Low Prevalence of Islet Autoantibodies in Patients With Gestational Diabetes Mellitus

Dozio, Nicoletta; Beretta, Andrea; Belloni, Cristina; Castiglioni, M.; Rosa, Susanna; Bosi, Emanuele; Bonifacio, Ezio

doi:10.2337/diacare.20.1.81

Cited by 38 publications

(46 citation statements)

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“…This finding is consistent with a series of studies performed in Finnish [57], other Scandinavian [59], Italian [60,61], German [62] and US [63] women with GDM. These studies link the given polymorphism to the disease with a reported frequency of the polymorphism varied from 2.2% to 9.5%.…”

Section: Gad65absupporting

confidence: 95%

Genetics in Gestational Diabetes Mellitus: Association with Incidence, Severity, Pregnancy Outcome and Response to Treatment

Lambrinoudaki

Vlachou²,

Creatsas³

2010

CDR

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Constant advances in gene mapping technology have allowed research to focus from rare monogenic disorders on common complex diseases involving multiple susceptibility genes-environment interactions. Gestational diabetes mellitus (GDM) is a heterogeneous pathogenic condition affecting 2-5% of all pregnant women during pregnancy. GDM is considered to result when genetic predisposition is triggered by increased insulin resistance during pregnancy leading to what seems to be one of the primary characteristics of GDM, the pancreatic b-cell impairment. Genetic predisposition to GDM has been suggested given the occurrence of the disease within family members. Furthermore, GDM is reported to be often present in women with maturity onset diabetes of the young (MODY) gene mutations. In addition, candidate susceptibility gene variants have been suggested to increase the risk of GDM. These genes include glucokinase (GCK), HLA antigens, insulin receptor (INSR), insulin-like growth factor-2 (IGF2), HNF4A, insulin gene (INS-VNTR), plasminogen activator inhibitor 1 (PAI-1), potassium inwardly rectifying channel subfamily J, member 11 (KCNJ11), hepatocyte nuclear factor-4a (HNF4A). Identification of the possible underlying genetic factors of GDM would eventually enrich our knowledge on the pathophysiologic mechanism of the disease and contribute to the individualization of both prevention and treatment of complications for the mother and fetus. However, so far, little is known about the genetic basis of GDM and its potential clinical significance. This review focuses on possible gestational diabetes mellitus susceptibility genes and their association with the disease incidence and severity as well as the pregnancy outcome and the response to treatment.

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Section: Gad65absupporting

confidence: 95%

Genetics in Gestational Diabetes Mellitus: Association with Incidence, Severity, Pregnancy Outcome and Response to Treatment

Lambrinoudaki

Vlachou²,

Creatsas³

2010

CDR

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“…The frequency of ICAs found in this study lies within the prevalence range of 1.6-12.4% previously reported by others (6,7,(24)(25)(26)(27)30), using standardized immunofluorescence techniques. As for GADAs, the prevalence in the GDM-A subgroup (5.4%) was similar, compared with a Caucasian GDM-A population from Spain (6%) (28), but higher, compared with two GDM-A populations from Denmark (2.2%) (29) and Northern Italy (0%) (27). Possible reasons for this variability may be differences in the ethnic origin of the patient populations, differences in the criteria used for the diagnosis of GDM, and differences in the control population used to establish the normal range of antibodies in pregnancy.…”

Section: Discussionsupporting

confidence: 62%

Prediction of Type 1 Diabetes Postpartum in Patients With Gestational Diabetes Mellitus by Combined Islet Cell Autoantibody Screening: A Prospective Multicenter Study

