Occupational asthma induced by ethylene oxide.
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Asthma↗
Biomedical subjects
O Michel
Publications and source records attributed to O Michel.
Blood inflammatory response to inhaled endotoxin in normal subjects.
Previously we have reported that in asthmatics an inhalation of 20 micrograms lipopolysaccharide (LPS) produces a bronchial obstruction associated with an inflammatory blood response. The aim of the present study was to evaluate this response in normal subjects. Eight normal non-atopic subjects were challenged by inhalation of a solution containing 20 micrograms LPS (from Escherichia coli 026:B6) a week after bronchial challenge with control solution. The lung function response was evaluated by the changes in forced expiratory volume in one second (FEV1), in specific conductance and in airway resistance while the blood inflammatory response was evaluated by serial measures of total white blood cells (WBC) and polymorphonuclear neutrophils (PMN) count, luminol enhanced-chemiluminescence (luminol-CL, as a marker of the PMN degree of activation), C-reactive protein (CRP), haptoglobin, complement fraction C3, tumour necrosis factor-alpha (TNF-alpha) and adrenocorticotropic hormone (ACTH). No response in lung function was observed for 6 h after the LPS inhalation. The count in WBC and PMN increased 300 (P < 0.01) and 360 (P < 0.01) min after the LPS challenge associated with an increase in the level of luminol-CL (P < 0.001). This rise in luminol-CL level was significant at 120 min (P < 0.05) before any change in the PMN count. After 24 and 48 h the acute-phase protein CRP raised significantly (P < 0.01), the other proteins C3 and haptoglobin being unchanged. A slight increase in ACTH was observed 240 and 360 min (P < 0.05) after the LPS challenge while the TNF alpha detectable level was not modified.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Inhalation↗
Protective effect of sodium cromoglycate on lipopolysaccharide-induced bronchial obstruction in asthmatics.
Lipopolysaccharides (LPS, the major part of endotoxins) are bacterial proinflammatory substances which can induce in asthmatic patients after inhalation a bronchial obstruction with an increase in both histamine bronchial hyperresponsiveness and blood inflammatory markers. The aim of the present study was to evaluate whether an acute inhalation of sodium cromoglycate, an anti-inflammatory and membrane-stabilizating agent, can block the LPS-induced lung function response. Using a double-blind placebo-controlled crossover method, 7 asthmatic subjects were submitted, at 4 days' interval, to a bronchial challenge test with either solvent solution or LPS (20 micrograms) preceded by inhalation of sodium cromoglycate (10 mg) or placebo. Compared to the solvent reaction, LPS induced a significant bronchial obstruction [measured by both the forced expiratory volume in 1 s (FEV1) and the airway resistances] beginning at the 60th minute and lasting more than 300 min (p < 0.01, 2-way ANOVA). On the other hand, acute pretreatment with sodium cromoglycate significantly inhibited the LPS-induced bronchial obstruction. The total lung capacity did not change significantly after LPS inhalation. Thus, this study showed that in asthmatics the LPS-induced FEV1 response is blocked by acute treatment with sodium cromoglycate. Sodium cromoglycate could be an active treatment in asthmatics exposed to house dust containing endotoxin.
Administration, Inhalation↗
Electron microscopic location of mRNA in the rat kidney: improved post-embedding in situ hybridization.
We determined the optimal technical conditions for post-embedding non-radioactive in situ hybridization applied to ultrastructural location of collagen I mRNA in rat kidney. The signal-to-noise ratio was improved by enhancing hybridization efficiency and distinguishing nonspecific labeling. Probes were labeled with digoxigenin or biotin and detected after hybridization by immunogold or peroxidase techniques. Under these conditions, the signal was located in fibroblasts. With digoxigenin, clusters of gold particles were observed on the endoplasmic reticulum (ER) or scattered throughout the cytoplasmic matrix and nuclei. With the enzymatic method, diaminobenzidine deposits were found on the ER but endogeneous peroxidase partly interfered with the results. Gold particles were less numerous in fibroblast cytoplasm with biotin than with digoxigenin. Moreover, gold particles condensed on fibroblast and tubular cell mitochondria when biotin was used, a phenomenon shown to be due to endogenous biotin by means of a histochemical method. The digoxigenin-immunogold system appeared to be the best method. The biotin system was subject to limitations such as interference from endogenous biotin and poor sensitivity, and mRNA localization was more precise and reliable by the immunogold method than by the enzymatic method.
