- Email: [email protected]
FOLATE DEFICIENCY AND DEMYELINATION IN AIDS
509 increase from 7 deaths in 1978 to 97 in 1982, with an incidence of 17per 100 000 inhabitants in 198 1.1 The 118 deaths from opioid overdose in Barcelona constitute one-third of all deaths by toxic substances recorded in the city during these 6 years, a figure that accords with Conso’s statement that heroin overdose is responsible for 30% of poisoning deaths in large cities.4 Opioids (above all, heroin) have now become the primary agent responsible for deaths of a toxic origin in young people in Barcelona. Opioids were associated with 50 % of all the fatal poisonings in 1985 while in 1982 they came third in the list of leading causes of death by poisoning and in 1981 sixth. This change is attributable both to an increase in the number of heroin addicts5 (in Spain, up from 79 000 in 1980 to 125 000 in 19841) and to changes in the purity of street heroin, which is influenced primarily by the drug’s country of
origin.2 Department of Forensic Medicine and Toxicology, University of Barcelona, 08014 Barcelona, Spain
P. REIG P. SANZ G. MARTÍ J. CORBELLA
J. Recuperación de heromómanos, definición, criterios y problemas de los estudios de evaluación y seguimiento. Med Clin (Barc) 1986; 87:
Large scale randomised trials should be possible but will be extremely difficult. This is because, despite scientific proof, many parents (fed by the media) and their doctors2 fervently believe in monitor use. The first attempt at such a trial is to be applauded.3 The final conclusion of that trial is, however, crucial-parents are most helped by caring professionals who devote time and skill to their anxieties. This is the important point in all the discussions, whether it is with or without alarms, scales, or other intervention. Simple prescription of a monitor is not enough.’4 Rotunda Hospital, Dublin, Ireland
K. P. DUNNE T. G. MATTHEWS
National -Institute of Health Consensus Development Conference on infantile apnoea and home monitoring: Sept 29-Oct 1, 1968. Pediatrics 1987; 79: 292-99. 2. Swift PG. Apneoa monitoring and cot deaths. Arch Dis Child 1987; 62: 98-99. 3. Emery JL, Waite AJ, Carpenter RJ, Limench SR, Blake D Apnoea monitors compared with weighing scales for siblings after cot death Arch Dis Child 1985; 60: 1055-60 4. Dunne KP, Matthews TG. Clinical presentation and management of "near-miss’ SIDS. Pediatrics 1987; 79: 889-93 1. Consensus statement.
1. Sánchez-Carbonell
377-82. 2. Samkoff JS, Baker SP. Recent trends in fatal poisonings by opiates in the United States. Am J Publ Health 1982; 11: 1251-56. 3. Ruttenber AJ, Luke JL. Heroin-related deaths: New epidermologic insights. Science 1984; 226: 14-20 4. Conso F. Intoxications aigues medicamenteuses. Encycl Méd Chir 1982; 12: 7. 5 Freixa F, Masferrer J, Sala LL. Aspectos sociosanitarios de la drogodependencia por heroína. Med Clin (Barc) 1984; 82: 30-32.
