1259 VIABILITY OF PREMATURE FETUS
SIR,-We agree with Dr Goldenberg and Dr Nelson that obstetricians should be aware of the changing prognosis for the prematurely born infant (April 8, p. 764). Indeed it seems paradoxical that physicians should know their hospital’s cassarean-section rate, a statistic of dubious relevance as an indicator of obstetric care, while they are often unaware of their agerelated infant-survival statistics. Many factors probably contribute to improving perinatal survival, including antepartum
care, intrapartum monitoring, availability of neonatal-care services. Survival also depends upon fetal age and weight. But, as intimated by Goldenberg and Nelson, outcome probably also depends upon the fetal weight anticipated by the obstetrician. Unfortunately, gestational age or weight cannot always be determined accurately before delivery. The outlook for a 1200 g baby may, therefore, be better if the obstetrician believes it weighs 1500 g and takes all precautions to prevent fetal distress and provide timely intervention should this be necessary. The same 1200 g fetus may have a far different prognosis if intervention is not considered in the mistaken impression that the fetus is but 800 g. Much needs to be done to improve the reliability of the estimations of fetal weight and age. Ultrasound may ultimately provide such reliability. For the present we would
and the
Family of affected
child.
. are members with Becker’s muscular dystrophy.
’
(normal liquid blood-sample gave a serum-c.p.K. >2000 < 117). The parents of this child wish to defer a muscle biopsy until he shows symptoms. However, there is a family history of Becker’s muscular dystrophy: the boy’s maternal grandmother’s sister’s son and his mother’s maternal grandfather have pseudohypertrophic muscular dystrophy (see figure). It is thus possible that cases of Becker’s muscular dystrophy can be detected at 5 days of age and confirmed at 6 months. Department of Community Health, University of Auckland, Auckland, New Zealand
L. M. DRUMMOND A. M. O. VEALE
HYPERTENSIVE RESPONSE TO LABETALOL IN PHÆOCHROMOCYTOMA
SiR,—Dr Briggs and colleagues (May 13,
p.
1045) report
a
labetalol which
they suggest may hypertensive response result from presynaptic alpha-receptor antagonism. This is an unlikely explanation. Stimulation of presynaptic alpha-receptors reduces peripheral neuronal noradrenaline released Alpha-blocking drugs vary in their relative affinities for the pre-synaptic and postsynaptic sites.2 Predominant presynaptic blockade3 may contribute to the blood-pressure rise seen with yohimbine.4 Labetalol has both beta and alpha blocking properties but it is predoof labetalol minantly a beta-blocker.5.6 The alpha antagonism is largely postsynaptic in the guineapig ileum.’7 Effective beta-blockade in phaeochromocytoma uncovers previously masked postsynaptic alpha effects, and may be dangerous.8 The most likely mechanism in this patient is that labetalol possessed inadequate postsynaptic alpha-blocking effects until augmented by phenoxybenzamine or phentolamine. Finally it is suggested that a change in posture may have to
further contributed to the pressure rise. Plasma-noradrenaline increases on standing,9 but such changes are small relative to the tumour-related five-fold elevation. The supine pressure (300/160 mm Hg) was not further increased after standing (260/165 mm Hg) so a posture related breakthrough of postsynaptic blockade is also unlikely. Department of Clinical Pharmacology, Royal Postgraduate Medical School, London W12
G. A. FITZGERALD
1. Starke, K. Rev. Physiol. Biochem. Pharmac 1977, 77, 1. 2. Borowski, E., Ehrl, H., Starke, K. Arch. Pharmac 1976, 293, R2. 3 Starke, K , Borowski, E., Endo, T. Eur. J. Pharmac. 1975, 34, 385. 4 Garfield, S L., Gershon, S., Sletten, I., Sundland, D. M., Ballou, S. Int. J. Neuropsychiat. 1967, 3, 426. 5 Brittain, R. T., Levey, G. P. Br. J. Pharmac. 1976, 3, suppl., p. 681. 6. Aggrebeck, M., Guellden, G., Hangune, J. ibid 1978, 62, 543. 7. Drew, G. M. ibid. 1977, 59, 573. 8. Ross, E. J., Prichard, B. N., Kaufman, L., Robertson, A. I. G., Harries, B J Br. Med. J. 1976, i, 191
suggest that neonatal survival statistics be set out on the basis of the estimated fetal weight or estimated age. We further recommend that before the obstetrician decides, on the basis of local neonatal survival statistics, that a baby is too immature to intervene an ultrasound examination be done to determine gestational age. With these recommendations, the decision to intervene would be less subjective and the tabulated results would provide a more reliable picture of survival potential in the very small fetus. Departments of Obstetrics and Gynecology and Pediatrics, Cedars-Sinai Medical Center, Los Angeles, California 90048, U.S.A.
