Importance of Disaccharide Intolerance in the Treatment of Cœliac Disease

Arthur, Ann; Cottom, Dennis; Clayton, Barbara E.; Seakins, J. W. T.; Platt, J. W.

doi:10.1016/s0140-6736(66)90699-4

Cited by 53 publications

(21 citation statements)

References 8 publications

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“…Only by determining in vivo hydrolysis and absorption kinetics can it be decided which stage is rate-limiting. A clinical trial of a lactose-free diet (Arthur et al, 1966) does not clirify the question; first, because the common " primary" lactase deficiency may frequently be superimposed on mucosal damage, and, secondly, because in reducing lactose (and/or sucrose) intake total carbohydrate may be reduced and thus decrease the load on the sugar pump.…”

Section: Discussionmentioning

confidence: 99%

Jejunal disaccharidases and some observations on the cause of lactase deficiency.

McMichael¹,

Webb²,

Dawson³

1966

BMJ

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We tried to obtain information about the time of onset and the first signs from relatives and neighbours in all cases, but found it difficult to obtain accurate data. In 34 cases no one could state exactly when deterioration had shown itself. In the others the period varied from one year to 10. There wag, however, absolutely no connexion between the duration and the degree of social deterioration. Cases of one year's duration were just as bad as those with a much longer history.The vulnerable individuals "at risk," who are potential candidates for developing the syndrome and in whose cases preventive community measures ought to be taken, are old people of the independent and domineering type living alone, with poor or non-existent social links with their local community. Their personality makes contact with them difficult, but much can be done with tact and perseverance, and this should be an easier task in the pre-breakdown stage.The key figures in prevention are the family doctor and community workers, such as the health visitor, the welfare services visitor, and the mental welfare officers, as they are usually the first to become-aware of the situation. They should be alive to the importance of precipitating factors-bereavement and physical ill-health or trauma, for instance.There is usually no organization to which cases can be reported and from which efficient action can be obtained. Our survey has demonstrated the need for such a service to be made available for these cases. We would like to suggest that in every area someone, preferably medical, should be designated to deal with all such cases from both the preventive and the therapeutic aspects. Psychiatric advice should be available.The question arises why old people, exposed to apparently comparable stresses, develop different patterns of symptoms. In some instances there is this syndrome of senile breakdown in standards, in others a senile paranoid psychosis, and in yet others one of the psychiatric senile states which are at present lumped together under the diagnosis of senile psychosis or senile dementia, while others show no obvious abnormal symptoms.Why in some cases do we find both the syndrome and a psychiatric illness, whereas in others the syndrome occurs without psychotic symptoms ?The contrast between the environmental conditions of the senile paranoid individual retaining a scrupulous regard for standards of cleanliness and hygiene and the sufferer from the breakdown syndrome is a most striking one. More extensive investigation of the latter could throw further light on the psychoses of the senium.We regard this investigation as merely a preliminary one of a condition which requires and should repay further study. SummaryA group of 72 individuals exhibiting evidence of personal and environmental lack of hygiene and deterioration in social standards was studied over a period of four years.The incidence was of the order of 0.5 per 1,000 population over 60. Most of the patients were over 70 years old, and women far outnumbered men.Isolation, ...

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Section: Discussionmentioning

confidence: 99%

Jejunal disaccharidases and some observations on the cause of lactase deficiency.

McMichael¹,

Webb²,

Dawson³

1966

BMJ

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“…11s montrent en effet une rtduction modtrCe de l'activitt phosphatasique alcaline [43, 321 et un fort dtficit des activitts maltasique et saccharasique [2,37,391. Mais ces difftrences peuvent &re expliqutes par la diminution importante de la surface tpithtliale dans les muqueuses alttrtes.…”

Section: A Rechuteunclassified

Étude histochimique de la muqueuse duodéno-jéjunale dans la maladie coeliaque

Frézal

Rey

et al. 1967

Pediatr Res

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ExtractEighteen peroral intestinal biopsies were obtained from children with celiac disease. A marked impairment ofthe enzymatic equipment was noted in the mucosa of patients with untreated celiac disease. The surface epithelium is clearly deficient in ATP-ase, 5-nucleotidase, monoamine oxidase, leucine aminopeptidase, glucose-6-phosphatase and lactase activities. The histochemical reactions for acid phosphatase, non specific esterases, a-glucosidases and deshydrogenases are often less affected. Only alkaline phosphatase activity seems unaltered in the surface epithelium.After the start of a gluten-free diet, an improvement in the patient's clinical condition occurs within a few weeks. At the same time, there is an increase in the activity of some enzymes. The histochemical reaction for ATP-ase shows a rapid improvement. This reaction is almost normal in specimens taken 2, 3 and 5 weeks after gluten withdrawal, but it is still negative in a biopsy performed one week after the removal of gluten from the diet. I n addition, the histochemical stains for several other enzymes, such as 5-nucleotidase and leucine aminopeptidase also return towards normal in a short time.Contrariwise lactase activity remains very low for several months after the beginning of the glutenfree diet. Sometimes the lactase deficiency may be responsible for clinical disturbances, i. e. 'a secondary intolerance to lactose'. I n such cases, lactose exerts some 'toxic effect' on the mucosa and prevents the restoration of the villi. Therefore, it is necessary to withdraw lactose as well as gluten from the diet. This intolerance to lactose is nevertheless transient and disappears after the mucosa is repaired.I t should be emphasized that there is a marked discrepancy between the histologic improvement, the evolution of the enzymatic abnormalities and the clinical response after gluten withdrawal. In most cases, the biological and clinical disturbances progressively disappear in three to five weeks. The morphologic changes of the duodeno-jejunal mucosa persist much longer. Before the first two months, there is no evident improvement in the histologic appearance of the mucosa. About three months after the start of dietary treatment, the villi are noticeable again, but are still short and broad (partial villous atrophy). Complete repair may require several months and sometimes more than one year. I n striking contrast, some enzymatic activities reappear very quickly. This improvement in some histochemical reactions seems to correlate closely with the rapid clinical response and, therefore, suggests that the histoenzymatic abnormalities play a prominent role in the absorptive failure of celiac disease.When the patients are put again on a normal diet, histological studies constantly show the reappearance of the mucosal lesions (subtotal villous atrophy), whereas the evolution of both clinical disturbances and histoenzymatic abnormalities is variable. Sometimes a clinical and biological relapse occurs and the histochemical reactions are again impaired. ...

