NON-INVASIVE TEST FOR SMALL-INTESTINAL MUCOSAL DAMAGE
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1379 be indicated in this disease if intravenous urography is deemed necessary. Division of Maternal-Fetal Medicine, Los Angeles County/University of Southern California Medical Center Women’s Hospital, 5K22, Los Angeles, California 90033, U.S.A. DAVID B. COTTON NON-INVASIVE TEST FOR SMALL-INTESTINAL MUCOSAL DAMAGE SIR,-Dr Menzies and colleagues (Nov. 24, p. 1107) de- scribe an oral test of intestinal permeability incorporating two sugars of differing molecular size. We were pleased to see that their results confirmed our earlier work describing a similar test making use of the same principle. Their suggestion that the technique seems to provide a non-invasive test for small- intestinal mucosal damage appears to be borne out by the results of some further work which we have carried out on our test,2 in which we showed that it was both sensitive and specific for mucosal disease and potentially of value as a screening test for coeliac disease. Menzies et al. object to our choice of the disaccharide cello- biose on the ground that it is subject to the action of intestinal disaccharidases.3 We preferred cellobiose to lactulose on the ground that cellobiose is readily obtainable in pure form, whereas pure lactulose is prohibitively expensive and the sugar is usually obtained in an impure syrup formulation (’Dupha- lac’). Moreover, we have experimental evidence to suggest that the slight susceptibility of cellobiose to intestinal disacchari- dase produces no discernible effect on its absorption and recov- ery. In this experiment, six normal volunteers and eleven coeliacs (eight treated, three untreated) took part. Each carried out a standard cellobiose/mannitol test’ and also a similar test in which the 5 g cellobiose was replaced by 5 g lactulose, the two tests being performed within a week of each other in all cases, but not necessarily in the same order. The recoveries of both 1. Cobden I, Dickinson RJ, Rothwell J, Axon ATR. Intestinal permeability assessed by excretion ratios of two molecules: Results in coeliac disease. Br Med J 1978; ii: 1060. 2. Cobden I, Rothwell J, Axon ATR. Intestinal permeability and screening test for cœliac disease. Gut 1979; 20: A456. 3. Dahlquist A. Specificity of the human intestinal disaccharidases and implica- tions for herediatry disaccharide intolerance. J Clin Invest 1962; 41: 463-70. Percentage recoveries of cellobiose and lactulose in six controls and eleven creliacs who carried out paired tests. Ce=cellobiose; Lu=lactulose. sugars were compared for each patient (see figure). There is no significant difference between the recoveries of the two sugars. The fact that there was no significant difference between the recoveries of cellobiose and lactulose suggests that, in the con- text of this test, disaccharidase function has no effect on cello- biose absorption, since lactulose is known not to be hydrolysed by the small-intestinal mucosa.4 The reason for this may be in the low susceptibility of cellobiose to hydrolysis, intestinal "cellobiase" activity being approximately one-fifth of its lac- tase activity. Alternatively, the extreme hypertonicity of the test (1500 mosmol/1) might in some way protect cellobiose from the activity of intestinal disaccharidases. Gastroenterology Unit, General Infirmary, Leeds LS1 3EX I. COBDEN J. ROTHWELL A. T. R. AXON SUDDEN INFANT DEATH AND LOW TEMPERATURE SIR,-Zoglo et al.5 have shown that the seasonal variation in sudden infant-death syndrome (SIDS) is almost unaffected by seasonal fluctuations in birth rate, since these are small, but that the length of a month may affect monthly death rates by over 10%. The seasonal variation of SIDS is thought to be primarily due to temperature.6-8 In our study of SIDS in Cardiff during 1955-74 there were 286 deaths (91 207 live births). The local night minimum temperatures on the days of deaths were com- pared with the frequency distribution of all night minimum temperatures during the twenty-year period and were found to be significantly lower than would be expected by chance =60-7; p<0.001). The strong association between SIDS and night minimum temperature (r= -.81) is shown in the figure. A four-fold increase in the daily death rate accompanies a 26°C fall in temperature (+17°C to-9°C). SillS and night vninirnilrn temperature Cardiff 1955-74. We have examined our data again to see whether this "sea- sonal" variation in SIDS is restricted to infants aged four months and over, as reported from Australia by Beal.9 The Cardiff data demonstrate a strong association between SIDS and the temperature that is not dependent on the age of the infant. Department of Bacteriology, Queen Elizabeth Hospital, Birmingham ROBERT BONSER Department of Community Medicine, Welsh National School of Medicine, Cardiff CF4 4XN ROBERT WEST 4. Dahlquist A, Gryboski JD. Inability of the human small intestinal lactase to hydrolyse lactulose. Biochim Biophys Acta 1965; 110: 635-36. 5. Zoglo DP, Luckey DW, Fraikor AL. Birth rate and sudden infant death. Lancet 1979, ii: 260. 6. Kraus AS, Steel R, Langworth JR. Sudden unexpected death in infancy. Can J Publ Health 1967; 58: 364. 7. Collier HOJ. Sudden death in infancy. Lancet 1971; i: 343. 8. Bonser RSA, Knight BH, West RR. Sudden infant death syndrome in Car- diff: Association with epidemic influenza with temperature—1955-1974. Int J Epidemiol 1978; 7: 335-40. 9. Beal SM. Seasonal variation in sudden infant death syndrome. Lancet 1979; i: 1257.
