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Biomedical subjects

M Marre

Publications and source records attributed to M Marre.

At least 91 records · Page 5Linked to original sources
PubMed1994

Microalbuminuria.

Microalbuminuria indicates slightly elevated urinary albumin excretion. In most cases, microalbuminuria is of glomerular origin and indicates initial glomerulosclerosis. Microalbuminuria has a high predictive value for nephropathy in insulin-dependent diabetes subjects and for premature mortality due to cardiovascular disease in non-insulin-dependent diabetes subjects and in the general population. All cardiovascular risk factors can be determinants for microalbuminuria constitution, especially the genetic determinants of these risk factors. Thus, microalbuminuria can be an indicator to summarize renal or cardiovascular risk, or both, in various populations. Treatment interventions were performed using microalbuminuria as the endpoint. So far, the most convincing results were obtained with angiotensin I-converting enzyme inhibitors to prevent nephropathy in insulin-dependent diabetes subjects.

Albuminuria↗
PubMed1994

Relationships between angiotensin I converting enzyme gene polymorphism, plasma levels, and diabetic retinal and renal complications.

Insulin-dependent diabetes mellitus (IDDM), cardiovascular morbidity, and vital prognosis are linked to diabetic nephropathy, which is probably determined by renal hemodynamic abnormalities and by a genetic predisposition. Angiotensin I converting enzyme (ACE) regulates systemic and renal circulations through angiotensin II formation and kinins metabolism. Plasma and cellular ACE levels are genetically determined; an insertion/deletion polymorphism of the ACE gene is strongly associated with ACE levels, subjects homozygote for insertion (genotype II) having the lowest plasma values. We studied the relationship between the ACE gene polymorphism or plasma levels and microcirculatory disorders of IDDM through two independent studies: one involved 57 subjects with or without diabetic retinopathy, and the other compared 62 IDDM subjects with diabetic nephropathy to 62 diabetic control subjects with the same characteristics (including retinopathy severity) but with normal kidney function. The ACE genotype distribution was not different in diabetic subjects with or without retinopathy and in a healthy population. Conversely, an imbalance of ACE genotype distribution, with a low proportion of II subjects, was observed in IDDM subjects with diabetic nephropathy compared with their control subjects (P = 0.006). Plasma ACE levels were mildly elevated in all diabetic groups, independently of retinopathy, but they were higher in subjects with nephropathy than in those without nephropathy (P = 0.0022). The II genotype of ACE gene is a marker for reduced risk for diabetic nephropathy.

Adolescent↗
PubMed1994

Combined analysis of islet cell antibodies that cross-react with mouse pancreas, antibodies to the M(r) 64,000 islet protein, and antibodies to glutamate decarboxylase in type I diabetic patients.

OBJECTIVE: A combined analysis of whether islet cell autoantibodies (ICAs) are cross-reactive with mouse pancreas, with glutamate decarboxylase (GAD) antibodies, and with 64K antibodies was performed in a large sample of recently diagnosed type I diabetic patients. The disappearance rates of these different autoantibodies were compared in some patients after onset of the disease. The aims were to determine patterns in GAD/64K antibodies with regard to cross-species reaction of ICA and to assess whether GAD could contribute to ICA positivity in mouse and human pancreases and whether the simultaneous search for all the antibody specificities enhances the detection of autoimmune stigma. RESEARCH DESIGN AND METHODS: ICA detected by immunofluorescence in human and mouse pancreases, antibodies immunoprecipitating the 64K rat islet antigen, and antibodies immunotrapping brain GAD activity were quantified at diagnosis of diabetes in 95 patients and in sequential samples during 1 year after diagnosis in 13 patients. The contribution of GAD to ICA positivity in mouse and human pancreases was evaluated by the analysis of correlations between tests and by the ability of brain homogenate to block ICA reactivity in pancreases from both species. RESULTS: ICAs were detected in human pancreases in sera from 63 (66%) patients, among which 61% bound also to a mouse pancreas. GAD and 64K antibodies were strongly correlated (P < 0.0001) and were detected in 69 and 73% of the patients, respectively. All but two patients with ICA in human pancreas also displayed either ICA in mouse pancreas or GAD/64K antibodies. Among 32 patients without ICA in human pancreas, 54% displayed either GAD/64K antibodies or ICA in mouse pancreas. Only 16% of the patients displayed neither ICA nor GAD/64K antibodies. A correlation (P < 0.005) was found between ICA in human and mouse pancreases. GAD or 64K antibodies were strongly correlated with ICA in human pancreas (P < 0.0001), but not with ICA in mouse pancreas. After preincubation of six sera with GAD-containing brain homogenate, ICA titers were unaffected in mouse pancreas but reduced in human pancreas. ICA titers in mouse pancreas were decreased after 3 months (P < 0.01) in diabetic patients, contrasting with the stability of ICA in human pancreas and GAD antibodies by 1 year after diagnosis. CONCLUSIONS: According to cross-species reaction, we confirm the heterogeneity of ICA in a large series of type I diabetic patients, ICAs that cross-reacted with mouse pancreas being more frequent than ICAs without cross-species reactivity. GAD and 64K antibodies were also present in a majority of patients. The simultaneous search for all the antibody specificities enhances the detection of autoimmune stigma so that only a few patients did not display any autoantibody at diagnosis. GAD is not the target of ICAs in mouse pancreas, whereas GAD accounts for ICA positivity in human pancreas. The conclusion that ICAs in mouse pancreas are not GAD-reactive is reinforced by the fact that they are more transient after onset of diabetes than are GAD antibodies or the complex mixture of ICAs in human pancreas.

