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Biomedical subjects

C Lebrun

Publications and source records attributed to C Lebrun.

At least 37 records · Page 2Linked to original sources
PubMed2003

[Castleman's disease located in the central nervous system].

A 26-year-old woman complained of trijeminal nevralgy and ocular symptoms revealing a paracavernal tumor which had progressed for three months. Histopathological analysis after partial resection led to the diagnosis of Castleman's disease. Six months later, the patient was considered cured after focal adjuvant radiotherapy. Castleman's disease is a lymphoproliferative disorder. Solitary intracranial involvement is unusual. Unlike multifocal disease, localized Castleman's disease has an excellent prognosis.

Adult↗
PubMed2003

[Intravenous immunoglobulins for relapsing-remitting multiple sclerosis after failure of treatment with other immuno-modulators].

Intravenous immunoglobulins are used in the treatment of different autoimmune diseases. Recent trials suggest their efficacy in relapsing remitting multiple sclerosis. We report the results of an efficacy and safety trial using monthly intravenous injections of immunoglobulins for patients with secondary progressive multiple sclerosis. Eighteen patients in clinical progression, who have been previously treated with immunomodulatory or immunosuppressive drugs, were given monthly intravenous immunoglobulin infusions (0.4 g/kg/d for 5 days). At the beginning, the mean EDSS score was 6.77. At the end of the study, an improvement of EDSS was noted in 61.1 p. cent of patients, with less than 1 and 0.75 for secondary and primary progressive diseases respectively. No worsening was reported. Surprisingly, some patients had partial improvement of neurological functions which were considered as sequelae. Indications for intravenous immunoglobulins in the treatment of the multiple sclerosis need to be evaluated.

Adjuvants, Immunologic↗
PubMed2003

[Chemotherapeutic neurotoxicity].

Not uncommonly, damage to the nervous system occurs as a complication of antineoplastic therapy. Neurotoxicity can be induced by synergistic or additive effects of cytotoxic treatments and nervous system exposure is related to routes and doses. Improvements in treating systemic malignancy have been accompanied by reports of neurologic toxicity that has important impact on quality of life and may even limit use of the treatment. Neurological toxicity may be a dose-limiting factor that prevents more aggressive use of that form of treatment. With the increasing use of multi-modality therapy, dose-intensive therapy and experimental therapy, the incidence of neurological toxicity continues to rise. It points out the need for continuous clinical evaluation to detect their appearance. When neurological complications are diagnosed late, they are rarely reversible. Neuroprotective agents are still under evaluation.

Animals↗
PubMed2001

Solid state and solution studies of lanthanide(III) complexes of cyclohexanetriols, models of the coordination sites found in sugars.

This report covers studies in trivalent lanthanide complexation by two simple cyclohexanetriols that are models of the two coordination sites found in sugars and derivatives. Several complexes of trivalent lanthanide ions with cis,cis-1,3,5-trihydroxycyclohexane (L(1)()) and cis,cis-1,2,3-trihydroxycyclohexane (L(2)()) have been characterized in the solid state, and some of them have been studied in organic solutions. With L(1)(), Ln(L)(2) complexes are obtained when crystallization is performed from acetonitrile solutions whatever the nature of the salt (nitrate or triflate) [Ln(L(1)())(2)(NO(3))(2)](NO(3)) (Ln = Pr, Nd); [Ln(L(1)())(2)(NO(3))H(2)O](NO(3))(2) (Ln = Eu, Ho, Yb); [Ln(L(1)())(2)(OTf)(2)(H(2)O)](OTf) (Ln = Nd, Eu). Lanthanum nitrate itself gives a mixed complex [La(L(1)())(2)(NO(3))(2)][LaL(1)()(NO(3))(4)] from acetonitrile solution while [La(L(1)())(2)(NO(3))(2)](NO(3)) is obtained using dimethoxyethane as reaction solvent and crystallization medium. With L(2)(), Ln(L)(2) complexes have also been crystallized from methanol solution [Ln(L(2)())(2)(NO(3))(2)]NO(3), (Ln = Pr, Nd, Eu). Single-crystal X-ray diffraction analyses are reported for these complexes. Complex formation in solution has been studied for several triflate salts (La, Pr, Nd, Eu, and Yb) with L(1 )()and L(2)(), respectively in acetonitrile and in methanol. In contrast to the solid state, both structures Ln(L) and Ln(L)(2) equilibrate in solution, as was demonstrated by low-temperature (1)H NMR and electrospray ionization mass spectrometry experiments. Competing experiments in complexing abilities of L(1)() and L(2)() with trivalent lanthanide cations have shown that only L(2)() exhibits a small selectivity (Nd > Pr > Yb > La > Eu) in methanol.

