Search PubMed⌕ Search

Biomedical subjects

B Bouhanick

Publications and source records attributed to B Bouhanick.

At least 19 recordsLinked to original sources
PubMed2006

Characteristics and six-month outcomes in a cohort of 8288 diabetic and non-diabetic patients with previous history of acute coronary syndrome or stroke: the French PREVENIR 3 survey.

AIMS: To evaluate the cardiovascular prognosis of 1845 Diabetic Patients (DP) and 6443 Non-Diabetic Patients (NDP) in secondary prevention. METHODS: Patients were recruited prospectively if they had had a previous history of ischemic stroke or acute coronary syndrome (ACS) i.e. Myocardial Infarction (MI) or Unstable Angina (UA) within a period of five years preceding inclusion. For each patient, the number of hospitalizations and vital status were recorded each month over a 6-month period (mean follow-up: 4.8 months). RESULTS: 306 patients (9.5/100--person years; 95% CI, 8.5 to 10.6) had undergone at least one subsequent event (hospitalization for ACS, ischemic stroke, or cardiovascular death). A majority of these events were non-fatal ACS (n=248). The cumulative incidence rate of subsequent events was higher in DP: 12.6/100- person years (10.0 to 15.2) than in NDP: 8.6/100--person years (7.5 to 9.8). DP were significantly at higher risk of subsequent cardiovascular events (OR: 1.34; P=0.025) after adjustment for confounding factors. 93% of coronary DP and NDP underwent a recurrent event affecting the same location. When the index episode was a stroke, 71% of DP had a subsequent stroke vs. 47% of NDP. CONCLUSION: in secondary prevention, the risk of mortality and subsequent vascular events is independently higher in French DP than in NDP. The locations affected by each type of subsequent cardiovascular event seemed correlated to the baseline diagnosis, whatever the diabetic status, even when the frequency of subsequent strokes increased (not significantly) in DP when compared to NDP.

Aged↗
PubMed2005

'Glucose control-related' and 'non-glucose control-related' effects of insulin on weight gain in newly insulin-treated type 2 diabetic patients.

Insulin use is common in type 2 diabetes and is frequently accompanied by weight gain, the composition of which is poorly understood. The present study evaluates insulin-induced body composition changes. Body weight and composition of thirty-two type 2 diabetic patients undergoing their first 12 months of insulin therapy were compared with those observed in thirty-two type 2 diabetic patients previously treated on insulin (minimum 1 year). Body composition was determined by simultaneous body water spaces (bioelectrical impedance analysis) and body density measurements. After 6 months, glycosylated Hb (HbA1c) significantly improved in the newly treated group (P<0.0001), but remained stable in those treated previously. HbA1c did not differ between 6 and 12 months in the two groups. Body weight significantly (P=0.04) changed over 12 months in those newly treated only (+2.8 kg), essentially comprising fat-free mass (P=0.044). Fat mass remained unchanged (P=0.85) as did total body water, while extracellular: total body water ratio tended to increase in those newly treated (P=0.059). Weight changes correlated with HbA1c changes (R2 0.134, P=0.002) in the initial 6 months only. Insulin therapy leads to weight gain (2.8 kg), predominantly fat-free mass, over 12 months. After 6 months, newly treated patients continued gaining weight despite an unchanged HbA1c, suggesting the potential anabolic role of insulin in subsequent gains. Therefore, in the initial 6 months, weight gain can be attributed to a 'glucose control-related effect' and further gain appears to be due to a 'non-glucose control-related' effect of insulin treatment.

Adipose Tissue↗
PubMed2004

Heterogeneity of diabetes phenotype in patients with 3243 bp mutation of mitochondrial DNA (Maternally Inherited Diabetes and Deafness or MIDD).

