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RUBELLA VACCINATION
1397
logic. " Adrenoceptor ", on the other hand, seems etymologically unsound: there is no valid reason for and
omitting the "
re
".
Perhaps
we
should settle for " p-
adrenoreceptor blocker " (P-blocker for short) and
"
p-
adreno-antagonist ". We strike similar difficulties when we consider the " agonists ". An agonist is defined (by Dorland’s Medical Dictionary-the shorter O.E.D. does not recognise the word) as a prime mover, in the sense of skeletal muscle action on limbs. By extrapolation it has taken on the meaning of a drug which has a particular action, and we do not mean by this the effect that the drug has on the receptor but the effect that it has through the receptor. " p-adreno-receptor agonist " thus seems meaningless and " p-adrenergic agonist " is probably somewhat tautological. Strictly speaking " p-adrenergist" though might be enough, " " " &bgr;-adreno-agonist would also be acceptable; &bgr;-adrenoreceptor stimulator " may be the most accurate. The importance of all this is rather doubtful, but there would be some advantages in having a standard terminology. If there are to be moves in this direction, then let us make sure that the new terminology is better than the old. Some general discussion in your columns might be useful. Department of Medicine, Wellcome Medical Research Institute, University of Otago, Dunedin, New Zealand.
F. O. SIMPSON.
RUBELLA VACCINATION
SiR,—The problem of inadvertent rubella vaccination in pregnancy raised by Dr Keele (Dec. 1, p. 1273) can be
largely avoided by the very screening test he would like exclude. Some 70-80% of women will not need vaccine because they are already naturally immune. For the remaining 20-30%, questioning on menstrual history and advice on contraception should, as Dr Keele suggests, be adequate. Even from an economic point of view, it may be more expensive to vaccinate all women than to prescreen and vaccinate only those who require it. Screening programmes for rubella immunity are, of course, only fully successful when the results are communicated to
to
the
women
themselves.
Virus
Regional Laboratory, City Hospital, Greenbank Drive, Edinburgh EH10 5SB.
WINIFRED THOMSON.
PALPABLE LIVERS AND SPLEENS IN NEWBORN INFANTS
SIR,—The traditional textbooks of paediatrics
1-3
state
that the liver and spleen are often palpable in normal newborn infants. However, estimates of the frequency with which the liver and spleen can be palpated in the first days of life are not given in these sources. We therefore undertook a brief survey of 60 newborn infants born during the summer of 1973 at the St. Louis Maternity Hospital to determine how often the liver and the spleen could be felt in this random selection. Infants with jaundice secondary to Rh and ABO incompatibilities, as well as infants with heart-failure, were excluded. All infants were examined by one observer (K. B.) under the supervision of P. C. Every patient was examined twice, once on the second day and once on the third day. The liver was palpable in 53% of the patients. The presence of a palpable liver and spleen was related to the birth-weights of the infants. 80% of the patients of low birthweight 1. McKay, R. J., Nelson, W. E., Vaughn, V. C. (editors). Textbook of Pediatrics; p. 356. Philadelphia, 1969. 2. Hardy, J., Cooke, R. E. The Biologic Basis of Pediatric Practice; p. 1487. New York, 1968. 3. Grossman, M., Barnett, H. Pediatrics; p. 82. New York, 1972.
(less than 2500 g.) had a palpable liver at some time during the second or third day of life. However, only 15 °o of infants weighing more than 2500 g. had a palpable liver during the course of this study. In no case was the liver greater than 2 cm. from the right costal margin. 15% of the infants had a palpable spleen. All the infants whose spleens could be felt had birth-weights greater than 2500 g. Department of Pediatrics, Washington University School of Medicine, St. Louis Children’s Hospital, St. Louis, Missouri 63110.
KAREN BOWYER PRA-ON CHAVALITDHAMRONG RICHARD E. MARSHALL.