HOME MONITORING FOR INFANTILE APNOEA
SIR,-Your July 18 editorial states that the 1986 National Institutes of Health (NIH) consensus development conference on infantile apnoeal advocated home monitoring for premature infants with apnoea. This is incorrect. The NIH conference made the following points about apnoea of prematurity: (1) there is no evidence that it is an independent risk factor for infantile apnoea; (2) there is evidence that it is not an independent risk factor for sudden infant death syndrome (SIDS); (3) there is no evidence that it causes subsequent morbidity; and (4) infants with a history of apnoea of prematurity constitute only 2-4% of total SIDS cases. The NIH conference advocated home monitoring for preterm infants with symptoms of residual neonatal disease, such as bronchopulmonary dysplasia. In low birth-weight premature infants with prolonged central apnoea continuous cardiorespiratory monitoring does not predict SIDS.2 Nonetheless, babies born weighing less than 1 kg have a 5-10 times greater risk of SIDS than the normal term baby.3 Clearly prematurity per se is the risk factor in this group of babies. Hopefully the NIH conference report will advise on home and hospital monitoring based on gestation and birthweight parameters. National Maternity Dublin 2, Ireland
Hospital,
CHRISTOPHER FITZPATRICK
1 Consensus statement. National Institutes of Health consensus development conference on infantile apnea and home monitoring, Sept 29-Oct 1, 1986. Pediatrics 1987; 79: 292-99. 2 Southall DP, Richards JM, Rhoden KJ, et al. Prolonged apnea and cardiac arrhythmias in infants discharged from neonatal intensive care units: Failure to predict an increase risk for sudden infant death syndrome. Pediatrics 1982; 70: 844-51. 3. Peterson DR. Sudden unexpected death in infants: an epidemiological study. Am J
Epidemiol 1966, 84: 478-82.
18 editorial is potentially misleading. of heart rate and respiration (pneumograms) are not predictive of sudden infant death syndrome and should not be used to screen those who should receive apnoea ala=s.1 Your contention that "the small group of infants in which such changes [of heart rate and respiration] have been demonstrated may benefit from cardiorespiratory monitoring" may lead to the opposite conclusion. This is not supported by the NIH report which only claims that pneumograms may occasionally be helpful in clinical management (eg, distinguishing false from true apnoea monitor alarms). You also fail to grasp the problems of a scientific evaluation of apnoea alarms.
SIR,-Your July
Recordings
FOLATE DEFICIENCY AND DEMYELINATION IN AIDS
SIR,-Dr Smith and colleagues (July 25, p 215) suggest that dihydroneopterin produced by y-interferon-stimulated macrophages has antifolate activity. However, there is little dihydroneopterin in such macrophages, they do produce large amounts of neopterin,l from dihydroneopterin oxidation by macrophage-derived oxidants.2,3 Folate catabolism in man occurs by chemical oxidation, and CSF folate depletion is most probably due
to
folate catabolism by an enhanced oxidative process.
Molecular Sciences, Aston University, Birmingham B4 7ET
J.
A. BLAIR J. HEALES
S. R.
C, Batchelor JR, Fuchs D, et al. Immune response associated production of neopterin release from macrophages primarily under the control of &ggr;-interferon. J Exp Med 1984; 160: 310-16. 2. Nathan CF, Horowitz CR, De La Harpe J, et al. Administration of recombinant interferon to cancer patients enhances monocyte secretion of hydrogen peroxide. 1. Huber
Proc Natl Acad Sci USA 1985; 82: 8686-90. 3. Heales SJR, Blair JA, Meinschad C, Ziegler J. Inhibition of monocyte luminol department luminescence by tetrahydrobiopterin and the free radical oxidation of tetrahydrobiopterin, dihydrobiopterin and dihydroneopterin. Cell Biochem Function (in press).
