Immunological Diseases and Pregnancy

Scott, James S.

doi:10.1136/bmj.1.5503.1559

Cited by 50 publications

(11 citation statements)

References 69 publications

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“…The idea that insulin antagonism, due to the transplacental passage of antibodies, could cause transient neonatal diabetes was put forward by Scott (1966). The suggestion rested on the fact that passively acquired maternal antibodies persist in the newborn for approximately 12-16 weeks, a period similar to the common duration of transient neonatal diabetes.…”

Section: Discussionmentioning

confidence: 99%

Transient Neonatal Diabetes Mellitus in Sibs

Ferguson¹,

Mliner²

1970

Archives of Disease in Childhood

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The infant was breast-fed and sucked well. However, he failed to gain weight, and on the 15th day began to vomit occasionally. On the 19th day he was transferred to the Children's Ward for further investigation. He then weighed 2065 g., was marasmic, wide-eyed, and thirsty, with a rectal temperature of 39*4 'C.( Fig.). Blood sugar, 720 mg./100 ml.; CSF sugar, 405 mg./100 ml.; CSF protein, chloride, and cell count normal; blood urea, 77 mg./100 ml.; urine contained 2% sugar but no ketones.A subcutaneous infusion of 1/5 normal saline was given. All urine voided was collected and tested for sugar and acetone. Soluble insulin was given two or three times daily in doses ranging from 2 to 6 units.Ketones were never found in the urine. Administered insulin totalled 12 units daily for most of the first fortnight, but thereafter the dose gradually fell. No attempt was made to keep the urine entirely sugarfree because of the particular dangers of hypoglycaemia in infancy. However, at 5 weeks a brief hypoglycaemic convulsion occurred which was terminated by intravenous glucose. From the start of treatment there was immediate clinical improvement and a steady gain in weight.At 6 weeks intermittent vomiting, abdominal distension, fever, and diarrhoea developed, associated on three occasions (2, 3, and 6 January 1964) with serum potassium over 7 mEq/l., and with low sodium and chloride levels. On these dates blood sugar levels of 550, 770, and 60 mg./100 ml. were recorded. The 24-hour urinary 17-oxosteroid and total oxogenic steroid excretion (5-6 January) were 0 * 15 and 0 * 64 mg., respectively. Blood urea was 30 mg./100 ml. and blood culture was negative. There was a tachycardia of 200/min., and the systolic blood pressure in the arm by the flush technique was 75 mm. Hg. Adrenal insufficiency was suspected and desoxycorticosterone acetate 1 mg. daily and subcutaneous 1/5 normal saline were administered from [7][8][9][10]

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Section: Discussionmentioning

confidence: 99%

Transient Neonatal Diabetes Mellitus in Sibs

Ferguson¹,

Mliner²

1970

Archives of Disease in Childhood

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“…Assuming, however, that ideological thinking will be overcome and more unbiased intellectual curiosity returns to the investigation of autoimmune-associated female infertility, one can predict not only great progress in the understanding of how the immune system promotes (and/or inhibits) female fertility, but also a better understanding of autoimmunity and allograft tolerance. Scott noted, decades previously, that pregnancy could represent the ideal 'research animal' for the investigation of abnormal autoimmune function [58]. We hopefully should be able to follow up on his suggestion.…”

Section: Five-year Viewmentioning

confidence: 91%

“…All of this demonstrates that certain physiological pathways of the immune system, if properly defined and isolated, may lend themselves to diagnostic and/or therapeutic use [6]. As Scott noted many years ago, pregnancy may represent an almost ideal experimental model for the investigation of abnormal autoimmunity [58].…”

Section: Flares and Pregnancymentioning

confidence: 99%

Female infertility due to abnormal autoimmunity: frequently overlooked and greatly underappreciated. Part I

Gleicher¹,

Weghofer²,

Barad³

2007

Expert Review of Obstetrics & Gynecology

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When the impact of abnormal autoimmune function on female fertility is objectively examined, an unexpectedly large contribution is (auto)immune related. This may be surprising since many authorities have been dismissive of (auto)immune-associated infertility. In this article, we therefore summarize the link between abnormal autoimmune function and female infertility, based on literature searches. Abnormal autoimmune function affects female fertility at numerous levels of the reproductive process. As with autoimmune conditions in general, abnormal autoimmune function affecting fertility is often difficult to diagnose since it frequently presents subclinically, without overt clinical symptoms. It also demonstrates other characteristics of abnormal autoimmunity, such as familial occurrence and genetic predisposition, environmental cofactors contributing to phenotypic expression of genetic risk and cyclicity of occurrence, often characterized by gestational exacerbation patterns. Proven treatments for autoimmune-associated infertility have not been established to date. This fact should, however, not preclude efforts to reach correct diagnoses, since only accurate diagnoses can lead to appropriately conducted clinical trials.Expert Rev. Obstet. Gynecol. 2(4), 453-464 (2007) "Fashions are the only induced epidemics, proving that epidemics can be induced by tradesmen." Bernard Shaw Bernard Shaw's quotation astutely comments on both the fickleness of fashion and the general fickleness of thought. By utilizing epidemics as acronyms for periodic, irrational behavior, he reminds us that fashionable behavior permeates all spheres of life, including, of course, the science of medicine.The thinking on autoimmune abnormalities in reproductive medicine is a good example. A highly popular topic during the 1980s and early 1990s, autoimmunity fell out of fashion by the end of the last decade. Some prominent individuals [1,2] and professional organizations [3] succeeded to a large degree in relegating the concept that abnormal autoimmune function can adversely affect female fertility to the dustbin of undistinguished, and failed, ideas. This article aims to balance an, at times quite opinionated, discourse [2,4]. As this twopart series of articles will demonstrate, abnormal autoimmune function can indeed interfere with successful human reproduction at quite a number of different levels.

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“…There are several diseases known to be mediated by transplacentally acquired maternal antibody-for example, haemolytic disease of the newborn and neonatal thyrotoxicosis attributable to transplacentally acquired long acting thyroid stimulator. 29 On the other hand, we are not aware of published evidence that a fetus may produce antiidiotype antibodies to matemal antibody or that maternal antibody can lead to disease many years later. Though speculative, this mechanism is at least suggestive of processes which would be extremely difficult to detect except through such a study population as ours.…”

Section: Discussionmentioning

confidence: 99%