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CARIES-RESISTANT TEETH
1297 the disease and is not an inherent abnormality in the platelets of these patients. Thus increased adhesiveness is just as likely to result from as it is to cause the damage to the central nervous system. We have still to resolve whether it is young or old platelets that are more adherent to glass. The evidence available so far suggests that young platelets are more adhesive than old, and therefore high adhesiveness may indicate increased platelet turnover. Platelet adhesiveness to glass is a highly artificial reaction, and no-one has any idea what is actually measured by the techniques which are used. A study of the beads in the method I have outlined reveals that platelets adhere both to glass and to each other in large aggregates. Therefore aggregation as well as adhesion is being measured by this method. Whatever the snags inherent in these techniques there is no doubt that these findings are exciting and do reopen the question of vascular changes in the pathogenesis of multiple sclerosis. Radcliffe Infirmary, A. A. SHARP. Oxford.
CARIES-RESISTANT TEETH SIR,-May I refer to your annotation (Nov. 6) ? The observation that some teeth are relatively resistant to caries was made many years ago by Professor Pickerill of New Zealand when dealing with the problem of caries among New Zealanders, including Maoris. He attributed the relative immunity of the Maoris to something in the local environment of the teeth on eruption, and this led him to direct attention to Nasmyth’s membrane. Some years later, Dr. Pincus of Melbourne drew attention also to this membrane, and suggested that protein intake-certain aminoacids-was important in its
development
to
give adequate protection
to
newly erupted
teeth for an optimum period in their new local environment. Hence the wheel of events seems to have come round again with a few modifications from which perhaps a fresh start can be made. Montebello Hospital, H. ARTHUR JONES. Natal, South Africa. THIAZIDES AND CEREBRAL ISCHÆMIA draws attention to the occurrence of apparent transient cerebral ischaemia associated with postural hypotension in atherosclerotic patients receiving thiazide diuretics. A similar reversible reaction to chlorothiazide has been observed in children, and it seems likely that the cause may be cerebral ischaemia. This reaction was seen in a child accidentally poisoned by chlorothiazide.11 Bass and Beisel2 described two children who became comatose after swallowing a large amount of chlorothiazide. There was no disturbance of blood-pressure or serum-electrolytes, and they recovered spontaneously. When the investigators performed animal studies on monkeys, those on high dosage became lethargic and depressed, although their serum and urine electrolyte-levels were no different from those of unaffected monkeys on low dosage. Two children were affected by chlorothiazide given as an antidiuretic for nephrogenic diabetes insipidus.33 The first, aged 2 years, became pale, drowsy, and confused for 12 hours, during which time the electroencephalogram (E.E.G.) showed a slight, diffuse, abnormal slow-wave pattern which had reverted to normal 5 days later. The other patient, aged 6 months, became comatose, with extreme generalised pallor, but recovered quickly during physical examination, and soon afterwards had a normal E.E.G. and electrocardiogram; in all, he had four such attacks while the drug was being given. Both children had normal blood-pressure and serum-electrolyte levels in the attack, and at the time their body-weight was stable following a satisfactory antidiuretic response to treatment. Another child of 12 years was given chlorothiazide in an
SIR,-Dr. Barham Carter’s letter (Nov. 27)
1. 2. 3.
Rougraff, M. E. Penn. mec.J. Bass, J. W., Beisel, W. R. Am. O’Doherty, N. J., Rosser, J.,
1959, 62, 694. J. Dis. Child. 1963, 106, 620. Slater, R. J. Can. med. Ass. J. 1962,
86, 559.
attempt 4.
to
curb the
polyuria
of chronic
glomerulonephritis.44
O’Doherty, N. J., Rosser, J., Slater, R. J. Unpublished.
His fluid turnover was significantly decreased, but from the 2nd day of treatment he was confused and had severe syncopal attacks which persisted until the drug was stopped. At the height of the attack his E.E.G. and serum-electrolytes were normal. It seems very likely that these children suffered from transient cerebral ischasmia due to a direct action of chlorothiazide, both with normal doses and during intoxication with the drug. Pædiatric Department,
Guy’s Hospital, London, S.E.1.
