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B Vialettes

Publications and source records attributed to B Vialettes.

At least 37 records · Page 2Linked to original sources

[Dietary assessment in current clinical practice: how to conciliate rapidity, simplicity and reliability?].

Dietary interviews and food diaries are traditionally used for nutritional assessments. In clinical practice, these methods are time consuming, require high training, and thus remain poorly used. Furthermore, the results are frequently impaired by the underreporting phenomenon which can be due either to underrecording (failure to record what is eaten) or to undereating (volontary food restriction during the assessment period). These difficulties can be overcome by using rapid questionnaires based on 2 principles: 1) underreporting is less for proteins than for other macronutrients; 2) in developed countries, calories from proteins are relatively stable and contribute approximately to one sixth of the total daily energy intake. Estimations given by the rapid questionnaire lead to less misleading results than those provided by 7 day-food records. On the other hand, the rapid questionnaire gives an estimate of specific dietary behaviors such as nibbling, festive meals and consumption of salted entrées, sweet desserts and caloric beverages. In conclusion, helpful and simple recommendations for correcting main nutritional errors can be drawn from estimation of the above mentioned specific behaviors that correspond to a daily average of 500 kcalories.

Alcohol Drinking↗

Can fructosamine be a surrogate for HbA(1c) in evaluating the achievement of therapeutic goals in diabetes?

OBJECTIVE: To determine if fructosamine can be used as a surrogate for HbA(1c) to monitor whether therapeutic goals in diabetes mellitus are achieved when HbA(1c) cannot be used for this purpose (hemoglobinopathies, anemia...). MATERIAL AND METHODS: Blood samples of 76 diabetic patients and 30 healthy subjects characterized by the absence of any risk of interference in the interpretations of HbA(1c) and fructosamine were studied in order to, first, deduce from the correlation a prediction of HbA(1c) from the fructosamine values, second, to evaluate the predictive value of such predicted HbA(1c) in the determination of poor metabolic control as defined by UKPDS and DCCT studies. RESULTS: The correlation between predicted HbA(1c) and actual fructosamine was fair (r=0.88) in diabetic patients but not in control subjects (r=0.01). It was therefore only possible to estimate HbA(1c) from fructosamine in diabetic patients. Nevertheless, the range of positive and negative predictive values of estimated HbA(1c) to detect a poor metabolic control defined by two thresholds of HbA(1c) (7%, 7.5%) was 91-93% and 86-87%, respectively. Then, even in this highly selected population, the risk of misclassification was around 10% when fructosamine was used to estimate HbA(1c). These results were unchanged when fructosamine was corrected by plasma protein level. CONCLUSIONS: This study shows the limitations to use fructosamine in place of HbA(1c) to evaluate the efficacy of antidiabetic treatments, even in a selected population.

Adult↗

Specific deficiency of p56lck expression in T lymphocytes from type 1 diabetic patients.

Peripheral T lymphocyte activation in response to TCR/CD3 stimulation is reduced in type 1 diabetic patients. To explore the basis of this deficiency, a comprehensive analysis of the signal transduction pathway downstream of the TCR/CD3 complex was performed for a cohort of patients (n = 38). The main result of the study shows that T cell hyporesponsiveness is positively correlated with a reduced amount of p56(lck) in resting T lymphocytes. Upon CD3-mediated activation, this defect leads to a hypophosphorylation of the CD3zeta-chain and few other polypeptides without affecting the recruitment of ZAP70. Other downstream effectors of the TCR/CD3 transduction machinery, such as phosphatidylinositol 3-kinase p85alpha, p59(fyn), linker for activation of T cells (LAT), and phospholipase C-gamma1, are not affected. In some patients, the severity of this phenotypic deficit could be linked to low levels of p56(lck) mRNA and resulted in the failure to efficiently induce the expression of the CD69 early activation marker. We propose that a primary deficiency in human type 1 diabetes is a defect in TCR/CD3-mediated T cell activation due to the abnormal expression of the p56(lck) tyrosine kinase.

