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Biomedical subjects

P Chatelain

Publications and source records attributed to P Chatelain.

At least 55 records · Page 3Linked to original sources
PubMed1998

Short stature associated with intrauterine growth retardation: final height of untreated and growth hormone-treated children.

Short term studies have demonstrated the acceleration of growth velocity after the administration of GH in short children born with intrauterine growth retardation (IUGR). We report the final heights of 70 IUGR children whose short stature was attributed to idiopathic GH deficiency (peak plasma GH <10 ng/mL at 2 provocative tests) and treated with GH at a mean dosage of 0.4 +/- 0.1 U/kg x week during an average of 4.6 +/- 2.5 yr. They were compared to a control group of 40 untreated short children born with IUGR, without GH deficiency. At the time of evaluation, age, auxological data, and pubertal status were similar in the 2 groups (height, -2.9 +/- 0.8 and -2.8 +/- 0.7 SD score). Final heights were comparable in both groups of children (-2 +/- 0.7 and -2.2 +/- 1.1 SD score). A multivariate analysis identified 4 independent predictors of final height, namely target height, age and body mass index at evaluation, and GH treatment. Treatment was associated with a gain of 0.6 SD score, suggesting a final height gain of about 3.4 cm. Fifty-three of 70 treated children were reevaluated after completion of growth, and 43 of 53 had a peak plasma GH level of 10 ng/mL or more. Auxological characteristics of these 53 patients were not different from those of nonreevaluated patients. We believe that the transient character of the GH deficiency in most patients and the nonstringent initial criteria used for the diagnosis of GH deficiency render the spontaneous growth potentials identical in the 2 groups of patients. Our data, therefore, suggest that GH treatment at this dosage has a limited effect on the final height of short children born with IUGR.

Adolescent↗
PubMed1998

[Ameloblastic carcinoma. Apropos of a case].

Ameloblastic carcinoma is an exceptionally rare odontogenic tumor. Ameloblastoma is considered malignant if there is evidence of metastasis or histological features of malignancy. Present classification of these tumors is debated. Several authors use the term malignant ameloblastoma for tumours that metastasize despite "benign" histological features whereas ameloblastic carcinoma is referred to as a tumor with malignant histological features regardless of its metastatic potential. We report a case of mandibular ameloblastic carcinoma with cervical lymph node metastasis in a 70-year-old man, documented by MRI and CT. We discuss current knowledge on these tumors.

Adenocarcinoma↗
PubMed1997

Long-term results of growth hormone treatment in France in children of short stature: population, register based study.

OBJECTIVES: To describe the growth of children treated with growth hormone and to evaluate the prognostic factors for height at the end of treatment. DESIGN: Register based cohort study. SETTING: French national register of all children treated with growth hormone. SUBJECTS: 3233 short stature children (3165 of whom were deficient in growth hormone) who were treated with growth hormone (excluding children with Turner's syndrome) and whose treatment started between 1973 and 1989, last data being recorded in December 1993. MAIN OUTCOME MEASURES: Annual changes in height, and height at the end of treatment. RESULTS: Mean height SD score at the end of treatment, after a mean of 4.3 years, was -2, corresponding to gain in mean height SD score of 1 and to a height SD score of 1.1 below target height. In all, 923 children prematurely stopped taking growth hormone treatment, mainly because of insufficient response (insufficient growth) or tiredness. Variables that predicted height at the end of treatment were age, target height, aetiology of short stature, use of puberty inhibitors, and type of growth hormone. CONCLUSIONS: The outcome of children of short stature with growth hormone deficiency who were treated with growth hormone has been less favourable than initially assumed. Growth hormone treatment has not restored normal growth to these children. The highly demanding nature and high costs of this treatment require an optimised prescription, and this remains to be determined.

Adolescent↗
PubMed1997

[Thrombolysis in acute myocardial infarct in everyday clinical practice].