N. J. O’DOHERTY.
TETANUS PROPHYLAXIS SIR,-In your leading article (Nov. 13) you mention only one of the hazards of antitetanus serum (A.T.s.)-namely, serum shock. Dr. Freeman (Nov. 27) refers to the serious neurological complications which may also occur. Antitetanus serum does not always prevent tetanus, and there is an increased risk of serum sickness and other reactions among those who have had previous serum experience.1-3 With serum administration another important disadvantage, which is well documented, is that serum-antitoxin-levels decline at a greatly accelerated rate if the recipient has had previous injections of horse serum 4-7; this is of practical importance, since once a patient has been sensitised to horse serum by previous injection the rate of antitoxin decline may be so rapid after subsequent injection that the prophylactic effect may be valueless. The antitoxin may be eliminated within the incubation period of tetanus, and the patient is left unprotected. Dr. Freeman, because of the danger of neurological complications, rightly disagrees with the recommendation of Trinca,a which you cite, that bovine antiserum should be used for patients sensitive to horse serum. A further objection to this recommendation is that serum sickness has been reported following the administration of tetanus antitoxin of bovine origin to a patient sensitive to horse serum.9 There is no doubt that active immunisation with tetanus toxoid is the best means of protecting against tetanus, but unimmunised children and adults continue to appear with wounds which, after surgical debridement, may call for antitoxin and/or antibiotic administration in addition. As mentioned, tetanus antitoxin is not without danger, but it has been reported 10 that penicillin has replaced foreign sera as the commonest cause of fatal anaphylactic shock. Tetanus has followed the use of antitetanus serum even when administered at the time of injury, and it has followed the use of antibiotics even when combined with antitetanus serum 11; so obviously these methods of preventing tetanus are not always effective. It is surprising that doctors remain so apathetic about active immunisation, and it would be of interest to know the proportion of doctors who are themselves protected against tetanus by active immunisation. Tetanus toxoid is a very effective and safe immunising agent, and if the entire population were actively immunised against tetanus, and an adequate record system were available, then the problem of tetanus prophylaxis would be solved. One thing is clear: the efficacy of active immunisation in preventing tetanus should be brought to the attention of the public by adequate health education, and doctors should advise their patients to have this protection. It is especially important that patients with infantile eczema and bronchial 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Goodall, E. W. Lancet, 1918, i, 323. Newell, C. E., McVea, C. Sth. med. J., Bgham, Ala. 1940, 33, 962. Moynihan, N. H. Lancet, 1955, ii, 264. Glenny, A. T., Hopkins, B. E. J. Hyg., Camb. 1922, 21, 142; ibid. 1923, 22, 12. Hooker, S. B., Follensby, E. M. J. Immun. 1931, 20, 269. Talmage, D. W., Dixon, F. S., Bokantz, S. C., Dammin, G. J. ibid. 1951, 67, 243. Parish, H. J., Cannon, D. A. Antisera, Toxoids, Vaccines and Tuberculins in Prophylaxis and Treatment; Edinburgh, p. 66. 1962. Trinca, J. C. Med. J. Aust. 1965, ii, 113 Reisman, R. E., Rose, N. R., Arbesman, C. E. J. Am. med. Ass. 1961, 176, 1004. Kern, R. A., Wimberley, N. A. Am. J. med. Sci. 1953, 266, 357. Ellis, M. Proc. R. Soc. Med. 1965, 58, 224.
CARIES-RESISTANT TEETH SIR,-May I refer to your annotation (Nov. 6) ? The observation that some teeth are relatively resistant to caries was made many years ago by Professor Pickerill of New Zealand when dealing with the problem of caries among New Zealanders, including Maoris. He attributed the relative immunity of the Maoris to something in the local environment of the teeth on eruption, and this led him to direct attention to Nasmyth’s membrane. Some years later, Dr. Pincus of Melbourne drew attention also to this membrane, and suggested that protein intake-certain aminoacids-was important in its
development
to
give adequate protection
to
newly erupted
teeth for an optimum period in their new local environment. Hence the wheel of events seems to have come round again with a few modifications from which perhaps a fresh start can be made. Montebello Hospital, H. ARTHUR JONES. Natal, South Africa. THIAZIDES AND CEREBRAL ISCHÆMIA draws attention to the occurrence of apparent transient cerebral ischaemia associated with postural hypotension in atherosclerotic patients receiving thiazide diuretics. A similar reversible reaction to chlorothiazide has been observed in children, and it seems likely that the cause may be cerebral ischaemia. This reaction was seen in a child accidentally poisoned by chlorothiazide.11 Bass and Beisel2 described two children who became comatose after swallowing a large amount of chlorothiazide. There was no disturbance of blood-pressure or serum-electrolytes, and they recovered spontaneously. When the investigators performed animal studies on monkeys, those on high dosage became lethargic and depressed, although their serum and urine electrolyte-levels were no different from those of unaffected monkeys on low dosage. Two children were affected by chlorothiazide given as an antidiuretic for nephrogenic diabetes insipidus.33 The first, aged 2 years, became pale, drowsy, and confused for 12 hours, during which time the electroencephalogram (E.E.G.) showed a slight, diffuse, abnormal slow-wave pattern which had reverted to normal 5 days later. The other patient, aged 6 months, became comatose, with extreme generalised pallor, but recovered quickly during physical examination, and soon afterwards had a normal E.E.G. and electrocardiogram; in all, he had four such attacks while the drug was being given. Both children had normal blood-pressure and serum-electrolyte levels in the attack, and at the time their body-weight was stable following a satisfactory antidiuretic response to treatment. Another child of 12 years was given chlorothiazide in an
SIR,-Dr. Barham Carter’s letter (Nov. 27)
1. 2. 3.
