Biomedical subjects

P Bonfils

Publications and source records attributed to P Bonfils.

At least 37 records · Page 2Linked to original sources

PubMed2003

[Adrenal insufficiency after treatment of nasal polyposis].

OBJECTIVE: Assessment of hypothalamic-pituitary-adrenal (HPA) axis after long term and uncontrolled corticosteroid treatment in nasal polyposis. PATIENTS AND METHODS: A short synacthen test was performed in ten patients who received uncontrolled doses of corticosteroids in a population of 128 patients treated for nasal polyposis. RESULTS: Mean yearly dose of oral prednisone administered in short-term treatment varied between 1280 and 7300 mg. Mean daily dose of inhaled beclomethasone varied between zéro and 2000 microg. Morning plasmatic cortisol was abnormal in seven the patients before and after the stimulation (respectively 140 nmole/l and 359 nmole/l). DISCUSSION: High and uncontrolled doses of corticosteroids in nasal polyposis affect HPA axis.

Adrenal Insufficiency↗

PubMed2002

[Normative data of the Biolfa(R) olfactory test].

OBJECTIVES: To evaluate the feasibility of the Biolfa(R) olfaction test and establish normative values. PATIENTS AND METHODS: The new Biolfa(R) olfaction test includes a quantitative test to measure the olfactory threshold of three substances in a concentration range from 1 to 9 and a semi-quantitative test to assess olfactory "acuteness" for eight substances. Substances used for this test entail non-significant trigeminal stimulation. A population of 28 women and 24 men without olfactory dysfunction were tested. RESULTS: The olfactory threshold obtained with the quantitative test ranged from 5.86 to 9.54 for women, and from 6.4 to 9.6 for men. Analysis of the thresholds identified with the semi-quantitative test enabled establishing normative values for recognition of the eight substances. These values were reported on a diagram to allow partial translation of each subject's olfactory "acuteness". Olfactory threshold and smell identification ability were statistically superior for women. CONCLUSION: The Biolfa(R) olfaction test is the first allowing determination of both the olfactory threshold and quantification of smell identification ability. Normative values were obtained in this study to detect disease states.

Feasibility Studies↗

PubMed2001

Efficacy and tolerability of budesonide aqueous nasal spray treatment in patients with nasal polyps.

OBJECTIVE: To assess the efficacy and tolerability of once-daily treatment with budesonide aqueous nasal spray in patients with nasal polyps. DESIGN: Randomized, double-blind, placebo-controlled, parallel-group study. SETTING: Sixteen hospital clinics. PATIENTS: One hundred eighty-three patients with moderate-sized nasal polyps causing clinically significant symptoms during a 1-week run-in period. INTERVENTIONS: Patients were randomized to receive 1 of the following 4 budesonide aqueous nasal spray treatments: 128 microg once daily in the morning and placebo in the evening, 128 microg twice daily, 256 microg once daily in the morning and placebo in the evening, or placebo for 8 weeks. Nasal polyp size was scored and peak nasal inspiratory flow was measured at clinic visits at the beginning and end of the run-in period and after 4 and 8 weeks' treatment. Patients recorded daily peak nasal inspiratory flow, symptom scores (ie, blocked nose, runny nose, and sneezing) and sense of smell on diary cards. MAIN OUTCOME MEASURES: Mean change in nasal polyp size at the end of treatment; mean changes in combined and individual symptom scores. RESULTS: All doses of budesonide aqueous nasal spray significantly (P<.01) reduced polyp size; no significant differences were noted between the 4 treatment groups. The mean improvement in clinic peak nasal inspiratory flow at 8 weeks was 65.9 L/min with budesonide aqueous nasal spray, 128 microg twice daily; 71.6 L/min with budesonide aqueous nasal spray, 256 microg once daily; and 54.6 L/min with budesonide aqueous nasal spray, 128 microg once daily (all P<.001 vs placebo). Combined and individual symptom scores and sense of smell improved significantly in all budesonide-treated groups; the effect on symptoms became apparent within 1 to 2 days of the first dose. Budesonide aqueous nasal spray was well tolerated. CONCLUSIONS: Doses of budesonide aqueous nasal spray, 128 microg once daily, were found to be effective in the treatment of nasal polyps, and doses of budesonide aqueous nasal spray, 256 microg once daily, did not show any significant additional efficacy.