Journal Article↗
PubMed2001

[The Roseland prosthesis].

Total joint replacement of the trapezio-metacarpal (TMC) joint is one of the procedures available for the surgical treatment of degenerative osteoarthritis or rheumatoid arthritis of the first carpometacarpal joint. A four French Alpine surgeon group, (C. Lebrun, P. Massart, F. Moutet and C. Sartorius) have developed a new cementless total TMC joint prosthesis: the Roseland prosthesis. Such a device tries to improve the biomechanical conditions of the La Caffinière's implant, which was introduced in 1973. Clinical data of a 24 patients with a 38 month mean follow-up series are reported.

Adult↗
PubMed2001

Nitroso-urea-cisplatin-based chemotherapy associated with valproate: increase of haematologic toxicity.

BACKGROUND: The incidence of haematologic toxicity of valproate (VPA) ranges from 1% to 32% and consists mainly of asymptomatic, dose-dependent thrombopenia. We describe a potentiation of haematologic side-effects of nitroso-urea (NU) when prescribed in association with VPA. PATIENTS AND METHODS: We followed a cohort of 70 patients (58 men, 22 women, mean age: 56 years, range 20-75 years). Patients with high-grade gliomas were treated with up-front chemotherapy regimen consisting of fotemustine (d3: 100 mg/m2), cisplatin (d1-3: 33 mg/m2) and etoposide (d1-3: 75 mg/m2) followed by whole brain radiotherapy at progression. Sixty patients required anti-epileptic drugs (AED) for either a single, well-documented epileptic seizure, or immediatly initiated after neurosurgical procedures. AED included VPA (35 of 60), phenobarbital (PB) (17 of 60), carbamazepine (CBZ) (2 of 60) and phenytoin (PHT) (3 of 60). Two patients had both PB and CBZ and one PB and PHT. RESULTS: Haematologic toxicity (grade 3-4 thrombopenia, neutropenia or both) was observed in 37 of 70 (52.85%) patients. Among them 24 (65%) had VPA. Group C were patients treated with fotemustine alone with or without VPA (23 patients). CONCLUSION: When prescribed in association with a fotemustine-cisplatin regimen, VPA treatment results in a three-fold higher incidence of reversible thrombopenia, neutropenia or both. Haematologic side-effects decrease after AED modification during the continued chemotherapy. This adverse event should be managed with caution.

Adult↗
PubMed2001

[Acute polyradiculoneuritis and dysautonomia: contribution of assaying catecholamines and their methoxylated metabolites].

Guillain-Barré syndrome is an acute demyelinating polyradiculoneuritis usually evolving with rapid, functional recovery. In severely paralysed patients, cranial nerve palsy and autonomic nervous system dysfunctions are common. Lesions of the spinal roots predominate but segmentary demyelination of peripheral nervous system reflects various clinical subtypes. Twelve patients (42,8 p. cent) had clinical dysautonomia. Ten had an increase of urinary methoxylated metabolites. Patients exempt of dysautonomia had normal biological parameters. The elevated level of urinary methoxylated metabolites is statistically correlated to clinical dysautonomia and can be used as a biological marker to monitoring demyelinating polyradiculoneuritis.

Autonomic Nervous System Diseases↗
PubMed2001

[Beta-interferon clinical trials using MRI in patients with multiple sclerosis].

Magnetic resonance imaging has revolutionized management of patients with multiple sclerosis. This tool provides information on a dynamic process never visualized before, optimizing diagnostic capacities and formalizing the course of the lesion load. Follow-in clinical assessment and performance testing, MRI constitutes a second line tool for following the course of patients with multiple sclerosis in phase II and III trials. We reviewed the correlations between the radiological and clinical findings and the methodology of published trials on beta interferons in remitting, secondarily progressive and early onset multiple sclerosis.

Brain↗
PubMed2001

[Therapeutic indications in spasticity symptoms of multiple sclerosis].

Spasticity is reported in 90 p. 100 of multiple sclerosis patients causing pain, spasms, loss of function and difficulties in nursing care. A variety of oral and parenteral medications are available. Review of comparative efficacy and tolerability of anti-spastic agents is performed in order to guide rational prescribing.