Adolescent↗

Mitochondrial DNA variations in patients with maternally inherited diabetes and deafness syndrome.

Mitochondrial DNA (mtDNA) variants have been implicated in the pathogenesis of diabetes. A mutation in the tRNA leucine gene at position 3243 has been previously reported in mtDNA of maternally inherited diabetes and deafness (MIDD) patients. Because the true prevalence of the mitochondrial origin in diabetes may be underestimated, we searched for potentially diabetogenic anomalies of mtDNA in 9 patients highly suspected of mitochondrial diabetes selected on maternally inheritance and clinical features. In order to detect high levels of mutant DNA, the mtDNA of muscle sample of 2 patients was totally sequenced and the 22 tRNA genes and flanking sequences of 7 patients were analyzed. A new homoplasmic mutation at position 8381 was found in the ATPase 8 gene of mtDNA of a MIDD patient. The prevalence of three homoplasmic variations (G1888A, T4216G, A4917G) was significantly higher in the small group of MIDD patients compared to controls and other subjects groups. This study demonstrated in our patients sample the high frequency of homoplasmic variations, which could play a role by themselves or in combination, in the pathogenesis of diabetes.

Adult↗

Dietary fat clearance in type V hyperlipoproteinaemia secondary to a rare variant of human apolipoprotein E: the apolipoprotein E3 (Arg 136-->Ser)

This present case report describes two siblings with severe type V hyperlipoproteinaemia, diagnosed very early in life and due to the combination of the common apolipoprotein (Apo) E2 allele and rare mutant variant of ApoE, ApoE3 (Arg 136-->Ser). Phenotyping of ApoE falsely identified E2/E2 phenotype. The presence of mutated ApoE was suspected on an unusual restriction polymorphism of a Hha 1 restriction site and confirmed by sequence analysis of the cloned polymerase chain reaction fragment of exon 4 and familial segregation study. The severity of the hypertriacylglycerolaemia was modulated by the lipid content of the diet. A low-fat diet enriched in medium-chain triacylglycerol (TAG) decreased but did not normalize plasma TAG levels in both affected patients of the pedigree. A standardized lipid-enriched test meal showed a marked impairment of TAG-rich lipoprotein (TRL) clearance, especially the exogeneous TRL bearing ApoB-48 which still represented 79% of total TRL 7 h after the fat load. Finally, differences between the male and female siblings with the existence of a consanguine relationship in their parents suggested the involvement of other genetic factors in modulating the severity of phenotypic expression. This observation reinforces the usefulness of genotyping of ApoE for the characterization of genetic hypertriacylglycerolaemia and selection of the appropriate diet and treatment.

Adult↗

Humoral immunity against glutamic acid decarboxylase and tyrosine phosphatase IA-2 in Lambert-Eaton myasthenic syndrome.

Some beta-cell-specific autoantigens also are present in the central nervous system. Furthermore, stiff man syndrome, an autoimmune neurological disease, is frequently associated with diabetes and shares with this one an anti-GAD and IA-2 humoral immunoreactivity. We wondered whether these autoantibodies could be found in other neurological diseases with a present or supposed autoimmune origin. So, anti-GAD65 (GAD65A) and anti-IA-2 (IA-2A) autoantibodies were assayed in various neurological diseases. There was a higher prevalence of such antibodies in Lambert-Eaton myasthenic syndrome (LEMS) (GAD65A, 35%; IA-2A, 21%; double positivity, 18%) compared to amyotrophic lateral sclerosis (18%, 12%, and 12%, respectively) and multiple sclerosis (10%, 3%, and 3%, respectively). In LEMS, the humoral reaction was more frequent and/or appeared earlier in the paraneoplastic forms. The detection of such autoantibodies in patients with small-cell lung carcinoma (SCLC) without LEMS suggests that these autoantigens, GAD65 and IA-2, could be produced by SCLC tissue.

Adolescent↗

[Is scuba diving allowed in diabetic patients treated with insulin?].

