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Biomedical subjects

Roberto Lanes

Publications and source records attributed to Roberto Lanes.

17 recordsLinked to original sources
PubMed2006

Coronary artery calcification, serum lipids, lipoproteins, and peripheral inflammatory markers in adolescents and young adults with type 1 diabetes.

OBJECTIVE: To determine whether coronary artery calcification (CAC), elevated fasting lipids, and lipoproteins and peripheral inflammatory markers are present in insulin-dependent diabetic adolescents and young adults several years after diagnosis. STUDY DESIGN: Hispanic insulin-dependent diabetics (n = 32) diagnosed a mean of 7.8 +/- 4.5 years ago (range, 3 to 16 years), with a mean glycosylated hemoglobin concentration at the time of the study of 8.8% +/- 2.3% and a mean chronological age of 16.1 +/- 4.4 years, were evaluated. Healthy patients (n = 15) with a chronological age (CA) of 15.2 +/- 2.2 years served as control subjects. CAC was assessed by multiple slice computed tomography, and total CAC score in Agatston units was calculated. Fasting lipids, C-reactive protein, apolipoprotein (Apo) A, Apo B, and metalloproteinase-9 (MMP-9) concentrations were measured in all subjects. RESULTS: Neither adolescents with type 1 diabetes nor healthy control subjects presented with evidence of CAC. Fasting lipids, Apo A, Apo B, CRP, and MMP-9 concentrations were similar between diabetic subjects and control subjects. However, 34.4% and 25.0% of our type 1 diabetic subjects had elevated total and LDL cholesterol levels (>200 and >130 mg/dL, respectively), whereas 15.6% and 28.1% had elevated triglyceride and Apo B concentrations (>150 mg/dL and >100 mg/dL, respectively). In addition, 28.1% and 34.4% presented with elevated CRP and MMP-9 levels (>2 mg/L and >80 ng/mL, respectively). Total, LDL and HDL cholesterol, triglycerides, Apo B, CRP, and MMP-9 concentrations correlated positively with duration of the disease and with glycosylated hemoglobin levels. CONCLUSIONS: Although the study adolescents with type 1 diabetes did not present any radiologic evidence of CAC at this stage of the disease, they remain a high-risk group for the development of microvascular and macrovascular artery disease, as risk factors such as elevated lipoproteins and proinflammatory markers are already present in a significant percentage of patients studied.

Adolescent↗
PubMed2006

Growth hormone deficiency, low levels of adiponectin, and unfavorable plasma lipid and lipoproteins.

OBJECTIVE: To examine the impact of adolescent growth hormone deficiency (GHD) on circulating adiponectin levels and the relation between adiponectin, fasting insulin, plasma lipid, and lipoprotein levels. STUDY DESIGN: Twelve children with GHD on GH treatment with a chronological age (CA) of 14.4 +/- 2.0 years and 12 untreated adolescents with GHD with a CA of 14.9 +/- 2.3 years were studied. Adiponectin concentrations were measured in all patients, and the association of adiponectin with fasting insulin, total, LDL, and HDL cholesterol, triglycerides, apolipoprotein A-1, and apolipoprotein B was evaluated. Twelve healthy adolescents served as control subjects. RESULTS: Adiponectin levels were significantly lower in untreated GHD adolescents than in treated GHD subjects or in control subjects (P < .008). Total and LDL cholesterol, triglycerides, and Apo B concentrations were increased in untreated GHD adolescents, whereas HDL cholesterol levels were similar in all three groups. Insulin levels were significantly increased in treated GHD adolescents when compared with control subjects (P < .05) but similar to those with untreated GHD. Adiponectin was found to be negatively associated with body mass index, waist-to-hip ratio, and with Apo B, total cholesterol, triglycerides, and LDL cholesterol concentrations in untreated GHD adolescents, whereas a positive correlation between adiponectin and HDL cholesterol was noted in both untreated and treated GHD subjects. Adiponectin correlated inversely with fasting insulin levels in untreated and treated GHD adolescents. CONCLUSIONS: GHD in adolescence is associated with low levels of adiponectin and with an unfavorable plasma lipid and lipoprotein profile. Our data suggest that treatment with GH may improve the abnormalities seen.

