Biomedical subjects
Publications and source records attributed to M Radermecker.
We report the case of a tracheal fibrolipoma in a 40-year-old man successfully treated by laser photocoagulation. The clinical and pathological aspects, as well as the therapeutical options of this rare upper airway benign tumor are discussed.
We investigated the effects of intravenous injection of methylprednisolone (MPR) compared with placebo (saline) on ex vivo leucocytic histamine release in eight healthy volunteers. All subjects received in a randomized and a single-blind manner the placebo and MPR, 20 mg and 125 mg, each injection given in 2 week intervals. On each occasion blood samples were taken just before and 24 h after the intravenous injection to determine circulating leucocyte counts and leucocytic histamine release induced by anti-IgE (1/2000) and FMP (Formyl-Methionyl-Phenylalanine) (10(-5) M) and its modulation by IL-3 (2 ng/ml). MPR 20 mg and 125 mg significantly increased circulating leucocyte counts (P < 0.05 and P < 0.001 respectively) but decreased leucocytic histamine content (P < 0.05 and P < 0.001 respectively) by 24 h. Placebo had no effect. As for circulating basophils, after 24 h they were decreased by 125 mg MPR (P < 0.05) but increased by 20 mg (P < 0.05). Anti-IgE-induced HR was significantly inhibited by 125 mg MPR (P < 0.05) but not by 20 mg MPR or by the placebo. In contrast, neither MPR (20 mg and 125 mg) nor placebo significantly reduced FMP-induced HR. The strong potentiation by IL-3 of HR evoked by anti-IgE and FMP at baseline (P < 0.001) persisted 24 h after injection of MPR or placebo (P < 0.001 except P < 0.05 for anti-IgE-induced HR after 125 mg MPR).(ABSTRACT TRUNCATED AT 250 WORDS)
We report the effect of interleukin-3 (IL-3) and of other cytokines on antigen-induced basophil histamine release in wasp-venom-allergic subjects. Leukocytes from 12 patients with documented anaphylactic sensitivity to wasp venom were preincubated in the presence or absence of IL-3, granulocyte/macrophage-colony stimulating factor (GM-CSF), IL-5, IL-8, or stem cell factor (SCF). Washed cells were then exposed to venom and to other secretagogues, and histamine release in the supernatant was measured fluorometrically. Preincubation of leukocytes with IL-3, GM-CSF, or IL-5 (0.02-2 ng/ml), but not with IL-8 and SCF, caused a dose-dependent enhancement of antigen-induced basophilic histamine release in all subjects tested. Mean maximum increase was about 100% for IL-3, IL-5, and GM-CSF. The priming effect of IL-3 was rapid, persisted up to 12 h, and was not accompanied by a change in cellular histamine. IL-3 had a comparable enhancing effect when basophils were triggered with anti-IgE or N-formylmethionylphenylalanine (FMP). By contrast, IL-3 had no effect on substance-P-induced histamine release. The significant enhancement of basophil releasability to antigen in wasp-venom allergy by very low concentrations of IL-3, GM-CSF, and IL-5 suggests that cytokines in the basophil (mast-cell?) microenvironment could be critical factors in determining the variability of sting reactions in Hymenoptera-venom-allergic subjects.
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To investigate the possible role of mast cell or basophil histamine release in mediating platelet-activating factor (PAF) airway obstruction, we studied the effect of inhaled PAF (30 micrograms, single dose) on plasma histamine, bronchial caliber, and leukocyte and platelet counts in six patients with mild or moderate allergic asthma (mean age, 27 +/- 1.3 years; mean FEV1, 95 +/- 5 percent of predicted; mean PC20 methacholine, 1.46 +/- 0.36 mg/ml). Specific conductance (SGaw) FEV1, FEF25-75 percent, differential leukocyte and platelet counts, and plasma histamine (radioimmunoassay) were measured before and 5, 10, 15, and 20 min after PAF inhalation. Mean basal plasma histamine level was 0.28 +/- 0.04 ng/ml. Inhalation of PAF caused a fall in SGaw peaking at 5 min (43 +/- 9 percent) and a fall in FEV1 and FEF25-75 peaking at 10 min (19 +/- 10 percent and 30 +/- 13 percent, respectively). There was also a rapid and transient fall in circulating neutrophils at 5 min (from 3,096 +/- 204/mm3 to 2,551 +/- 158/mm3, p < 0.05) followed by a rebound neutrophilia. In contrast, plasma histamine level did not change significantly at any time measured. Conversely in the same asthmatics, a rapid rise in plasma histamine level (from 0.29 +/- 0.03 ng/ml at baseline to 0.53 +/- 0.06 ng/ml at 5 min; p < 0.01) was observed after an allergenic challenge (Dermatophagoides pteronyssinus) causing a fall in FEV1 peaking at 10 min (22 +/- 4 percent). Thus, inhaled PAF may induce airway obstruction and neutropenia in asthmatics without any significant change of plasma histamine level. These results indicate that it is unlikely that lung mast cells or basophils degranulate during PAF-induced bronchoconstriction.