CHRONIC CASSAVA TOXICITY: POSSIBLE RELATIONSHIP TO CHRONIC PANCREATIC DISEASE IN MALNOURISHED POPULATIONS
SiR,-The clinical syndromes well recognised
to be chronic cassava toxicity include degenerative neurological diseases (tropical ataxic neuropathy) and endemic goitre.1 The presence of cyanogenetic glucosides in cassava appear to be responsible for these syndromes. The hydrocyanic acid in tapioca or cassava is concentrated in the outer integument of the tuber and the intensity of exposure to the toxin is influenced by the method adopted for cooking.22 The concentration of the toxic glycoside varies, depending on a number of factors such as the kind of plant, weather, and soil.3 Hydrocyanic acid is detoxified in the body by the enzyme rhodanese in the presence of sulphur-containing aminoacids, depleting further the levels of these aminoacids in malnourished patients. The other mode of detoxification of cyanide is by combination with hydroxycobalmin (B12) in the liver to form non-toxic
related
to
cyanocobalmin. In southern India, in the State of Kerala, chronic pancreatic disease associated with pancreatic calcification
and diabetes mellitus is known
to occur
in endemic pro-
portions.4-6 Its xtiology is obscure, but it does not appear to be solely attributable to protein malnutrition. The diet of this population group is mostly made up of carbohydrate derived from cassava. Even though no definite experimental study incriminating cassava as a potential pancreatic toxin is recorded in the literature, epidemiological association between tapioca consumption and the high incidence of chronic pancreatic disease in India has been observed for many years by physicians in Kerala. It is interesting to note that a similar pancreatic syndrome in diabetes in Nigeria was observed by Kinnear.7 The rural population in Nigeria consume large quantities of cassava. Similar cases of juvenile or adolescent pancreatitis have been reported from a number of Asian and African countries. 8 9 The concept of toxic pancreatic injury accords with current knowledge of pancreatic disease. Pancreas is vulnerable to a number of exogenous toxins, including certain drugs and chemicals.1O The susceptibility of the pancreas to toxic agents is accentuated by protein malnutrition. The combined effect on the pancreas of a nutritionally deficient diet and toxin is greater than the influence of either factor alone. 1. Lancet, 1973, ii, 245. 2. Oke, O. L. Nature, 1966, 212, 1055. 3. Oke, O. L. World Review of Nutrition and Dietetics; vol. IX, p. 227. Basle, 1968. 4. GeeVarghese, P. J., Pillai, V. K., Joseph, M. P., Pitchumoni, C. S. J. Ass. Phys. Ind. 1962, 10, 173. 5. GeeVarghese, P. J., Pitchumoni, C. S., Nair, S. R. ibid. 1969, 17, 417. 6. Pitchumoni, C. S., GeeVarghese, P. J. Proceedings of World Congress on Diabetes in the Tropics, Bombay, 1966, p. 240. 7. Kinnear, T. W. G. E. Afr. med. J. 1963, 40, 288. 8. Banwell, J. G., et al. Gut, 1967, 8, 388. 9. Pitchumoni, C. S. Am. J. clin. Nutr. 1973, 26, 374. 10. Dreiling, D. A., Janowitz, H. J., Perrier, C. F. Pancreatic Inflammatory Disease, p. 64. New York, 1964.
logic. " Adrenoceptor ", on the other hand, seems etymologically unsound: there is no valid reason for and
omitting the "
re
".
Perhaps
we
should settle for " p-
adrenoreceptor blocker " (P-blocker for short) and
"
p-
adreno-antagonist ". We strike similar difficulties when we consider the " agonists ". An agonist is defined (by Dorland’s Medical Dictionary-the shorter O.E.D. does not recognise the word) as a prime mover, in the sense of skeletal muscle action on limbs. By extrapolation it has taken on the meaning of a drug which has a particular action, and we do not mean by this the effect that the drug has on the receptor but the effect that it has through the receptor. " p-adreno-receptor agonist " thus seems meaningless and " p-adrenergic agonist " is probably somewhat tautological. Strictly speaking " p-adrenergist" though might be enough, " " " &bgr;-adreno-agonist would also be acceptable; &bgr;-adrenoreceptor stimulator " may be the most accurate. The importance of all this is rather doubtful, but there would be some advantages in having a standard terminology. If there are to be moves in this direction, then let us make sure that the new terminology is better than the old. Some general discussion in your columns might be useful. Department of Medicine, Wellcome Medical Research Institute, University of Otago, Dunedin, New Zealand.
F. O. SIMPSON.
RUBELLA VACCINATION
SiR,—The problem of inadvertent rubella vaccination in pregnancy raised by Dr Keele (Dec. 1, p. 1273) can be
largely avoided by the very screening test he would like exclude. Some 70-80% of women will not need vaccine because they are already naturally immune. For the remaining 20-30%, questioning on menstrual history and advice on contraception should, as Dr Keele suggests, be adequate. Even from an economic point of view, it may be more expensive to vaccinate all women than to prescreen and vaccinate only those who require it. Screening programmes for rubella immunity are, of course, only fully successful when the results are communicated to
to
the
women
themselves.
Virus
Regional Laboratory, City Hospital, Greenbank Drive, Edinburgh EH10 5SB.
WINIFRED THOMSON.