OBJECTIVE: In patients with maternally inherited diabetes and deafness (MIDD), due to 3 243 A > G mutation of mitochondrial DNA (mtDNA), diabetes may present with variable phenotypes. OBJECTIVE: To ascertain the existence of two distinct phenotypes, MIDD1 and MIDD2, in a series of patients with MIDD. DESIGN: Multicenter prospective study. PATIENTS: 77 patients with diabetes and the mtDNA 3243 mutation and 139 control patients with type 1 (T1D) or type 2 (T2D) diabetes, matched according to initial presentation of diabetes, age at onset, sex, and duration of diabetes (24 T1D and 115 T2D, including 55 treated with insulin). MEASUREMENTS: Anthropometric characteristics (height, body weight, body mass index [BMI], sex), family history of diabetes, and characteristics of diabetes (age at onset, treatment, hemoglobin A1c [HbA1c]), extrapancreatic manifestations. RESULTS: In 13 cases (17%, MIDD1), diabetes presented as insulin-dependent from the onset, with ketoacidosis in 6 cases. In 64 cases (83%, MIDD2), diabetes resembled T2D, and was treated with diet in 12 cases, oral hypoglycemic agents in 21 cases, or insulin in 31 cases. Compared with patients with MIDD2, patients with MIDD1 were characterized by lower age at onset of first manifestation of MIDD (25.4 +/- 9.6 vs 33.7 +/- 13.2 Years, P<0.0005), lower body weight (49.1 +/- 7.4 vs 56.3 +/- 10.9 kg, P<0.0025), lower BMI (18.2 +/- 2.3 vs 20.9 +/- 3.6 kg/m2, P<0.0005), and higher HbA1c levels (9.5 +/- 2.0 vs 7.5 +/- 1.6%, P<0.0005). Frequency of family history of diabetes and of extrapancreatic manifestations was the same in both MIDD subtypes. No difference was found within the MIDD2 subtype when comparing patients treated with or without insulin. Compared with matched controls, patients with MIDD had a lower BMI (MIDD1/T1D 18.2 +/- 2.3 vs 24.0 +/- 3.6 kg/m2 and MIDD2/T2D 20.9 +/- 3.6 vs 30.2 +/- 5.9 kg/m2, P<0.0025). Lastly, male patients with MIDD had a shorter height than controls (MIDD1/T1D: 166.1 +/- 3.2 vs 177.3 +/- 6.6 cm and MIDD2/T2D: 168.4 +/- 7.2 vs 173.6 +/- 6.6 cm P<0.025). CONCLUSIONS: These results confirm the existence of two different phenotypes in MIDD, MIDD1 and MIDD2, which may be related to the severity of the mitochondrial disease. The role of other genetic and/or environmental factors in the variable phenotype of MIDD remains to be elucidated.

Adult↗
PubMed2004

Effect of insulin treatment on the body composition of Type 2 diabetic patients.

OBJECTIVE: Insulin is used commonly in Type 2 diabetes and is often accompanied by weight gain. The composition of this weight gain is poorly understood. Predominant increases in fat mass could increase cardiovascular risks. The aim of the study was to evaluate insulin-induced body composition changes. RESEARCH DESIGN AND METHODS: Body weight and composition of 35 Type 2 diabetic patients during their first 6 months of insulin therapy was compared with those in 34 Type 2 diabetic individuals treated with insulin for at least 1 year prior to commencing the study. Body composition was determined by the simultaneous measurement of body water spaces and body density. RESULTS: Over 6 months, glycaemic control improved in the new treatment group only (HbA(1c): 7.26 +/- 0.81 vs. 9.66 +/- 1.60%; P < 0.0001), remaining stable in the previously treated group (7.67 +/- 1.25 vs. 7.76 +/- 1.26%; P = NS). Weight significantly increased over time in the newly treated group (+1.7 kg; P = 0.04), but not in the previously treated group (-0.3 kg). It comprised of both fat (+0.85 kg) and fat-free mass (+0.55 kg). Total body water remained unchanged. Using bioelectrical impedance analysis, the gain in fat mass was +2.2 kg; P = 0.048. CONCLUSIONS: Over 6 months, insulin therapy leads to a weight gain of 1.7 kg because of an increase in both fat and fat-free mass. When body composition is determined by bioelectrical impedance analysis, the results are biased by fluctuations in hydration.

Aged↗
PubMed2003

Description of microangiopathy in children with type 1 diabetes mellitus: a 19-year retrospective study.

BACKGROUND: The aim of the study was to estimate the outcome of patients with type 1 diabetes followed in a university hospital in the paediatric department and then in the adult diabetic department for at least 10 years. METHODS: We made a retrospective analysis of 50 patients (28 women and 22 men) with type 1 diabetes with disease duration of 19 +/- 6 years and analysed whether retinopathy and nephropathy had progressed, had remained unchanged or had improved or normalised. RESULTS: The mean age of diabetes onset was 8 +/- 4 years (1-16). Ketoacidosis revealed diabetes in 36% of the children. Mean HbA(1c) was 8.6 +/- 1.8%, and was over 8.5% in 34% of the patients. The mean age at onset of puberty (Tanner stage II) was 12 +/- 1 years in girls and 13 +/- 1 years in boys. Mean HbA(1c) was 7.9 +/- 1.2% during the year before onset of puberty and 8.7 +/- 1.1% in the following 3 years, corresponding to a 10% pubertal increase in HbA(1c). Retinopathy was seen in 50% of the patients at a mean age of 22 +/- 5 years, 15 +/- 6 years after onset of diabetes. Mean HbA(1c) was 9.7 +/- 1.6% in patients with proliferative retinopathy, 9.0 +/- 1.5% in patients with non proliferative retinopathy, and 8.1 +/- 1.3% in those without (p=0.02, proliferative versus no retinopathy, p > 0.05 non proliferative versus no retinopathy). Microalbuminuria was diagnosed in 26% of the patients. Mean HbA(1c) was 9.3 +/- 2.1% in patients with microalbuminuria versus 8.1 +/- 1.3% in those with normoalbuminuria (p=0.02). CONCLUSIONS: Glycemic control was similar in patients with non proliferative retinopathy and those without. Proliferative retinopathy and nephropathy were both related to the level of glycemic control.