Adolescent↗
PubMed1993

[Microalbuminuria. Signification and value].

The term microalbuminuria means a slightly elevated urinary albumin level. It indicates an abnormal passage of plasma albumin into urine through the glomerular filter. Its prognostic significance was first established in diabetics: in insulin-dependent diabetics microalbuminuria predicts a renal disease, while in non-insulin-dependent diabetics it predicts an excessive cardiovascular mortality. Recently, microalbuminuria has been shown to predict cardiovascular morbidity and mortality in the general population, especially in elderly subjects. Pathogenetic mechanisms common to both atherosclerosis and renal failure may account for the predictive value of microalbuminuria in the above-mentioned conditions.

Albuminuria↗
PubMed1993

Antihypertensive efficacy and acceptability of perindopril in elderly hypertensive patients.

The antihypertensive efficacy and acceptability of perindopril, an angiotensin-converting enzyme (ACE) inhibitor, was evaluated in 2,927 elderly (> or = 70 years) hypertensive patients in general practice, as part of an open 6-month trial conducted on a total of 23,460 patients with mild-to-moderate hypertension. Patients were ambulatory and selected if diastolic blood pressure (DBP) was between 94 and 115 mm Hg and no serious illness or ACE inhibitor intolerance was known. Perindopril was started at 2 or 4 mg once daily and, if supine DBP remained > 90 mm Hg, the daily dose could be doubled after 1 or 3 months (or a diuretic added if perindopril titration reached 8 mg). At entry, the 2,927 patients (65% females) were on average 74 years old, body weight was 68.2 kg, duration of hypertension was 9.4 years, and prior antihypertensive treatment was present in 78%. Percentage of normal DBP (< or = 90 mm Hg) was 69% at 1 month, 86% at 3 months (in patients on perindopril alone), and 94% at 6 months. At 6 months the reduction of systolic blood pressure and DBP was 28 and 16.6 mm Hg, respectively. Of the 2,927 patients at entry, 8.6% dropped out during the trial, including 6.1% due to side effects. Cough was the most common symptom (8.9%) leading to withdrawal in 3.4% of cases. In one patient, serum creatinine increased (3-fold at 1 month), but overall no significant variation of renal function occurred, as shown by stable plasma creatinine and potassium levels.

Aged↗
PubMed1993

Comparison of reduction in microalbuminuria by enalapril and hydrochlorothiazide in normotensive patients with insulin dependent diabetes.