Scuba diving is usually prohibited in diabetic patients at risk of hypoglycemic attacks (i.e. IDDM and NIDDM treated with sulfonylureas) due to the particular severity of these episodes in a hostile environment. In fact, diabetic subjects can perform this popular leisure activity without extra-risk, provided strict requisites in aptitude, practice and environment are enforced. These limitations lead to the establishment of practical guidelines, as proposed in this paper.

Diabetes Mellitus, Type 1↗

[Considerations on delocalized HbA1c assays].

Availability and knowledge of HbA(1c) value during consultation is an important feature for diabetologists, that permits a better adaptation of therapy and a better motivation of patients. This expectation explains the request for delocalized assays of HbA(1c), even though life prognosis is not affected, like in the other cases of point of care testing. One of the most frequent solutions is the use of immunological delocalized HbA(1c) assays. Technically, these methods have to meet the same criteria as those used in laboratories. They have to be standardized, and controlled according to the "Guide de Bonne Exécution des Analyses de Biologie Médicale" (GBEA) rules. Solutions chosen for delocalization must respect specific skills of clinicians and biologists and cope with cost limitations. This paper reviews rationales for delocalized HbA(1c) assays, steps of their implementation, and their use in practical routine, with a special emphasis given on the necessary complementarity between clinicians and biologists.

Biomarkers↗

Constitutive impaired TCR/CD3-mediated activation of T cells in IDDM patients co-exist with normal co-stimulation pathways.

IDDM is a T cell-mediated autoimmune disease which is paradoxically associated with T cell functional deficiencies. The proliferative response of PBMC under CD3-, Vbeta2-, Vbeta8- and Vbeta7-stimulation was investigated in IDDM and NIDDM patients, non-diabetic first-degree relatives and control subjects. Despite normal surface expression of the TCR/CD3 complex, the TCR/CD3-mediated proliferation of PBMC from IDDM patients was significantly impaired compared to control subjects (P<0.05). This defect was specific for the autoimmune disease, constitutive and not linked to the class II MHC genotype, to metabolic disturbances or to presence of specific autoantibodies. Inefficient activation of T cells was not related to a lower capacity of CD28 to transduce co-stimulative signals because proliferative responses under CD2/CD28 stimulations were similar in IDDM and control groups. The IL-2/IL-2 receptor system was functional because unstimulated PBMC proliferated in response to increasing amounts of IL-2. Nevertheless, despite normal expression of CD25, addition of IL-2 did not normalize the proliferative defect linked to IDDM. In conclusion, excluding a faulty co-stimulation pathway, these results are in favour of a constitutive defect in the CD3/TCR transduction machinery, increasing sensitivity to apoptosis or anergy in T cells from IDDM patients.

Adult↗

Prevalence of macular pattern dystrophy in maternally inherited diabetes and deafness. GEDIAM Group.

OBJECTIVE: To evaluate the prevalence of macular pattern dystrophy (MPD) in maternally inherited diabetes and deafness (MIDD), a new subtype of diabetes mellitus that cosegregates with a mutation of mitochondrial DNA (i.e., the substitution of guanine for adenine at position 3243 of leucine transfer RNA) and to report the clinical characteristics of MPD. DESIGN: Prospective cohort study. PARTICIPANTS: Forty-six patients from 29 families with an adenine-to-guanine mutation of mitochondrial DNA were recruited from a French collaborative multicenter study. Thirty-five patients had MIDD, 8 were asymptomatic children of MIDD patients, and 3 had MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes). The 33 MIDD patients with diabetes were matched for diabetes duration and gender with 33 patients with "common" type-2 diabetes to compare the prevalence of diabetic retinopathy (DR) in both series. METHODS: All patients had a full ophthalmologic examination and fundus photographs. MAIN OUTCOME MEASURES: The presence and severity of MPD and DR were assessed in each patient. RESULTS: Thirty MIDD patients (85.7%) of 35 exhibited bilateral MPD characterized by linear pigmentation surrounding the macula and optic disc. In 24 of these 30 patients, visual acuity was 20/25 or more in both eyes. The prevalence of DR was 6% in MIDD patients with diabetes versus 15% for patients with common type-2 diabetes (a difference that was not significant, P = 0.23). The fundus of each of the eight asymptomatic children was normal. MPD was present in one of the three cases of MELAS. CONCLUSION: The prevalence of MPD in MIDD is high. Its detection may be helpful for the diagnosis of this new subtype of diabetes, for which specific treatments may be proposed.

