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Biomedical subjects

A Vambergue

Publications and source records attributed to A Vambergue.

17 recordsLinked to original sources
PubMed2006

Follow-up study of two sisters with type A syndrome of severe insulin resistance gives a new insight into PCOS pathogenesis in relation to puberty and pregnancy outcome: a case report.

We report two sisters with profound insulin resistance associated with a novel heterozygous missense mutation in exon 19 (His1130Arg) of the insulin receptor gene. The eldest was seen after puberty at age 15 and she presented a severe form of polycystic ovary syndrome (PCOS) with biological hyperandrogenism (HA) mimicking a virilizing tumour. However, she has been able to ovulate under clomiphene citrate (CC) and to achieve two uneventful pregnancies. The patient had no glucose tolerance abnormality during pregnancies. The outcome of pregnancy was good except for a low birthweight. The youngest sister was seen earlier in life (at age 11) before puberty. First, she developed polycystic ovaries (PCO), seen under ultrasound scan, and later also developed full PCOS. This second finding gave us the opportunity to observe that PCO developed before and at the beginning of puberty despite low LH levels. We postulate that the development of PCO was the consequence of an LH-independent intra-ovarian HA likely induced by the severe hyperinsulinism in the context of genetic abnormalities.

Adolescent↗
PubMed2002

Pregnancy induced hypertension in women with gestational carbohydrate intolerance: the diagest study.

OBJECTIVE: To determine the relationship between pregnancy induced hypertension (PIH) and gestational glucose intolerance. METHODS: A 50g, 1h glucose loading test was offered to all pregnant women between 24 and 28 weeks of gestation in 15 centres in northern France during 8 months in 1992. If the test was positive (> or =7.2 mmol/l), the woman underwent a 3h oral glucose tolerance test (OGTT) as soon as possible. Using the criteria of Carpenter and Coustan, gestational diabetes mellitus (GDM) was defined by two abnormal values (n=218) and gestational mild hyperglycemia (GMH) by one abnormal value (n=130). Each control group was defined by a 50g, 1h loading test result of <7.2 mmol/l (n=108).PIH included gestational hypertension (GH) and preeclampsia (PE). GH was defined as a diastolic pressure of more than 85 mmHg on at least two occasions arising during pregnancy. PE was defined as GH with proteinuria > or =500 mg/24h. RESULTS: The rate of PIH in the three groups (GDM; GMH and control group, C) was, respectively 17.0, 10.8, and 4.6%. All the six PE occurred in the GDM group. Univariate analysis showed significantly higher rate of hypertension in women with a history of PE, increasing body mass index before pregnancy (BMI) and glucose intolerance. In multivariate analysis with adjustment for primiparity, independent risk factors for PIH were a history of PE, BMI>27 and GDM, contrary to GMH and maternal age. CONCLUSIONS: PIH appears to be linked to the level of glucose intolerance during pregnancy, independently of other known factors of hypertension.

Adult↗
PubMed2002

CTLA-4 49 A/G dimorphism and type 1 diabetes susceptibility: a French case-control study and segregation analysis. Evidence of a maternal effect.

Several studies have demonstrated an association of cytotoxic T lymphocyte-associated molecule 4 (CTLA-4) (IDDM 12) alanine 17 with type 1 diabetes, but we wished to study the parental effect of CTLA-4 49 A/G dimorphism in diabetic families. The CTLA-4 exon 1 polymorphism (49 A/G), HLA-DRB1 and insulin gene (INS) variable number tandem repeats (VNTR) were analysed in 134 type 1 diabetic patients vs. 273 control subjects. The segregation analysis for transmission was carried out in 70 informative diabetic families using the transmission distortion test (TDT). All genotyping was performed by PCR-RFLP. CTLA-4 49 G allele frequency was not increased in diabetic patients compared to controls (41 vs. 38%, not significant). The distribution of GG, AG and AA CTLA-4 genotypes was similar in the two groups (13, 57 and 30% vs. 11, 54 and 35%, respectively) and was independent of HLA-DRB1 or INS VNTR polymorphism. The CTLA-4 49 G allele showed weak distorted transmission to the diabetic offspring, whereas random transmission was observed in unaffected offspring. This distortion is attributable to a maternal effect (71% compared to the 50% expected ratio; tdt = 4.8; P < 0.03). The combined transmission of maternal CTLA-4 G with HLA-DRB1*03 (90%; tdt = 6.4; P < 0.01) and VNTR class I (80%; tdt = 5.4; P < 0.02) enhanced the susceptibility effect of each marker separately. We noted a slight CTLA-4 49 G and HLA-DRB1*04 distortion of transmission shared in paternal and maternal diabetic meiosis. In non-diabetic offspring, the CTLA-4 49 A allele confers a protective effect in the presence of maternal HLA-DRB1*03 and paternal HLA-DRB1*04 alleles. Despite the absence of a positive association of the CTLA-4 49 G allele with type 1 diabetes, our segregation analysis supports the hypothesis of a modulation by CTLA-4 49 G/A dimorphism of the susceptibility conferred by maternal HLA-DRB1*03 inheritance. This potential parental effect needs to be confirmed in a larger data set.