OBJECTIVE: To compare the effects of sodium depletion and of angiotensin I converting enzyme inhibition on microalbuminuria in insulin dependent diabetes. DESIGN: Randomised, double blind, double dummy parallel study of normotensive diabetic patients with persistent microalbuminuria (30-300 mg/24 h) treated with enalapril or hydrochlorothiazide for one year after a three month, single blind placebo period. SETTING: Diabetic clinic in a tertiary referral centre. PATIENTS: 10 diabetic patients with low microalbuminuria (30-99 mg/24 h) and 11 with high microalbuminuria (100-300 mg/24 h). INTERVENTIONS: 11 subjects (six with low microalbuminuria, five with high microalbuminuria) were given enalapril 20 mg plus placebo hydrochlorothiazide once daily and 10 (four with low microalbuminuria, six with high microalbuminuria) hydrochlorothiazide 25 mg plus placebo enalapril once daily. MAIN OUTCOME MEASURES: Monthly assessment of urinary albumin excretion and mean arterial pressure; plasma active renin and aldosterone concentrations and renal function studies at 0, 6, and 12 months. RESULTS: Median urinary albumin excretion decreased from 59 (range 37-260) to 38 (14-146) mg/24 h with enalapril and from 111 (33-282) to 109 (33-262) mg/24 h with hydrochlorothiazide (analysis of variance, p = 0.0436). During the last three months of treatment with enalapril five patients had persistent normoalbuminuria (2-3 times below 30 mg/24 h), five low microalbuminuria, and one high microalbuminuria; in the hydrochlorothiazide group one had normoalbuminuria, three low microalbuminuria, and six high microalbuminuria (chi 2 test = 6.7; p = 0.03). Mean arterial pressure did not differ before (98 (SD 7) with enalapril v 97 (9) mm Hg with hydrochlorothiazide) or during treatment (88 (7) with enalapril v 90 (7) mm Hg with hydrochlorothiazide (analysis of variance, p = 0.5263)). Glomerular filtration rate did not vary. The aldosterone to active renin ratio was decreased by angiotensin I converting enzyme inhibition and increased by sodium depletion, showing treatment efficacy. CONCLUSION: Angiotensin I converting enzyme inhibition by enalapril effectively reduces microalbuminuria in normotensive diabetic patients whereas hydrochlorothiazide is not effective. Changes in blood pressure and activity of the renin-angiotensin-aldosterone system may contribute to these different effects.

Adolescent↗
PubMed1993

Hypertension and diabetes mellitus.

The association of arterial hypertension and diabetes mellitus is frequent: one third of patients attending a diabetic clinic. Excess hypertension frequency is marked in type II, non insulin-dependent diabetes, a condition often associated with other vascular risk factors such as obesity and lipid disorders. Insulin resistance is a common feature between type II diabetes, hypertension and other risk factors. In type I, insulin-dependent diabetes, hypertension is often linked to diabetic nephropathy. There is a genetic basis for diabetic nephropathy, which may share a common background with familial hypertension. Apart from possible genetic predispositions to hypertension diabetes association, chronic hyperglycaemia can lead to alteration in functional and structural properties of blood and vessels, which both contribute to elevated vascular resistance and blood pressure. From a therapeutic viewpoint, blood pressure values above 140/90 mmHg are not tolerable in diabetic subjects under 40 years of age. Due to their renal haemodynamic effects, angiotensin I converting enzyme inhibitors may be of special interest to protect kidney function in diabetic subjects.

Adult↗
PubMed1993

[Detection of subjects at risk of type 1 diabetes. GOFEDI. Groupe Ouest-France pour l'Etude du Diabète Insulino-dépendant].

The so-called type 1 (insulin-dependent) diabetes is an autoimmune disease occurring in genetically predisposed subjects. The clinical onset of the disease is preceded by a subclinical period during which insulin-producing cells are progressively destroyed by immunological effectors. This prediabetic phase can be detected by the presence of autoantibodies directed against islet cells and sometimes associated with anti-insulin antibodies in children, and later on by the disappearance of the early insulin secretion peak in response to intravenous glucose. It is at this prediabetic phase that immunomodulators specific to the antipancreas process and devoid of side-effects will be used, when available, and that an early insulin therapy will be instituted.

Biomarkers↗
PubMed1992

[Converting enzyme inhibitors in diabetes].

ACE inhibitors are used on a large scale basis in hypertensive diabetics, while the association between diabetes and hypertension is frequent and harmful. This is due to their excellent tolerance and efficacity. No specific advantage has been reported in their use regarding tolerance, i.e., they may not alter insulin sensitivity consistently. Conversely, ACE inhibitors may offer the specific advantage of protecting kidney function against diabetic microangiopathy, since their effects on glomerular haemodynamics seem independent from their hypotensive effect.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Serum lipids and urinary albumin excretion in non insulin-dependent diabetics.