Adult↗

Relationship between HLA-DQ and -DR genotypes and clinical characteristics in a French population of Type 1 diabetic patients.

AIMS: The present study was designed to look for a heterogeneity in the association between Type 1 diabetes mellitus (DM) and class II alleles of major histocompatibility complex (MHC) according to clinical presentation and C-peptide secretion during the first year of the disease, in a population living in south of France. METHODS: HLA DRB1 and DQB1 genotypes were determined in 129 Caucasoid patients with Type 1 DM and compared to a control group (n = 88). In a subgroup of 46 young adult diabetic patients, basal and postglucagon C-peptide secretion was followed during the first year of the disease (at 0, 1, 3, 6, 9 and 12 months). RESULTS: The two main haplotypes associated with Type 1 DM were DRB1*04DQB1*0302 and DRB1*03DQB1*02. The genotypes DRB1* 04DQB1 *0302/DRB1*04DQB1*0302 and DRB1 *03DQB1*02/DRB1*04DQB1* 0302 were associated with an early onset of diabetes, while homozygosity for DRB1*03DQB1*02 was characterized by later onset. Levels of residual insulin secretion in patients genotyped DRB1*03DQA1*0501DQB1* 02/DRB1* 04DQA1*0301DQB1*0302 were higher than in patients genotyped DRB1* 3DQA1*0501DQB1*02/DRB1*XDQA1*XDQB1*X or DRB1* XDQA1* XDQB1*X/DRB1*XDQA1*XDQB1*X. CONCLUSIONS: This study confirms some clinical heterogeneity of Type 1 DM linked to HLA DR and DQ genotypes, and leads to a paradoxical finding: DQB1*02/ DQB1*0302 combination predisposes to an early onset in the whole population but residual secretion of insulin disappears more slowly in a subgroup of young adults with recently diagnosed diabetes. These data suggest that interrelations between MHC genotype and diabetogenic process could be different at various ages of life.

Adolescent↗

Influence of obesity and body fat distribution on postprandial lipemia and triglyceride-rich lipoproteins in adult women.

We know that upper body obesity is associated with metabolic complications, but we don't know how regional body fat distribution influences postprandial lipemia in obese adults. Thus, this study explored the respective effects of android or gynoid types of obesity and fasting triglyceridemia on postprandial lipid metabolism and especially triglyceride-rich lipoproteins. Twenty-four obese and 6 lean normotriglyceridemic women (control), age 24-57 yr, were enrolled. Among obese women with an android phenotype, 9 exhibited normal plasma triglyceride levels (mean: 1.38 mmol/L) (NTAO), and 7 displayed a frank hypertriglyceridemia (mean: 2.40 mmol/L) (HTAO). The 8 patients with a gynoid phenotype had normal triglyceride levels (mean: 1.00 mmol/L) (GO). All were given a mixed test meal providing 40 g triglycerides. Serum and incremental chylomicron triglycerides 0-7 h areas under the curve (AUCs) as well as triglyceride levels in apoB-48-containing triglyceride-rich lipoprotein (TRLs) or chylomicrons were significantly higher in HTAOs and NTAOs than in GOs and controls postprandially. The size of chylomicron particles was bigger in controls and GOs than in HTAOs and NTAOs postprandially. Android obese subjects showed abnormally elevated fasting apoB-48 and apoB-100 triglyceride-rich lipoprotein (TRL) levels. Most abnormalities that were found correlated to plasma levels of insulin and apoC-III. In conclusion, an abnormal postprandial lipid pattern is a trait of abdominal obesity even without fasting hypertriglyceridemia.

