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A de Leiva

Publications and source records attributed to A de Leiva.

At least 19 recordsLinked to original sources

Physical training decreases plasma thrombomodulin in type I and type II diabetic patients.

AIMS/HYPOTHESIS: Endothelial damage is an early step in the pathogenesis of atherosclerosis and its improvement through physical training can contribute to the known reduction of cardiovascular risk associated with exercise. An increase in some endothelium-dependent haemostatic parameters, considered as markers of endothelial damage, has been observed in diabetic patients. METHODS: The effect of a three-month physical exercise programme on thrombomodulin, tissue factor pathway inhibitor, plasminogen activator inhibitor, tissue-type plasminogen activator and von-Willebrand factor was evaluated in 14 well-controlled patients with Type I (insulin-dependent) diabetes mellitus and 13 patients with Type II (non-insulin-dependent) diabetes mellitus (HbA1c 6.5 +/- 0.8 and 7.4 +/- 0.8%, respectively). A matched control group was also studied. RESULTS: Thrombomodulin at baseline was higher in both Type I and Type II diabetic patients than in their respective matched control subjects (50.0 +/- 16 vs 31.1 +/- 8.7 microg/l, p < 0.05; 51.0 +/- 10 vs 28.5 +/- 11 microg/l, p <0.05, respectively). After the exercise programme, thrombomodulin plasma concentrations had decreased (p < 0.05) in both groups of patients, with final thrombomodulin values being similar to those observed in their control groups (38.2 +/- 11 microg/l for Type I and 34.6 +/- 12 microg/l for Type II patients). The thrombomodulin decrement correlated with baseline thrombomodulin and VO2max increase in Type I diabetic patients. A decrease in tissue factor pathway inhibitor was also observed in Type II diabetic patients. CONCLUSION/INTERPRETATION: We conclude that the normalisation of plasma thrombomodulin concentrations in Type I and Type II diabetic patients after physical training might reflect the improvement in endothelial function associated with physical exercise.

Adolescent↗

Apo(B)-dependent dyslipidemic phenotypes in type 1 diabetic patients.

BACKGROUND: The prevalence of apo(B)-dependent dyslipidemic phenotypes, which are associated with cardiovascular disease, is increased in normocholesterolemic type 2 diabetic patients. Our aim was to determine the impact of including apo(B) in the evaluation of normocholesterolemic type 1 diabetic patients. METHODS: A total of 123 type 1 diabetic patients (47% male, age 36.6+/-12.5 years) were included. The apo(B) cut-off point (1.14 g/l) was obtained from a group of 53 normolipidemic control subjects of similar age and gender distribution; for low density lipoprotein cholesterol (LDLc), triglycerides, and high density lipoprotein cholesterol (HDLc), we used the cut-off points recommended by the National Cholesterol Education Program. LDLc was determined by ultracentrifugation or Friedewald's equation, depending on triglyceride concentrations, and apo(B) by immunoturbidimetry. RESULTS: A total of 113 (92%) type 1 diabetic patients were normocholesterolemic, and 13% of these were dyslipidemic. The frequency of hyperapo(B) was similar in normocholesterolemic patients and controls (6.2 vs. 9.4%, respectively). Diabetic patients with hyperapo(B) had poorer glycemic control, higher total cholesterol, triglycerides, and LDLc, and a lower HDLc and LDLc/apo(B) ratio. CONCLUSIONS: Unlike type 2 diabetes, type 1 diabetes is not associated with an increased prevalence of hyperapo(B)-dependent dyslipidemic phenotypes. Thus, only in patients with poor glycemic control who display other components of diabetic dyslipidemia, typical for type 2 diabetes, does determining apo(B) concentrations provide additional information in type 1 diabetes.

Journal Article↗

Prevalence and phenotypic distribution of dyslipidemia in type 1 diabetes mellitus: effect of glycemic control.