Adenine↗
PubMed2002

[Pathophysiology of gestational diabetes].

During pregnancy, a number of maternal metabolic changes occur early and continue throughout pregnancy which help optimize the transfer of nutrients to the fetus. During normal pregnancy, there are a decrease in insulin sensibility which is physiological, progressive and reverse. For glucose tolerance to be maintained in pregnancy it is necessary for maternal insulin secretion to increase sufficiently to counteract the fall in insulin sensitivity. The metabolic characteristic of women with gestational diabetes is insufficient insulin secretion to counteract the pregnancy related fall in insulin sensitivity. There are a lot of factors that could explain the mechanism of insulin secretion and insulin sensitivity during normal pregnancy and gestational diabetes mellitus. Although glucose tolerance normalizes shortly after pregnancy with gestational diabetes in the majority of women, the risk of developing overt diabetes, especially type 2 diabetes is markedly increased. The mechanisms which could explain gestational diabetes are the same as type 2 diabetes mellitus. We could speculate that these two diseases are identical for alterations in carbohydrate metabolism, but at different stages.

Diabetes, Gestational↗
PubMed2002

[Maternal and fetal outcome].

Gestational diabetes, a glucose tolerance disorder of variable severity which occurs or is diagnosed for the first time during pregnancy, constitutes a public health problem because of its frequency (1 to 6% of all pregnancies) and its short-or long term consequences for the foetus and/or the mother. There is as yet still no consensus concerning screening and diagnosis criteria, therapeutic management and the reality of the disease. This population is a high risk population of diabetes mellitus, especially of type 2 diabetes. We could think that the introduction of specific prevention programs in this group could delay or avoid diabetes mellitus and its complications. The mechanisms which could explain gestational diabetes are the same as type 2 diabetes mellitus. We could speculate that these two diseases are identical for alterations in carbohydrate metabolism, but at different stages. It has been reported that the offspring of gestational diabetics mothers are at risk of obesity and glucose intolerance. Therapeutic management of the mother and/or the offspring should be better defined. The screening for gestational diabetes provides an opportunity of identify a large population of women and children at risk of diabetes. It should be possible to avoid diabetes mellitus by specific therapeutic programs in these populations.

Diabetes Mellitus, Type 2↗
PubMed2001

Factor VII, tissue factor pathway inhibitor, and monocyte tissue factor in diabetes mellitus: influence of type of diabetes, obesity index, and age.

Changes of the tissue factor (TF) pathway of blood coagulation have been described in diabetes and could be involved in its vascular complications. In order to evaluate the influence of the type of diabetes and of the obesity index and age on these changes, factor VII coagulant activity, factor VII antigen, activated factor VII, monocyte TF expression, and plasma Tissue Factor Pathway Inhibitor (TFPI) were examined in 18 Type 1 and 16 Type 2 diabetic patients compared to non-diabetic control subjects matched for age, sex, and obesity index (Types 1 and 2 controls, respectively). Multicomplicated patients were excluded. FVIIc, FVIIAg, and FVIIa were higher in Type 2 diabetic patients and controls than in Type 1 diabetic patients and controls (P< .03). However, FVIIc and FVIIAg were lower in diabetic patients than in their matched controls (P< .03). Monocyte expression of TF was not different between Types 1 and 2 diabetic patients and their matched controls except for LPS-stimulated monocyte TF activity which was lower in Type 2 diabetic patients than in Type 2 controls (P< .05). Plasma TFPI was slightly but significantly higher in Type 1 diabetic patients than in Type 1 controls (P= .01) and was correlated to glycemia. However, both in Type 2 diabetic patients and controls, TFPI was higher than in Type 1 controls and was correlated with BMI (P< .0003). These results indicate that in not multicomplicated patients, the increase of FVII and TFPI was highly dependent on obesity index and age rather than on diabetes by itself.