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“…Az LI és gluténérzékenység együttes előfordulását 1965-ben írták le gyermekekben és olyan gyakorinak találták, hogy lisztérzékenységben laktózmentes étrendet javasoltak [49]. Utóbb vékonybél-biopsziával és laktóztoleran-cia-teszttel coeliakiás gyermekek 8,5%-ában igazolták az LI-t [50].…”

Section: Laktózintolerancia éS Coeliakiaunclassified

A laktózintoleranciáról: Múlt és jelen – I. rész

Buzás¹

2015

Orvosi Hetilap

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A tejcukor-érzékenység a leggyakoribb felszívódási zavar. A szerző a betegség történetének ismertetése után leírja a laktózintolerancia megjelenését a fajfejlődés során, majd vázolja a laktóz biokémiai jellegzetességeit. Az emberi és bakteriális laktáz enzim tulajdonságainak ismertetése után az epidemiológiai részben kitér a kórkép egyenlőtlen föld-rajzi eloszlására, régebbi és jelenlegi hazai elterjedésére. A felnőttkori laktózintoleranciát a 2. kromoszómán található laktáz gén felett elhelyezkedő MCM6 gén polimorfi zmusa okozza: meghatározása polimeráz láncreakcióval lehetsé-ges. A tejcukor-érzékenység extraintestinalis tünetei kevésbé ismertek. Az invazív diagnosztikai módszerek (laktázak-tivitás mérése vékonybél-biopsziából, laktóztolerancia-teszt) bár pontosak, átadták helyüket a nem invazív módsze-reknek: a H 2 -kilégzési teszt arany strandardnak számít. A genetikai tesztet egyre kiterjedtebben használják hazánkban is, és a közeljövőben a metánkilégzési teszt is elérhető lehet. A tejcukor-érzékenység társulhat gyulladásos bélbeteg-ségekkel, lisztérzékenységgel és irritábilis bél szindrómával: meg kell állapítani, hogy létezik-e patogenetikai összefüg-gés e betegségek között a helyes diéta és terápia megválasztása céljából. Orv. Hetil., 2015, 156(38), 1532-1539.Kulcsszavak: coeliakia, gyulladásos bélbetegség, irritábilis bél, laktáz, laktóz, polimorfi zmus, tejcukor-érzékenység Lactose intolerance: past and present. Part I Lactose intolerance is the most prevalent intestinal malabsorption disorder. After presentation of its history, the author describes the emergence of lactose intolerance during the evolution of species, and the biochemistry of lactose as well as features of human and bacterial lactase enzymes are then described. The unequal distribution of lactose intolerance in different continents and population is discussed, followed by presentation of past and present prevalence data in Hungary. Adult-type hypolactasia is caused by a polymorphism of the MCM6 gene located upstream from the lactase gene on the long arm of the chromosome 2. It can be determined with the polymerase chain reaction. The intestinal symptoms of lactose intolerance are well known, but its extra-intestinal manifestations are less recognised. Invasive diagnostic methods (determination of lactase activity from small intestinal biopsies, lactose tolerance test), are accurate, but have been replaced by the non-invasive methods; their gold standard is the H 2 breath test. Genetic testing is being used more and more frequently in Hungary too, and, presumably, the methane breath test will be also available in the near future. Lactose intolerance can be accompanied by infl ammatory bowel diseases, coeliac disease and irritable bowel syndrome; it could be established whether this association is causal or not in order to start a correct diet and therapy. Rövidítések A = adenin; BL = bakteriális laktáz; C = citozin; CD = Crohnbetegség; CU = colitis ulcerosa; EC = (enzyme classifi cation) az enzimek osztályozása; G = guanin; IBD = gyulladá...

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Importance of Disaccharide Intolerance in the Treatment of Cœliac Disease

Cited by 53 publications

References 8 publications

Jejunal disaccharidases and some observations on the cause of lactase deficiency.

Jejunal disaccharidases and some observations on the cause of lactase deficiency.

Étude histochimique de la muqueuse duodéno-jéjunale dans la maladie coeliaque

A laktózintoleranciáról: Múlt és jelen – I. rész

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