BACKGROUND: Data on the prevalence of dyslipidemia in type 1 diabetes mellitus are scarce and are based on total triglyceride and total cholesterol concentrations alone. OBJECTIVE: To assess the effect of glycemic optimization on the prevalence of dyslipidemia and low-density lipoprotein cholesterol (LDL-C) concentrations requiring intervention in patients with type 1 diabetes. PATIENTS: A total of 334 adults with type 1 diabetes and 803 nondiabetic control subjects. METHODS: Levels of glycosylated hemoglobin, total cholesterol, total triglyceride, high-density lipoprotein cholesterol (HDL-C), and LDL-C were assessed at baseline and after 3 to 6 months of intensive therapy with multiple insulin doses. RESULTS: Levels of LDL-C greater than 4.13 mmol/L (>160 mg/dL) and total triglyceride greater than 2.25 mmol/L (>200 mg/dL) and low HDL-C levels (<0.9 mmol/L [<35 mg/dL] in men or <1.1 mmol/L [<45 mg/dL] in women) were found in 16%, 5%, and 20% of patients and 13%, 6%, and 9% of controls, respectively (P<.001 for HDL-C). Diabetic women showed more hypercholesterolemia than nondiabetic women (15.6% vs 8.5%; P =.04). After glycemic optimization (mean +/- SD glycosylated hemoglobin decrease, 2.2 +/- 1.96 percentage points), the prevalence of LDL-C levels greater than 4.13 mmol/L (>160 mg/dL) became lower in diabetic men than in nondiabetic men (9.7% vs 17.5%; P =.04), but women showed frequencies of dyslipidemia similar to their nondiabetic counterparts. The proportion of patients with LDL-C concentrations requiring lifestyle (>2.6 mmol/L [>100 mg/dL]) or drug (>3.4 mmol/L [>130 mg/dL]) intervention decreased from 78% and 42% to 66% and 26%, respectively. CONCLUSIONS: Low HDL-C is the most frequent dyslipidemic disorder in patients with poorly controlled insulin-treated type 1 diabetes, and a high proportion show LDL-C levels requiring intervention. Less favorable lipid profiles could explain the absence of sex protection in diabetic women. The improvement caused by glycemic optimization puts forward intensive therapy as the initial treatment of choice for dyslipidemia in poorly controlled type 1 diabetes.

Adolescent↗

Assessment of insulin sensitivity and beta-cell function from measurements in the fasting state and during an oral glucose tolerance test.

AIMS/HYPOTHESIS: We aimed to find if the relation between insulin sensitivity and beta-cell function assessed from fasting and OGTT measurements has a physiological shape (hyperbolic with the reference methods). METHODS: Healthy women without diabetic first-degree relatives underwent a 75 g OGTT with plasma glucose and insulin (n = 35) concentrations being measured at 0, 30, 60 and 120 min. Beta-cell function and insulin sensitivity were estimated using previously described indices from fasting (1 for beta-cell function, 6 for insulin sensitivity) and OGTT measurements (3 for beta-cell function and 5 for insulin sensitivity). A hyperbolic relation was tested for the 21 beta-cell function-insulin sensitivity pairs using a non-lineal regression method. RESULTS: The assessment of beta-cell function from OGTT was impossible in seven women and one had outlier indices. For the remaining 27 women, only 8 combinations adjusted to a hyperbolic relation. The best adjustment was achieved using the fasting glucose to insulin ratio as the estimation of insulin sensitivity and the homeostasis model assessment (HOMA) index (single fasting sample) as the estimation of beta-cell function (r2 0.802, k 869.71, p < 0.001). CONCLUSION/INTERPRETATION: In this group of healthy women, the estimation of insulin sensitivity and beta-cell function by most methods using OGTT-derived glucose and insulin measurements did not adjust to a hyperbolic relation but all fasting indices combinations did. Beta-cell function estimated with the HOMA index and insulin sensitivity with fasting glucose to insulin ratio had the best adjustment.

Adult↗

Effect of physical exercise on lipoprotein(a) and low-density lipoprotein modifications in type 1 and type 2 diabetic patients.