Adiponectin↗
PubMed2006

Relationship between different fasting-based insulin sensitivity indices in obese children and adolescents.

OBJECTIVES: To evaluate insulin sensitivity from data obtained from baseline values and from an oral glucose tolerance test (OGTT) in normal and obese children and adolescents. STUDY DESIGN: We recruited 89 children 4-10 years old and 82 adolescents 11-18 years old divided into moderately obese (Mod OB), severely obese (Severe OB), and non-obese (Non-OB) controls. We evaluated the relationship between four simple measures of insulin sensitivity: homeostatic model assessment (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), fasting glucose to insulin ratio (FGIR), and fasting insulin resistance index (FIRI), with an insulin sensitivity measure derived from the standard 2-hour OGTT, the composite whole body insulin sensitivity index (ISI Comp). RESULTS: The strongest correlation was between QUICKI and ISI Comp and between FGIR and ISI Comp, (correlations [r] 0.81-0.85 in the Mod OB and 0.63-0.67 in the Severe OB). The relationship between HOMA-IR and ISI Comp and between FIRI and ISI Comp did not appear to be as strong (correlations [r] -0.36 and -0.53 in Mod OB and Severe OB, respectively). Moderately obese and severely obese children had fasting and 2-hour insulin levels 2-3 fold higher than the control group. CONCLUSIONS: QUICKI and FGIR, are strongly correlated with OGTT measures of insulin sensitivity in children and adolescents with different degrees of obesity. These simple fasting-based indices may help the pediatrician identify patients at risk of developing insulin resistance.

Adolescent↗
PubMed2005

Endothelial function, carotid artery intima-media thickness, epicardial adipose tissue, and left ventricular mass and function in growth hormone-deficient adolescents: apparent effects of growth hormone treatment on these parameters.

OBJECTIVE: The purpose of this study was to determine whether GH-deficient (GHD) adolescents have abnormalities of cardiac and vascular function detectable during the teenage years. DESIGN/METHODS: Ten GHD children on GH treatment with a chronological age (CA) of 14.6 +/- 1.7 yr and 12 untreated GHD adolescents with a CA of 15.0 +/- 3.0 yr were studied. Cardiac mass and function, carotid artery intima-media thickness, flow-mediated endothelium-dependent vasodilation (percent change from baseline diameter during hyperemia), and hyperemia-induced blood flow increase of the brachial artery (percent change from baseline) and epicardial adipose tissue were evaluated by echocardiography. Fourteen healthy adolescents served as controls. RESULTS: Untreated GHD adolescents present with a reduced left ventricular mass when compared with controls (P < 0.05) and a lower flow-mediated endothelium-dependent increase in the diameter of the brachial artery during hyperemia than both controls and treated GHD subjects (P < 0.02), whereas their epicardial adipose tissue is significantly higher than that of healthy controls (P < 0.02). Interventricular septum thickness, posterior wall thickness, left ventricular ejection fraction, and carotid artery intima-media thickness were similar in all three groups. Hyperemia-induced blood flow increase was greater in treated GHD adolescents than both untreated subjects and controls (P < 0.001). Body mass index correlated positively with epicardial adipose tissue in all three groups and with carotid intima-media thickness in treated and untreated GHD adolescents. CONCLUSIONS: GHD adolescents have a reduced left ventricular mass and vascular abnormalities manifested by lower flow-mediated endothelium-dependent vasodilation. These findings together with an increase in epicardial adipose tissue, a good indicator of abdominal/visceral fat, may contribute to an increased cardiovascular risk in the long term. An improvement in endothelial function and a reduction in arterial stiffness appear to occur after GH replacement.

Adipose Tissue↗
PubMed2004

Decreased final height of children with growth deceleration secondary to poor weight gain during late childhood.

Eighteen healthy, short children with normal growth during most of their childhood were evaluated after a sustained fall in weight and reduced linear growth. Growth was followed after nutritional counseling until final height. This report demonstrates the need for an appropriate-for-age weight gain in growing children as a relatively minor but prolonged caloric restriction, leading to a sustained fall in weight centiles, will affect growth velocities long term and may lead to reduced final heights.