Adolescent↗
PubMed2002

West syndrome and mitochondrial diabetes: relationship or coincidence?

West syndrome occurs in infancy and in early childhood. It is characterized by intractable seizures occurring almost daily, severe psychomotor retardation, poor prognosis and EEG abnormalities, known as hypsarrhythmia. We report here the case of a 28-year-old patient, who was diagnosed with West syndrome when he was 8 months old and with diabetes mellitus when he was 25 years old. Sequencing analyses and restriction analyses were suggestive of mitochondrial diabetes. Four years after the diagnosis of diabetes, this patient's diabetes is still controlled by diet and biguanides.

DNA, Mitochondrial↗
PubMed2002

Proliferative retinopathy in patients with type 1 diabetes of less than 5 years' duration.

The position statement about diabetic retinopathy postulates that at least 3-5 years of duration of diabetes are needed for the retinopathy to occur, and initial retinal examination should be performed within 3-5 years after the initial diagnosis. We report here the case of a 18 year-old type 1 diabetic woman with a proliferative retinopathy discovered 2 years after the onset of a clinical diabetes. The hypothesis of a Latent Autoimmun Diabetes in Adults (LADA) could not be excluded and we propose, particularly in this context, to detect a diabetic retinopathy at the onset of diabetes.

Adolescent↗
PubMed2001

Maternally inherited diabetes and deafness: a multicenter study.

BACKGROUND: Maternally inherited diabetes and deafness (MIDD), which is seen in 0.5% to 2.8% of patients with type 2 diabetes mellitus, is related to a point mutation at position 3243 of mitochondrial (mt) DNA. Its clinical description is incomplete. OBJECTIVE: To study the clinical presentation and complications of diabetes in patients with MIDD and to identify clinical characteristics that may help select diabetic patients for mtDNA mutation screening. DESIGN: Multicenter prospective descriptive study. SETTING: 16 French departments of internal medicine, diabetes and metabolic diseases, or both. PATIENTS: 54 patients with type 2 diabetes mellitus and the mtDNA 3243 mutation. MEASUREMENTS: Characteristics of diabetes, metabolic control (glycosylated hemoglobin level), complications of diabetes, and involvement of other organs. RESULTS: On average, patients with MIDD were young at diabetes onset and presented with a normal or low body mass index. None were obese. Seventy-three percent of probands had a maternal family history of diabetes. Diabetes was non-insulin-dependent at onset in 87% of patients; however, 46% of patients had non-insulin-dependent disease at onset but progressed to insulin therapy after a mean duration of approximately 10 years. Neurosensory hearing loss was present in almost all patients. Eighty-six percent of patients who received an ophthalmologic examination had macular pattern dystrophy (a specific retinal lesion). Forty-three percent of patients had myopathy, 15% had cardiomyopathy, and 18% (9 of 51) had neuropsychiatric symptoms. Although the prevalence of diabetic retinopathy was 8% among patients who received an ophthalmologic examination, lower than expected after a mean 12-year duration of diabetes, prevalence of kidney disease was 28%. This suggests that a specific renal involvement was the result of mitochondrial disease. CONCLUSIONS: Maternally inherited diabetes and deafness has a specific clinical profile that may help identify diabetic patients for mtDNA testing.

Adolescent↗
PubMed2000

Oral insulin administration and residual beta-cell function in recent-onset type 1 diabetes: a multicentre randomised controlled trial. Diabète Insuline Orale group.