To evaluate the effect of physical exercise on blood pressure, the lipid profile, lipoprotein(a) (Lp(a)), and low-density lipoprotein (LDL) modifications in untrained diabetics, 27 diabetic patients (14 type 1 and 13 type 2) under acceptable and stable glycemic control were studied before and after a supervised 3-month physical exercise program. Anthropometric parameters, insulin requirements, blood pressure, the lipid profile, Lp(a), LDL composition, size, and susceptibility to oxidation, and the proportion of electronegative LDL (LDL(-)) were measured. After 3 months of physical exercise, physical fitness improved (maximal O2 consumption [VO2max], 29.6 +/- 6.8 v 33.0 +/- 8.4 mL/kg/min, P < .01). The body mass index (BMI) did not change, but the waist circumference (83.2 +/- 11.8 to 81.4 +/- 11.2 cm, P < .05) decreased significantly. An increase in the subscapular to triceps skinfold ratio (0.91 +/- 0.37 v 1.12 +/- 0.47 cm, P < .01) and midarm muscle circumference ([MMC], 23.1 +/- 3.4 v 24.4 +/- 3.7 cm, P < .001) were observed after exercise. Insulin requirements (0.40 +/- 0.18 v 0.31 +/- 0.19 U/kg/d, P < .05) and diastolic blood pressure (80.2 +/- 10 v 73.8 +/- 5 mm Hg, P < .01) decreased in type 2 diabetic patients. High-density lipoprotein cholesterol (HDL-C) increased in type 1 patients (1.48 +/- 0.45 v1.66 +/- 0.6 mmol/L, P < .05), while LDL cholesterol (LDL-C) decreased in type 2 patients (3.6 +/- 1.0 v3.4 +/- 0.9 mmol/L, P < .01). Although Lp(a) levels did not vary in the whole group, a significant decrease was noted in patients with baseline Lp(a) above 300 mg/L (mean decrease, -13%). A relationship between baseline Lp(a) and the change in Lp(a) (r = -.718, P < .0001) was also observed. After the exercise program, 3 of 4 patients with LDL phenotype B changed to LDL phenotype A, and the proportion of LDL(-) tended to decrease (16.5% +/- 7.4% v 14.0% +/- 5.1%, P = .06). No changes were observed for LDL composition or susceptibility to oxidation. In addition to its known beneficial effects on the classic cardiovascular risk factors, regular physical exercise may reduce the risk of cardiovascular disease in diabetic patients by reducing Lp(a) levels in those with elevated Lp(a) and producing favorable qualitative LDL modifications.

Adolescent↗

Normalisation of tissue factor pathway inhibitor activity after glycaemic control optimisation in type 1 diabetic patients.

UNLABELLED: Increased plasma concentrations of various markers of endothelial damage have been observed in type I diabetic patients, particularly in those with microangiopathy. OBJECTIVE: To evaluate the effect of near-normalisation of glycaemic control on different markers of endothelial injury involved in haemostasis in poorly-controlled type 1 diabetic patients. MATERIAL AND METHODS: TFPI, thrombomodulin (TM), plasminogen activator inhibitor, tissue-type plasminogen activator and von Willebrand factor were measured in 14 poorly-controlled type 1 diabetic patients free of diabetes-related complications (8 men, 6 women; mean age 29.8 +/- 9.9 years) before (baseline) and after 3 months of intensive therapy and in 14 sex-, age- and BMI-matched control subjects. RESULTS: After a mean follow-up of 107 +/- 49 days (56-210), HbA1c decreased from 11.2 +/- 2.3 to 6.7 +/- 0.7% (p <0.0001). TFPI activity at baseline was higher than in the control group (126.9 +/- 34 vs 92.0 +/- 13%, p <0.005) and decreased after good glycaemic control was achieved (p <0.005), becoming similar to that in the control group (91.0 +/- 16.5%). The TFPI descent correlated with the variations observed in HbA1c (p <0.05; r = 0.54). TM levels at baseline were significantly higher than in the control group (42.3 +/- 9.1 vs 29.00 +/- 10.9; p <0.005) and did not change. The remaining parameters studied were similar between patients and controls and did not change after glycaemic optimisation. CONCLUSIONS: Optimisation of glycaemic control normalises the increased activity of TFPI but not the higher TM levels observed in poorly-controlled type I diabetic patients without chronic complications.