Adult↗
PubMed2001

Higher carbohydrate intake is associated with decreased incidence of newborn macrosomia in women with gestational diabetes.

OBJECTIVE: To study the influence of energy and macronutrient intake on infant birthweight in women with gestational diabetes mellitus undergoing intensive management. DESIGN: This prospective study evaluated the impact of intensive management of gestational diabetes on maternal and fetal morbidity, and addressed the relationship between food intake and infant birthweight. SETTING: Fifteen maternity hospitals in northern France. SUBJECTS: Ninety-nine women with gestational diabetes or gestational mild hyperglycemia diagnosed between 24 and 34 weeks of gestation were surveyed. After 1 was excluded because of a premature birth and 18 were excluded as underreporters, 80 women were included in the final analysis. Diet intake was assessed by a dietary history at the first interview, and by two 3-day diet records at the 3rd and 7th week after diagnosis. RESULTS: In a forward-stepwise regression analysis (controlling for maternal age; smoking; parity; prepregnancy BMI; pregnancy weight gain; gestational duration; infant sex; fasting and 2-hour postprandial serum glucose; insulin therapy; and energy, fat, protein and carbohydrate intake during treatment) infant birthweight was positively associated with gestational duration (beta = +0.34, P<.002), and negatively with smoking (beta = -0.27, P<.02) and carbohydrate intake (beta = -0.24, P<.03). There were no large-for-gestational-age infants among women whose carbohydrate intake exceeded 210 g/day. CONCLUSION: For women with gestational diabetes undergoing intensive management, higher carbohydrate intake is associated with decreased incidence of macrosomia. APPLICATION: These findings suggest that nutrition counseling in gestational diabetes must be directed to maintain a sufficient carbohydrate intake (at least 250 g per day), which implies a low-fat diet to limit energy intake. A careful distribution of carbohydrate throughout the day and the use of low-glycemic index foods may help limit postprandial hyperglycemia.

Adult↗
PubMed2001

[What is the approach to gestational diabetes in 2001?].

In 2001, gestational diabetes (GD) remains the subject of much debate, particularly as regards screening and diagnosis, therapeutic management and effects on perinatal outcome. It continues to be defined as a disorder of glucose tolerance occurring for the first time during pregnancy, whatever the outcome during the post-partum period. There is as yet still no consensus concerning screening and diagnosis criteria, partly due to the existence of a continuum between maternal blood glucose levels and perinatal outcome, which means that any threshold is necessarily arbitrary. There is no general agreement concerning therapeutic management. As regards diet, there are insufficient randomised prospective studies that could serve to establish minimum required calorie intakes and various regimen. Intervention studies should provide more accurate information concerning the role of diet in therapeutic strategies. It is also necessary to define the role of other therapeutic alternatives such as insulin analogues, or more recently, the sulphonylureas. Nevertheless, although there is still a large debate, the physiopathological mechanisms are becoming increasingly clear. GD and type 2 diabetes appear to be the same entity, with the former constituting an early sign of the latter. Long-term management of women with GD and treatment modalities also require better definition, since these patients are at risk for diabetes, mainly type 2.

Blood Glucose↗
PubMed2000

Is mild gestational hyperglycaemia associated with maternal and neonatal complications? The Diagest Study.