BACKGROUND: Oral administration of autoantigens can slow the progression of beta-cell destruction in non-obese diabetic mice. We investigated whether oral administration of recombinant human insulin could protect residual beta-cell function in recent-onset type 1 diabetes. METHODS: We enrolled 131 autoantibody-positive diabetic patients aged 7-40 years within 2 weeks of diagnosis (no ketoacidosis at diagnosis, weight loss <10%, polyuria for <6 weeks). They were randomly assigned 2.5 mg or 7.5 mg oral insulin daily or placebo for 1 year, in addition to subcutaneous insulin therapy. Serum C-peptide concentrations were measured in the fasting state and after stimulation, to assess beta-cell function. Autoantibodies to beta-cell antigens were assayed. Analyses were by intention to treat. FINDINGS: Baseline C-peptide and haemoglobin A1c concentrations were similar in the three groups. During follow-up, there were no differences between the groups assigned 2.5 mg or 7.5 mg oral insulin or placebo in subcutaneous insulin requirements, haemoglobin A1c concentrations, or measurements of fasting (mean at 12 months 0.18 [SD 0.17], 0.17 [0.17], and 0.17 [0.12] nmol/L) or stimulated C-peptide concentrations (glucagon-stimulated 0.39 [0.38], 0.37 [0.39], and 0.33 [0.24] nmol/L; meal-stimulated 0.72 [0.60], 0.49 [0.49], and 0.57 [0.51 nmol/L]. Neither age nor C-peptide concentration at entry influenced treatment effects. No differences were seen in the time-course or titres of antibodies to insulin, glutamic acid decarboxylase, or islet antigen 2. INTERPRETATION: At the doses used in this trial, oral administration of insulin initiated at clinical onset of type 1 diabetes did not prevent the deterioration of beta-cell function.

Administration, Oral↗
PubMed2000

Lack of relationship in long-term type 1 diabetic patients between diabetic nephropathy and polymorphisms in apolipoprotein epsilon, lipoprotein lipase and cholesteryl ester transfer protein. Genétique de la Nephropathie Diabétique Study Group. Données Epidémiologiques sur le Syndrome d'Insulino-Résistance Study Group.

BACKGROUND: Genetic susceptibility contributes to the risk of diabetic nephropathy. Lipid disorders may favour diabetic nephropathy. Thus polymorphisms in lipid metabolism are candidates for the genetic component of risk for diabetic nephropathy. METHODS: We searched for a contribution of the genetic polymorphisms of lipoprotein lipase (LPL), cholesteryl ester transfer protein (CETP) and apolipoprotein epsilon (Apo E) to the development of diabetic nephropathy by studying 494 type 1 diabetic patients with proliferative retinopathy and various stages of diabetic nephropathy (GENEDIAB Study). The selection process ensured that all patients had expressed their risk of chronic complications due to uncontrolled diabetes. Thus the nephropathy stages were largely influenced by genetic background. The lipid profile included fasting plasma total cholesterol (TC), triglycerides (TG), apolipoprotein A1 (Apo A1) and B (Apo B), and lipoprotein (a) (Lp(a)). Genetic polymorphisms were determined by PCR-based detection of Apo epsilon (e2/e3/e4), LPL (mutation Asn 291 Ser) and CETP (TAQ:IB B1/B2). RESULTS: One hundred and fifty-seven patients (32%) had no nephropathy, 104 (21%) incipient nephropathy, 126 (25%) established nephropathy and 107 (22%) advanced nephropathy. There was a significant relationship between the stages of diabetic nephropathy and TC (P=0.002), TG (P<0.0001), Apo B (P=0.0007) or Lp(a) (P=0. 038), but not Apo A1. However the genetic polymorphism distributions of LPL, CETP and Apo epsilon did not differ in terms of renal complications. The study power to reject the null hypothesis was 58% for the Apo epsilon genotypes. CONCLUSION: These results support no or only marginal effects of a genetic basis for lipid disturbances encountered in diabetic nephropathy.

Adult↗
PubMed2000

Normal and abnormal day-to-day variability of urinary albumin excretion in control and diabetic subjects.

Urinary albumin excretion (UAE) is very variable from day to day. This variability, more or less potent, might by itself have a patho-physiological significance. We analyzed day-to-day UAE in 207 elderly (60-75 years) inpatients (134 with and 73 without diabetes mellitus) attending the department of internal medicine of the Angers University hospital. Twenty-four-hour urine was collected 3 times during a 5-10 day hospitalization period. One-hundred-fifty-one patients (73%) displayed normoalbuminuria (UAE<30 mg/24 h in 2 or 3 measures) while 56 patients (27%) had microalbuminuria (UAE within 30-300 mg/24 h in 2 or 3 measures). As the raw data of UAE was not normally distributed, we transformed UAE into the variable z=log (log (k + UAE)) where k is an integer and looked for a k value for which z might be normally distributed. We found that z was actually normally distributed for k=2. Mean value and coefficient of variation of z in the 3 measurements were used to define the level and the temporal intra-individual variability of UAE. Expressed in term of z, the day-to-day intra-individual variability of UAE showed a potent change (from large variability to small variability) at the particular level z=1.25, corresponding to UAE=30.8 mg/24 h. This value is precisely the level currently used to define microalbuminuria in diabetic subjects. It is remarkable that the day-to-day variability of UAE collapses when UAE crosses the level which has been used to define microalbuminuria.

