Biomedical subjects
Publications and source records attributed to M Mairesse.
Diagnosis of allergy diseases is at first linked to a detailed history, in which professional activities as well as the environment take an important place. Fishing activity as well as aquarium-related activities may be the origin of a symptomatology which is, often IgE-mediated, respiratory and skin localised: the responsible agents are most often insects in their larval form, crustaceans and worms.
STUDY OBJECTIVE: To assess the frequency of cystic fibrosis transmembrane conductance regulator (CFTR) gene mutations in patients with allergic bronchopulmonary aspergillosis (ABPA). DESIGN: Case-control study. All subjects in the study were screened for the presence of 13 mutations in the CFTR gene (R117H, 621 + 1G(-)>T, R334 W, Delta F508, Delta I507, 1717-1G(-)>A, G542X, R553X, G551D, R1162X, 3849 + 10kbC(-)>T, W1282X, and N1303K). Moreover, they were also screened for the presence of the 5T variant in intron 8. SETTING: University hospital and community-based hospital. PATIENTS: Twenty-one white patients with ABPA participated in the study. The presence of CFTR mutations was also investigated in 43 white subjects with allergic asthma who did not show sensitization to Aspergillus fumigatus and in 142 subjects seeking genetic counseling for diseases other than cystic fibrosis (CF). RESULTS: Six patients with ABPA were found to be heterozygous for one CFTR mutation, including Delta F508 (n = 2), G542X (n = 1), R1162X (n = 1), 1717-1G(-)>A (n = 1), and R117H (n = 1). The 5T allele was not detected in ABPA patients. None of the ABPA patients showed sweat chloride concentrations > 60 mEq/L. The frequency of CFTR mutation carriers was significantly higher in ABPA patients (6 of 21 patients; 28.5%) than in control asthmatic subjects (2 of 43 subjects; 4.6%; p = 0.01) and in subjects seeking genetic counseling (6 of 142 subjects; p < 0.001). CONCLUSION: These findings indicate that in patients without a clinical diagnosis of CF, CFTR gene mutations could be involved in the development of ABPA, in association with other genetic or environmental factors.
BACKGROUND: We have previously shown in several allergy models that allergic and tolerance status with respect to allergens is associated with a somewhat different dominant specificity of IgG antibodies. The objective was to test this hypothesis in the compelling model of ultrarush venom immunotherapy (VIT), which induces clinical tolerance after only a few hours of treatment. METHODS: Antibody titers and specificity were evaluated through solid-phase ELISA using streptavidin-biotin technology in 12 patients allergic to wasp venom before and during the ultrarush procedure (at 12 h, 24 h, and 15 days). The results were compared with those from another group of 20 patients treated with venom injections for at least 2 years. RESULTS: No significant change was observed in IgG titers during the early phase of VIT. The capacity of individual sera to prevent the antigen binding of pooled IgG from allergic patients changed rapidly, with mean percentage inhibitions falling from 80+/-15%, before starting VIT, to 26+/-14%, 35+/-15%, and 34+/-5% after 12 h, 24 h, and 15 days of treatment, respectively (P<0.001 by one-way ANOVA). The capacity of individual sera to prevent the antigen binding of pooled IgG from patients receiving prolonged VIT changed, with mean percent inhibitions increasing from 47+/-8%, before starting VIT, to 76+/-7%, 83+/-6%, and 87+/-6% after 12 h, 24 h, and 15 days of treatment, respectively (P<0.001 by one-way ANOVA). CONCLUSIONS: During the initial phase of ultrarush VIT, a change in IgG specificity, i.e., a change in the set of epitopes dominantly recognized by IgG on wasp-venom antigens, occurred concomitantly with early clinical tolerance and was already detectable a few hours after the onset of treatment. Although it may be an epiphenomenon, this change represents the earliest humoral modification described so far during this procedure. The mechanism is unknown, but it appears to be a selective depletion of the highest avidity antibody fraction by the venom injected in large doses at this stage of therapy. Finally, our data now show the previously documented association between a particular IgG specificity and the clinical status (allergy vs tolerance) to be true also with ultrarush VIT, a model in which the clinical ability to display allergic symptoms is rapidly reversed.
The authors emphasize the effectiveness of spiral CT in the diagnosis of typical endobronchial carcinoid. The tumor was found in a 25-year-old man referred for evaluation of steroid-resistant asthma. Successful diagnosis and complete local staging of the right intermediate bronchus tumor were obtained by two successive single apnea spiral acquisitions: a high resolution series (HRCT) with Multiplanar Reconstruction (MPR) and 3D virtual endoscopic views was completed by a dynamic angiographic series (angio-CT) with multiplanar Maximal Intensity Projections (MIP). The CT findings are compared with macroscopic anatomic views and major features of bronchial carcinoid are shortly addressed.