We prospectively included in a database all thrombolyzed acute transmural myocardial infarction patients admitted to our hospital from November 1986 to September 1995. Six hundred and twenty-seven patients (497 males) with a mean age of 61 +/- 12 years (range 26-88 years) were included. 87% were having their first acute myocardial infarction. Different thrombolytic regimens were applied in the emergency room but the vast majority (92%) received t-PA. The median delay between the onset of pain and admission was 2 h 0 min (10 min-22 h). The median admission to treatment time was 40 min (5 min-6 h 20 min). The latter has been shortened (median 55 min from 1986 to 1989 versus 35 min from 1990 to 1995, p < 0.05) during the study period. The rate of intracerebral hemorrhage was 2.4% (confidence interval 1.1-3.5%) and no significant predictor could be found, although patients with cerebral bleeding tended to be slightly older (66 +/- 9 years vs 61 +/- 13 years, p = ns). The rate of false diagnosis was only 4.6%, even when patients with a final diagnosis of unstable angina and/or aborted acute myocardial infarction were included. The in-hospital mortality was 8.8%, a rate similar to those reported in the literature. Using multivariate analysis, negative prognostic factors were higher age (p < 0.001), advanced Killip class at admission (p < 0.001) and elevated peak CPK levels (p < 0.001). These results confirm that thrombolysis for acute myocardial infarction in the emergency room can be done with a short admission-to-treatment time and with an acceptably low rate of false diagnosis. However, our intracerebral hemorrhage rate was clearly higher than generally reported in the literature and may be explained by a different patient selection from that in large randomized studies.

Adult↗
PubMed1997

Feasibility of intracoronary beta-irradiation to reduce restenosis after balloon angioplasty. A clinical pilot study.

BACKGROUND: With the aim of decreasing the incidence of restenosis after coronary balloon angioplasty, we developed a technique of intracoronary beta-irradiation using an endoluminally centered pure metallic 90Y source. The purpose of the present study was to evaluate the clinical feasibility and safety profile of this approach with a dose of 18 Gy delivered to the inner arterial surface. METHODS AND RESULTS: Between June 21 and November 15, 1995, fifteen patients (6 women and 9 men; mean age, 71 +/- 5 years) underwent intracoronary beta-irradiation immediately after a conventional percutaneous transluminal coronary angioplasty (PTCA) procedure. The PTCA/irradiation procedure was technically feasible in all attempted cases, and the delivery of the 18 Gy dose was accomplished without complications. In 4 patients, the intervention was completed through intra-arterial stent implantation because of dissection induced by the initial PTCA. During the follow-up period of 178 +/- 17 days (range, 150 to 225 days), no complication occurred that could be attributed to radiation therapy. No aneurysm or angiographically detectable thrombus was observed in any of the irradiated arterial segments. The clinical event rate (4 of 15 patients underwent further target lesion revascularization) and the angiographic follow-up (6 of 15 patients had a > 50%-diameter stenosis at the previously treated site) did not suggest a marked impact on the expected restenosis rate. CONCLUSIONS: This early experience demonstrates that our approach is feasible, and no side effects attributable to radiation were noted during a 6-month period of follow-up. Whether higher doses of beta-irradiation will favorably affect post-PTCA restenosis in patients must await further evaluation.

Aged↗
PubMed1997

New device for compression of the radial artery after diagnostic and interventional cardiac procedures.