Acrylic Resins↗
Morphometric detection of incipient glomerular lesions in diabetic nephropathy in rats. Protective effects of ACE inhibition.
BACKGROUND: Glomerulosclerosis is the main renal lesion complicating diabetes in humans and in experimental models. Angiotensin I-converting enzyme (ACE) inhibitors are effective in preventing the development of diabetic nephropathy. Incipient glomerular lesions were explored in streptozotocin-diabetic rats at a stage when glomerulosclerosis was not yet established. The modulation of such early glomerular lesions by a new ACE inhibitor (Trandolapril (T) at high or low doses was assessed. EXPERIMENTAL DESIGN: Five groups of rats were designed as follows: (a) nondiabetic control rats, (b) diabetic rats, (c) diabetic rats treated with 0.1 mg/kg/day of T, (d) diabetic rats treated with 1 mg/kg/day of T, and (e) nondiabetic rats treated with 1 mg/kg/day of T. The rats were killed at 1, 3, and 6 months after the beginning of the treatment. The kidneys were studied using a powerful morphometric technique at optical microscopic level with an image analyzer to measure the following glomerular parameters to assess the development of incipient glomerular lesions: (a) total glomerular surface area, (b) glomerular tuft surface area, (c) mesangial surface area, (d) ratio of the mesangial surface area to the glomerular tuft surface area, and (e) mean thickness of the Bowman's capsule. In parallel, albuminuria was measured. RESULTS: The results showed the development of glomerular hypertrophy in parallel with the increase in glomerular mesangial domain and in albuminuria with diabetes. They also demonstrated that ACE inhibitor given at a high dose is significantly effective in reducing glomerular hypertrophy and the expansion of the mesangial domain. ACE inhibitor given at a low dose tended to reduce glomerular hypertrophy and the expansion of the mesangial domain. Furthermore, ACE inhibitor at both doses completely abolished the albuminuria increase, maintaining the levels of albuminuria within the range of young nondiabetic rats. CONCLUSIONS: Using morphometric image analysis, incipient glomerular changes can be detected before glomerulosclerosis is patent in experimental diabetes. Moreover, they can be easily and reliably quantified by this technique, allowing comparison among experimental groups. These changes can be prevented by ACE inhibition.
Angiotensin-Converting Enzyme Inhibitors↗
[Expert assessment within the scope of the sudden deafness disease picture].
Claims for medical liability mostly arise when a patient believes that his sudden deafness was not accurately diagnosed, diagnosed too late or insufficiently or was not well treated. Guided by seven expert opinions potential problems in indemnity were depicted. A clear misdiagnosis of sudden hearing loss (e.g., a hearing loss taken for eustachian tube disorder) will lead to an accusation of malpractice if the doctor cannot prove an accurate otological examination and appropriate diagnostic studies. The burden of proof lies with the doctor. A further consequence of a missed diagnosis is a delay in treatment. In the literature the good prognostic factor of early treatment has been stressed but without delineating a clearcut line between "in time" and "too late". An accusation of malpractice by insufficient treatment (pills instead of infusions) has risen. Since an unequivocal treatment is not established and various modalities of therapy are still controversial, disputes could be settled more easily. The validity of "no treatment" may be considered but requires accurate diagnosis and the patient must give informed consent. Such a procedure is justifiable, even from an ethical standpoint, when the patient fully understands and agrees.
Adult↗
Effects of prostaglandin E2 on the fluctuating hearing loss in Ménière's disease.
To elucidate the possible mediating role of prostaglandins as underlying mechanism of the acute audiologic effects of furosemide in patients with Ménière's disease, the hearing threshold shift after a 1 hour infusion of a commercially available prostaglandin E2 derivative (120 ng/kg body weight) was determined in 10 patients. Prostaglandin E2 produced a transient hearing improvement comparable to the effects obtained in the furosemide test with 1.2 mg/kg bw in the same patients. The effectiveness of a prostaglandin infusion on hearing levels may be a further sign of the involvement of this mediator in hearing processes.