SERUM OSMOLALITY IN CRITICALLY ILL PATIENTS
SiR,—Several biological and nutritional variables are used to establish the course and prognosis of critically ill patients. Dr Inaba and colleagues (June 13, p 1331) suggest the need to monitor the serum osmolality gap (the difference between the measured and calculated plasma osmolality) as a predictive variable. With the aim of characterising the metabolic alterations in patients in intensive care who had acute multiorgan failure (respiratory, renal, and haemodynamic function failure, and sepsis) and who needed artificial nutrition, we determined plasma antidiuretic hormone (ADH) and glucose and other metabolic variables, and made 273 determinations of serum osmolality by direct osmometry. Blood samples were obtained from the central (right atrium, superior vena cava, and pulmonary artery) and peripheral circulation at 2 and 24 h, and in the early morning on days 5 and 10. Although progressive hyperglycaemia occurred, neither central nor peripheral serum osmolality levels increased significantly (table). Plasma ADH remained normal. 10 of the 11I patients survived despite acute multiorgan failure. The clinical course and serum osmolality levels recorded in our patients were similar to the findings of Inaba and colleagues. Their group III surviving patients, despite acute multiorgan failure, had lower serum osmolality than non-surviving cases. Our results also agree with the previous finding of only minor changes in serum osmolality in patients with acute renal failure.2 Although we did not estimate the serum osmolality gap in our patients,_ multiple determinations of serum osmolality during the acute phase of
origin.2 Department of Forensic Medicine and Toxicology, University of Barcelona, 08014 Barcelona, Spain
P. REIG P. SANZ G. MARTÍ J. CORBELLA
J. Recuperación de heromómanos, definición, criterios y problemas de los estudios de evaluación y seguimiento. Med Clin (Barc) 1986; 87:
Large scale randomised trials should be possible but will be extremely difficult. This is because, despite scientific proof, many parents (fed by the media) and their doctors2 fervently believe in monitor use. The first attempt at such a trial is to be applauded.3 The final conclusion of that trial is, however, crucial-parents are most helped by caring professionals who devote time and skill to their anxieties. This is the important point in all the discussions, whether it is with or without alarms, scales, or other intervention. Simple prescription of a monitor is not enough.’4 Rotunda Hospital, Dublin, Ireland
K. P. DUNNE T. G. MATTHEWS
National -Institute of Health Consensus Development Conference on infantile apnoea and home monitoring: Sept 29-Oct 1, 1968. Pediatrics 1987; 79: 292-99. 2. Swift PG. Apneoa monitoring and cot deaths. Arch Dis Child 1987; 62: 98-99. 3. Emery JL, Waite AJ, Carpenter RJ, Limench SR, Blake D Apnoea monitors compared with weighing scales for siblings after cot death Arch Dis Child 1985; 60: 1055-60 4. Dunne KP, Matthews TG. Clinical presentation and management of "near-miss’ SIDS. Pediatrics 1987; 79: 889-93 1. Consensus statement.
1. Sánchez-Carbonell
377-82. 2. Samkoff JS, Baker SP. Recent trends in fatal poisonings by opiates in the United States. Am J Publ Health 1982; 11: 1251-56. 3. Ruttenber AJ, Luke JL. Heroin-related deaths: New epidermologic insights. Science 1984; 226: 14-20 4. Conso F. Intoxications aigues medicamenteuses. Encycl Méd Chir 1982; 12: 7. 5 Freixa F, Masferrer J, Sala LL. Aspectos sociosanitarios de la drogodependencia por heroína. Med Clin (Barc) 1984; 82: 30-32.
HOME MONITORING FOR INFANTILE APNOEA
SIR,-Your July 18 editorial states that the 1986 National Institutes of Health (NIH) consensus development conference on infantile apnoeal advocated home monitoring for premature infants with apnoea. This is incorrect. The NIH conference made the following points about apnoea of prematurity: (1) there is no evidence that it is an independent risk factor for infantile apnoea; (2) there is evidence that it is not an independent risk factor for sudden infant death syndrome (SIDS); (3) there is no evidence that it causes subsequent morbidity; and (4) infants with a history of apnoea of prematurity constitute only 2-4% of total SIDS cases. The NIH conference advocated home monitoring for preterm infants with symptoms of residual neonatal disease, such as bronchopulmonary dysplasia. In low birth-weight premature infants with prolonged central apnoea continuous cardiorespiratory monitoring does not predict SIDS.2 Nonetheless, babies born weighing less than 1 kg have a 5-10 times greater risk of SIDS than the normal term baby.3 Clearly prematurity per se is the risk factor in this group of babies. Hopefully the NIH conference report will advise on home and hospital monitoring based on gestation and birthweight parameters. National Maternity Dublin 2, Ireland
Hospital,
CHRISTOPHER FITZPATRICK
1 Consensus statement. National Institutes of Health consensus development conference on infantile apnea and home monitoring, Sept 29-Oct 1, 1986. Pediatrics 1987; 79: 292-99. 2 Southall DP, Richards JM, Rhoden KJ, et al. Prolonged apnea and cardiac arrhythmias in infants discharged from neonatal intensive care units: Failure to predict an increase risk for sudden infant death syndrome. Pediatrics 1982; 70: 844-51. 3. Peterson DR. Sudden unexpected death in infants: an epidemiological study. Am J
Epidemiol 1966, 84: 478-82.