Recently the transradial route has emerged as a valuable alternative to the femoral approach for coronary angiography and angioplasty. However, sheath and catheter size and their immediate removal after the procedure, combined with aggressive antiplatelet and anticoagulant therapies, have favored mechanical compression of the radial artery to achieve satisfactory hemostasis. We report on our initial clinical experience with a new device specially designed for prolonged controlled mechanical compression of the radial artery (the RadiStop radial compression system, RADI Medical Systems AB, Uppsala, Sweden). A total of 159 consecutive patients (mean age 60 +/- 11 yr, 130 males) who required either coronary angiography (group 1, 103 patients) or ad hoc or elective coronary angioplasty (group 2, 56 patients) via the right radial route had local hemostasis with the RadiStop system. In group 1, 4F and 5F sheaths and catheters were used, whereas in group 2, 6F systems were inserted in the radial artery. Hemostasis was achieved with the device in all patients but was considered difficult to obtain in 4 patients (2.5%). Twenty-eight patients (18%) considered the device uncomfortable or painful, but no release of pressure was necessary. The mean compression time was 151 +/- 82 min (114 +/- 64 min in group 1, and 223 +/- 64 min in group 2; P = 0.0001). There were 23 local complications (15%). In 7 patients (4.4%), the radial pulse was absent after compression and at discharge, without major clinical consequences. In one patient, recurrent bleeding occurred 2 hr after compression, requiring a new compression session. In 15 patients, a small local hematoma was observed. Neither heparin dosage nor the use of a 6F sheath affected the rate of radial artery patency in this survey. We conclude that the use of this device for mechanical compression of the radial artery after coronary angiography and angioplasty is efficient, and that its use is related to an acceptable rate of local complications.

Aged↗
PubMed1997

A new densitometric approach to the assessment of mean coronary flow.

RATIONALE AND OBJECTIVES: The authors present an angiographic method to measure absolute coronary blood flow in patients. METHODS: The left or right coronary tree is three-dimensional (3D)-reconstructed from biplane coronary angiograms. This allows the determination of the intravascular volumes needed for flow measurement. The 3D distance traveled by the contrast medium during one cardiac cycle is determined by appropriately thresholding the "concentration-distance", curves computed on two pairs of images taken one cardiac cycle apart. RESULTS: The angiographic flow measurements were compared with nearly simultaneous flow determinations obtained with an intracoronary ultrasonic Doppler flow velocity measuring device. The mean relative difference between the Doppler and the 3D measurements was 11% and the two sets of flow values correlated well (r = 0.81). CONCLUSIONS: A method for the determination of mean coronary flow is presented. The procedure is simple and can be incorporated easily into clinical routine.

Blood Flow Velocity↗
PubMed1997

Growth hormone treatment of short children born small for gestational age: reappraisal of the rate of bone maturation over 2 years and metanalysis of height gain over 4 years.

A minority of children born small for gestational age (SGA) fail to achieve sufficient catch-up growth during infancy and remain short throughout childhood, apparently without being growth hormone (GH) deficient. A previous metanalysis of four trials revealed that GH treatment over a period of 2 years induced a dose-dependent acceleration of linear growth and, to a lesser extent, of the rate of bone maturation in short, prepubertal children born SGA. The rate of bone maturation and the change in height SDS for bone age from the previous 2-year metanalysis have been re-analysed according to chronological age (two prepubertal age groups: group A, 3.0-5.9 years old; group B, 6.0-8.9 years old). The rate of bone maturation was slower in younger than in older prepubertal children; this difference was more marked in children receiving high-dose (0.2 or 0.3 IU/kg/day) GH treatment (p < or = 0.01). Accordingly, the change in height SDS for bone age was increased by high-dose GH treatment in both age groups (p < or = 0.01), and was more pronounced in younger than in older children (1.45 +/- 0.28 versus 0.63 +/- 0.20; p < or = 0.01). Height SDS data from 100 short, prepubertal children born SGA have been analysed over 4 years. The change in height SDS appeared to be related to the average dose of GH. A mean GH dose of 0.1 IU/kg/day over 4 years was administered either as 0.1 IU/kg/day for 4 years (continuous) or as 0.2 IU/kg/day for 2 years, followed by 2 years without GH treatment (discontinuous). After 4 years of treatment, the increase in height SDS for the continuous and discontinuous treatment schedules was similar, being 1.42 +/- 0.10 SDS and 1.58 +/- 0.17 SDS, respectively. In a second regimen, a mean GH dose of 0.2 IU/kg/day over 3 years was administered either as 0.2 IU/kg/day for 3 years (continuous) or as 0.3 IU/kg/day for 2 years, followed by 1 year without GH treatment (discontinuous). After 3 years, the increase in height SDS with the continuous and discontinuous treatment schedules was similar, being 2.01 +/- 0.18 SDS and 2.22 +/- 0.16 SDS, respectively. GH administration was well tolerated in all treatment groups. In conclusion, the rate of bone maturation in short, prepubertal children born SGA treated with GH appeared to depend not only on the dose of GH, but also on the age of the child. GH treatment resulted in a prolonged increase in height SDS, the magnitude of the rise being dependent on the average GH dose rather than on the continuous or discontinuous mode of GH administration.