The increase of urinary albumin excretion has a predictive value for cardiovascular disease in insulin-dependent and non insulin-dependent diabetics. To study the relationship between urinary albumin excretion and serum lipids, 380 non insulin-dependent diabetics, 40 to 75 yr old, with urinary albumin excretion from 0 to 200 mg/l, and normal serum creatinine (less than 150 mumol/l), were surveyed. Urinary albumin excretion, was related positively to age (r2 = 0.014; p = 0.02), to systolic blood pressure (r2 = 0.073, p = 0.0001) and diastolic blood pressure (r2 = 0.052, p = 0.0001); a negative correlation existed with HDL-cholesterol (r2 = 0.043, p = 0.0001) and Apoprotein A1 (r2 = 0.044, p = 0.0001). A stepwise regression analysis was performed and resulted in three independently contributing variables related to urinary albumin excretion: First systolic blood pressure (F = 36), second Apoprotein A1 (F 24), third hemoglobin A1C (F = 6). The presence of hypertension or insulin therapy did not modify these findings. In conclusion, serum lipid seems an important determinant of urinary albumin excretion in non insulin-dependent diabetics.

Adult↗
PubMed1992

[Increase of activity of angiotensin-converting enzyme in insulin-dependent diabetic patients with permanent microalbuminuria].

Angiotensin I Converting Enzyme (ACE), which is synthesized by vascular endothelial cells, can be elevated in some diabetic subjects. To study if serum ACE can be elevated in subjects with high risk for malignant microangiopathy, 34 normotensive type I, insulin-dependent diabetic subjects with persistent microalbuminuria (30-300 mg/24 h) were compared for serum ACE activity (Liebermann's method) with 30 normotensive, normoalbuminuric type I, insulin-dependent diabetic subjects of same age (33 +/- 15 (M +/- SD) vs 39 +/- 14 years), sex (13 F/21 M vs 15 F/15 M), stage of retinopathy (14 vs 16 nil/11 vs 7 background/6 vs 4 preproliferative/3 vs 3 proliferative), HbA1c (7.7 +/- .9 vs 8.2 +/- 1.0%). Serum ACE activity of diabetic subjects were also compared with 120 age and sex related healthy controls. Serum ACE activity was higher in type I, insulin-dependent diabetic subjects with microalbuminuria than in those with normoalbuminuria (406 +/- 114 vs 359 +/- 97 IU/l; p = 0.05), or in controls (307 +/- 95 IU/l; p = 0.0001). Normoalbuminuric subjects also had higher ACE activity than controls (p = 0.02). In diabetic subjects, serum ACE activity was not related to diabetes duration (r = 0.1; ns), stage of retinopathy (r = 0.06; ns), HbA1c (r = 0.02; ns), or to blood pressure (r = 0.03; ns), but was related to urinary albumin excretion (r = 0.28; p = 0.03) in diabetic subjects. However, stage of retinopathy was related to diabetes duration (r = 0.74; p = 0.0004) and to age (r = 0.42; p = 0.003) in these subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

[Increase of angiotensin converting enzyme activity during oral load of glucose].

Elevated serum angiotensin I-converting enzyme activity may occur in diabetic subjects. This may signal alteration of vascular endothelium. To study the effect of acute glucose change on serum Angiotensin Converting Enzyme (ACE), we performed an oral glucose tolerance test in 17 obese subjects (7M/10F), (Body Mass Index, (BMI): 31 +/- 1 kg/m2), aged 48 +/- 3 years. We measured serum ACE activity (Lieberman's method), active renin (RIA Pasteur kit), and aldosterone (RIA, Cis-International kit), before and 2 hours after oral glucose intake (75 g), and plasma glucose and insulin every 30 min. After oral glucose tolerance test, subjects were classified as 6 Non Insulin-Dependent Diabetic (NIDD), 8 Glucose intolerant (GI), and 3 NormoGlycaemic (NG) subjects. Active renin did not vary after glucose loading (14 +/- 2 vs 15 +/- 2 pg/ml) nor aldosterone (104 +/- 14 vs 133 +/- 18 pg/ml), while ACE activity rose significantly (229 +/- 25 vs 277 +/- 28 IU/l; p = 0.02). Serum ACE activity were different in the 3 groups before glucose loading (NIDD: 266 +/- 37, GI: 252 +/- 32, NG: 90 +/- 21 IU/l; Kruskal-Wallis H = 7.03; p = 0.03), but not after 2 hours (NIDD: 297 +/- 42, GI: 275 +/- 36, NG: 204 +/- 113 IU/l; ns).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

[Comparison of 3 methods of measurement of blood pressure in insulin-dependent diabetic patients with or without incipient diabetic nephropathy].

