctors call "blue attacks" are as serious as they look, deserve elaborate breath-holding investigation, and are an important potential cause of neurological damage or sudden death. Their studies have confirmed pure prolonged expiratory apnoea as a mechanism for reflex syncopes of early life unaccompanied by asystole. They have also shown that in early infancy some of these episodes may appear "white" rather than "blue", but they will not easily dislodge the term "breath-holding", which has survived despite the knowledge that such attacks often begin in the neonatal penod2 before the emergence of voluntary action in the usual sense.
message
(Sept 14,
What is disturbing is Southall and colleagues’ attitude to these children and the inferences they draw. "... during most of the observed episodes, it was considered essential to attempt resuscitation". What effect did this have on the parents? It is the opposite of the approach recommended in asystolic reflex anoxic seizures where, once an attack has been reproduced by ocular compression, "the doctor does not touch the child at all. If he does, the mother will continue to believe that her child may die in an attack, and cannot be blamed for continuing potentially dangerous practices". The published evidence on death after one of these reflex syncopes is confined to a single case in which vomit was blown into the child’s lungs.3Ihave been involved in one unpublished fatality, but in this instance the repeated severe breathholding attacks (prolonged expiratory apnoea) appeared at necropsy to have a neurological basis, with malformation of the brainstem and cerebellum and fourth ventricle outlet obstruction. Southall et al refer to ataxic cerebral palsy in 3 cases, with nerve deafness in 2 of them, but this suggests pre-existing neurological abnormality. Even in the non-handicapped, the frequent coexistence2 of "blue breathholding" and a tendency to asystole favours an aberrant brainstem reflex rather than a primary pulmonary lesion. Repeated acute cerebral hypoxia sufficient to flatten the EEG for many seconds does not appear to have any serious consequences: the epidemiological data could be improved, but follow-up information, not cited by Southall et al, fits in with the view that sequelae do not
occur.2 The mother of an affected child whom I saw earlier this month would not have understood the oxygen saturation curves. Fortunately she had not heard the message of Southall’s article on the radio-if she had it might have been much more difficult to convince her that her boy would not die or be brain-damaged, as she had silently feared. Fraser of Allander Unit and EEG Department, Royal Hospital for Sick Children,
J. B. P. STEPHENSON
Glasgow G3 85J
Stephenson JBP. Reflex anoxic seizures and ocular compression. Dev Med Child Neurol 1980; 22: 380-86 2. Laxdal T, Gomez MR, Reiher J. Cyanotic and pallid syncopal attacks in children (breath-holding spells). Dev Med Child Neurol 1969; 11: 755-63. 3 Paulson G Breath holding spells: a fatal case. Dev Med Child Neurol 1963; 5: 246-51. 1.
MANAGEMENT OF INTUSSUSCEPTION IN CHILDHOOD
Singh (Aug 24, p 444) question the management in your Aug 3 editorial on acute intussusception in childhood (AIC). They suggest that the higher success rate of hydrostatic reduction reported from the USA and Scandinavia, compared with UK series,I.4 may be explained by earlier referral of children with bellyache to the radiologist, with SIR,-Mr Poston and
conclusions
Mr
on
consequent increased, sometimes unnecessary, use of barium insertion per rectum. Many such intussusceptions might, they think, have reduced spontaneously. Even so, is that not preferable to a late referral, which may lead to (equally unnecessary) surgery? In Malmö county in Sweden we found an incidence of AIC of 2 -55 per 1000 live births during a period of twelve years.The table shows further data on AIC, together with those from nine other surveys published during the past twelve years. The surveys, totalling 1230 patients, were comparable with respect to age and sex distribution, frequency of cardinal features, and the 24 h availability of a trained radiologist. As suggested by several workers 1,2,9,10 the remarkably different figures for attempt rates and success rates with hydrostatic reduction may reflect the considerable variation in duration of symptoms. In the studies listed in the table, in which various methods of recording symptom duration were used, about half the cases presented within 24 h. But, as pointed out in your editorial and by others,5-8 a strict threshold of duration of illness should not by itself be used as an indicator for primary surgical treatment, provided there is no associated peritonitis or profound hypovolaemic shock, which, with perforation and frank intestinal obstruction, are the only absolute contraindications to barium enema. Others who have correlated the site of the intussusception