Body Height↗
PubMed1997

Identification of a large-scale mitochondrial deoxyribonucleic acid deletion in endocrinopathies and deafness: report of two unrelated cases with diabetes mellitus and adrenal insufficiency, respectively.

In recent years, a broad variety of chronic diseases have been related to different mitochondrial DNA (mtDNA) rearrangements. We have investigated two 16-yr-old unrelated girls with unexplained endocrine disorders for a mtDNA mutation. One initially presented with an adrenal crisis at the age of 4 yr. Complete adrenal insufficiency for nearly 15 yr was the main clinical manifestation, along with insiduous growth retardation and sensorineural hearing loss since age 6. The other girl presented with ketoacidosis at the age of 15 yr. She exhibited incomplete deafness since age 6 and poor growth. In both patients, brain magnetic resonance imaging abnormalities and raised cerebrospinal fluid protein concentration indicated mild leucodystrophy. Biopsy of skeletal muscle showed a mitochondrial dysfunction; molecular analysis using a PCR screening procedure revealed a 7.4 kb deletion of the mtDNA in skeletal muscle but not in leucocytes. Direct sequence analysis of the junctional regions showed that the deletion spanned 7.436 kb (nucleotide 8649 to nucleotide 16084). The relative amount of deleted mtDNA estimated by Southern blot analysis was 25 and 15%, respectively. No deletion was present in leukocytes obtained from the asymptomatic mothers. The presence of the same mutation in different patients with various endocrine conditions supports the view that the 7.4 kb mtDNA deletion should be considered as one of the candidate causes for phenotypically uncommon cases of endocrinopathies, specially in children with deafness. This is the first report of a mitochondrial disease with primary adrenocortical insufficiency as the clinical onset.

Adolescent↗
PubMed1997

Management of Coronary Restenosis via the Radial Artery: An Elegant Approach to the AchillesÕ Heel of PTCA.

In spite of many efforts, the most effective treatment for restenosis after coronary angioplasty remains repeat angioplasty. Although the second procedure is known to be at lower risk, it is usually performed by the same technique, thus requiring hospitalization. In such a group of patients, the feasibility of using the radial route for repeat coronary angiography and angioplasty when needed and the safety of early discharge were evaluated prospectively. Coronary angiography via the radial artery was attempted in 51 patients referred within 6 months of initial coronary angioplasty with the clinical suspicion of restenosis. Successful cannulation of the radial artery was possible in 48 (94%). Following placement of a 4 Fr arterial sheath, coronary angiography was completed successfully in all but one patient. Restenosis was confirmed angiographically in 25 patients (one via the femoral route) and a new lesion was observed in 3. Repeat angioplasty was attempted via the radial route (25 patients) or via the femoral route (one patient) using a fixed-wire balloon catheter through the 4 Fr diagnostic catheter (n=22). Angioplasty via the radial route including elective stent implantation (5 patients) was a technical success in 92% of the patients. Immediate arterial sheath withdrawal and mechanical compression of the radial artery provided satisfactory hemostasis after 186 +/- 126 minutes. The radial pulse was absent post-procedure without clinical consequence in 3 patients (6%). Of the 46 patients without a femoral artery puncture, 39 (85%) were discharged the same day without any cardiac or local complications. Thus, early discharge after repeat coronary angiography and angioplasty for restenosis is feasible and safe using the transradial route in the majority of patients.

Journal Article↗
PubMed1997

[Early percutaneous coronary angioplasty in unstable angina].