Administration, Intranasal↗

PubMed2001

[Esophagectomy for squamous cell carcinoma of the esophagus isolated or associated with head and neck cancer: long-term survival].

STUDY AIM: Esophageal squamous cell carcinomas are frequently associated with head and neck cancers. This retrospective study was conducted to compare the long-term outcome of the patients with a double cancer and of the patients with a solitary esophageal cancer after curative management. PATIENTS AND METHODS: From 1989 to 1999, 114 patients with an esophageal carcinoma were included in the study. Among them, 52 had an associated head and neck cancer (metachronous: n = 17 and synchronous: n = 35). Curative treatment was achieved in all patients. The patients were divided in "solitary" and "associated" group. RESULTS: Age, sex distribution, tumor location and histological findings were similar in the two groups. The esophageal resection was an esopharyngolaryngectomy (n = 13), a subtotal esophagectomy with cervical anastomosis (n = 92) and a Lewis-Santy esophagectomy with thoracic anastomosis (n = 9). Operative mortality (8 versus 7.7%), anastomotic leaks rate (14.5 versus 21%) and pneumonia rate (21 versus 9.6%) were not significantly different in the two groups. The mean hospital stay was 27 days. The mean follow-up was 85 +/- 50 months. Five-year survival rates were not significantly different in the two groups (p = 0.6411). In univariate survival analysis the only significant predictive factors were the depth of esophageal tumor invasion (p = 0.0002) and node involvement (p = 0.0373). The presence of head and neck cancer did not affect survival after esophagectomy. CONCLUSION: With an aggressive therapeutic plan, the survival of patients with an esophageal cancer associated to head and neck cancer was similar to the survival of patients with an isolated esophageal carcinoma. Long term esophageal survey seems to be useful to detect more superficial esophageal carcinomas in patients with head and neck cancer.

Aged↗

PubMed2001

Functional anatomy of auditory brainstem nuclei: application to the anatomical basis of brainstem auditory evoked potentials.

Brainstem auditory evoked potentials (BAEP) are used routinely in clinical practice to evaluate the normality of the lower auditory system. The objective of this review is to describe the functional anatomy of the structures implicated in BAEP generation (cochlear nerve and the auditory brainstem nuclei). Indications and results of BAEP in clinical practice are presented and correlated with auditory structures, which generate each waveform of BAEP.

Auditory Pathways↗

PubMed2001

Lymphocele of the thoracic duct presenting as a left supraclavicular mass: a case report and review of the literature.

Surgical injuries and blunt trauma are the main causes of thoracic duct lesions. Cervical chylous fistula and chylothorax occur frequently after lesions of the cervical portion of the thoracic duct. On the other hand, thoracic duct cyst is a very rare entity, especially in its cervical portion. The authors reported a case of thoracic duct cyst, presenting as an asymptomatic left cervical mass. Diagnosis was suggested by computerized axial tomography and confirmed by histological analysis, after surgical removal of the cyst. After review of the literature, the authors recommended surgical treatment of cervical thoracic duct cysts in order to prevent potential complications as traumatic or spontaneous rupture.

Clavicle↗

PubMed2001

Origin of cubic difference tones generated by high-intensity stimuli: effect of ischemia and auditory fatigue on the gerbil cochlea.