Body Height↗
PubMed2004

Peripheral inflammatory and fibrinolytic markers in adolescents with growth hormone deficiency: relation to postprandial dyslipidemia.

OBJECTIVE: To determine whether peripheral inflammatory and fibrinolytic markers are elevated in growth hormone-deficient (GHD) adolescents and associated with increased postprandial lipoproteins. STUDY DESIGN: Fifteen GHD children on GH treatment with a chronologic age of 12.7 +/- 2.5 years and 10 untreated GHD adolescents with a chronologic age of 13.0 +/- 2.6 years were studied. Triglycerides (TG), C-reactive protein (CRP), fibrinogen, interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) were measured in the fasting state and 4 hours after ingesting a high-fat meal; 15 healthy adolescents served as controls. RESULTS: Fasting and postprandial TG of untreated GHD children were higher than those in treated subjects and healthy controls. Fasting TNF-alpha, CRP, and fibrinogen concentrations of untreated GHD adolescents were higher than those in healthy controls, but similar to those of GH-treated GHD adolescents. Although fibrinogen levels increased after a high-fat meal in GHD adolescents, CRP, TNF-alpha, and IL-6 concentrations did not increase further. Fasting and postprandial TG of untreated GHD adolescents were positively associated with fasting and postprandial CRP, and with postprandial TNF-alpha and IL-6 concentrations. Fasting TG also correlated positively with fasting fibrinogen concentrations in untreated and treated GHD adolescents. CONCLUSIONS: The pronounced inflammatory response seen in GHD adolescents seems to be associated with the presence of elevated levels of fasting and postprandial TG, which may result in an increased susceptibility for premature atherosclerosis.

Adolescent↗
PubMed2004

Female pseudohermaphroditism with phallic urethra in the offspring of a mother with an adrenal tumor.

BACKGROUND: Female pseudohermaphroditism is a disorder in which 46,XX females with ovaries do not develop as normal women. This disorder is caused by overexposure of a female fetus to androgens during intrauterine life. We describe a masculinized female infant who was born to a mother who had virilizing signs. PATIENT REPORT: The patient had a normally formed phallus and a completely fused scrotum. Baseline as well as stimulated adrenal hormones and testosterone values were in the normal range in the infant. No androgens were given to the mother during pregnancy. Serum 17-OHP, DHEA-S, and testosterone levels were all elevated in the mother. Imaging studies revealed a tumor mass over the left kidney pole. Histologically it was an adrenal tumor. CONCLUSIONS: Although a maternal adrenal tumor is a rare cause of female pseudohermaphroditism, the physician must bear this in mind when confronted with a newborn or infant with 46,XX karyotype and cryptorchidism with a phallic urethra.

Adrenal Gland Neoplasms↗
PubMed2004

Accelerated versus slowly progressive forms of puberty in girls with precocious and early puberty. Gonadotropin suppressive effect and final height obtained with two different analogs.