BARRY S. SCHIFRIN JEFFREY POMERANCE
PATHOGENESIS OF ATOPIC ALLERGY
SIR,-Most studies of T-lymphocyte levels in atopic sub-jects, using sheep-erythrocyte (E)-rosette formation to identify the T cells, have shown an abnormal deficit of these cells,but Hsieh,’ Hovmark,2 Ghazanshahl et al,3 and now Dr Thomson and his colleagues (May 6, p. 984) were unable to detect this deficit. We have shown in asthmatic subjects that subnormal levels of E-rosetting cells are detected in serum-free medium, and that if the lymphocytes are pre-incubated with fetal calf serum (F.C.S.) or with thymoslll (calf thymic hormone extract), the ’1--cell deficit is abolished.4 F.c.s., like thymosm, appears to induce "null" cells to become E-rosette forming cells.5 We suggest that by pre-incubating lymphocytes in medium containing F.C.S.,6 Thomson and his colleagues converted many null cells into E-rosetting cells and thus underestimated the T-cell deficit in their asthmatic patients. All the author, who have reported normal T-cell levels in atopics have at some stage incubated lymphocytes with F.c.s., possibly concealing a 1 Hsieh, K -H. Ann Allergy, 1976, 37, 383. 2 Hovmark, A. Acta derm vener Stockh 1977, 57, 237 3. Ghazanshahi, S , Townley, R, Chaperone, E, Villacorte, G Ann
Allergy,
1976, 36, 324 N. A., Caballero, F, Campbell, M. A, Chooi, M., Lane, A M, Hugh-Jones, K, Timlin, D. M., Hobbs, J R Clin. exp. Immun in the
4. Byrom,
press
5 6
N. A , Campbell, M A., Staughton, R. C D., T imlin, D M, Lancet, 1977, ii, 1132 Sandilands, G. P, Gray, K, Cooney, A , Browning, J D., Anderson, J. R
Byrom,
Clin.
exp
Immun
1975, 22, 493.
SIR,-We agree with Dr Goldenberg and Dr Nelson that obstetricians should be aware of the changing prognosis for the prematurely born infant (April 8, p. 764). Indeed it seems paradoxical that physicians should know their hospital’s cassarean-section rate, a statistic of dubious relevance as an indicator of obstetric care, while they are often unaware of their agerelated infant-survival statistics. Many factors probably contribute to improving perinatal survival, including antepartum
care, intrapartum monitoring, availability of neonatal-care services. Survival also depends upon fetal age and weight. But, as intimated by Goldenberg and Nelson, outcome probably also depends upon the fetal weight anticipated by the obstetrician. Unfortunately, gestational age or weight cannot always be determined accurately before delivery. The outlook for a 1200 g baby may, therefore, be better if the obstetrician believes it weighs 1500 g and takes all precautions to prevent fetal distress and provide timely intervention should this be necessary. The same 1200 g fetus may have a far different prognosis if intervention is not considered in the mistaken impression that the fetus is but 800 g. Much needs to be done to improve the reliability of the estimations of fetal weight and age. Ultrasound may ultimately provide such reliability. For the present we would
and the
Family of affected
child.
. are members with Becker’s muscular dystrophy.
’
(normal liquid blood-sample gave a serum-c.p.K. >2000 < 117). The parents of this child wish to defer a muscle biopsy until he shows symptoms. However, there is a family history of Becker’s muscular dystrophy: the boy’s maternal grandmother’s sister’s son and his mother’s maternal grandfather have pseudohypertrophic muscular dystrophy (see figure). It is thus possible that cases of Becker’s muscular dystrophy can be detected at 5 days of age and confirmed at 6 months. Department of Community Health, University of Auckland, Auckland, New Zealand
L. M. DRUMMOND A. M. O. VEALE
HYPERTENSIVE RESPONSE TO LABETALOL IN PHÆOCHROMOCYTOMA
SiR,—Dr Briggs and colleagues (May 13,
p.