Pulmonary alveolar proteinosis is a rare idiopathic diffuse airspace disease characterized by intraalveolar accumulation of large quantities of lipoproteinaceous material. The clinical presentation and course are variable and the definite diagnosis is made by biopsy or broncho-alveolar lavage (BAL) that also constitutes the unique and empiric treatment. We report the extremely typical HRCT features of the disease found in a series of five patients diagnosed in our institution over a ten-year period. The HRCT signs and their evolution are discussed. A continuous spectrum of findings going from isolated ground glass opacities to lobular consolidation is found, but the most common and invariably present pattern consists of ground glass areas with superimposed smooth septal thickening; these areas have a patchy or geographic distribution--often termed the "crazy-paving" pattern--and are unlike pulmonary findings in any other disease.
Pulmonary sequestration is a rare congenital anomaly that consists of abnormal pulmonary tissue for which the arterial supply is usually derived from the aorta or its major branches. Considering clinical and anatomical aspects two types of sequestration, intralobar and extralobar, have been described. The definite diagnosis requires exact visualization of the anomalous feeding and draining vessels and this condition is essential when surgical treatment is necessary because of recurrent pulmonary infections. We report on 3 cases of intralobar sequestration successfully and extensively diagnosed in adults by spiral angioCT. Our series includes one symptomatic left case confirmed by surgery and two rare fortuitous asymptomatic right cases. In the three cases, the pulmonary abnormal tissue, the arterial supply and venous drainage were clearly identified. We conclude that, probably more than MRI, spiral angio-CT can presently be considered the first choice procedure to diagnose and evaluate pulmonary sequestration; the equal performance of spiral CT in imaging lung and vessels makes classical angiography unnecessary.
BACKGROUND: We have previously reported that, in addition to modifying IgG levels and subclass distributions, wasp venom immunotherapy (VIT) rapidly changes IgG antibody specificity. OBJECTIVES: We investigated whether such a change can be documented in the IgG response to the major bee venom allergen, phospholipase A2 (PLA2), from patients allergic to bees treated with VIT; whether it is coupled to the shift in IgG subclass distribution (IgG4 predominance) usually observed during VIT; and whether it restores the specificity displayed by IgG antibodies from nonallergic individuals. METHODS: Antibody specificity was evaluated in 17 patients allergic to bee venom in competitive ELISAs by using streptavidin biotin technology. Patients were tested before and during specific immunotherapy (at 15 days and 6 months) and compared with another group of 17 patients treated with venom injections for at least 2 years (VIT patients) and 30 healthy individuals. RESULTS: The capacity of individual sera to prevent PLA2 binding of pooled IgG from allergic patients changed rapidly with mean percentage inhibitions falling from 84% +/- 14% before starting VIT to 27% +/- 13% and 28% +/- 7% after 15 days and 6 months of treatment, respectively (p < 0.001 by one-way analysis of variance [ANOVA]). IgG titers were only slightly increased. The capacity of individual sera to prevent the binding of pooled IgG from patients receiving VIT changed rapidly with mean percentage inhibition increasing from 60% +/- 12% before starting VIT to 85% +/- 6% and 82% +/- 6% after 15 days and 6 months of treatment, respectively (p < 0.001 by one-way ANOVA). Similar results were found regardless of whether pooled IgG1 or pooled IgG4 were used. CONCLUSION: VIT results in a rapid change in the antigenic reactivity of anti-PLA2 IgG antibody of human allergic sera, restoring, although not completely, the specificity peculiar to lgG from healthy individuals. This suggests that allergic status and immunoprotection correlate with the preferential expression of distinct IgG specificities, which appear equally distributed over the IgG1 and IgG4 antibody subclasses. It is, however, not known whether the shift in IgG specificity is one of the operative mechanisms of VIT.
The authors report a case of an intrapulmonary tumour which on histological analysis was found to be a malignant Triton tumour after surgical excision. The tumours proved to be of nervous tissue origin and was a rare variant of malignant tumours of the surrounding of peripheral nerves with rhabdomyoblastic heterologous differentiation which is rarely described in the lungs. The characteristics of the tumour as well as therapeutic approaches are discussed followed by a review of the literature. A particular aspect of the case presented was to realise that there was a right to left shunt and this is also discussed.
The anatomoclinical exercise consists in the discussion of the etiology of an isolated pulmonary nodule in an asymptomatic patient.