Incipient diabetic nephropathy is characterized by a urinary albumin excretion (UAE) between 30-300 mg/24 h and a slightly elevated blood pressure. We measured blood pressure in 14 insulin-dependent diabetic subjects (IDDs) with persistent microalbuminuria (group A) and 50 IDDs with persistent normoalbuminuria (group B) using 3 different methods: 1) Sphygmomanometer, by a nurse, on supine position since 10 min, on the third day of hospitalization; 2) automatic device (Dinamap), on supine position, every 5 min, during 30 min; 3) ambulatory blood pressure (Spacelab 90202 every 15 min between 8 a.m. and 8 p.m.; values obtained with this last method were compared to the mean values of healthy subjects of same age. Recorded UAE was the median value of 3 twenty-four-hours urines. Blood pressure was not different among the two groups with any of the three methods: 1) SBP/DBP A: 136 +/- 14/81 +/- 9 vs B: 131 +/- 13/78 +/- 8 mmHg; ns; 2) SBP/MBP/DBP A: 134 +/- 17/96 +/- 12/79 +/- 10 vs B: 127 +/- 13/90 +/- 10/74 +/- 10 mmHg; ns; 3) A: 132 +/- 12/97 +/- 11/84 +/- 9 vs B: 127 +/- 11/91 +/- 9/82 +/- 12 mmHg; ns. There were no concordance between microalbuminuria/normoalbuminuria and systolic or diastolic blood pressure higher/lower than the mean of the healthy subjects (X2 = 1.6; ns). However, UAE was significantly related to MBP measured with 1): r = 0.29; p = 0.027, but not with 2): r = 0.24; ns, nor with 3): r = 0.26; ns. These results suggest that: 1-blood pressure of IDDs should be measured in standardized conditions; 2-diurnal ambulatory blood pressure recording does not predict incipient nephropathy in these subjects.

Albuminuria↗
PubMed1991

Scotopization and the Nagel-II anomaloscope.

The term scotopization refers to the intrusion of rod activity in colour vision when assessed under photopic observation conditions. Scotopization is an important symptom of cone dystrophies. The detection of scotopization is not easy. With the Nagel-II anomaloscope scotopization can be detected in two ways. One method is new and this method is described in the present paper.

Color Perception Tests↗
PubMed1991

Acute insulin response to intravenous glucose, glucagon and arginine in some subjects at risk for type 1 (insulin-dependent) diabetes mellitus.

The relationships between first-phase insulin secretion to i.v. glucagon and i.v. arginine were studied in 19 healthy adult volunteers (Group I) and in 21 subjects at risk for Type 1 (insulin-dependent) diabetes mellitus with either a "normal" (n = 11; Group IIa) or a "low" insulin response to i.v. glucose (n = 10; Group IIb). Groups I and IIa displayed similar insulin responses to the three secretagogues. In contrast, Group IIb demonstrated lower insulin responses to both glucagon and arginine than control subjects (p less than 0.007 and p less than 0.04 respectively) or than "normo-responders" to glucose (p less than 0.007 and p less than 0.04 respectively). In Group IIb however, arginine-stimulated insulin release was increased compared to the response to glucose (p less than 0.006), while glucagon and glucose led to non-statistically different responses. Five "low-responders" developed Type 1 diabetes. As a group, they displayed lower responses to glucagon and to arginine than subjects who up to now have not developed the disease (p less than 0.05 and p less than 0.0003 respectively). In the subjects who progressed to diabetes, the responses to glucose and glucagon were similarly blunted. In the "low-responders" who have not developed the disease, no statistical difference could be detected between mean responses to glucagon and glucose, but four out of these five subjects had a glucagon-stimulated response within the control range and higher than their corresponding response to glucose. Arginine led to a higher stimulation than glucose, in subgroups that either progressed to diabetes (p less than 0.006) or did not (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