PALPABLE LIVERS AND SPLEENS IN NEWBORN INFANTS
SIR,—The traditional textbooks of paediatrics
1-3
state
that the liver and spleen are often palpable in normal newborn infants. However, estimates of the frequency with which the liver and spleen can be palpated in the first days of life are not given in these sources. We therefore undertook a brief survey of 60 newborn infants born during the summer of 1973 at the St. Louis Maternity Hospital to determine how often the liver and the spleen could be felt in this random selection. Infants with jaundice secondary to Rh and ABO incompatibilities, as well as infants with heart-failure, were excluded. All infants were examined by one observer (K. B.) under the supervision of P. C. Every patient was examined twice, once on the second day and once on the third day. The liver was palpable in 53% of the patients. The presence of a palpable liver and spleen was related to the birth-weights of the infants. 80% of the patients of low birthweight 1. McKay, R. J., Nelson, W. E., Vaughn, V. C. (editors). Textbook of Pediatrics; p. 356. Philadelphia, 1969. 2. Hardy, J., Cooke, R. E. The Biologic Basis of Pediatric Practice; p. 1487. New York, 1968. 3. Grossman, M., Barnett, H. Pediatrics; p. 82. New York, 1972.
(less than 2500 g.) had a palpable liver at some time during the second or third day of life. However, only 15 °o of infants weighing more than 2500 g. had a palpable liver during the course of this study. In no case was the liver greater than 2 cm. from the right costal margin. 15% of the infants had a palpable spleen. All the infants whose spleens could be felt had birth-weights greater than 2500 g. Department of Pediatrics, Washington University School of Medicine, St. Louis Children’s Hospital, St. Louis, Missouri 63110.
KAREN BOWYER PRA-ON CHAVALITDHAMRONG RICHARD E. MARSHALL.
CHRONIC CASSAVA TOXICITY: POSSIBLE RELATIONSHIP TO CHRONIC PANCREATIC DISEASE IN MALNOURISHED POPULATIONS
SiR,-The clinical syndromes well recognised
to be chronic cassava toxicity include degenerative neurological diseases (tropical ataxic neuropathy) and endemic goitre.1 The presence of cyanogenetic glucosides in cassava appear to be responsible for these syndromes. The hydrocyanic acid in tapioca or cassava is concentrated in the outer integument of the tuber and the intensity of exposure to the toxin is influenced by the method adopted for cooking.22 The concentration of the toxic glycoside varies, depending on a number of factors such as the kind of plant, weather, and soil.3 Hydrocyanic acid is detoxified in the body by the enzyme rhodanese in the presence of sulphur-containing aminoacids, depleting further the levels of these aminoacids in malnourished patients. The other mode of detoxification of cyanide is by combination with hydroxycobalmin (B12) in the liver to form non-toxic
related
to
cyanocobalmin. In southern India, in the State of Kerala, chronic pancreatic disease associated with pancreatic calcification
and diabetes mellitus is known
to occur
in endemic pro-
portions.4-6 Its xtiology is obscure, but it does not appear to be solely attributable to protein malnutrition. The diet of this population group is mostly made up of carbohydrate derived from cassava. Even though no definite experimental study incriminating cassava as a potential pancreatic toxin is recorded in the literature, epidemiological association between tapioca consumption and the high incidence of chronic pancreatic disease in India has been observed for many years by physicians in Kerala. It is interesting to note that a similar pancreatic syndrome in diabetes in Nigeria was observed by Kinnear.7 The rural population in Nigeria consume large quantities of cassava. Similar cases of juvenile or adolescent pancreatitis have been reported from a number of Asian and African countries. 8 9 The concept of toxic pancreatic injury accords with current knowledge of pancreatic disease. Pancreas is vulnerable to a number of exogenous toxins, including certain drugs and chemicals.1O The susceptibility of the pancreas to toxic agents is accentuated by protein malnutrition. The combined effect on the pancreas of a nutritionally deficient diet and toxin is greater than the influence of either factor alone. 1. Lancet, 1973, ii, 245. 2. Oke, O. L. Nature, 1966, 212, 1055. 3. Oke, O. L. World Review of Nutrition and Dietetics; vol. IX, p. 227. Basle, 1968. 4. GeeVarghese, P. J., Pillai, V. K., Joseph, M. P., Pitchumoni, C. S. J. Ass. Phys. Ind. 1962, 10, 173. 5. GeeVarghese, P. J., Pitchumoni, C. S., Nair, S. R. ibid. 1969, 17, 417. 6. Pitchumoni, C. S., GeeVarghese, P. J. Proceedings of World Congress on Diabetes in the Tropics, Bombay, 1966, p. 240. 7. Kinnear, T. W. G. E. Afr. med. J. 1963, 40, 288. 8. Banwell, J. G., et al. Gut, 1967, 8, 388. 9. Pitchumoni, C. S. Am. J. clin. Nutr. 1973, 26, 374. 10. Dreiling, D. A., Janowitz, H. J., Perrier, C. F. Pancreatic Inflammatory Disease, p. 64. New York, 1964.