OBJECTIVES: To distinguish which children with precocious puberty (PP) and early puberty (EP) should be treated and which followed without therapy. To determine the effect of GnRH analog treatment on the final height of treated patients and compare the effect of two different analogs on gonadotropin suppression and final height. STUDY DESIGN: Sixteen females with PP or EP with a mean chronological age (CA) of 8.8 +/- 1.4 years and a mean bone age (BA) of 10.8 +/- 1.3 years were treated for a mean of 2.7 +/- 1.0 years with a GnRH analog (triptorelin or leuprolide acetate; group A), while 21 girls with a mean CA of 8.5 +/- 1.0 years, a mean BA of 9.7 +/- 1.4 years and a predicted adult height of >155 cm were followed without therapy (group B). Criteria for treatment were one of: a. predicted adult height (PAH) of <155 cm initially or at any time during follow up; b. PAH over 155 cm with a dramatic decrease in PAH over a 6-month follow-up period; c. advanced and rapidly progressing breast development for age (Tanner 3 before the age of 9 years). RESULTS: GnRHa therapy suppressed gonadotropins in group A, while gonadotropins increased gradually in group B. Height velocity (HV) decreased in group A, while it remained accelerated in group B; BA increased a mean of 1.7 +/- 0.5 years in group A and 3.2 +/- 0.3 years in group B. This resulted in a height increase in group A from a baseline PAH of 153.7 +/- 1.2 cm to a final height (FH) of 160.9 +/- 4.0 cm (p <0.001), clearly above their target height (TH) of 157.7 +/- 4.2 cm. The height of group B children did not change over time (164.1 +/- 4.1 cm before therapy and 166.0 +/- 6.0 cm at FH), both above their TH. The mean leuprolide acetate dose utilized in this study decreased during treatment, while both the initial and final triptorelin dose remained unchanged. Adequate gonadotropin suppression (peak level of LH and FSH of <2 IU/l after i.v. GnRH stimulation) was noted with both leuprolide acetate and triptorelin, although LH suppression was slightly more pronounced with triptorelin. BA advanced 1.8 +/- 0.4 years during leuprolide acetate treatment and 1.5 +/- 0.3 years with triptorelin, so that FH increased a mean of 5.5 +/- 1.3 cm with leuprolide acetate and 8.7 +/- 2.2 cm with triptorelin. CONCLUSIONS: PAH of <155 cm before or during therapy, PAH of >155 cm with a dramatic decrease in predicted height over a 6-month follow-up period and/or advanced and rapidly progressing breast development in girls with PP or EP were useful parameters in deciding which patients to treat. GnRHa therapy suppressed gonadotropins, HV and bone maturation in children with an accelerated form of PP or EP, resulting in a significant height increase. Final height remained stable over time in untreated patients. Adequate gonadotropin suppression was noted with both analogs, although with the doses of analog used in our study, LH and BA suppression were more pronounced with triptorelin, resulting in a larger height gain.

Body Height↗
PubMed2004

Long-term outcome of growth hormone therapy in children and adolescents.

Growth hormone (GH) has been available for more than 4 decades for the treatment of GH deficiency. Initially, GH was extracted from the pituitary glands of human cadavers, but its use was discontinued following the transmission of the Creutzfeldt-Jakob virus. After the development of recombinant GH (somatropin) in 1985, an 'unlimited' commercial source of GH has been available, allowing for the treatment of a large number of short GH-deficient and -sufficient children. Refinements in both the dosage and the frequency of administration of GH have allowed GH-deficient children to reach nearly normal final heights, although mostly they are still below their target heights. Decreased bone mineral densities and increased concentrations of fasting and postprandial lipids, coagulation factors, and several independent cardiovascular risk factors have been reported in GH-deficient children and adolescents and appear to improve with GH administration. The short-term administration of GH to mostly non-GH-deficient short children with Turner syndrome, chronic renal insufficiency (CRI), intrauterine growth retardation (IUGR), and idiopathic short stature (ISS) has resulted in increased growth velocities. In addition, the final height of patients with Turner syndrome and CRI appears to improve with the long-term administration of GH. Final height data are still lacking in adolescents with IUGR, but height standard deviation score and final height predictions appear to improve with therapy. Based on the incomplete and inconclusive available data, one must conclude that GH treatment of children with ISS cannot be advised. The use of GH at replacement doses in children with GH deficiency has resulted in rare and generally reversible adverse effects. The long-term administration of pharmacologic GH doses to short, mostly non-GH-deficient children must, however, still be viewed with caution, as long-term complications cannot as yet be fully evaluated. GH therapy must be individualized and should be limited only to children with severe short stature or a significantly decreased growth velocity, to children under considerable stress due to their short stature, and to patients in whom low GH or low insulin-like growth factor-1 secretion might be the rate-limiting factors for growth. The cost of the medication and the inconvenience of daily GH injections to otherwise mostly healthy short children must also be taken into account.

Adolescent↗
PubMed2004

Metabolic abnormalities in growth hormone deficiency.

