Prevalence and Predictive Value of Islet Cell Antibodies and Insulin Autoantibodies in Women with Gestational Diabetes

Damm, Peter; Kühl, Claus; Buschard, Karsten; Jakobsen, B. K.; Svejgaard, A.; Sodoyez-Goffaux, F; Shattock, Marion; Bottazzo, G. F.; Mølsted‐Pedersen, Lars

doi:10.1111/j.1464-5491.1994.tb02035.x

Cited by 82 publications

(75 citation statements)

References 22 publications

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“…The same negative association between DR2, which is in linkage disequilibrium with DQB1*0602, and GDM has been reported in some studies [6,8]. Most previous studies, however, have reported an association with the high-risk HLA-DR3 and -DR4.…”

Section: Discussionsupporting

confidence: 79%

The type 1 diabetes protective HLA DQB1*0602 allele is less frequent in gestational diabetes mellitus

et al. 2009

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Aims/hypothesis We tested whether gestational diabetes mellitus (GDM) is associated with HLA-DQ genotypes. Methods A total of 764 mothers with non-autoimmune (GAD65, insulinoma-associated protein 2 [IA-2] and insulin autoantibody-negative) GDM were ascertained between September 2000 and August 2004 in the population-based Diabetes Prediction in Skåne (DiPiS) study. HLA-DQB1 genotypes were determined in these mothers and in 1191 randomly selected non-diabetic control mothers also negative for islet autoantibodies. The data were analysed in relation to maternal age, country of birth, number of pregnancies/ siblings and pregnancy weight gain. Results The frequency of type 1 diabetes high-risk HLA-DQ alleles (DQB1*0201, DQB1*0302) did not differ between GDM mothers and controls. In contrast, the low-risk DQB1*0602 allele was less prevalent (OR 0.64, 95% CI= 0.51-0.80, p=0.0006) in GDM than in control mothers. The difference in DQB1*0602 frequency between GDM mothers and controls remained after multiple logistic regression analysis correcting for maternal age, country of birth, number of pregnancies/siblings and weight gain during pregnancy (OR 0.67, 95% CI 0.51-0.88, p=0.009). Conclusions/interpretation The negative association between mothers who have non-autoimmune GDM and HLA-DQ*0602 suggest that this allele may protect not only from type 1 diabetes but also from GDM.

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Section: Discussionsupporting

confidence: 79%

The type 1 diabetes protective HLA DQB1*0602 allele is less frequent in gestational diabetes mellitus

et al. 2009

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“…Between 17 and 63 % of women whose glycosuria during pregnancy is attributable to glucose intolerance will subsequently become diabetic, depending on the series quoted [12]. Of these, a proportion (around 20 % according to one study [13]) will develop Type I diabetes, emphasizing the principle to be established here that prediabetes of Type I and Type II differ only in tempo and not in outcome. Both represent a period of accelerated beta cell loss.…”

Section: Pathophysiology Of Diabetesmentioning

confidence: 95%

The accelerator hypothesis: weight gain as the missing link between Type I and Type II diabetes

2001

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Diabetes is currently of two types. Type I (insulin-dependent) diabetes mellitus is an autoimmune disorder of childhood, characterised by acute onset, ketoacidosis and insulin dependency. Type II diabetes is a metabolic disorder of middle-life, slow in onset and non-insulin-dependent.The definitions need urgent revision. More than half of the patients with Type I diabetes present in adulthood, when their onset is slow and many do not develop acidosis or require insulin for many years [1]. Type II diabetes occurs in teenagers [2], sometimes with keto-acidosis [3], and insulin-dependency frequently ensues given time. Clinically, there is little other than tempo to distinguish two types of diabetes. The HypothesisThe`Accelerator Hypothesis' argues that Type I and Type II diabetes are one and the same, distinguishable only by their rate of beta cell loss and the accelerators responsible. The first accelerator, a constitutionally (intrinsically) high rate of beta-cell apoptosis, is necessary for diabetes to develop but in itself rarely Diabetologia (2001) AbstractBlood glucose concentrations are controlled by a loop incorporating two components, the beta cells which secrete insulin and the insulin-sensitive tissues (liver, muscle, adipose) which respond to it. Loss of blood glucose control might result from failure of the beta cells to secrete insulin, resistance of the tissues to its action, or a combination of both. The distinctions between Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus are becoming increasingly blurred both clinically and aetiologically, where beta-cell insufficiency is the shared characteristic. The`Accelerator Hypothesis' identifies three processes which variably accelerate the loss of beta cells through apoptosis: constitution, insulin resistance and autoimmunity.None of the accelerators leads to diabetes without excess weight gain, a trend which the`Accelerator Hypothesis' deems central to the rising incidence of both types of diabetes in the industrially developed world. Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. The rising blood glucose (glucotoxicity) accelerates beta-cell apoptosis directly in all and, by inducing beta-cell immunogens, further accelerates it in a subset genetically predisposed to autoimmunity. Rather than overlap between two types of diabetes, the`Accelerator Hypothesis' envisages overlay. Body mass is central to the development and rising incidence of all diabetes. Only tempo distinguishes the`types'. The control of weight gain, and with it insulin resistance, could be the means of minimising both.

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“…However, the risk factors are unable to predict all cases of subsequent type 2 diabetes: the biggest risk factor is a GDM pregnancy. The prevalence of type 1 diabetes identified 1-10 years after GDM in mostly European studies is 2.3-9.3% (Table 2) (40 -42,45) and can usually be predicted by detection of ␤-cell-related autoantibodies during or after the GDM pregnancy (26,46,(53)(54)(55)(56)(57)(58).…”

mentioning

confidence: 99%

Gestational Diabetes After Delivery

Dang-Kilduff²,

2007

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Prevalence and Predictive Value of Islet Cell Antibodies and Insulin Autoantibodies in Women with Gestational Diabetes

Cited by 82 publications

References 22 publications

The type 1 diabetes protective HLA DQB1*0602 allele is less frequent in gestational diabetes mellitus

The type 1 diabetes protective HLA DQB1*0602 allele is less frequent in gestational diabetes mellitus

The accelerator hypothesis: weight gain as the missing link between Type I and Type II diabetes

Gestational Diabetes After Delivery

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