Cubic difference tone (CDT) otoacoustic emissions are thought to arise from the feedback loop allowing outer hair cells to enhance the sensitivity and tuning of the organ of Corti. The existence of residual CDTs during complete cochlear ischemia is therefore disturbing. That stimulus intensities must exceed 50-60 dB SPL for residual CDTs to be recorded and for level notches to be present in CDT growth functions is often cited as evidence for a two-component, "active/passive" model: one component, the residual one, would originate from a passive, hardly vulnerable mechanism and thus be unsuitable for hearing screening purposes. This model was probed in gerbil ears after complete interruption of the cochlear blood flow. Cochlear potentials and CDTs were controlled simultaneously through continuous monitoring of CDT level and phase for 50 and 60 dB SPL stimuli and group-delay measurements. After a clear initial decay, CDT levels elicited at 60 dB SPL plateaued for several minutes at about 20 dB below initial level, and when early level notches were observed, CDT phase changes remained minor. The CDT group delays decreased by less than 30%. Later CDT level notches were associated with sharp phase reversals but the similarity between CDT characteristics before and after a notch was hardly consistent with a two-component interpretation. When mild sound overexposure (pure tone, 90-95 dB SPL, 15-30 min) had been performed prior to ischemia, little or no ischemic CDT came from the frequency bands where auditory fatigue had been detected (within 1 kHz), irrespective of the stimulus intensity. It suggests that instead of being passive, residual ischemic CDTs were vulnerable and produced according to a near-normal tonotopy by the same mechanisms that were sensitive to auditory fatigue. All the results lined up with a simple feedback model of cochlear function assuming a single CDT source related to mechano-electrical transduction in outer hair cells. More parsimonious than a two-component model, it posits that although early stages of ischemia dramatically impair the overall performance of the cochlea, the nonlinear mechanical stages responsible for the existence of CDTs keep working albeit at higher intensities.

Acoustic Stimulation↗

PubMed2001

Catheter-related upper extremity deep venous thrombosis in cancer patients: a prospective study based on Doppler US.

PURPOSE: This prospective study extending for more than 3 years had two objectives: (a) to use Doppler ultrasonography (US) to estimate the incidence of asymptomatic catheter-related upper extremity deep venous thrombosis (DVT) in a large population and (b) to study the effect of the catheter position as an individual risk factor for catheter-related DVT. MATERIALS AND METHODS: Between October 1995 and June 1998, a total of 145 patients who had oropharyngeal tract cancer and who were fitted with the same totally implantable central venous catheters (CVCs) were included in the study. Follow-up included (a) estimation of the position of each catheter tip on a chest radiograph obtained immediately after surgery and (b) regular monthly Doppler US screening for catheter-related DVT. RESULTS: Seventeen patients developed catheter-related DVT; 13 of them were asymptomatic. The mean interval between CVC implantation and detection of thrombosis was 42.2 days. Correct positioning of the distal catheter tip was associated with a significantly lower rate of catheter-related DVT. Only five of 87 patients with a correctly positioned distal catheter tip (ie, either in the superior vena cava or at the junction between the right atrium and the superior vena cava) developed thrombosis, compared with 12 of 26 patients with a misplaced catheter (P <.001). The side on which the CVC was implanted did not influence the catheter-related DVT rate. CONCLUSION: The rate of asymptomatic catheter-related DVT is high and could be lowered with correct initial CVC positioning.

Adult↗

PubMed2001

[Smell dysfunction in nasal and paranasal sinus disease: a review of the literature (I)].

Substantial advances have been achieved during the last decade in our understanding of the biological bases of the sense of smell, as well as in the clinical identification, diagnosis, and management of dysosmia. Nasal obstruction can result from inflammatory, neoplastic, traumatic, and developmental alterations within the nasal cavity. All these processes, if they result in bilateral restriction of airflow to the olfactory neuroepithelium, presumably alter the ability to smell. Rhinitis, nasal polyposis, and rhinosinusitis are accompanied by decreased ability to smell. Benign and malignant neoplasms can obstruct the nasal chamber and thereby alter airflow to the olfactory receptors without damaging the olfactory neuroepithelium. The purpose of this synthesis is to provide an advanced review of the literature in order to describe the basis of smell alterations in nasal polyposis and chronic rhinosinusitis.