Aged↗
PubMed2000

Hereditary factors in the development of diabetic renal disease.

The role of genetics in diabetic renal disease has been suspected on the basis of follow-up and familial studies. Barely half of Type 1 patients who develop a diabetic retinopathy also develop nephropathy, and the relative risk of nephropathy for a diabetic proband is around 3 if a sib is affected. Candidate genes for diabetic nephropathy can be divided into two categories: those affecting glucose metabolism in target organs of diabetic microangiopathy, and those affecting renal changes in response to hyperglycaemia. The role of angiotensin-I-converting enzyme (ACE) insertion/deletion (I/D) polymorphism has been suspected for several years. Evidence of its possible role in the development and progression of diabetic renal disease is presented here.

Diabetes Mellitus, Type 1↗
PubMed2000

[Normal and abnormal daily variability of urinary excretion of albumin].

Urinary albumin excretion (UAE) is very variable from day to day. We analyzed day-to-day UAE in 207 elderly (60-75 years) inpatients (134 with and 73 without diabetes mellitus) attending the department of internal medicine of the Angers University hospital. Twenty-four-hour urine was collected 3 times during a 5-10 day hospitalization period. One-hundred-fifty-one patients (73%) displayed normoalbuminuria (UAE < 30 mg/24 h in 2 or 3 measures) while 56 patients (27%) had microalbuminuria (UAE within 30-300 mg/24 h in 2 or 3 measures). As the raw data of UAE was not normally distributed, we transformed UAE into the variable z = log(log(k+ UAE)) where k is an integer. We found that z has a gaussian distribution for k = 2. Mean value and coefficient of variation of z in the 3 measurements were used to define the level and the temporal intra-individual variability of UAE. Expressed in term of z, the day-to-day intra-individual variability of UAE showed a potent change (from large variability to small variability) at the particular level z = 1.25, corresponding to UAE = 30.8 mg/24 h, which is precisely the level currently used to define microalbuminuria in diabetic subjects.

Aged↗
PubMed2000

[Differences in glycemic balance (but not weight) correlate positively with changes in absolute cardiovascular risk in diabetic patients].

Coronary Risk Profile (CRP), assessed according to the Framingham equation takes the presence of diabetes into account, but not the glycaemic control or the body overweight. We have performed an observational survey to study the respective roles of changes in body weight or glycaemic control on calculated CRP, in a given subject, by an effect on several items of the CRP equation (systolic blood pressure, total and HDL cholesterol) which can be modified by blood glucose or weight. We have studied the CRP of 179 type 1 and 208 type 2 diabetes patients, admitted in the department of diabetology of the Angers Hospital, twice (interval < 3 years; 1.6 +/- 0.8 yr). The patients yielded no coronary heart disease, their age ranged from 30 to 74 yr (mean +/- SD: 53 +/- 13), they were not on antihypertensive or lipid lowering medication. Glycaemic control was assessed by glyco-haemoglobin (HbA1c), systolic blood pressure (SBP) was measured with an automatic device (Dinamap). Total and HDL cholesterol were determined by an enzymatic method, in fasting patients. Only age at first examination was taken into account to compute CRP. Initially, SBP was 131 +/- 17 mmHg, total and HDL cholesterol were 2.20 +/- 0.47 et 0.56 +/- 0.20 g/L, respectively. SBP was positively correlated with body weight (Rho = 0.310; p < 0.0001), but not with HbA1c. Median 5 yr CRP was 5% (range: < 1%-25%). Between both admissions, mean change in body weight, HbA1c and 5 yr CRP was +1.0 kg (range: -27 à +29), -0.2% (range: -4.5 à +7.6) et -0.01% (range: -10 à +13) respectively. Change in CRP between both admissions was associated with change in HbA1c (Rho = 0.109; p = 0.0315) but not in body weight (Rho = 0.072; p = 0.1588). This result was explained by the effect of the change in HbA1c on total cholesterol (Rho = 0.151; p = 0.003), (no effect on SBP or HDL cholesterol: Rho = 0.008 and Rho = 0.019; NS, respectively). These results suggest that, in diabetic patients, changes in glycaemic control affect their CRP by an effect on total cholesterol, but the changes in body weight do not affect their CRP.

Adult↗