AIMS: To evaluate the maternal and neonatal complications rates of mild gestational hyperglycaemia (MGH) compared to a control group in France. METHODS: A systematic screening by a 50-g glucose challenge test was offered to all women between 24 and 28 weeks of gestation in 15 maternity units. If the 50-g glucose challenge test was > or = 7.2 mmol/l, a 100-g 3-h oral glucose tolerance test (OGTT) was performed. MGH (n = 131) was defined by one abnormal value on the 3-h OGTT (Carpenter and Coustan criteria). The control group (n = 108) was defined by a 50-g glucose challenge test below 7.2 mmol/l. Women with MGH received no treatment or specific advice during the pregnancy. Large for gestational age (LGA) was defined by a birth weight of at least the 90th percentile on French standard growth curves. RESULTS: Women with MGH were older than the controls (28.8 (5.8) vs. 27.0 (5.2); P < 0.05) and had a higher body mass index (24.8 (4.8) vs. 23.0 (3.9); P < 0.01). The rate of pregnancy-induced hypertension and Caesarean section were not different between the MGH and control group. The rate of LGA was significantly higher in the MGH group than the control group (22.1% vs. 11.4%; P < 0.05). After adjustment for confounding factors of macrosomia (pre-pregnancy body mass index > 27, maternal age > 35, multiparity and educational level), there was a persistent relationship between LGA and MGH (odds ratio 2.50; 95% confidence interval (1.16-5.40); P < 0.05). MGH was more frequently associated with adverse maternal and fetal outcome than in the controls (53.4% vs. 28.7%; P < 0.01). CONCLUSIONS: This study suggested that the increased rate of adverse maternal and fetal outcome, especially LGA, was associated with untreated mild gestational hyperglycaemia women compared to a control group. This link to lower degrees of hyperglycaemia during pregnancy is independent of confounding factors.

Birth Weight↗
PubMed2000

Autoimmune markers in slow type 1 diabetes: confrontation to type 1 diabetes.

UNLABELLED: Slow onset type 1 diabetes is an heterogeneous entity. Its clinical features may mimick type 2 diabetes but its pathophysiological mechanisms are close to type 1 diabetes. AIM OF THE STUDY: To find out the frequencies, levels and associations of ICA, GADab and IA-2ab in type 2 diabetic patients with atypical phenotype. To compare it to type 1 diabetes. PATIENTS AND METHODS: ICA, GADab and IA-2ab were determined in: - 61 patients (age at diagnosis 48.2 +/- 10, range 36-73 years) with an initial diagnosis of type 2 diabetes but having at least one symptom suggesting a slow type 1 diabetes (loss of weight, absence of obesity at diagnosis or secondary failure of oral hypoglycaemic agents). - 70 patients with type 1 diabetes (age 18 +/- 8.9, range 2-35 years). Clinical data evaluated in slow type 1 were maximal BMI, BMI and loss of weight at diagnosis and autoimmune disease. Fasting C-peptide and insulinemia were also assessed. RESULTS: (Slow type 1 diabetes versus type 1 diabetes). ICA (43% vs 70%; p <0.01) and IA-2ab (16% vs 75%; p <0.01) were more frequent in type 1. GADab were as frequent (62% vs 74%). Association of the three antibodies (15.7% vs 58.5%; p <0.05) were more frequent in type 1. Prevalence of GADab alone (27.5% vs 7.5%; p <0.05) was higher in slow type 1 diabetes and with higher levels (median 55.5 UI/ml vs 17 UI/ml; p <0.01). There was no difference for levels of ICA (25.5 UJDF/ml vs 28 UJDF/ml) or IA-2ab (11.5 UI/ml vs 38.5 UI/ml). BMI of GADab positive patients was lower. Delay of insulinotherapy was shorter in GADab or ICA positive patients. We did not find any relationship between antibodies presence and fasting C-peptide or insulinemia. CONCLUSION: Slow type 1 diabetes should be evoked in atypical type 2 diabetes. Slow onset type 1 diabetic patients have different autoimmune patterns suggesting a different pathophysiological process. GADab and ICA are useful markers to predict future insulinopenia.

Adult↗
PubMed1997

Gestational diabetes mellitus and HLA class II (-DQ, -DR) association: The Digest Study.