Anti-Inflammatory Agents↗

PubMed2001

[Smell dysfunction in nasal and paranasal sinus disease: a review of the literature (II)].

Chronic Disease↗

PubMed2000

[Chemicals toxic to the olfactory system. Analysis and description].

AN IMPORTANT PROBLEM: Occupational exposure to chemical products can have toxic effects on the olfactory system. An important number of patients have experienced olfactory disorders subsequent to the development of the chemical industry and atmospheric pollution. EPIDEMIOLOGY DATA: Straightforward data are difficult to collect because several cofactors other than the toxic product are involved. Two lists of toxic products can be made. The first list includes products for which scientific data is available and the second products for which data is lacking. Olfactory tests also differ between authors and countries. TWO TYPES OF TOXICITY: Acute, accidental toxicity is evidenced by the lesions caused by inhalation of high-doses of strongly toxic agents. Chronic intoxication caused by lower concentrations of these inhaled agents does not produce a trigeminal reflex leading to a modified respiratory rate reducing the airborne aggression. APPROXIMATIONS: Clinical data describing the olfactory toxicity of certain industrial and chemical compounds are very significant but often cannot prove a cause and effect relationship. Data obtained with experimental models in rodents are difficult to extrapolate to humans.

Air Pollutants, Occupational↗

PubMed2000

[Evaluation of the hypothalamo-hypopituitary axis after long-term inhalation corticotherapy for nasal polyposis].

OBJECTIVE: To assess the hypothalamic-pituitary-adrenal (HPA) axis after long-term intranasal corticosteroid treatment in nasal polyposis. PATIENTS AND METHODS: A short synacthen test was performed in 24 patients who received the highest dose of inhaled beclomethasone among a population of 392 patients treated for nasal polyposis with inhaled corticosteroid therapy and short-term oral corticosteroids. RESULTS: Mean yearly dose of oral prednisone administered in short-term treatment was 371 mg/year. The amount of short-term oral prednisone decreased during the treatment. Mean daily dose of inhaled beclomethasone was 2861 micrograms/day, decreasing during treatment. Morning plasma cortisol was normal in all patients before and after stimulation (163 +/- 44 and 1 +/- 60 micrograms/ml respectively). Nolomethasone dose and plasma cortisol level before or after stimulation. DISCUSSION: The high dose of inhaled beclomethasone used to treat nasal polyposis does not affect the HPA axis. Some authors in the literature contest the validity of short synacthen test to detect HPA axis suppression. This test does however detect severe impairments of the HPA axis in outpatients.

Administration, Inhalation↗

PubMed2000

[Olfactory disorders due to medications: analysis and review of the literature].

INTRODUCTION: Olfactory disorders caused by medicinal drug intake are an uncommon occurrence. However, such an etiology should be systematically taken into account and investigated, as olfactory loss may be reversible once the particular treatment has been stopped. CURRENT KNOWLEDGE AND KEY POINTS: An analysis of the literature shows that of the large number of drugs that are apparently responsible for olfactory disorders, this adverse side effect has in fact only been observed in animal study populations, and no clinical case report has been made on the subject. The real toxicity to man is therefore only hypothetical. Of the 150,000 cases recorded in the pharmacovigilance centers in France, only 68 have reported olfactory complications (0.05% of cases), and only 22% of the medical files on this disorder reach a satisfactory level of plausibility. Cardiovascular drugs are mainly implicated in the development of olfactory disorders. Of these, certain drugs in particular should be mentioned: conversion enzyme (ACE) inhibitors which are responsible for taste disorders, some betablockers, and a calcium antagonist (a dihydropyridine derivative). Olfactory disorders have also been reported following administration of drugs used in anesthesia, in cancerology, endocrinology (carbimazole), in immunology (interferon), in the treatment of infectious diseases (ciprofloxacine, dioxycycline, terbinafine), and in rheumatology (D-penicillamine). FUTURE PROSPECTS AND PROJECTS: It is frequently difficult to establish a direct relationship between drug exposure and an olfactory disorder, and it is often not easy to determine with any certainty the causative role of the drug in the development of this disorder.