Adult↗
Relation between the bronchial obstructive response to inhaled lipopolysaccharide and bronchial responsiveness to histamine.
BACKGROUND: Bronchoconstriction has developed after inhalation of lipopolysaccharide in a dose of 20 micrograms in asthmatic patients and of 200 micrograms in normal subjects. This study set out to determine whether the bronchial response to lipopolysaccharide was related to non-specific bronchial responsiveness and atopy. METHODS: Sixteen subjects with a fall in specific airway conductance of 40% (PD40sGaw) after inhaling up to 900 micrograms histamine inhaled 20 micrograms lipopolysaccharide (from Escherichia coli type 026:B6) a week after bronchial challenge with a control solution of saline. The bronchial response over five hours was measured as change in FEV1 and area under the FEV1-time curve. RESULTS: FEV1 fell significantly more after lipopolysaccharide than after diluent inhalation, the difference in mean (SE) FEV1 being 4.6% (5.4%); response was maximal 60 minutes after lipopolysaccharide inhalation and lasted more than five hours. Histamine PD20FEV1 and PD40sGaw correlated with the fall in FEV1 after lipopolysaccharide inhalation. There was no difference in the proportions of responders and non-responders to lipopolysaccharide who were atopic. CONCLUSION: Lipopolysaccharide induced bronchial obstruction is associated with non-specific responsiveness but not with atopy.
Administration, Inhalation↗
Inflammatory response to acute inhalation of endotoxin in asthmatic patients.
Inhalation of 20 micrograms endotoxins (from the membrane of Gram-negative bacteria) has been reported to induce a bronchial obstructive response in asthmatic subjects. The aim of the present study was to evaluate in asthmatic patients the possibility of an inflammatory response to inhaled endotoxins. Eight patients with mild asthma were submitted to bronchial challenge tests, in a single-blind trial, on Day 1 with control solution and on Day 7 with 20 micrograms endotoxin of Escherichia coli (026:B6). Local inflammatory response was indirectly evaluated by the degree of bronchial hyperresponsiveness (BHR) expressed as PD20 FEV1 histamine (the dose of histamine inducing a 20% decrease in FEV1) at 0, 6, 24, and 48 h and 7 days. Systemic inflammation was investigated by sequential blood determinations of total (and differential) white cells, complement anaphylatoxin C5a, interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and C-reactive protein (CRP). A significant (p < 0.01) bronchial obstructive response was demonstrable 45 min after lipopolysaccharide (LPS) inhalation, lasting 5 h. Comparing the level of BHR after control inhalation, a significant (p < 0.05) increase in BHR was shown 6 h after LPS, partially normalized at 24 and 48 h. A short peak in TNF-alpha at 60 min (p < 0.05) and an increase in total white blood cells (p < 0.01) and neutrophil polymorphonuclear neutrophils at 360 min (p < 0.05) and of CRP at 24 and 48 h (p < 0.05 and p < 0.01) were significant. The other blood parameters did not change significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Inhalation↗
Hearing loss as a sequel of lumbar puncture.
Only a few case reports have been published about hearing impairment following lumbar puncture, and not all were thoroughly documented by audiograms. We present nine cases of hearing loss following myelography, lumbar puncture, and spinal anesthesia. We speculate that this rare complication arises only in persons with a wholly or partially patent cochlear aqueduct, and occurs via the release of perilymphatic fluid in the cerebrospinal space. Hearing loss was seen in eight of the nine patients in the lower frequencies, and in six of the nine patients on both sides. Recovery to normal hearing was noticed in six of the nine patients. Transient hearing loss may occur more often than it is generally assumed, and the symptom can remain unnoticed. Since not all of these hearing losses proved to be fully reversible, we suggest informing patients about this complication for medicolegal reasons.
Adult↗
[Response to the publication by B. Panning: "Inner ear hearing loss after lumbar puncture. A complication required in patient education?"].
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Anesthesia, Spinal↗
Probational treatment of sudden deafness with prostacyclin: a pilot study.
