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DYSBIOTIC ENTERIC FLORA SYNDROME

SIR,-It is well known that bacteria within the small-intestinal lumen may interfere with the absorption ofcertain nutrients-fat and vitamin B12 having been

particularly studied. An investigation by Campbell et al.,ltogether with previous work, 2 indicates that the mere

presence of increased bacterial numbers need not result in

recognisable malabsorption. It appears, not surprisingly,that the nature of the flora as well as the number of

organisms is important.There is confused terminology for the situation where

an altered intestinal microflora does interfere with absorptivefunction. This has been variously referred to as theblind-loop syndrome, stagnant-loop syndrome, con-

taminatated small-bowel syndrome, or simply as small-bowel bacterial overgrowth. Perhaps the most widelyused at present is the stagnant-loop syndrome, which hasthe merit of emphasising stasis as the commonest factorunderlying the fully developed syndrome. Nevertheless,stasis is not obligatory and an abnormal flora resulting inmalabsorption also occurs in some patients with achlor-hydria, and in conditions which give colonic bacteriaincreased access to the small intestine such as enterocolicfistula or after surgical disruption of the ileocsecal valvemechanism.3 3 Blind-loop syndrome is even more of aminomer in that it takes no cognisance of such predis-posing factors as scleroderma or intestinal stricture.Contaminated small-bowel syndrome has the disadvantageof being inexplicit, giving no hint of the nature of the" contamination". Small-bowel bacterial overgrowthsyndrome appears to be the most accurately descriptivelabel in current use, but it is rather cumbersome.In contrast to the normal symbiotic flora of the small

intestine, the fascal-Iike flora which results in impairedintestinal absorption could be termed dysbiotic. Haenelhas used the expressions eubiotic and dysbiotic with refer-ence, respectively, to normal and to disturbed gastrointestinalmicroflora, without necessarily implying that diseaseresults from the latter. 4 It is proposed here that themalabsorption syndrome which results from an alteredsmall-intestinal bacterial flora be termed the "dysbioticenteric flora syndrome" (D.E.F. syndrome). A more concise(but less explicit) suggestion is the " enteric dysbioticsyndrome ".Attempts to alter nomenclature should, of course, be

1. Campbell, C. B., Cowen, A. E., Harper, J. Aust. N.Z. Jl Med.1973, 3, 339.

2. Gorbach, S. L., Banwell, J. G., Jacobs, B., Chatterjee, B. D.,Mitra, R., Sen, N. N., Guha Mazumder, D. N. Am. J. clin. Nutr.1970, 23, 1545.

3. Tabaqchali, S. Scand. J. Gastroent. 1970, 5, suppl. 6, 139.4. Haenel, H. Am. J. clin. Nutr. 1970, 23, 1433.

discouraged unless the benefits of the new terminologyoutweigh the nuisance and confusion of change. To

suggest that diabetes mellitus be renamed the relative

insulinopsnic syndrome would be clearly fatuous: theolder term is concise, of historical interest, and in anycase too well entrenched. However, the plethora of labelsalready attached to the abnormal flora-induced malabsorp-tion indicates that none is really satisfactory and there isjustification for review.

Anatomy Department C,University of Copenhagen,

2200 Copenhagen N, Denmark. NEVILLE D. YEOMANS.

AVOIDING PITFALLS IN GENETIC STUDIES

SiR,—There has been some recent interest in the highincidence of false paternity among certain populations inBritain. Edwards 1,2 showed that as many as 50% ofpremaritally conceived children were not fathered by themother’s husband, and Philipp 3 found that 30% ofchildren in a selected group used for the study of Rh andABO inheritance were similarly placed. There are obviouslynumerous consequences for this. Our attention was

drawn to this problem during the genetic studies of thefamily of a child with pseudocholinesterase-activitydeficiency, who presented with prolonged apncea aftersuxamethonium.4 None of the other members of the

family had previously had an anaesthetic.During the course of these studies we used the blood-

groups to assess the validity of the family situation. Theresults are shown in the table, where it is seen that althoughthe mother and eldest son appear to be heterozygous, it isevident that the index patient could not have been fatheredby her legal father, neither could the youngest sibling, whowas unaffected. The gene is therefore presumably carriedby another man (who was not available for study).

Since pseudocholinesterase-activity deficiency, like anyother inborn error, is inherited in autosomal-recessivefashion, the possibility of such a socially modified birth rankphenomenon must be considered in the investigation offamilies affected, and it is suggested that blood-groupsshould be used more frequently in the investigation of suchfamilies.

Department of Pædiatrics,St. Stephen’s Hospital,London SW10 9TH.

SAMUEL MALKA ABBOLEONARD SINCLAIR.

1. Edwards, J. H. Br. J. prev. soc. Med. 1957, 11, 78.2. Edwards, J. H. in Law and Ethics of A.I.D. and Embryo Transfer:

Ciba Foundation Symposium 17, p. 66. Amsterdam, 1973.3. Philipp, E. E. ibid.4. Kimbrough, R. D., Suggs, J. E. New Engl. J. Med. 1973, 14, 751.

EXCLUSION OF PATERNITY ON RH PHENOTYPE