Combined Modality Therapy↗
PubMed2001

[Therapeutic indications in symptoms of bladder and sphincter disorders in multiple sclerosis].

Bladder and bowel dysfunction is common in multiple sclerosis. After accurate diagnosis of dysfunction, a management program with anticholinergic or alphabloquers drugs is mandatory. Intermittent catheterization, surgical treatment, or electrostimulation are proposed in most severe cases. Therapies for intestinal disorders are more limited. Management of symptoms and different therapies are reviewed.

Combined Modality Therapy↗
PubMed2001

[Therapeutic indications in symptomatic cognitive and psychopathological disorders in multiple sclerosis].

Cognitive impairment and psychiatric disorders occur in about 60 p. cent of multiple sclerosis patients. In general, impairment develops in established cases, although it can present early in the disease course. The pattern of neuropsychological deficits is characterized by deficits in attention, memory and executive functions; No specific treatment seems to be effective in cognitive impairment but appropriate strategies could limit the negative impact on this disease. Depressive states are twice frequent and usual antidepressant drugs seems to demonstrate some efficacy.

Cognition Disorders↗
PubMed2000

Effects of S 18986-1, a novel cognitive enhancer, on memory performances in an object recognition task in rats.

(S)-2,3-dihydro-[3,4]cyclopentano-1,2,4-benzothiadiazine-1,1-dioxi de (S 18986-1) is a new compound that facilitates post-synaptic responses by modulating alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor-mediated synaptic responses and thus promotes long-term potentiation and potentiates (S)-AMPA-induced release of noradrenaline in rat brain slices. In the present study, the effects of S 18986-1 were evaluated on cognitive functions by using a one-trial object-recognition test in the Wistar rat, a test which measures a form of episodic memory in rodents. Recognition was measured by the ability of treated rats to discriminate between a familiar and a new object after a 24-h retention delay. Oral administrations with S 18986-1 (0.3 to 100 mg/kg) 1 h before each session of the test improved object recognition at concentrations as low as 0.3 mg/kg. Under the same conditions, the nootropic drug aniracetam was active at a dose of 10 mg/kg by i.p. route. S 18986-1 was still effective on the object-recognition test when it was administered 4 h before each of the three sessions. Furthermore, subchronic oral pretreatment (7 days) with S 18986-1 (0.3 to 30 mg/kg) also increased the recognition of the familiar object indicating that the animals failed to develop tolerance to repeated administrations with S 18986-1. Finally, the recognition of the familiar object was improved when S 18986-1 was administered before the recognition trial whereas the rats failed to recognise the familiar object when S 18986-1 was administered before the sample presentation trial only. Taken together, the results indicated that S 18986-1 facilitated a form of episodic memory in the rat, by improving the recognition of a familiar information (retention). Furthermore, S 18986-1 was long-acting and demonstrated a good oral bioavailability. These data confer on S 18986-1, a potential role in improving episodic memory impaired in neurodegenerative diseases and during aging.

Administration, Oral↗
PubMed2000

Up-front chemotherapy with fotemustine (F) / cisplatin (CDDP) / etoposide (VP16) regimen in the treatment of 33 non-removable glioblastomas.

Despite combinations of surgery, radiotherapy (RT) and chemotherapy used in the treatment of glioblastomas, mean and median survival rates in most patients remain 12 months or less after diagnosis. RT and nitrosourea after surgery are the standard combination for glioblastomas. They may induce acquired resistance and, consequently, non-operable glioblastomas is a unique biological and clinical situation allowing evaluation of intrinsic chemosensitivity. We assess the fotemustine (F) (100 mg/m2 day 1)/ cisplatin (CDDP) (33 mg/m2 days 1-3)/etoposide (VP16) (75 mg/m2 days 1-3) monthly regimen for efficacy in non-removable glioblastomas at presentation. Between 1995 and 1998, 33 consecutive patients with symptomatic non-removable histologically proven glioblastomas were treated: none of them had previously received chemotherapy, irradiation or surgical debulking. Objective response was evaluated by contrast enhancement with magnetic resonance imaging (MRI) scan after each treatment. Toxicity was moderate and mainly haematological (grade III-IV thrombopenia = 20/171 cycles; leucopenia = 25/171). Neutropenic fever was rare and no intracranial haemorrhages or treatment-related deaths were noted. Nausea and vomiting (grade 1), and asymptomatic hearing loss were common. Peripheral neuropathy occurred in 3 patients. Objective response rates were 9/33 (27%) (stabilisation = 17/33). Mean survival time was 14.4 (11.2 months in the 26 deceased patients) with a median survival of 10 months. Median survival rates at 6 and 12 months were 88% and 42%, respectively. 7/33 patients are still alive with median survival of 34.6 months. 7/33 (4/7 alive) were long-term survivors (range: 19-67 months). Neoadjuvant chemotherapy in non-resectable patients is safe allowing delayed RT. Phase II chemotherapy trials should include studies with a subgroup of non-resectable tumours.