Sudden idiopathic hearing loss has occasionally been supposed to be caused by a disturbed microcirculation in the inner ear of unknown origin. Little is known about the regulation of cochlear blood flow and the effectiveness of drugs in cochlear microcirculation. Because animal experiments gave evidence that prostacyclin (PGI2) might be one biochemical substratum of local regulators in the flow of blood in the stria vascularis, 11 patients with sudden idiopathic hearing loss were treated once for 6 h with prostacyclin (10 ng/kg body weight/min) in a first open clinical trial. In most cases prostacyclin increased hearing level (mean value: 7.4 dB/frequency/day) more than a standard therapy with pentoxifylline. The substitution of PGI2 could be another indication of a rheologic disorder--whether per se or within a larger context of inflammation-like interaction--in the inner ear of patients with sudden hearing impairment.
Adult↗
[Placebo-controlled double-blind study of the treatment of sudden hearing loss with a stable prostacyclin analog].
A placebo-controlled, double-blind study with the stable prostacyclin analog Taprosten (CG4203, Grünenthal, Aachen, FRG) on the treatment of sudden hearing loss was conducted in 22 patients in the ENT Department of the University of Cologne. The hospital ethical committee gave permission for the trial. After informed consent had been obtained, the patients (13 male, 9 female, age 21-74 yrs.) were treated with Taprosten (25 ng/kg bodyweight/minute intravenously) or with 30 ml saline solution (NaCl 0.9%) for 6 hours during 5 days. Hearing thresholds were controlled by pure tone audiometry and speech discrimination test each day before and after treatment. All the data obtained (dB hearing loss) by pure tone audiometry was averaged for 7 frequencies. Differences were calculated between the hearing loss before and after treatment. Differences were considered significant if p less than or equal to 0.01. No significant difference could be seen in hearing recovery after Taprosten and placebo during the 5 days of treatment. Evaluation of the individual frequencies showed no prevalence of higher or lower frequencies. Although the impression was that hearing loss recovered better within the first days of treatment with Taprosten, no statistical proof could be found. In both groups the percentage of complete recovery did not differ (about 70%). The reason for the lack of significant statistical differences was the high standard deviation of the averaged hearing loss and the very high spontaneous recovery. Even if, in this placebo-controlled study, we could not prove the efficacy of a prostaglandin treatment for sudden hearing loss, the need for multicentred placebo-controlled studies with more patients is evident.
Adult↗
[Endoscopically-controlled endonasal orbital decompression in malignant exophthalmos].
In 6 patients with endocrine ophthalmopathy, indications, surgical technique and results of the endoscopic controlled endonasal orbital decompression are described in comparison to the common surgical procedures. When medical and radiation therapy fail, indications for decompression are a) loss of visual acuity or visual field defects, b) increasing strabismus, c) severe keratopathy due to eyelid retraction. The endoscopic-controlled endonasal surgical decompression technique is proceeded in three steps. First, an endonasal ethmoidectomy with resection of the middle turbinate is performed and the medial wall of the maxillary sinus is widely opened. Second, the medial and inferior wall of the orbital walls are removed, preserving the infraorbital nerve. In the last step, the periorbital area is incised and the orbital fat herniates. The advantages of this procedure consist in the absence of exterior scars and the known morbidity of a Caldwell-Luc antrotomy. The results were documented by computed tomographic scans (CT), magnetic resonance imaging (MRI), Hertel measurements, evaluation of ocular motility and ophthalmoscopy. An average of 3-4 mm improvement in Hertel-measurements could be reached. All patients had a postoperative improvement of visual acuity. 2 patients developed more significant diplopia postoperatively, whereas in all other patients ocular motility either improved or rested unaffected. Therefore, the endoscopic controlled endonasal procedure allows to obtain comparable results to the common extranasal and transantral procedures without the disadvantages of the latter.
Aged↗
Domestic endotoxin exposure and clinical severity of asthma.