Adolescent↗

Gestational diabetes mellitus: metabolic control during labour.

The purpose of this study was to assess, in women with gestational diabetes mellitus (GDM): 1) metabolic control during labour using a standardised protocol; 2) the influence of therapy during pregnancy in intrapartum metabolic control and insulin requirements; and 3) the impact of maternal glycaemia during labour on neonatal hypoglycaemia. An observational study of 85 women with GDM (54 insulin-treated) was performed. Intrapartum metabolic management included i.v. glucose and insulin infusions, urinary ketone measurement and hourly capillary blood glucose (CBG) monitoring. Mean CBG from arrival to delivery was 4.7 +/- 1.1 mmol/l with 83% of mean CBG values within the target range (2.8-6.9 mmol/l). Mean CBG and insulin requirements were unrelated to therapy during pregnancy, but hypoglycaemia (CBG<2.8 mmol/l) was more frequent in women receiving insulin during pregnancy (40.7 vs 19.4 %, p<0.01). In several logistic regression models, CBG during labour was predictive of neonatal hypoglycaemia. We conclude that in women with GDM, the use of a standardised intrapartum management protocol is associated to fair metabolic control, that insulin requirements during labour are unrelated to therapy during pregnancy and that high CBG during labour increases the risk of neonatal hypoglycaemia.

Adult↗

Postpartum thyroiditis in women with hypothyroidism antedating pregnancy?

In women with hypothyroidism, levothyroxine (LT) requirements after delivery are assumed to return to prepregnancy values. The occasional observation of discordances prompted this study. Forty-one women (31 receiving LT replacement therapy and 10 receiving suppressive therapy for thyroid carcinoma) were followed during the first year after delivery. A control group of 31 nonpregnant women with hypothyroidism (n = 21) or thyroid carcinoma (n = 10) were also followed during a similar period. Twenty-three patients of 41 (56.1%) had discordant requirements at follow-up after delivery vs. 3 of 31 in the control group (9.7%; P < 0.001). The patterns of discordance in the postdelivery group were hyperthyroidism in 12, increase in LT dose in 5, hyper- and hypothyroidism in 5, and recurrence of Graves' disease in 1 women. Those in the control group were increase in LT dose, hyperthyroidism, and hypo- and hyperthyroidism. The rate of patients with discordant prepregnancy-postpartum LT doses was higher in the noncarcinoma subgroup (67.7% vs. 20.0%; P < 0.01), whereas in the control group, both subgroups displayed a similar rate of discordance (9.5% vs. 10%; P = NS). In conclusion, this study documents that women with hypothyroidism antedating pregnancy display changes in LT requirements in the first year after delivery that suggest postpartum thyroiditis.

Autoimmune Diseases↗

IDDM12 (CTLA4) on 2q33 and IDDM13 on 2q34 in genetic susceptibility to type 1 diabetes (insulin-dependent).

Type 1 diabetes (insulin-dependent) is a multifactorial disease with polygenic susceptibility. The major genetic component (IDDM1) resides within the HLA region, but several non-HLA loci have been implicated in the genetic susceptibility. In the present study, we have analysed two such loci, IDDM12 (CTLA4) on 2q33 and IDDM13 on 2q34, in Danish (n = 254) and Spanish (n = 39) type 1 diabetic multiplex families. No significant evidence of linkage of IDDM12 was observed in any of the two studied data sets. However, when the present data were combined with previously published data, they strengthened the evidence of linkage at this locus, p = 0.00002. For the IDDM13 region, we found some positive evidence of linkage of the D2S137-D2S164-D2S1471 markers (p-values 0.007, 0.02, and 0.007, respectively) using transmission disequilibrium testing (TDT) and the Tsp version of the TDT. Importantly, random transmission of all tested alleles was observed in unaffected offspring (p > 0.3). Stratification for HLA (high risk and non-high risk genotypes) in the Danish families did not reveal heterogeneity at IDDM12 or IDDM13. In conclusion, our data on an entirely new family data set did not support the existence of IDDM12 as a type 1 diabetes susceptibility locus in the Danish population. In addition, we found support for evidence of linkage and association of the IDDM13/D2S137-D2S1471 region (approximately 3.5 cM) to type 1 diabetes, however, further studies are needed to substantiate this observation.