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LY 186655 (Tibenelast, Lilly) is a new phosphodiesterase inhibitor, not derived from the xanthine, possessing bronchodilating activity in animals. The aim of this work was to study the effect of LY 186655 and theophylline on histamine release from human leukocytes, skin and lung fragments. Histamine was measured using a spectrofluorometric method. Both drugs (3 x 10(-5)-3 x 10(-3) M) exhibited a dose-dependent inhibition on anti-IgE (1/2000)-induced histamine release from human leukocytes. At 3 x 10(-3) M, theophylline was significantly more effective than LY 186655 (mean inhibition 94 and 42%, respectively). On lung fragments, theophylline and LY 186655 (3 x 10(-5)-3 x 10(-3) M) caused strong and comparable inhibitory effects on anti-IgE (1/500)-induced histamine release with a mean inhibition reaching maximally 65%. Histamine release induced by compound 48/80 (1 mg/ml) on sliced human foreskin was reduced with both drugs (3 x 10(-3) M) by about 37%. We conclude that LY 186655 inhibits in vitro immunological histamine release from human lung and cutaneous mast cells as well as basophils with a similar pattern of activity to theophylline.
To clarify the mechanism of chemotactic deactivation of polymorphonuclear neutrophils (PMN) following incubation with the synthetic dipeptide N-formylmethionyl phenylalanine (FMP), we tested the hypothesis that histamine, which is released from leukocytes during incubation with FMP, could explain this inhibition. Human PMN were incubated in the presence or absence of FMP (10(-7) to 10(-5) M) and histamine measured fluorometrically in the supernatant. Washed PMN were then tested in Boyden chambers against FMP (10(-5) M) and other chemoattractants. Incubation of leukocytes with FMP caused a nonpreferential PMN deactivation which was proportionally and kinetically related to FMP-induced histamine release. No histamine release or chemotactic deactivation was observed in the absence of Ca2+ and Mg2+. The inhibitory effect of the peptide was significantly prevented by an H2 blocker or when using basophil-depleted PMN suspensions. Histaminase abolished the capacity of FMP-incubated leukocyte supernatants to decrease PMN chemotaxis. Preincubation of leukocytes with anti-IgE or a sensitizing allergen caused a significant PMN chemotactic deactivation. These results show that histamine which is released during leukocyte incubation with FMP, contributes, at least in part, to the chemotactic deactivation of PMN.
Two women, aged 44 and 29 years, respectively, were admitted to the hospital in early 1987 for recurrent pneumothorax, dyspnea and a diffuse reticulonodular pattern evidenced on the chest x-ray film. Lung biopsy confirmed LAM in both patients. Both were treated sequentially with medroxyprogesterone and a LHRH agonist (buserelin) to achieve reversible medical castration. Neither subjective nor objective improvement was noted after 13 and 5 months, respectively, of buserelin therapy (900 micrograms/day, nasal spray) despite an effective suppression of the pituitary-gonadal axis. Medroxyprogesterone also was ineffective. Buserelin thus failed to control pulmonary LAM in these two patients, in spite of effective medical castration.
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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.