Animals↗

PubMed2000

[Olfactory disorders and general pathology. Analysis and review of the literature].

INTRODUCTION: Disturbances of the sense of smell have been documented in many general pathologies. The actual etiology of such impairments is often difficult to determine. The aim of the authors is to review the literature on olfactory disorders in general diseases. CURRENT KNOWLEDGE AND KEY POINTS: Acute and chronic liver disorders are frequently associated with hyposmia, which can be improved by vitamin A intake. Renal insufficiency could induce hyposmia according to the severity of the renal disease. Olfactory disorders seem to regress after transplantation but not after dialysis. Patients with AIDS--especially neurological forms--often present with taste and smell impairments. Smell alteration can also be noted in hypothyroidism and pseudohypoparathyroidism. In addition, taste and smell impairments have been described in patients with adrenal insufficiency or Cushing's disease. Subsequent to glucocorticoid therapy, adrenal insufficiency can induce regressive olfactory hypersensitivity. Olfactory impairments in diabetic patients can be associated with diabetic macrovascular manifestations due to ischemic alterations in the olfactory neuroepithelium. Impairment of the sense of smell has been described in many systemic diseases such as Horton's arteritis and Sjögren's syndrome. FUTURE PROSPECTS AND PROJECTS: Olfactory disorders should be investigated in patients presenting one of the above-mentioned diseases.

Acquired Immunodeficiency Syndrome↗

PubMed2000

On the spectral periodicity of transient-evoked otoacoustic emissions from normal and damaged cochleas.

The spectral quasi-periodicity of transient-evoked otoacoustic emissions (TEOAE) is well acknowledged since Zwicker described a preferred spacing of 0.4 bark between consecutive peaks in the spectrum of otoacoustic emissions from normal ears. While there is scarce evidence of any anatomical reason for this regularity, several functional models of the cochlea have predicted that the structure of emission spectra reflects important characteristics of cochlear filters. In an attempt to check such predictions, the average regularity of TEOAE spectra was studied in three groups of human subjects, normally hearing adults, healthy neonates, and adults suffering from noise-induced hearing loss. Significant differences in emission periodicities were found. Around 1 kHz, the preferred spacing was close to 130 Hz in normally hearing adult ears and neonates. In contrast, no clear periodicity was found in the group of damaged ears, even though they had clinically normal pure-tone audiometry below 2 kHz. Around 4 kHz, the preferred spacing was close to 240 Hz in normal adults and neonates, whereas TEOAEs were absent in many impaired ears. A phenomenological model assuming that TEOAEs stem from the responses of a slightly disarrayed bank of highly tuned filters predicts that the filter width would be the same in healthy young adults and neonates. In contrast, ears suffering from high-frequency hearing loss could exhibit early damaged filters. The proposed method might provide an objective assessment of parameters otherwise difficult to evaluate, especially in neonatal cochleas.

Adult↗

PubMed2000

[Signs and symptoms, etiologies and clinical course of parosmia + in a series of 84 patients].