Abatacept↗

[An endemic goiter study of a population in the Pyrenees (Cerdanya-Girona)].

INTRODUCTION: To evaluate the iodine deficiency, the scholar population is the most usually studied. However, the survey in general population offers information about the most affected groups. Our work was made in the frame of a health survey of Cerdanya (12,200 inhabitants), and five years after salt iodination. AIMS: Aims.--1) Prevalence evaluation of endemic goiter and urinary iodine excretion in Cerdanya population (> 6 y.). 2) Measurement of iodine concentration in drinking water. MATERIAL AND METHODS: 492 individuals were randomly recruited (46.5% men and 53.5% women). A questionnaire and estimation of thyroid size (Pérez) were performed. Urinary iodine excretion was determined (Benotti) in 25% of the subjects. Measurement of iodine concentration in drinking water were performed. RESULTS: Goiter prevalence (> or = Ia) was 28.7% (IC 95%: 24.8-32.6). The prevalence was higher in women (35.3% vs 21%/p < 0001). Goiter prevalence > Ia was 7.9% (IC 95%: 5.6-10.2) and for nodular goiter 3.4% (IC 95%: 1.9-4.9). In our population the goiter prevalence = Ia, decreased with age, but no significant changes age-related for goiter > or = Ib was observed. In women > or = 45 years and previous pregnancy, the prevalence was higher (35.6% vs 17.6%. p < 0.05). Median urinary iodine was 165 micrograms/l. In 81% of the population the fish consumption was higher than once a week. Mean iodine concentration in drinking water was 2.04 mg/l (2.1 SD). CONCLUSIONS: After promote iodinated-food consumption, good results with a decrease in goiter prevalence and a increase in urinary iodine excretion were observed. Pregnancy increases the risk of goiter development. Although young people was more affected, the good level of urinary iodine excretion was the best indicator to expect progressive goiter disappearance. The low iodine concentrations in Cerdanya water drinking, explains the iodine deficiency in this area.

Adolescent↗

Plasma homocysteine is related to albumin excretion rate in patients with diabetes mellitus: a new link between diabetic nephropathy and cardiovascular disease?

The high risk of cardiovascular disease in patients with diabetes mellitus, particularly in those with nephropathy, is not completely explained by classical risk factors. A high plasma homocysteine concentration is an independent risk factor for cardiovascular disease but information on its association with diabetes is limited. Fasting homocysteine concentrations were measured in the plasma of 165 diabetic patients (75 with insulin-dependent [IDDM]; 90 with non-insulin-dependent diabetes [NIDDM]) and 56 non-diabetic control subjects. Other measurements included the prevalence of diabetic complications, glycaemic control, lipid and lipoprotein levels, vitamin status and renal function tests. Patients with NIDDM had higher homocysteine levels than control subjects, whereas IDDM patients did not (9.2 +/- 4.5 vs 7.7 +/- 2 micromol/l, p < 0.01; and 7.0 +/- 3 vs 7.4 +/- 2 micromol/l, NS). Univariate correlations and multiple regression analysis showed albumin excretion rate to be the parameter with the strongest independent association with homocysteine. Patients with both types of diabetes and nephropathy had higher plasma homocysteine concentrations than those without nephropathy. Increases of homocysteine in plasma were related to increases in the severity of the nephropathy. Fasting hyperhomocysteinaemia was considered as the mean of the plasma homocysteine for all control subjects (7.5 +/- 2.1 micromol/l) + 2 SD (cut-off = 11.7 micromol/l). Nephropathy was present in 80 % of diabetic patients with fasting hyperhomocysteinaemia. In conclusion, increases in fasting homocysteine in diabetic patients are associated with increased albumin excretion rate, especially in those with NIDDM, thus providing a potential new link between microalbuminuria, diabetic nephropathy and cardiovascular disease.

Adult↗