Celiac Syndrome

Andersen, Dorothy H.

doi:10.1001/archpedi.1946.02020300069004

Cited by 141 publications

(11 citation statements)

References 14 publications

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“…In a recent paper on the genetics of the disease, Andersen and Hodges (1946) reviewed the literature and concluded that 'it occurs among siblings, twins and more distant relatives with a distribution which is compatible with the hypothesis that it is carried as a relatively infrequent hereditary trait.' They collected from the literature several instances in which one sibling suffered from congenital intestinal obstruction and another from proved pancreatic disease presenting one ofthe other cinical syndromes (Flax et al, 1942;Deem and McGeorge, 1941;Attwood and Sargent, 1942;Philipsborn et al, 1944).…”

Section: Featuresmentioning

confidence: 90%

Congenital Fibrocystic Disease of the Pancreas: A Report of Two Proved Cases of Dissimilar Clinical Types in Siblings

Macgregor¹,

Rhaney²

1948

Archives of Disease in Childhood

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Section: Featuresmentioning

confidence: 90%

Congenital Fibrocystic Disease of the Pancreas: A Report of Two Proved Cases of Dissimilar Clinical Types in Siblings

Macgregor¹,

Rhaney²

1948

Archives of Disease in Childhood

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“…Congenital malformations can occur in many other forms of nutritional deficiency, in infections, and in poisoning by drugs. T h e early and more recent workers who studied the effect of vitamin A deficiency (Hale, 1935;Andersen, 1941;Warkany & Schraffenberger, 1946) and excess (Cohlan, 1953;Giroud & Martinet, 1954) on the development of the foetus, can be honoured as pioneers in a field which extended far beyond their original interests.…”

Section: The Lesions In Hypervitaminosis Amentioning

confidence: 99%

Vitamin A deficiency and excess

Moore

1965

Proc. Nutr. Soc.

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Vol. 24Vitamin A 129 dubious but in practice the results are very good-partly in fact because errors tend to be compensated ! Correction procedures devised specially to meet difficulties over vitamin A assays are actually theoretically safer in most of the many other situations in which they have been used ! I suppose there are lessons here as well as an element of irony.T h e problem of the site and manner of conversion of p-carotene into vitamin A was another problem which had its ups and downs, but the importance of processes occurring in the lining of the gut is beyond doubt. There have been interesting quantitative aspects of the storage of esterified vitamin A in the liver and its release as alcohol into the blood. The human requirement for vitamin A has been another problem with its own chequered history of good work done under difficulties, and the Sheffield wartime experiment on volunteers has its niche in the history of the subject.T h e deficiency syndrome was at first (perhaps necessarily) oversimplified, but as time has gone on appreciation of its complexities has grown. Hypervitaminosis A has in some respects been as revealing as hypovitaminosis, and experiments with tissue cultures have enriched notions based on experiments with intact animals. Links with the incidence of congenital abnormalities have shown that vitamin A can be teratogenic as well as indispensable. The variety of deficiency signs shown by different species has enlarged and complicated our outlook.My colleagues, Howell, Pitt and Thompson, have studied vitamin A acid (retinoic acid) with results which have not lost any interest to me through familiarity. I am left with a feeling that despite the enormous-and in many ways deeply satisfyingbody of knowledge about vitamin A we are still short of essential biochemical information. It is not my place in an introduction to speculate about the possibility of new light on the mode of action of vitamin A. I am here to listen. I am convinced, however, that the intellectual consummation of half a century of research has still to come. When it does we may be surprised at the sign-posts on the road which escaped our attention but were there all the time! REFERENCE McCollum, E.

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“…Fanconi und M it arb eiter ko n n ten bereits 1947 ü b er 67 eigene Fälle, d a ru n te r 14mal Geschwister, berichten. N ach Andersen [1953] ist die zystische P ankreasfibrose in etw a 3% aller A utopsien von N eugeborenen und K indern im B abies-H ospital New Y ork anzutreffen, au f alle Ge b u rte n bezogen m ach t dies 1,7 Prom ille aus! In den betroffenen Fam ilien sind 22 und m ehr P ro zen t der G eschwister befallen.…”

Section: Familiäre Bronchiektasien Gleichzeitig M It Zystischer Pankrunclassified

Familiäres Vorkommen von Bronchiektasien

Kartagener¹,

Mülly²

1956

Respiration

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Celiac Syndrome

Cited by 141 publications

References 14 publications

Congenital Fibrocystic Disease of the Pancreas: A Report of Two Proved Cases of Dissimilar Clinical Types in Siblings

Congenital Fibrocystic Disease of the Pancreas: A Report of Two Proved Cases of Dissimilar Clinical Types in Siblings

Vitamin A deficiency and excess

Familiäres Vorkommen von Bronchiektasien

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