Vasopressin-neurophysin (hNpI), oxytocin-neurophysin (hNpII) and blood osmolality were assayed before any treatment in basal conditions in 35 patients suffering from lung carcinoma (20 oat cell, 6 undifferentiated and 9 well-differentiated epidermoid cell carcinomas). Plasma vasopressin (antidiuretic hormone, ADH) was also assayed in 7 of the 20 patients suffering from oat cell carcinoma. We found a close correlation (r = 0.98) between plasma ADH and hNpI levels in the 7 patients. Further, hNpI was elevated in 13 out of the 20 oat cell carcinoma patients and in none of the epidermoid-cell carcinoma group; however, searching for an abnormality of ADH secretion as reflected by a detectable plasma hNpI level together with subnormal plasma osmolality revealed 2 additional positive results in the oat cell carcinoma group, and 2 out of the 6 in the undifferentiated-cell carcinoma group. hNpII was increased together with an increase in hNpI in 6 oat cell carcinoma patients; it was specifically increased without hNpI increment in 2 additional oat cell carcinoma patients and in 2 patients of the undifferentiated-cell carcinoma group (different from the 2 positive for the hNpI-osmolality ratio). hNpI and hNpII were normal in the majority of undifferentiated and all of the differentiated epidermoid-cell carcinoma group. Hence, our results show that simultaneous measurements of hNpI, hNpII, and blood osmolality could detect abnormalities in 17 out of 20 oat cell carcinoma patients, in 4 of the 9 undifferentiated-cell carcinoma patients, but in none of the differentiated epidermoid-cell carcinoma patients, suggesting that the neurophysin assay can be used for the early detection of oat cell- and possibly other neuroendocrine-derived carcinomas.
The anatomical data concerning to the latissimus dorsi and its neurovascular pedicle are revised with its applications in reconstructive surgery. The use of this muscle in cardiomyoplasty depends upon a good understanding of its vascularisation and the intramuscular innervation. Our angiological study of the human latissimus dorsi demonstrates clearly the topographic distribution of the branches of the thoraco dorsal artery ant the peripheral blood supply after interrupting the intercostal and lumbar perforating vessels. These findings demonstrate the vascular reliability of the muscle for cardiomyoplasty.
We studied in vitro the effect of histamine on the chemotactic and phagocytic abilities of human blood monocytes and alveolar macrophages. The chemotactic response to activated autologous serum, leukotriene B4 or N-formyl-methionine-L-phenylalanine was similar for macrophages and monocytes. Incubation of monocytes with histamine in picomolar concentrations caused a significant chemotactic inhibition (about 25%). This effect was antagonized by cimetidine but not by promethazine. Histamine did not have an effect on alveolar macrophages chemotaxis or phagocytosis. Thus, histamine, in minute concentrations, exerts, in vitro, a partial inhibitory effect on monocyte chemotaxis through activation of H2-type receptors.
To better define the dose-effect relationship and the pharmacokinetics of almitrine, sixteen stable hypoxaemic COPD patients received random single oral administrations of almitrine bismesylate 50, 100 and 150 mg or placebo at two-week intervals in a double-blind manner. Resting ventilation, arterial blood gases and plasma almitrine levels were measured. No significant changes were seen after placebo administration. Almitrine 50 and 100 mg caused a significant dose-related improvement in arterial oxygen tension (PaO2) in thirteen of the sixteen patients. Almitrine 150 mg caused little if any additional PaO2 increment. PaO2 returned to near basal values after 24 h. Two patients responded to almitrine 100 and 150 mg only, whereas one patient did not respond at all. Mean PaO2 increases in the sixteen patients were 0.9 kPa (7 mmHg), 1.5 kPa (11 mmHg) and 1.6 kPa (12 mmHg) 3 h after 50, 100 and 150 mg, respectively. A significant mean 0.9 kPa (7 mmHg) decrease in arterial carbon dioxide tension (PaCO2) and a l.min-1 increase in ventilation were observed after almitrine 150 mg. Mean maximum almitrine plasma concentration and area under the curve correlated linearly with dose. The relationship between mean PaO2 improvement and mean almitrine plasma level was curvilinear with a flattening of the curve over plasma levels of 150 ng.ml-1. Almitrine plasma half-life was found to be 116-140 h.
The aim of this study was to specify the effect of therapeutic pulmonary lavage on the function of alveolar macrophages in a patient suffering from alveolar proteinosis; we have studied phagocytosis and chemotaxis in cells before and at different times after the lavage. Our results indicate a restoration of the functional properties of the alveolar macrophages in parallel with an improvement in pulmonary function and blood gases under the effects of treatment. These data are in favour with an inhibitory effect of the lipoprotein material on the function of alveolar macrophages and suggest that the deposit of this material is a determining factor in the alteration in the defense mechanisms of the lung.
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