1045) report
a
labetalol which
they suggest may hypertensive response result from presynaptic alpha-receptor antagonism. This is an unlikely explanation. Stimulation of presynaptic alpha-receptors reduces peripheral neuronal noradrenaline released Alpha-blocking drugs vary in their relative affinities for the pre-synaptic and postsynaptic sites.2 Predominant presynaptic blockade3 may contribute to the blood-pressure rise seen with yohimbine.4 Labetalol has both beta and alpha blocking properties but it is predoof labetalol minantly a beta-blocker.5.6 The alpha antagonism is largely postsynaptic in the guineapig ileum.’7 Effective beta-blockade in phaeochromocytoma uncovers previously masked postsynaptic alpha effects, and may be dangerous.8 The most likely mechanism in this patient is that labetalol possessed inadequate postsynaptic alpha-blocking effects until augmented by phenoxybenzamine or phentolamine. Finally it is suggested that a change in posture may have to
further contributed to the pressure rise. Plasma-noradrenaline increases on standing,9 but such changes are small relative to the tumour-related five-fold elevation. The supine pressure (300/160 mm Hg) was not further increased after standing (260/165 mm Hg) so a posture related breakthrough of postsynaptic blockade is also unlikely. Department of Clinical Pharmacology, Royal Postgraduate Medical School, London W12
G. A. FITZGERALD
1. Starke, K. Rev. Physiol. Biochem. Pharmac 1977, 77, 1. 2. Borowski, E., Ehrl, H., Starke, K. Arch. Pharmac 1976, 293, R2. 3 Starke, K , Borowski, E., Endo, T. Eur. J. Pharmac. 1975, 34, 385. 4 Garfield, S L., Gershon, S., Sletten, I., Sundland, D. M., Ballou, S. Int. J. Neuropsychiat. 1967, 3, 426. 5 Brittain, R. T., Levey, G. P. Br. J. Pharmac. 1976, 3, suppl., p. 681. 6. Aggrebeck, M., Guellden, G., Hangune, J. ibid 1978, 62, 543. 7. Drew, G. M. ibid. 1977, 59, 573. 8. Ross, E. J., Prichard, B. N., Kaufman, L., Robertson, A. I. G., Harries, B J Br. Med. J. 1976, i, 191
suggest that neonatal survival statistics be set out on the basis of the estimated fetal weight or estimated age. We further recommend that before the obstetrician decides, on the basis of local neonatal survival statistics, that a baby is too immature to intervene an ultrasound examination be done to determine gestational age. With these recommendations, the decision to intervene would be less subjective and the tabulated results would provide a more reliable picture of survival potential in the very small fetus. Departments of Obstetrics and Gynecology and Pediatrics, Cedars-Sinai Medical Center, Los Angeles, California 90048, U.S.A.
BARRY S. SCHIFRIN JEFFREY POMERANCE
PATHOGENESIS OF ATOPIC ALLERGY
SIR,-Most studies of T-lymphocyte levels in atopic sub-jects, using sheep-erythrocyte (E)-rosette formation to identify the T cells, have shown an abnormal deficit of these cells,but Hsieh,’ Hovmark,2 Ghazanshahl et al,3 and now Dr Thomson and his colleagues (May 6, p. 984) were unable to detect this deficit. We have shown in asthmatic subjects that subnormal levels of E-rosetting cells are detected in serum-free medium, and that if the lymphocytes are pre-incubated with fetal calf serum (F.C.S.) or with thymoslll (calf thymic hormone extract), the ’1--cell deficit is abolished.4 F.c.s., like thymosm, appears to induce "null" cells to become E-rosette forming cells.5 We suggest that by pre-incubating lymphocytes in medium containing F.C.S.,6 Thomson and his colleagues converted many null cells into E-rosetting cells and thus underestimated the T-cell deficit in their asthmatic patients. All the author, who have reported normal T-cell levels in atopics have at some stage incubated lymphocytes with F.c.s., possibly concealing a 1 Hsieh, K -H. Ann Allergy, 1976, 37, 383. 2 Hovmark, A. Acta derm vener Stockh 1977, 57, 237 3. Ghazanshahi, S , Townley, R, Chaperone, E, Villacorte, G Ann
Allergy,
1976, 36, 324 N. A., Caballero, F, Campbell, M. A, Chooi, M., Lane, A M, Hugh-Jones, K, Timlin, D. M., Hobbs, J R Clin. exp. Immun in the
4. Byrom,
press
5 6
N. A , Campbell, M A., Staughton, R. C D., T imlin, D M, Lancet, 1977, ii, 1132 Sandilands, G. P, Gray, K, Cooney, A , Browning, J D., Anderson, J. R
Byrom,
Clin.
exp
Immun
1975, 22, 493.