Eighty-four patients (72% females and 28% males) consulted between January 1995 and January 1998 for olfactory disorders with parosmia (erroneous olfactory response to stimuli). Parosmia occurred immediately after or during the course of acute rhinitis (n=70, 83%), head trauma (n=7, 9%), naso-sinus polyposis (n=5, 6%), chronic rhinitis (n=1) or frontal tumor (n=1). Quantitative and qualitative olfactory disorders were analyzed and products producing the parosmia were identified. The only cases where parosmia regressed concerned patients who developed parosmia after acute rhinitis (n=28 cases, 33%). The prognosis of parosmia appeared to be better when it was a secondary phenomenon: i) the percentage of improvements was higher though not significant (41% versus 26.7% compared with primary parosmia), ii) delay to improvement was shorter (8.4 +/- 2.1 months versus 14.5 +/- 4.4 months for primary parosmia, p<10(-4) ), iii) there were no cases of persistent parosmia where quantitative disorders improved (compared with 7 cases of persistent primary parosmia, p<0.05). In addition, the prognosis of associated quantitative disorders was the same for both primary and secondary parosmia. Only the delay to improvement appeared to be shorter in case of secondary parosomia (though the difference was not significant). Products which produced the parosmic perception were identified by nearly all the patients (85%). The most frequently cited products were coffee, perfume, certain fruits (melon, banana, citric fruits), tobacco or chocolate. All these products contain tannic acid, a water-soluble polyphenol with many biological properties (influence feeding habits and metabolism in the rate, antioxidant and antimutagenic properties). Thus acid tannic could induce parosmic perception due to its antioxidant properties susceptible of integrating the P-450 cytochromes of the mucosal cells or olfactory neuroepithelium supporting cells.

Adult↗

PubMed2000

[Description and analysis of olfactory disorders after head trauma. Review of the literature].

Olfactory disorders subsequent to head trauma can raise medicolegal problems when the olfactory deficit occurs after a work accident or a traffic accident and also raises the problem of psychological and functional tolerance when the patient consults late for a therapeutic solution. We studied the epidemiology of olfactory disorders after head trauma. Such disorders have been recognized since the XIX(th) century. Several studies have attempted to determine the prevalence of olfactory sequelae after head trauma. We then describe the pathophysiology of these lesions and emphasize that the degree of severity is related with the gravity of the head trauma and that the prevalence of these disorders varies considerably depending on the site of the trauma. Mechanisms which can lead to lesions of the olfactory system include, damage to the olfactory nerve bundles, naso-sinus lesions, or lesions of the cerebral olfactory centers. Brain MRI in anosmic patients after head trauma allows a visualization of intracranial lesions. The degree of reversibility of olfactory disorders after head trauma is imperfectly evaluated and discordant results have been reported. Some authors consider loss of olfaction is definitive. Others suggest an improvement in olfaction the year following head trauma. We reviewed the literature on these different elements. Expert opinions concerning patients complaining of olfactory disorders should relate this disorder to the initial trauma and determine the personal and occupational impact of the deficit. Attribution of cause must take into account all the clinical, radiological and psycho-olfactory factors.

Brain Damage, Chronic↗

PubMed2000

[Olfactory disorders in Alzheimer's disease and in Parkinson's disease. Review of the literature].

Olfactory disorders in Alzheimer's disease and Parkinson's disease have been the topic of a large body of work over the last decades. Work devoted to olfactory disorders in Alzheimer's disease includes over 300 papers providing clinical and fundamental data. Anatomy studies in Alzheimer's disease have demonstrated a specific concentration of lesions in peripheral and central olfactory structures (senile plaques, neurofibrillary degeneration) as well as lesions in layers II and III of the entorhinal cortex. These neuropathological findings led to the development of the hypothesis that olfactory disorders in Alzheimer's disease would result from a toxic process. Observed olfactory deficits involve both identification and recognition of odors and detection thresholds. Nevertheless, patients with Alzheimer's disease rarely consult for sensorial deficits as the other signs of the disease predominate. Neuropathology data on the olfactory system are much more sparse in Parkinson's disease. Lewy bodies suggestive of Parkinson's disease have been observed in the olfactory bulb and pathways, but, unlike Alzheimer's disease, the olfactory disorders appear to be stable, changing little over time, as opposed to the evolution of neurological symptoms and cognition impairment. Clinicians should be aware that olfactory disorders are an integral part of Alzheimer's disease and Parkinson's disease. Screening for sensorial impairment however is a secondary objective in the context of these neurodegenerative diseases.

Alzheimer Disease↗