Adult↗
PubMed2000

[Chemotherapy of malignant inoperable gliomas. The association of fotemustine-cisplatine-etoposide as neoadjuvants].

Efficiency of chemotherapy (CT) on non removable HGG has not been proven and neoadjuvant brain irradiation (RT) following biopsy is the standard treatment. We aimed to define whether combination of polychemotherapy and radiotherapy is synergistic in non removable HGG. It has been proven that F, CDDP and VP16 can reach therapeutic levels in brain after intravenous standard dose injections. The aim of this study was to assess that (i) neoadjuvant CT is safe; (ii) feasibility and efficacions of F (100 mg/m2.d1)/CDDP (100 mg/m2.d1-3 TD)/VP16 (75 mg/m2.d1-3) q21-28d regimen; (iii) Delayed RT is not unsafe: RT was performed when tumor progression or toxicity appeared. This study included 16 patients with symptomatic non removable HGG. Two of them had anaplastic gliomas and 14 glioblastomas multiforme. None of them had a prior chemotherapy regimen. Objective response was evaluated with CT scan or MRI during chemotherapy. Toxicity was moderate and mainly hematological (grade III-IV thrombopenia = 10/67 cycles; leukopenia = 13/67). Objective response rates were 5/16 (31 p. 100) (CR = 1; PR = 4; Median duration of response: 20 weeks). Median survival was 55 weeks in the 14 grade IV patients. Three/16 patients are still alived with respectively 22, 30, 40 months survival: These results confirm the neoadjuvant chemotherapy efficacy. It may be a useful tool before RT for non removable HGG.

Adult↗
PubMed1999

Overexpression of the FAD-binding domain of the sulphite reductase flavoprotein component from Escherichia coli and its inhibition by iodonium diphenyl chloride.

SiR-FP43, the NADPH- and FAD-binding domain of the Escherichia coli sulphite reductase flavoprotein component (SiR-FP), has been overexpressed and characterized. It folds independently, retaining FAD as a cofactor and the catalytic properties associated with the presence of this cofactor. Iodonium diphenyl chloride (IDP) was shown to be a very efficient inhibitor of SiR-FP43 and SiR-FP60, the monomeric form of SiR-FP, containing both FMN and FAD as cofactors (K(i) = 18.5 +/- 5 microM, maximal inactivation rate = 0.053 +/- 0.005 s(-1)). In both cases, inactivation was shown to result from covalent binding of a phenyl group to FAD exclusively, in marked contrast with previous results obtained with cytochrome P450 reductase (CPR), where FMN and a tryptophan were phenylated, but not FAD. However, our kinetic analyses are in agreement with the inhibition mechanism demonstrated with CPR [Tew (1993) Biochemistry 32, 10209-10215]. Nine different FAD phenylated adducts were isolated and, for the first time, two FAD phenylated adducts were identified directly after extraction from a protein. Taken together, our results have shown that flavoprotein inactivation by IDP is not a reliable indicator for a flavin radical intermediate in catalysis.

Base Sequence↗
PubMed1999

[Cancer in patients infected with the human immunodeficiency virus. The unusual aspects].

CANCER AND HIV INFECTION: As the HIV epidemic advances, the spectrum of non-AIDS defining malignancy is expanding. Recent reports suggest an increased incidence of skin cancers, squamous cell carcinomas of the anus, and Hodgkin's disease in HIV-infected patients. Other neoplasms encountered in this setting include oral mucosa, head and neck carcinoma without evidence of increased incidence. PARTICULAR FEATURES: The natural history of lung, testicle and skin cancer (excepting Kaposi sarcoma) as well as ENT cancer appears to be modified in HIV-infected patients. The main problem raised by these tumors is confounding infection which may lead to late diagnosis or an error in tumor staging.

HIV Infections↗