Growth hormone has been implicated in the regulation of cardiovascular function and growth hormone deficiency (GHD) has been postulated to be one of the main factors responsible for the increased morbidity and mortality from cardiovascular disease in both young and older patients with childhood- and adulthood-onset GHD. Growth hormone also influences bone turnover and mineral deposition. Subjects with growth hormone deficiency have been shown to have an increased cardiovascular risk as manifested by elevated fasting and postprandial lipids and by increased body fat. In addition, premature atherosclerosis, decreased fibrinolytic activity, increased peripheral insulin resistance, abnormal cardiac structure and impaired cardiac performance have also been reported in this group of patients. Short and long term growth hormone treatment has been shown to exert beneficial effects on several of these parameters. While most of these abnormalities have been reported in adult GHD patients, metabolic changes in GHD children and adolescents have only recently begun to be investigated in more detail.

Cardiovascular Diseases↗
PubMed2003

Molecular analysis in Turner syndrome.

OBJECTIVE: The frequency of Y-chromosome material is high in Turner syndrome (TS), but the ocurrence of gonadoblastoma seems to be low. We performed a study to evaluate whether DNA analysis might be a useful tool in the evaluation of patients with TS. SUBJECTS: Unrelated patients with TS (n = 52) of Venezuelan mestizo ethnic origin were diagnosed by cytogenetic analysis as having TS. METHODS: Clinical assessment, karyotyping, endocrine evaluation, fluorescence in situ hybridization, and polymerase reaction chain analysis of the Y-chromosome loci. RESULTS: We found that 7.69% (4 of 52) patients with TS had Y-chromosome material. A low occurrence of gonadoblastoma was also found (2 of 52 [3.85%]). Two patients showed a 45,X/46,XY karyotype, and gonadoblastoma in the gonadal biopsy specimen was not found. Two patients had no Y chromosome on initial karyotype; they were positive on lymphocyte DNA to Y-sequences specific. Both patients (45,X) had bilateral gonadoblastoma. The four patients with Y-chromosome material in peripheral blood lymphocytes had Y-chromosome sequences on gonadal DNA. Fluorescence in situ hybridization confirmed their Y-chromosome origin. CONCLUSIONS: Our results suggest that the detection of Y-chromosome material should be carried out in all patients with TS and not be limited to patients with TS with cytogenetically identifiable Y chromosome and/or virilization.

Child↗
PubMed2003

Cardiovascular risk of young growth-hormone-deficient adolescents. Differences in growth-hormone-treated and untreated patients.

OBJECTIVE: To determine whether postprandial lipids, coagulation factors and homocysteine levels are abnormal in young growth hormone (GH)-deficient (GHD) adolescents. METHODS: Fifteen GHD adolescents on GH replacement were studied. Ten untreated GHD adolescents and 15 healthy subjects served as controls. Fasting lipids, lipoprotein(a), fibrinogen, plasminogen activator inhibitor-1, homocysteine, folate and vitamin B12 levels were measured. Cholesterol and triglycerides were measured 4 h after a high fat meal. RESULTS: Fasting and postprandial triglycerides and homocysteine levels of untreated GHD patients were increased compared to those of GH-treated GHD subjects and healthy controls; fibrinogen concentrations were elevated in both treated and untreated adolescents. CONCLUSIONS: GHD adolescents present an abnormal fasting and postprandial lipid profile. In addition, the increased fibrinogen and homocysteine levels are suggestive of the accumulation of cardiovascular risk factors early on in life.

Adolescent↗
PubMed2002

The effect of short- and long-term growth hormone treatment on bone mineral density and bone metabolism of prepubertal children with idiopathic short stature: a 3-year study.

