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CARRAGEENAN AND THE HUMAN GUT
726 ENZYMATIC ACTIVITIES AND PROTEIN CONTENT IN THE INTESTINAL MUCOSA OF THE PATIENT AND OF A CONTROL GROUP OF 35 CHILDREN*
* These children had no symptoms of malabsorption and ranged in age from 1 month to 14 years. Permission for biopsy examination was obtained from the parents.
symptoms at the time of measles infection suggests a causal relationship, although specific lactase deficiency is an uncommon sequela to mucosal damage of infectious origin.144 It may be worth while looking for similar cases, especially in tropical areas where the intestinal symptoms of measles are more
prevalent.
supported by the N.F.W.O. of Belgium. G. CARPENTIER Department of Pædiatrics, F. D’HONDT. Heilig Hartkliniek, Lier.
This work
was
Department of Pædiatrics, St. Rafael
University Hospital, Leuven, Belgium.
SIR,-Over a year ago we first drew attention 16 to the fact that in four animal species ulcerative lesions in the colon had been produced by the oral administration of seaweed-derived carrageenans, degraded or undegraded. We were pleased to read the letter by Dr. Bonfils (Aug. 22, p. 414) about the effects of carrageenan on the human colon and in particular to learn that in none of his Ebimar ’-treated patients had ulcerative colitis developed. It is a pity, however, that the letter contained inadequate data to permit any valid scientific criticism of his observations. He refers to his experience with degraded carrageenan as contained in the French pharmaceutical preparation calledEbimar’. He gives no indication of the source of the carrageenan, whether derived from Chondrus crispus or Eucheuma spinosum, nor does he indicate that the French preparation also contains, we believe, aluminium hydroxide. In his observations on ebimar-treated patients it would have been helpful to have given the results of tests for occult blood in the faeces. We found that the presence of occult blood is an early and reliable indication of the onset of colonic ulceration in laboratory animals. The conclusions drawn from the experiment on 10 patients with ulcerative colitis would have been more valid if the administration of ebimar had been continued for longer than ten days. We assume that on ethical grounds it would be hard to justify a more prolonged experiment with a preparation known to be ulcerogenic to the colon in several animal species. ’
R. MARCUS.
JAMES WATT.
Gudmand-Hoyer, E., Dahlquist, A., Jarnum, S. Scand. J. Gastroent. 1964, 4, 377. 15. Eggermont, E., Hers, H. G. Eur. J. Biochem. 1969, 9, 488. 16. Marcus, R., Watt, J. Lancet, 1969, ii, 489. 14.
contributory.
University Departments of Pathology and Medicine, Edinburgh.
A. M. MOLLA E. EGGERMONT.
CARRAGEENAN AND THE HUMAN GUT
Clatterbridge Hospital, Bebington, Cheshire. Department of Pathology, University of Liverpool.
GLOMERULAR LESIONS IN ACUTE PANCREATITIS SiR,—We were interested to read of the findings of Dr. Simon and Dr. Giacobino (Sept. 26, p. 669). The observations of platelet aggregation, fibrin deposition, endothelial-cell proliferation, and occasional glomerular capillary thrombosis in rabbits after the injection of trypsin, and in patients with pancreatitis,l are, however, not confined to these animals nor to pancreatitis. Similar ultrastructural appearances may be seen in renalbiopsy specimens from patients with acute ischsemic renal failure from a wide variety of causes including hypovolxmia, hypotension, and infection.22 Furthermore, studies of coagulation and fibrinolysis in these patients reveal abnormalities which persist throughout the period The ultrastructural coagulation and of renal failure. fibrinolytic changes revert to normal with recovery. Since hypotension, hypovolaemia, and infection are common complications of pancreatitis, it is likely that trypsin is not the sole or main causal factor but one which may be only A. R. CLARKSON MARY K. MACDONALD V. FUSTER J. S. ROBSON J. D. CASH.
THE AT-RISK REGISTER
SIR,-Your interesting leader (Sept. 19, p. 595) draws attention to the need for a new approach to the problem of screening children for handicapping conditions not detectable at birth. As you point out, the hoped-for gains from the use of selective screening have not materialised, but this is only partly because expectations had been based on inadequate evidence. Probably more important is the fact that most evaluations seem to have been from areas with relatively high resources where one would expect the gain to be minimal. It would therefore be a pity if during the present swing away from the policy of selective screening its initial justification was forgotten. This was that, when the resources available for screening children are limited, it is a sensible policy to allocate more resources to those at highest risk of handicap. It is still true that there are areas where the shortage of suitably trained general practitioners and health visitors is such that it is just not possible to do as you recommend-namely, to see all children regularly until their early milestones have been passed. However, in the many arguments which have been advanced for and against selective screening, it has largely been forgotten that it is possible, and sensible, to steer a path between screening only a high-risk group and universal screening. Given data on the relationship between early predictors and later handicap, it is possible to estimate the optimal composition of a high-risk group; and division of resources (e.g., visits by health visitors) between high and low risk groups. By " optimal " is meant that allocation of resources which will detect the maximum number of handicapping conditions. This problem has been examined using the data of the National Child Development Study. We have shown:= that there is always some advantage to be gained by favouring the high-risk group. For example, it should be possible. in areas where resources are scarce, to increase the detection rate of serious handicaps by up to 500, simply bB "
’’
Chatelanat, F., Simon, G. Path. Microbiol. 1965, 28, 399. Clarkson, A. R., MacDonald, M. K., Fuster, V., Robson, J. S Cash, J. D. Q. Jl Med. (in the press). 3. Alberman, E. D., Goldstein, H. Br. J. prev. soc. Med. 1970, 24, 129. 1. 2.