Endotoxins are potent pro-inflammatory substances present in several natural environments and in commercial house dust extracts. To investigate the possible effect of chronic endotoxin exposure on asthma, 28 patients with perennial chronic asthma (20 allergic to house dust mite and eight intrinsic asthmatics) were evaluated during a 4-month period (lung function, clinical and immunological criteria). At the same time, two house dust samples were collected from each patient's home to determine total house dust weight (mg/m2), endotoxin concentration and house dust mite antigen content (evaluated indirectly by guanine content with HPLC method). The mean (+/- s.d.) endotoxin concentration, as measured by quantitative Limulus assay was 2.59 (+/- 3.41) ng/mg house dust, ranging from 0.12 to 20 ng/mg. The mean guanine content was 0.13 (+/- 0.16) mg/100 mg house dust. There was no correlation between endotoxin and house dust mite concentrations. Patients were compared according to the low or high grade exposure to dust, endotoxins and guanine. Compared with patients with low grade (less than or equal to 5.6 ng/ml) exposure, subjects exposed to high endotoxin concentrations (greater than 5.6 ng/ml) showed a significant increase in dyspnea (median 2.6 vs 3.3; P less than 0.05) and treatment (median 14 vs 44.3; P less than 0.01) scores, oral corticosteroid (median 0.0 vs 13.5 mg/24 hr; P less than 0.01) and beta 2-mimetics (median four vs eight puffs/day; P less than 0.01) intake, and a significant decrease in FEV1/FVC (median 84.5 vs 67% of predicted value; P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effect of endotoxin contamination on the antigenic skin test response.
Bacterial lipopolysaccharides (LPS), the major part of endotoxin, are proinflammatory substances present in the natural environment. Lipopolysaccharides enhance allergen-induced histamine release from human basophils of allergic subjects. The aim of this study was to assess the LPS activity on the allergy skin test response. Twenty patients allergic to house dust mite (HDM) underwent skin prick tests with LPS (E coli 026: B6 serotype) at concentrations of 1, 10, 100 micrograms/mL, with HDM extracts at different dilutions, and with solutions of LPS mixed with HDM. Endotoxin alone did not induce any immediate skin response; LPS had a synergistic effect on the HDM skin response both in terms of flare [27.4 +/- 2.8 mm, 26.6 +/- 3.3 mm, 28.1 +/- 2.5 mm versus 20.7 +/- 3.6 mm, respectively in presence of LPS 1 (P less than .02), 10 (P less than .05), 100 (P less than .01) micrograms/mL] and wheal response [6.4 +/- 1.0 mm, in presence of LPS 100 micrograms/mL versus 4.9 +/- 1.1 mm in absence of LPS (P less than .05)]. On the other hand, a possible LPS synergistic action on the histamine skin response was evaluated in ten normal subjects but the results were not significant. These findings show that LPS increases the allergy skin response probably due to a mechanism including a potentiation of the IgE receptor activation rather than an increase of the skin response to the release mediators.
Adult↗
[Postoperative inhalation treatment after paranasal sinus interventions. A placebo-controlled, double-blind and randomized study].
A placebo-controlled, double-blind study with Ems brine inhalations as postoperative treatment after endoscopic endonasal sinus surgery was conducted on 30 patients. After informed consent had been obtained, the patients were treated with either Ems brine or saline solution (200 ml) 3 times a day for 10 days. The parameters measured were rhinomanometry, X-ray films of the sinuses, endoscopy, saccharin clearance and a subjective evaluation by the physician and by the patient based on a visual analogue scale. The difficulty of choosing parameters for assessing the treatment was that comparable clinical studies and a single predictive parameter were not available. The bacteriological test and the saccharin clearance test were not significantly different between the two groups. Recovery, swelling, crusting, bleeding and signs of inflammation, opacity on sinus X-ray films, and nasal flow as measured by rhinomanometry were all significantly better in the group inhaling brine solution (P less than 0.05).
Adolescent↗
[Congenital cerebrospinal fluid pressure labyrinth].
The audiograms and CT scans of three children with a bilateral congenital mixed deafness are presented. Two children underwent an exploratory tympanotomy revealing a fixed stapes footplate: a perilymph gusher arose during platinotomy in both cases. The gusher was controlled successfully with a large fat graft in both children, and hearing remained unchanged. Two of the children were brothers: they had no other deformities except an enlarged fundus of the auditory canal on CT scans, and no clearly defined bony barrier to the vestibule, suggesting a cerebrospinal fluid fistula. Neither a patent nor an abnormal cochlear aqueduct could be detected in all three cases. It is likely that the three patients present an X-linked mixed deafness syndrome with fixation of the stapedial foot plate and perilymph gusher. A classification of congenital perilymph-CSF shunts is proposed.
Cerebrospinal Fluid Otorrhea↗