Rougraff, M. E. Penn. mec.J. Bass, J. W., Beisel, W. R. Am. O’Doherty, N. J., Rosser, J.,
1959, 62, 694. J. Dis. Child. 1963, 106, 620. Slater, R. J. Can. med. Ass. J. 1962,
86, 559.
attempt 4.
to
curb the
polyuria
of chronic
glomerulonephritis.44
O’Doherty, N. J., Rosser, J., Slater, R. J. Unpublished.
His fluid turnover was significantly decreased, but from the 2nd day of treatment he was confused and had severe syncopal attacks which persisted until the drug was stopped. At the height of the attack his E.E.G. and serum-electrolytes were normal. It seems very likely that these children suffered from transient cerebral ischasmia due to a direct action of chlorothiazide, both with normal doses and during intoxication with the drug. Pædiatric Department,
Guy’s Hospital, London, S.E.1.
N. J. O’DOHERTY.
TETANUS PROPHYLAXIS SIR,-In your leading article (Nov. 13) you mention only one of the hazards of antitetanus serum (A.T.s.)-namely, serum shock. Dr. Freeman (Nov. 27) refers to the serious neurological complications which may also occur. Antitetanus serum does not always prevent tetanus, and there is an increased risk of serum sickness and other reactions among those who have had previous serum experience.1-3 With serum administration another important disadvantage, which is well documented, is that serum-antitoxin-levels decline at a greatly accelerated rate if the recipient has had previous injections of horse serum 4-7; this is of practical importance, since once a patient has been sensitised to horse serum by previous injection the rate of antitoxin decline may be so rapid after subsequent injection that the prophylactic effect may be valueless. The antitoxin may be eliminated within the incubation period of tetanus, and the patient is left unprotected. Dr. Freeman, because of the danger of neurological complications, rightly disagrees with the recommendation of Trinca,a which you cite, that bovine antiserum should be used for patients sensitive to horse serum. A further objection to this recommendation is that serum sickness has been reported following the administration of tetanus antitoxin of bovine origin to a patient sensitive to horse serum.9 There is no doubt that active immunisation with tetanus toxoid is the best means of protecting against tetanus, but unimmunised children and adults continue to appear with wounds which, after surgical debridement, may call for antitoxin and/or antibiotic administration in addition. As mentioned, tetanus antitoxin is not without danger, but it has been reported 10 that penicillin has replaced foreign sera as the commonest cause of fatal anaphylactic shock. Tetanus has followed the use of antitetanus serum even when administered at the time of injury, and it has followed the use of antibiotics even when combined with antitetanus serum 11; so obviously these methods of preventing tetanus are not always effective. It is surprising that doctors remain so apathetic about active immunisation, and it would be of interest to know the proportion of doctors who are themselves protected against tetanus by active immunisation. Tetanus toxoid is a very effective and safe immunising agent, and if the entire population were actively immunised against tetanus, and an adequate record system were available, then the problem of tetanus prophylaxis would be solved. One thing is clear: the efficacy of active immunisation in preventing tetanus should be brought to the attention of the public by adequate health education, and doctors should advise their patients to have this protection. It is especially important that patients with infantile eczema and bronchial 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Goodall, E. W. Lancet, 1918, i, 323. Newell, C. E., McVea, C. Sth. med. J., Bgham, Ala. 1940, 33, 962. Moynihan, N. H. Lancet, 1955, ii, 264. Glenny, A. T., Hopkins, B. E. J. Hyg., Camb. 1922, 21, 142; ibid. 1923, 22, 12. Hooker, S. B., Follensby, E. M. J. Immun. 1931, 20, 269. Talmage, D. W., Dixon, F. S., Bokantz, S. C., Dammin, G. J. ibid. 1951, 67, 243. Parish, H. J., Cannon, D. A. Antisera, Toxoids, Vaccines and Tuberculins in Prophylaxis and Treatment; Edinburgh, p. 66. 1962. Trinca, J. C. Med. J. Aust. 1965, ii, 113 Reisman, R. E., Rose, N. R., Arbesman, C. E. J. Am. med. Ass. 1961, 176, 1004. Kern, R. A., Wimberley, N. A. Am. J. med. Sci. 1953, 266, 357. Ellis, M. Proc. R. Soc. Med. 1965, 58, 224.