et al. 1997

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Women with gestational diabetes mellitus (GDM) have a considerable risk of developing diabetes later in life. To determine the predictive value of autoantibody markers in gestational diabetic pregnancy for the development of type 1 diabetes postpartum, we tested 437 patients with GDM (289 women treated with diet only [GDM-A] and 148 requiring insulin treatment during pregnancy [GDM-B]) for antibodies to islet cells (ICAs), GAD (GADAs), and tyrosine phosphatase ICA512/IA-2 (IA2As). We prospectively followed them with repeated oral glucose tolerance tests and antibody determinations for up to 7 years postpartum (mean, 1.6 years; range, 0-7.2 years). The cumulative risk of diabetes up to 5 years postpartum was 17% (95% CI 12-22%). The risk of type 1 diabetes was 3% (2-5%) by 9 months and 7% (4-9%) 2 years after delivery. At delivery, 8.5% of all patients were ICA+, 9.5% were GADA+, 6.2% were IA2A+, and 18.1% were positive for at least one antibody (12.6% for GDM-A vs. 30.4% for GDM-B, P < 0.0001). During follow-up, GADAs persisted in 75%, ICAs in 35%, and IA2As in 30% of the subjects positive for the respective marker at delivery. By 2 years postpartum, 29% (19-39%) of patients positive for at least one antibody developed type 1 diabetes, compared with 2% (1-4%) of antibody-negative patients (P < 0.0001). Thereby, the risk for type 1 diabetes 2 years postpartum increased with the number of antibodies present at delivery from 17% (6-28%) for one antibody, to 61% (30-91%) for two antibodies, and to 84% (55-100%) for 3 antibodies. Risk of progression to type 1 diabetes postpartum was also associated with the status of parity. Women with one or more pregnancies before the index pregnancy had a higher risk for type 1 diabetes 2 years after delivery (14.7% [4.9.-24.5%]) than women having their first (i.e., index) pregnancy (5% [2.9-7.1%]) (P < 0.006). A comparison of different prediction strategies showed that single antibody screening with GADA yielded the highest sensitivity of 63% (45-75%), compared with ICA (48% [31-65%]) and IA2A (34% [13-47%]). Combined screening with two autoantibodies increased sensitivity to 74% (58-90%) and 75% (60-92%) when using GADA plus ICA or GADA plus IA2A, respectively. Screening with all three markers improved sensitivity further to 82% (67-100%). Beta-cell autoantibodies determined at delivery in women with GDM are highly predictive for the development of type 1 diabetes postpartum. Autoantibody screening in pregnant women with GDM from populations at high risk for type 1 diabetes should therefore be considered to allow early diagnosis and appropriate therapy.

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“…In contrast, Dozio et al [6] observed only low frequencies of islet cell autoimmunity (ICA, insulin autoantibody [IAA]) among GDM patients, similar to the prevalence found in women with normal glucose tolerance. None of Gestational diabetes mellitus (GDM) is a heterogeneous entity, including carbohydrate intolerance of variable severity with onset or first recognition during pregnancy.…”

Section: Pathogenesis Of Gdmmentioning

confidence: 66%

Current controversies in the mechanisms and treatment of gestational diabetes

Tamás

Kerényi²

2002

Curr Diab Rep

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Gestational diabetes mellitus (GDM) is a heterogeneous entity, including carbohydrate intolerance of variable severity with onset or first recognition during pregnancy. Insulin resistance and beta-cell dysfunction are thought to be major determinants of its development. Its pathomechanism in many ways resembles that of type 2 diabetes. There is an evolving body of evidence from the last decade presenting similarities between gestational diabetes and the metabolic (insulin resistance) syndrome. These new observations suggest that GDM might be an early manifestation of the metabolic syndrome. The desired treatment target of GDM is normoglycemia. It can be reached by dietary treatment; however, if it fails, maternal glycemic monitoring or combined fetal-maternal monitoring, or even insulin (if required) can help reach it. Multiple daily insulin regimens are becoming more widely accepted for the treatment of GDM. Insulin analogues, however, need some more evidence to support their usefulness and safety during pregnancy. The screening for GDM, the reclassification, regular care, and follow-up of these women after pregnancy are of the utmost importance to delay or prevent not only type 2 diabetes but cardiovascular complications as well.

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Low Prevalence of Islet Autoantibodies in Patients With Gestational Diabetes Mellitus

Abstract: Low-titer ICAs and IAAs are not infrequent in pregnant women, but multiple islet autoantibodies and antibodies to GAD65 or IA-2 were not found in GDM. These findings suggest that the serological characteristics of IDDM are rare in GDM.

Cited by 38 publications

References 0 publications

Genetics in Gestational Diabetes Mellitus: Association with Incidence, Severity, Pregnancy Outcome and Response to Treatment

Genetics in Gestational Diabetes Mellitus: Association with Incidence, Severity, Pregnancy Outcome and Response to Treatment

Prediction of Type 1 Diabetes Postpartum in Patients With Gestational Diabetes Mellitus by Combined Islet Cell Autoantibody Screening: A Prospective Multicenter Study

Current controversies in the mechanisms and treatment of gestational diabetes

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