18 editorial is potentially misleading. of heart rate and respiration (pneumograms) are not predictive of sudden infant death syndrome and should not be used to screen those who should receive apnoea ala=s.1 Your contention that "the small group of infants in which such changes [of heart rate and respiration] have been demonstrated may benefit from cardiorespiratory monitoring" may lead to the opposite conclusion. This is not supported by the NIH report which only claims that pneumograms may occasionally be helpful in clinical management (eg, distinguishing false from true apnoea monitor alarms). You also fail to grasp the problems of a scientific evaluation of apnoea alarms.
SIR,-Your July
Recordings
FOLATE DEFICIENCY AND DEMYELINATION IN AIDS
SIR,-Dr Smith and colleagues (July 25, p 215) suggest that dihydroneopterin produced by y-interferon-stimulated macrophages has antifolate activity. However, there is little dihydroneopterin in such macrophages, they do produce large amounts of neopterin,l from dihydroneopterin oxidation by macrophage-derived oxidants.2,3 Folate catabolism in man occurs by chemical oxidation, and CSF folate depletion is most probably due
to
folate catabolism by an enhanced oxidative process.
Molecular Sciences, Aston University, Birmingham B4 7ET
J.
A. BLAIR J. HEALES
S. R.
C, Batchelor JR, Fuchs D, et al. Immune response associated production of neopterin release from macrophages primarily under the control of &ggr;-interferon. J Exp Med 1984; 160: 310-16. 2. Nathan CF, Horowitz CR, De La Harpe J, et al. Administration of recombinant interferon to cancer patients enhances monocyte secretion of hydrogen peroxide. 1. Huber
Proc Natl Acad Sci USA 1985; 82: 8686-90. 3. Heales SJR, Blair JA, Meinschad C, Ziegler J. Inhibition of monocyte luminol department luminescence by tetrahydrobiopterin and the free radical oxidation of tetrahydrobiopterin, dihydrobiopterin and dihydroneopterin. Cell Biochem Function (in press).
SERUM OSMOLALITY IN CRITICALLY ILL PATIENTS
SiR,—Several biological and nutritional variables are used to establish the course and prognosis of critically ill patients. Dr Inaba and colleagues (June 13, p 1331) suggest the need to monitor the serum osmolality gap (the difference between the measured and calculated plasma osmolality) as a predictive variable. With the aim of characterising the metabolic alterations in patients in intensive care who had acute multiorgan failure (respiratory, renal, and haemodynamic function failure, and sepsis) and who needed artificial nutrition, we determined plasma antidiuretic hormone (ADH) and glucose and other metabolic variables, and made 273 determinations of serum osmolality by direct osmometry. Blood samples were obtained from the central (right atrium, superior vena cava, and pulmonary artery) and peripheral circulation at 2 and 24 h, and in the early morning on days 5 and 10. Although progressive hyperglycaemia occurred, neither central nor peripheral serum osmolality levels increased significantly (table). Plasma ADH remained normal. 10 of the 11I patients survived despite acute multiorgan failure. The clinical course and serum osmolality levels recorded in our patients were similar to the findings of Inaba and colleagues. Their group III surviving patients, despite acute multiorgan failure, had lower serum osmolality than non-surviving cases. Our results also agree with the previous finding of only minor changes in serum osmolality in patients with acute renal failure.2 Although we did not estimate the serum osmolality gap in our patients,_ multiple determinations of serum osmolality during the acute phase of