The risks of complications of percutaneous transluminal coronary angioplasty (PTCA) are increased in unstable angina. Medical treatment for a few days before PTCA is widely adopted to reduce the risk of thrombosis or occlusive dissection during and after the procedure. Over the last few years, the authors have adopted a strategy of early coronary angiography completed by immediate angioplasty when possible, without waiting for the eventual benefit of aspirin or heparin therapy. Their experience from 1988 to 1995 of 853 patients treated by PTCA (151/853 or 17.7%, with implantation of a stent) for unstable angina, was reviewed. Group I comprised 402 patients treated on the day of or the day after admission. Group II comprised 451 patients treated 2 days or more after admission. Patients in Group I were younger (62 +/- 11 vs 64 +/- 12, p < 0.001), and had single vessel disease more often (61 vs 52%, p < 0.005). The success rate of PTCA was similar in the 2 groups (85.3 vs 88.2%, NS), as was the rate of complications (death, infarction or coronary bypass surgery, 9.9 vs 7.3%, NS). The length of hospital stay was significantly shorter in Group I (6.1 +/- 5.6 vs 8.7 +/- 6.9 days, p < 0.0001). With the limitations inherent to all retrospective studies, these data suggest that an early interventional approach in unstable angina has a similar success rate with no more complications than angioplasty. This approach is associated with a deferred significant decrease in the duration of hospital stay.

Aged↗
PubMed1996

The impact of vessel orientation in space on densitometric measurements of cross sectional areas of coronary arteries.

Under ideal conditions, densitometric measurement of a coronary arterial cross section in biplane angiographic images should result in nearly equal cross sectional areas for both planes. However, quite appreciable discrepancies have been found by some authors in patients. In this study, the role of inadequate spatial orientation of the vessel axes relatively to the x-rays was assessed by use of a 3D technique applied to 60 stenoses (45 pre PTCA and 15 post PTCA) in simultaneously acquired digital biplane coronary angiograms of 27 CAD patients. The 3D technique yields two radius values per projection directly in mm at any arterial cross section of interest. This was used to determine the areas Ar(in mm2) of the reference cross sections. As with catheter calibration, these cross sections were thus assumed to be more or less circular, but out-of-plane effects and errors due to a catheter diameter determination in pixels were avoided. The areas of the stenotic sections were then determined densitometrically (in mm2) from the two projections (1 and 2) according to As1 = ArDs1/Dr1, resp. As2 = ArDs2/Dr2, where Dr1, Dr2, Ds1 and Ds2 are the conventional densitometric areas of the reference and stenotic cross sections measured in planes 1 and 2. As expected, the areas As1 and As2 correlated only moderately: As2 = 0.92 As1 + 0.7 mm2, r = 0.82, n = 60, SEE = 1.4 mm2. The 3D method also yielded the two spatial angles between the local vessel axis and the X-rays of both planes. These two angles were then used to correct each densitometric area for inadequate orientation. With the corrected densitometric areas As1c and As2c, the correlation improved to: As2c = 1.05 As1c + 0.03 mm2, r = 0.93, n = 60, SEE = 0.8 mm2. Inadequate orientation of the cross sections in space thus appears to be an important factor of inaccuracy in densitometric measurements of stenotic cross sections in patients.

Absorptiometry, Photon↗
PubMed1996

Three years of GH treatment in Turner's syndrome: complex effect of GH dosage on growth parameters. French Pediatric Clinics and Sanofi-Winthrop.

OBJECTIVE: There have been few studies of GH dose responses in Turner's syndrome. We have therefore compared the growth effect of two doses of subcutaneous GH: 0.45 (D1) or 0.90 (D2) IU/kg/week. DESIGN: Multicentre study with two parallel randomized groups treated with D1 or D2 dose for one year, then with D2 for the second and third years in both groups. PATIENTS: Ninety-seven girls with Turner's syndrome aged from 4.8 to 16.5 years. RESULTS: The first mean height velocity (HV) was significantly higher with D2. At one year the girls changed from D1 to D2 showed a further acceleration in HV. During second and third years HV remained above the mean for untreated Turner girls, in both groups. Mean cumulative height gains over the 3 years were 1.06 and 1.17 SDS/CA (Ranke's Turner standard) in groups G1 and G2 respectively. Bone maturation, over 36 months, was 33.7 (G1) and 31.9 (G2) months. CONCLUSION: These results suggest that, if a higher initial GH dose is associated with a greater net initial height gain, the duration of treatment might affect the long-term results. Intermittent treatment should be considered.