BACKGROUND: The evolution of the IgG response during venom immunotherapy (VIT) has been previously investigated in terms of antibody titres and subclasses. OBJECTIVES: The present work studied the evolution of IgG antibody fine specificity in wasp allergic patients treated with rush VIT. METHODS: Antibody specificity was evaluated in 51 wasp allergic patients in competitive ELISA using streptavidin biotin technology. Patients were tested before and during specific rush immunotherapy (at 15 days, 6 months, 12 months) and compared with 44 patients treated by venom injections for at least 2 years. RESULTS: The capacity of sera to prevent the antigen binding of pooled IgG from allergic patients changed rapidly with mean percentage inhibitions (+/-SD) falling from 70+/-11-51+/-18% after 15 days of treatment (P<0.001 by one way ANOVA). Similarly, the antigen binding capacity of pooled IgG from VIT patients was differently prevented by sera with mean percentage inhibitions increasing from 37+/-12-65+/-8 after 15 days of treatment (P< 0.0001 by one-way ANOVA). CONCLUSIONS: The immunodominance pattern of IgG epitopes recognized on wasp venom antigens by sera from wasp allergic patients changes soon after initiating rush VIT. Further studies will indicate whether, instead of measuring IgG titres, this marked change could be used as the basis of a new test for monitoring the outcome of VIT.
Two patients with pleural plaques developed pleural effusion and subsequent diffuse pleural fibrosis 50 and 39 yrs after their first exposure to asbestos. The diagnosis of benign asbestos pleural effusion was suggested, but the work-up finally suggested bromocriptine-induced pleural disease in both patients. These two cases illustrate that drug-induced pleural effusion is an important differential diagnosis of benign asbestos pleural effusion. It is, moreover, possible that pre-existing asbestos pleural lesions, or even asbestos exposure, increases the risk of developing bromocriptine-induced pleural disease.
In this study, we performed 150 desensitizations in 139 Hymenoptera venom allergic patients (109 Yellow jacket allergic patients, 19 Honey bee allergic patients and 11 patients sensitized to both insects, who received a dual desensitization). We used a rush protocol, allowing injection of a total cumulated dose of 125,1 (Honey bee) to 175,1 (Yellow jacket) microgram of venom in 30 hours. Patients were hospitalized, with all emergency precautions for treating systemic reactions. The protocol was well tolerated in 147/150 cases; 3 patients had a benign systemic reaction. Patients received monthly maintenance doses of 100 micrograms venom. 39 patients experienced a field sting during immunotherapy; 2 of them (5%) had a benign systemic reaction. Thus, our rush desensitization protocol seems to be safe and effective.
A case of rhinitis and environmental asthma caused by unroasted coffee has been reported in an adolescent living in a building in which there is an installation for roasting coffee. The diagnosis, suggested by the case history, is confirmed by the presence of specific IgE, by the positive result of the skin test using unroasted coffee extract and also of a broncho-provocation test entailing the manipulation of dust from the coffee roasting room. An amelioration of the room and work conditions is recommended.
The authors report 3 cases of azygos continuation of the inferior vena cava. This congenital malformation is due to the atresia of inferior vena cava in the retrohepatic segment. The abnormalities encountered on the chest film are described. The interest of TDM, ultrasound and cavography is discussed.
Contrast media related reactions are numerous and of variable gravity. We report a case of pulmonary edema related to the intravenous administration of contrast media. Cardiogenic and non cardiogenic pulmonary edema are pathophysiologic possibilities. High resolution CT findings associate patchy ground glass areas and smooth thickening of subpleural septa, both rapidly disappearing.
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Eighty nine patients with hypoxic chronic obstructive airways disease (COAD) were enrolled into the 1 year Vectarion International Multicentre Study-VIMS in 4 centres, Sheffield (UK), and Antwerp, Liege and Namur (Belgium). At the end of the year the remainder were invited to continue taking placebo or almitrine bismesylate (100-200 mg daily) in the same double blind manner for a further 12 months. In the almitrine treated patients mean arterial oxygen tension (Pao2) at the end of the treatment period improved from 7.5 (0.5) kPa to 8.2 (1.3) kPa (p less than 0.01) and arterial carbon dioxide tension (Paco2) fell from 6.1 (0.8) kPa to 5.8 (0.9) kPa (p less than 0.01). Forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and measurements of breathlessness were unchanged. In the placebo treated group changes in the above variables were not significant. Twenty nine patients withdrew from the almitrine group with seven deaths and six cases of peripheral neuropathy, and 22 patients withdrew from the placebo group with six deaths and two cases of peripheral neuropathy. Death rates between the groups were not significantly different. In conclusion, 2 yrs of almitrine treatment (100-200 mg daily) leads to a persistent slight improvement in PaO2 and PaCO2 but no benefit in survival was demonstrated. Patients in this study had a high incidence of drug related side-effects. Lower dose schedules should be investigated.