Adipose Tissue↗

Serum reg protein level is not related to the beta cell destruction/regeneration process during early phases of diabetogenesis in type I diabetes.

OBJECTIVE: In type I diabetes mellitus, early markers of beta cell damage are needed in order to detect the infraclinical development of the disease. The reg protein may be a good candidate, as the reg gene has been proposed to play a role in the pancreatic beta cell destruction/regeneration process during diabetogenesis in animal models of autoimmune diabetes. The aim of this study was to test the hypothesis whether serum reg protein level could be representative of either the destructive or regenerative process at the beta cell level during the early phases of type I diabetes in humans. DESIGN AND METHODS: We used a highly specific immunoassay to measure serum reg protein level in controls and in three groups of either diabetes prone or diabetic subjects: recently diagnosed diabetic patients, long-standing diabetic patients and islet cell antibody-positive non-diabetic subjects. RESULTS: We found no significant difference between the values observed in these three groups in comparison with control group (90.7+/-18.1ng/ml, 83.1+/-5.6ng/ml, 98.7+/-24.5ng/ml vs 85.5+/- 5.6ng/ml respectively). Moreover, when the insulin reserve was evaluated at 6 months in the recently diagnosed group, serum reg protein levels were not different between patients with or without residual insulin secretion (at onset: 103+/-42 vs 70.3+/-8. 5ng/ml respectively; at 6 months: 79.7+/-25.8ng/ml vs 81.6+/-15ng/ml respectively). In contrast, trypsin levels were significantly lower in every group of diabetic patients. Results were expressed as means +/- S.E.M. and groups compared by Student's t-test (P<0.05). CONCLUSIONS: We conclude that serum reg protein level cannot be used as a marker for the progression of the diabetogenic process in type I diabetes.

Adult↗

Disorganization of thymic medulla precedes evolution towards diabetes in female NOD mice.

The thymic medulla is a complex microenvironment which plays a crucial role in central tolerance induction. Using a quantitative histological analysis of non-obese diabetic (NOD) mice, we show that the medulla undergoes several structural modifications during the course of the disease in NOD mice. Indeed, the majority of 70-day-old NOD mice show a scattering of medullary epithelial cells in the cortex which is associated with a reduction in the size of the medulla in heavily disorganized thymuses. The severity of this phenotype is shown to correlate with the subsequent appearance of diabetes in older female NOD mice. This trait is mainly controlled by non-major histocompatibility complex NOD genes since C57BL/6 H-2g(7) congenic mice have a normal medulla. It persists in conditions where effector lymphocytes that lead to diabetes are inhibited in periphery. These results suggest that primary alterations of the thymic stroma might play a role in the progression towards diabetes in NOD mice.

Age Factors↗

HBA1c: clinical and biological agreement for standardization of assay methods. Report by the experts of ALFEDIAM (Association de Langue Française pour lEtude du Diabète et des Maladies Métabolique) and SFBC (Société Française de Biologie Clinique).

Glycohaemoglobin, and particularly haemoglobin A1c(HbA1c), assays have been used for many years to retrospectively evaluate the glycaemic control of diabetic patients. Cut-off values have been established for deciding treatment modifications. The techniques used in the laboratories however exhibit varying quality, and all of them are not yet standardized. The consequence is an under-utilization of this test, especially in non-hospital practice. In this context, working groups of Société Française de Biologie Clinique (SFBC), Association de Langue Française pour l'Etude du Diabète et des Maladies Métaboliques (ALFEDIAM) and Société Française d'Endocrinologie (SFE) have met together, in order to analyze the national status, and to propose practical recommendations for implementing a standardization process on the basis of international experiences. It is recommended to exclusively express results as HbA1c percentage, using methods standardized and certified by comparison to reference methods such as those using Diabetes Control and Complications Trial (DCCT) values. Simultaneously, contacts have been established with manufacturers, and the realisation of periodic quality control surveys was encouraged.

Clinical Laboratory Techniques↗