Transcript of NON-INVASIVE TEST FOR SMALL-INTESTINAL MUCOSAL DAMAGE
1379
be indicated in this disease if intravenous urography is deemednecessary.
Division of Maternal-Fetal Medicine,Los Angeles County/University of
Southern California Medical CenterWomen’s Hospital, 5K22,Los Angeles, California 90033, U.S.A. DAVID B. COTTON
NON-INVASIVE TEST FOR SMALL-INTESTINALMUCOSAL DAMAGE
SIR,-Dr Menzies and colleagues (Nov. 24, p. 1107) de-scribe an oral test of intestinal permeability incorporating twosugars of differing molecular size. We were pleased to see thattheir results confirmed our earlier work describing a similartest making use of the same principle. Their suggestion thatthe technique seems to provide a non-invasive test for small-intestinal mucosal damage appears to be borne out by theresults of some further work which we have carried out on ourtest,2 in which we showed that it was both sensitive and specificfor mucosal disease and potentially of value as a screening testfor coeliac disease.
Menzies et al. object to our choice of the disaccharide cello-biose on the ground that it is subject to the action of intestinaldisaccharidases.3 We preferred cellobiose to lactulose on theground that cellobiose is readily obtainable in pure form,whereas pure lactulose is prohibitively expensive and the sugaris usually obtained in an impure syrup formulation (’Dupha-lac’). Moreover, we have experimental evidence to suggest thatthe slight susceptibility of cellobiose to intestinal disacchari-dase produces no discernible effect on its absorption and recov-ery.
In this experiment, six normal volunteers and eleven coeliacs(eight treated, three untreated) took part. Each carried out astandard cellobiose/mannitol test’ and also a similar test inwhich the 5 g cellobiose was replaced by 5 g lactulose, the twotests being performed within a week of each other in all cases,but not necessarily in the same order. The recoveries of both
1. Cobden I, Dickinson RJ, Rothwell J, Axon ATR. Intestinal permeabilityassessed by excretion ratios of two molecules: Results in coeliac disease. BrMed J 1978; ii: 1060.
2. Cobden I, Rothwell J, Axon ATR. Intestinal permeability and screening testfor cœliac disease. Gut 1979; 20: A456.
3. Dahlquist A. Specificity of the human intestinal disaccharidases and implica-tions for herediatry disaccharide intolerance. J Clin Invest 1962; 41:463-70.
Percentage recoveries of cellobiose and lactulose in six controlsand eleven creliacs who carried out paired tests.
Ce=cellobiose; Lu=lactulose.
sugars were compared for each patient (see figure). There is nosignificant difference between the recoveries of the two sugars.The fact that there was no significant difference between the
recoveries of cellobiose and lactulose suggests that, in the con-text of this test, disaccharidase function has no effect on cello-biose absorption, since lactulose is known not to be hydrolysedby the small-intestinal mucosa.4 The reason for this may be inthe low susceptibility of cellobiose to hydrolysis, intestinal"cellobiase" activity being approximately one-fifth of its lac-tase activity. Alternatively, the extreme hypertonicity of thetest (1500 mosmol/1) might in some way protect cellobiosefrom the activity of intestinal disaccharidases.
Gastroenterology Unit,General Infirmary,Leeds LS1 3EX
I. COBDENJ. ROTHWELLA. T. R. AXON
SUDDEN INFANT DEATH AND LOW TEMPERATURE
SIR,-Zoglo et al.5 have shown that the seasonal variationin sudden infant-death syndrome (SIDS) is almost unaffectedby seasonal fluctuations in birth rate, since these are small, butthat the length of a month may affect monthly death rates byover 10%.The seasonal variation of SIDS is thought to be primarily
due to temperature.6-8 In our study of SIDS in Cardiff during1955-74 there were 286 deaths (91 207 live births). The localnight minimum temperatures on the days of deaths were com-pared with the frequency distribution of all night minimumtemperatures during the twenty-year period and were found tobe significantly lower than would be expected by chance=60-7; p<0.001). The strong association between SIDS and
night minimum temperature (r= -.81) is shown in the figure.A four-fold increase in the daily death rate accompanies a26°C fall in temperature (+17°C to-9°C).
SillS and night vninirnilrn temperature Cardiff 1955-74.
We have examined our data again to see whether this "sea-sonal" variation in SIDS is restricted to infants aged fourmonths and over, as reported from Australia by Beal.9 TheCardiff data demonstrate a strong association between SIDSand the temperature that is not dependent on the age of theinfant.
Department of Bacteriology,Queen Elizabeth Hospital,Birmingham ROBERT BONSER
Department of Community Medicine,Welsh National School of Medicine,Cardiff CF4 4XN ROBERT WEST
4. Dahlquist A, Gryboski JD. Inability of the human small intestinal lactase tohydrolyse lactulose. Biochim Biophys Acta 1965; 110: 635-36.
5. Zoglo DP, Luckey DW, Fraikor AL. Birth rate and sudden infant death.Lancet 1979, ii: 260.
6. Kraus AS, Steel R, Langworth JR. Sudden unexpected death in infancy. CanJ Publ Health 1967; 58: 364.
7. Collier HOJ. Sudden death in infancy. Lancet 1971; i: 343.8. Bonser RSA, Knight BH, West RR. Sudden infant death syndrome in Car-
diff: Association with epidemic influenza with temperature—1955-1974.Int J Epidemiol 1978; 7: 335-40.
9. Beal SM. Seasonal variation in sudden infant death syndrome. Lancet 1979;i: 1257.
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