OBJECTIVE: We recently reported that children with idiopathic short stature (ISS) have decreased lumbar spine bone mineral density (BMD) that increases after 1 year of GH therapy. The aim of this study was to confirm these short-term results and to evaluate the effect of long-term GH therapy on the BMD of children with ISS. PATIENTS AND DESIGN: We treated a group of 16 short, slow-growing but otherwise healthy non-GH-deficient prepubertal children (8 girls and 8 boys) with a chronological age of 9.5 +/- 0.9 years, a bone age of 8.1 +/- 1.2 years and a height of 124.3 +/- 6.3 cm (height-SDS of -2.1 +/- 0.6) with GH at a dose of 0.1 IU/kg/day for 3 consecutive years. MEASUREMENTS: Height was determined at 3-month intervals and annual growth velocities were calculated. Bone ages and BMD were measured every 12 months by dual-energy X-ray absorptiometry, as were serum concentrations of the carboxy-terminal propeptide of type 1 collagen (PICP) and the carboxy-terminal cross-linked telopeptide of type 1 collagen (ICPT). RESULTS: Growth velocity increased from 4.0 +/- 0.8 cm/year to 8.7 +/- 1.5 and 8.0 +/- 1.7 cm/year at 12 and 36 months of GH therapy, respectively, while height-SDS improved from -2.1 +/- 0.6 to -1.6 +/- 0.4 after 36 months of GH (P < 0.0001). Baseline lumbar spine BMD was decreased when compared to that of a control group of healthy children paired for gender, bone age and height (0.640 +/- 0.08 g/cm2vs. 0.730 +/- 0.08 g/cm2; P < 0.003). Lumbar spine BMD increased after 1 year of GH from 0.640 +/- 0.08 to 0.749 +/- 0.08 g/cm2 (P < 0.05), reaching levels similar to that of controls followed for 1 year without therapy (0.749 +/- 0.04 g/cm2vs. 0.760 +/- 0.08 g/cm2). During this period lumbar spine BMD increased 14.5% in the ISS subjects and 3.9% in the controls. Over the following 2 years of GH therapy the lumbar spine BMD of our ISS patients increased at a rate similar to that of the control population, so that after 3 years of consecutive GH therapy the lumbar spine BMD of ISS children was comparable to that of the controls (0.784 +/- 0.12 g/cm2vs. 0.785 +/- 0.09 g/cm2). Femoral neck BMD of our patients was similar to that of the controls at baseline and at 36 months. Following 1 year of GH treatment serum concentrations of PICP increased from 229.6 +/- 63.5 to 358.6 +/- 87.9 micro g/l, while levels of ICTP increased from 9.6 +/- 5.9 to 13.7 +/- 2.1 micro g/l. After 36 months of GH therapy, PICP and ICTP values had decreased to 303.3 +/- 67.2 micro g/l and 11.3 +/- 3.3 micro g/l, respectively, and were no longer significantly different from baseline. CONCLUSIONS: Children with ISS have decreased lumbar spine BMD, which normalized after 1 year of GH. Over the next 2 years of therapy lumbar spine BMD increased at a normal rate, so that after 3 consecutive years of GH the lumbar spine BMD of children with ISS was similar to that of controls. Bone turnover increased with treatment as indicated by a rise in bone formation and bone resorption markers.

Biomarkers↗
PubMed2002

Is insulin-like growth factor-1 monitoring useful in assessing the response to growth hormone of growth hormone-deficient children?

OBJECTIVE: To assess the relationship between insulin-like growth factor-1 (IGF-1), the growth hormone (GH) dose utilized to treat GH-deficient children and the changes noticed in height-standard deviation score (H-SDS) and height velocity (HV). STUDY DESIGN: We studied 24 prepubertal GH-deficient patients with a mean age of 10.5 +/- 1.8 years and a mean bone age (BA) of 8.4 +/- 2.1 years. H-SDS for chronologic age (CA) and BA before therapy were -2.6 +/- 0.8 and -1.2 +/- 0.8, whereas height velocity (HV)-SDS was -1.1 +/- 1.5. Serum IGF-1 and insulin-like growth factor binding protein-3 (IGFBP-3) levels were measured before, after 6 and 12 months of GH, and correlated with the GH dose used. Based on the increment of IGF-1 used during treatment, patients were divided into 2 groups: G1 (>1 SDS) and G2 (<1 SDS). HV-SDS and interval height increases were analyzed. RESULTS: HV-SDS, as well as H-SDS for CA and BA during the first year of treatment, were significantly greater than before therapy. IGF-1 SDS increased significantly during the first 6 months of therapy (P <.0003), but increased no further at 12 months despite the use of a higher GH dose (0.1 vs 0.14 IU/kg/day), whereas IGFBP-3 SDS increased at both 6 and 12 months. There was no correlation between the GH dose used and IGF-1 and IGFBP-3 levels. When patients were divided according to their IGF-1 increment during therapy, a significant increase in H-SDS for BA and in HV-SDS was noted only in group 2. CONCLUSIONS: The increment in IGF-1 SDS during therapy did not correlate with the interval height increase. IGF-1 measurement may be helpful in monitoring compliance and safety, but seems to be less useful in adjusting the GH dose needed to treat prepubertal GH-deficient children.