Adolescent↗
PubMed1996

Growth hormone treatment of short children born small for gestational age: metanalysis of four independent, randomized, controlled, multicentre studies.

A minority of children born small for gestational age (SGA) fail to achieve sufficient catch-up growth during infancy and remain short throughout childhood, apparently without being growth hormone (GH) deficient. The effect of GH administration was evaluated over 2 years in short prepubertal children born SGA. The children (n = 244), who were taking part in four independent multicentre studies, had been randomly allocated to groups receiving either no treatment or GH treatment at a daily dose of 0.1, 0.2 or 0.3 IU/kg (0.033, 0.067 or 0.1 mg/kg) s.c. At birth, their mean length SD score (SDS) was -3.6 and their mean weight SDS -2.6; at the start of the study, mean age was 5.2 years, bone age 3.8 years, height SDS -3.3, height SDS adjusted for parental height -2.4, weight SDS -4.7 and body mass index (BMI) SDS -1.4. The untreated children had a low-normal growth velocity and poor weight gain. Although bone maturation progressed more slowly than chronological age, final height prognosis tended to decrease, according to height SDS for bone age, GH treatment induced a dose-dependent effect on growth, up to a near doubling of height velocity and weight gain; BMI SDS was not altered. Bone maturation was also accelerated differentially; however, final height prognosis increased in all GH treatment groups. The more pronounced growth responses were observed in younger children with a lower height and weight SDS. In conclusion, GH administration is a promising therapy for normalizing short stature and low weight after insufficient catch-up growth in children born SGA. Long-term strategies incorporating GH therapy now remain to be established.

Age Determination by Skeleton↗
PubMed1996

Follow-up of three years of treatment with growth hormone and of one post-treatment year, in children with severe growth retardation of intrauterine onset.

Seventy-eight prepubertal, non-GH-deficient children aged 8.1 +/- 0.2 y, with very short stature (mean, -3.2 SD) of intrauterine onset, were treated for 3 y with GH [0.4 (dose D1) or 1.2 (dose D2) IU/kg/wk] and 66 were followed during a 4th y without GH therapy. A 2-y intermediary report had demonstrated a GH dose-dependent acceleration of growth. During the 3rd y on GH, patients D2 (1.2 IU/kg/wk) continued with the same dose, whereas patients D1 (0.4 IU/kg/wk) were randomized to either continue on D1 (group D1) or be increased to D2 (group D1D2). After 3 y on GH, patients' mean height (SD) reached -2.37 (D1), -2.17 (D1D2), and -1.58 (D2) with a total mean height gain of 0.77 (D1), 0.93 (D1D2) (difference NS), and 1.61 SD (D2 significantly higher than D1 and D1D2, p < or = 0.0001). During the off-treatment year, mean growth rate (cm/y) decreased to 3.4 in patients D1, 3.7 in D1D2, and 4.1 in D2 (NS). During the 4 y, bone age advanced of 4.6, 4.6, and 5.3 y in D1, D1D2, and D2, respectively, and puberty started in 34 patients (10 during the off-treatment year). Age at onset of puberty, apparently within normal range, did not relate either to the dose or the duration of treatment. Clinical and biologic tolerance of treatment was good. In conclusion this study demonstrates a GH dose-dependent effect on growth acceleration in persistent postnatal severe growth retardation of intrauterine onset. This effect was sustained for 3 y at 1.2 IU/kg/wk followed by a peculiar growth deceleration at treatment discontinuation. Additional studies are necessary to optimize long-term GH treatment regimen and to document its effects on final height.

Body Height↗