* These children had no symptoms of malabsorption and ranged in age from 1 month to 14 years. Permission for biopsy examination was obtained from the parents.
symptoms at the time of measles infection suggests a causal relationship, although specific lactase deficiency is an uncommon sequela to mucosal damage of infectious origin.144 It may be worth while looking for similar cases, especially in tropical areas where the intestinal symptoms of measles are more
prevalent.
supported by the N.F.W.O. of Belgium. G. CARPENTIER Department of Pædiatrics, F. D’HONDT. Heilig Hartkliniek, Lier.
This work
was
Department of Pædiatrics, St. Rafael
University Hospital, Leuven, Belgium.
SIR,-Over a year ago we first drew attention 16 to the fact that in four animal species ulcerative lesions in the colon had been produced by the oral administration of seaweed-derived carrageenans, degraded or undegraded. We were pleased to read the letter by Dr. Bonfils (Aug. 22, p. 414) about the effects of carrageenan on the human colon and in particular to learn that in none of his Ebimar ’-treated patients had ulcerative colitis developed. It is a pity, however, that the letter contained inadequate data to permit any valid scientific criticism of his observations. He refers to his experience with degraded carrageenan as contained in the French pharmaceutical preparation calledEbimar’. He gives no indication of the source of the carrageenan, whether derived from Chondrus crispus or Eucheuma spinosum, nor does he indicate that the French preparation also contains, we believe, aluminium hydroxide. In his observations on ebimar-treated patients it would have been helpful to have given the results of tests for occult blood in the faeces. We found that the presence of occult blood is an early and reliable indication of the onset of colonic ulceration in laboratory animals. The conclusions drawn from the experiment on 10 patients with ulcerative colitis would have been more valid if the administration of ebimar had been continued for longer than ten days. We assume that on ethical grounds it would be hard to justify a more prolonged experiment with a preparation known to be ulcerogenic to the colon in several animal species. ’
R. MARCUS.
JAMES WATT.
Gudmand-Hoyer, E., Dahlquist, A., Jarnum, S. Scand. J. Gastroent. 1964, 4, 377. 15. Eggermont, E., Hers, H. G. Eur. J. Biochem. 1969, 9, 488. 16. Marcus, R., Watt, J. Lancet, 1969, ii, 489. 14.
contributory.
University Departments of Pathology and Medicine, Edinburgh.
A. M. MOLLA E. EGGERMONT.
CARRAGEENAN AND THE HUMAN GUT
Clatterbridge Hospital, Bebington, Cheshire. Department of Pathology, University of Liverpool.
GLOMERULAR LESIONS IN ACUTE PANCREATITIS SiR,—We were interested to read of the findings of Dr. Simon and Dr. Giacobino (Sept. 26, p. 669). The observations of platelet aggregation, fibrin deposition, endothelial-cell proliferation, and occasional glomerular capillary thrombosis in rabbits after the injection of trypsin, and in patients with pancreatitis,l are, however, not confined to these animals nor to pancreatitis. Similar ultrastructural appearances may be seen in renalbiopsy specimens from patients with acute ischsemic renal failure from a wide variety of causes including hypovolxmia, hypotension, and infection.22 Furthermore, studies of coagulation and fibrinolysis in these patients reveal abnormalities which persist throughout the period The ultrastructural coagulation and of renal failure. fibrinolytic changes revert to normal with recovery. Since hypotension, hypovolaemia, and infection are common complications of pancreatitis, it is likely that trypsin is not the sole or main causal factor but one which may be only A. R. CLARKSON MARY K. MACDONALD V. FUSTER J. S. ROBSON J. D. CASH.
THE AT-RISK REGISTER
SIR,-Your interesting leader (Sept. 19, p. 595) draws attention to the need for a new approach to the problem of screening children for handicapping conditions not detectable at birth. As you point out, the hoped-for gains from the use of selective screening have not materialised, but this is only partly because expectations had been based on inadequate evidence. Probably more important is the fact that most evaluations seem to have been from areas with relatively high resources where one would expect the gain to be minimal. It would therefore be a pity if during the present swing away from the policy of selective screening its initial justification was forgotten. This was that, when the resources available for screening children are limited, it is a sensible policy to allocate more resources to those at highest risk of handicap. It is still true that there are areas where the shortage of suitably trained general practitioners and health visitors is such that it is just not possible to do as you recommend-namely, to see all children regularly until their early milestones have been passed. However, in the many arguments which have been advanced for and against selective screening, it has largely been forgotten that it is possible, and sensible, to steer a path between screening only a high-risk group and universal screening. Given data on the relationship between early predictors and later handicap, it is possible to estimate the optimal composition of a high-risk group; and division of resources (e.g., visits by health visitors) between high and low risk groups. By " optimal " is meant that allocation of resources which will detect the maximum number of handicapping conditions. This problem has been examined using the data of the National Child Development Study. We have shown:= that there is always some advantage to be gained by favouring the high-risk group. For example, it should be possible. in areas where resources are scarce, to increase the detection rate of serious handicaps by up to 500, simply bB "
’’
Chatelanat, F., Simon, G. Path. Microbiol. 1965, 28, 399. Clarkson, A. R., MacDonald, M. K., Fuster, V., Robson, J. S Cash, J. D. Q. Jl Med. (in the press). 3. Alberman, E. D., Goldstein, H. Br. J. prev. soc. Med. 1970, 24, 129. 1. 2.