Child↗
PubMed2002

Cardiac mass and function, carotid artery intima-media thickness and lipoprotein (a) levels in children and adolescents with type 1 diabetes mellitus of short duration.

OBJECTIVE: To evaluate cardiac mass and function, carotid intima-media thickness, and serum lipid and lipoprotein (a) (Lpa) levels in children and adolescents with type 1 diabetes mellitus (DM) of short duration. BACKGROUND: Diabetes mellitus has been found to be an important risk factor for macrovascular disease in adults. Increased serum lipids and Lpa levels have been reported in adolescents with type 1 DM; atherosclerotic vascular lesions involving a combination of fatty degeneration and vessel stiffening of the arterial wall and myocardial involvement impairing diastolic function may be present in adolescents and young adults with type 1 DM. DESIGN/METHODS: Twenty children and adolescents (10 males, 10 females) diagnosed with type 1 DM before 3.4 +/- 3.3 years with a mean age of 11.9 +/- 3.6 years were studied; their HbA1c levels were 8.0 +/- 1.9%. Twenty healthy non-diabetic controls, 10 males and 10 females, aged 12.1 +/- 3.4 years, matched for height and weight, participated in the study. Fasting blood samples were obtained for lipid and Lpa analysis. Patients underwent transthoracic M-mode and two-dimensional echocardiographic evaluation for measurement of left atrial and ventricular dimensions and left ventricular (LV) wall thickness and mass. Stroke volume and cardiac output were measured using pulsed Doppler echocardiography; carotid intima-media thickness was measured using high-resolution mode B ultrasound. RESULTS: Interventricular septal thickness (7.1 +/- 1.8 vs 7.0 +/- 1.5 mm), LV posterior wall thickness (7.1 +/- 1.4 vs 7.5 +/- 2.0 mm) and LV mass after correction for body surface area (70.6 +/- 27.4 vs 70.7 +/- 18.0 g/m2) were similar in patients and controls. Similarly, the LV ejection fraction at rest was similar in patients and controls (69.9 +/- 2.3 vs 70.0 +/- 0.6%), as were pulmonary venous flow velocities (0.56 +/- 0.09 vs 0.55 +/- 0.10 m/s for diastolic peak velocity, 0.54 +/- 0.08 vs 0.50 +/- 0.09 m/s for systolic peak velocity and 0.17 +/- 0.07 vs 0.19 +/- 0.05 m/s for atrial reversal filling). Carotid intima-media thickness (0.60 +/- 0.02 and 0.59 +/- 0.02 mm for the right and left carotid artery) was similar to that of controls (0.60 +/- 0.03 and 0.61 +/- 0.02 mm for the right and left carotid artery). Low density lipoprotein cholesterol and Lpa levels were increased in patients compared to controls (113.2 +/- 26.0 mg/dl and 20.1 +/- 11.7 mg/dl in patients vs 90.4 +/- 14.3 mg/dl and 9.8 +/- 2.9 mg/dl in controls; p <0.01), while total cholesterol, HDL cholesterol and serum triglyceride concentrations were similar to those in controls. CONCLUSIONS: Although children and adolescents with type 1 DM seem not to show alterations in cardiac mass and function or early atherosclerotic changes in the first few years after diagnosis, their cardiovascular risk is increased as they present with dyslipidemia at an early stage of the disease.

Adolescent↗