Gestational diabetes mellitus (GDM) and impaired glucose tolerance during pregnancy (IGT) are associated with an increased risk of perinatal morbidity and then further development of diabetes among 30-50% of affected women. This is a real public health problem that deserves investigation of phenotypic and genotypic predisposing markers. However, the involvement of genetic background in GDM and IGT remains unclear. In particular, association with HLA class II polymorphism has been poorly studied and has produced conflicting results. In attempt to clarify these discrepancies, we investigated HLA class II polymorphism in 95 GDM and 95 IGT women from the north of France using DNA amplification followed by restriction enzyme digestion (PCR-RFLP). Ninety-five pregnant women with normal glucose tolerance (NGT) were chosen as a control reference group. The distribution of HLA class II polymorphism was not found to be significantly different between GDM, IGT and NGT samples. In particular, we did not find any significant variation of DRB1*03 and DRB1*04 allele frequencies between these three groups. These data provide further evidence that insulin-dependent diabetes mellitus (IDDM) HLA class II susceptibility alleles cannot serve as genetic markers for susceptibility to glucose intolerance during pregnancy. However, GDM and IGT were not equivalent to the NGT control group and presented particular HLA patterns. In particular, we observed an increase of the DRB1*0701-DQA1*0201-DQB1*02 haplotype in GDM women (P = 0.02; Pc not significant) and an increase of DRB1*0101-DQA1*0101-DQB1*0501 and DRB1*1302-DQA1*0102-DQB1*0604 haplotypes in the IGT group (P = 0.02 and 8 x 10(-3), respectively; Pc not significant). In contrast, we found a decrease in the DRB1*1101 allele in IGT samples (P = 0.03; Pc not significant) and a decrease of DRB1*1103-*1104 alleles in the GDM group (P = 9 x 10(-3); Pc not significant). Although these findings are only descriptive, it points out the genetic heterogeneity of glucose intolerance during pregnancy.

Alleles↗
PubMed1997

[Gestational diabetes: long-term maternal consequences].

Gestational diabetes, a glucose tolerance disorder of variable severity which occurs or is diagnosed for the first time during pregnancy, constitutes a public health problem because of its frequency (1 to 6% of all pregnancies) and its short- or long-term consequences for the fetus and/or the mother. The classical maternal complications are gravidic hypertension, preeclampsia and cesarean section. The dominant short-term effects on the fetus are macrosomia and metabolic complications. Progression to diabetes mellitus (essentially non-insulin-dependent) represents a serious long-term risk for the mother. Systematic screening of gestational diabetes can prevent complications through an optimal care programme and target a very high risk population in order to delay or avoid the occurrence of diabetes and its complications.

Biomarkers↗
PubMed1996

[Results of sub-inguinal revascularization in the treatment of diabetic ischemic foot].

From January 1993 to August 1995, we performed 60 revascularizations of the lower limb using 65 bypasses in 55 patients (32 men, 23 women, mean age 66.6 yars) with diabetes. Trophic lesions of the foot existed in 57 of the revascularizations, and in 3 cases pain was provoked by the supine position. Supra-articular femoropopliteal bypass was performed in 8 cases, subarticular femoropopliteal bypasses in 25, femorotibial bypasses in 14 and paramalleolar bypasses in 18. There were 6 post-operative deaths. Six major amputations were required including 2 despite patent bypasses. Twenty-nine minor amputations were required for trophic disorders. There were 5 deaths after the postoperative period in which 4 major amputations were required despite patent bypasses in 2 cases. Retarded cicatrization was seen in 13 of the amputation stumps of areas of atrophism. Actuarial survival at 2 years was 77 +/- 6% with primary patency of 53 +/- 9.5% and secondary patency of 74 +/- 7%. The rate of success in saving the lower limb was 80.5 +/- 5.6%. Bypass revascularization has been effective in the treatment of the diabetic ischemic foot. Operative mortality was high, resulting from associated cerebral vascular events and coronary heart disease.

Aged↗
PubMedDate not supplied

[Lipids, hemostasis and diabetes].

Modifications of hemostasis and plasma lipids are an integral part of diabetes mellitus, and probably play a key role in the evolution of vascular complications. This review points to the important relationships between hemostasis and lipids and their modifications in diabetes, with a special attempt to link the abnormalities described with the pathogenic mechanisms of diabetes.

Animals↗