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Biomedical subjects

B Wallaert

Publications and source records attributed to B Wallaert.

At least 235 records · Page 13Linked to original sources
PubMed1990

[The in vivo penetration of erythromycin into alveolar macrophages].

In order to appreciate the in vivo penetration of erythromycin the alveolar spaces a broncho-alveolar lavage was carried out in 24 guinea pigs, 30 minutes, 1 hour 30 minutes and three hours after a single intraperitoneal injection of 50 mgms. of erythromycin. The erythromycin dose was assessed by a microbiological method in the alveolar macrophages and the supernatant of the broncho-alveolar lavage liquid. The intramacrophage concentrations of erythromycin were 3.9, 11.5 and 12 times higher than the serum concentrations at 30 minutes, 1 hour 30 and three hours respectively. The concentrations in the broncho-alveolar lavage liquid was always higher than the serum concentrations tacking account of the different dilutions estimated with relation to the glucose concentrations. At 30 minutes, 1 hour 30 minutes and three hours the alveolar macrophages contained 1.9; 7.6 and 6 times more erythromycin respectively than the lavage supernatant. From the first half hour of its administration the erythromycin was concentrated in the alveolar spaces, in particular within the macrophages. Already noted in vitro, this rapidity of erythromycin concentration in vivo in alveolar macrophages appears to be one of the reasons to explain its activity against micro-organisms developing within macrophages.

Absorption↗
PubMed1990

[Alveolar proteinosis in a facade plasterer. A sequential study of bronchoalveolar lavage and thoracic computerized tomography].

Alveolar proteinosis is a rare disease. We report a case occurring in a patient who smoked and was a facade plasterer who was treated with repeated pulmonary lavage. A mineral analysis of the lavage fluid recovered a significant amount of silica and iron oxide confirming the massive exposure of the patient to these minerals. The favourable outcome over the next 7 years was associated as regards respiratory function, with a progressive improvement in lung volumes and pulmonary output and of CO diffusion capacity, as regards broncho-alveolar lavage there was a regular increase in the cellularity and finally as regards CT scanning (at high resolution) there was a progressive clearing of the alveolar opacities only leaving the persistent opacities in the interstitium.

Adult↗
PubMed1990

[Study of the in vivo penetration of cotrimoxazole in alveolar macrophages].

Kinetic of cotrimoxazole was studied in serum, alveolar macrophages and BAL fluid from guinea pigs receiving sulfamethoxazole (SMX, 100 mg/kg) and trimethoprim (TMP, 20 mg/kg). Guinea pigs were killed by cervical dislocation 30 min, 1 h, 3 h, 6 h and 24 h after intraperitoneal injection. Lung lavage was performed to obtain alveolar macrophages and BAL fluid. TMP and SMX levels were assayed using high-performance-liquid chromatography. Highest SMX levels were obtained in serum at 30 min, in BAL fluid at 1 h and in alveolar macrophages at 3 h. Mean SMX/TMP ratios (30 min, 1 h, 3 h) was 26.5 +/- 0.8 in serum, 3.76 +/- 1.8 in BAL fluid and 1.15 +/- 0.02 in alveolar macrophages.

Animals↗
PubMed1990

[Rapidly progressive glomerulonephritis in pneumoconiotic coal miners].

We review a series of 11 silicotic coal miners demonstrating a progressive renal failure with a syndrome of rapidly progressive glomerulonephritis. Renal biopsies reveal crescentic glomerulonephritides associated three times with angeitis. These cases confirm that silica induced glomerulonephritides can be an occupational hazard and warrant further clinical and epidemiological research.

Adult↗
PubMed1989

[Churg-Strauss syndrome].

The Churg-Strauss syndrome is part of the necrotizing vasculitis group of diseases. Its clinical diagnosis rests on the occurrence of a severe asthma followed, more or less closely, by systemic manifestations that are predominantly neurological, cutaneous, gastrointestinal and cardiovascular. To these must be added pulmonary infiltrates, eosinophilia and increase in serum IgE's. Three histological criteria (necrotizing vasculitis of the small vessels, perivascular infiltration with numerous eosinophils and extravascular granulomas) enable this anatomico-clinical syndrome to be identified, but the granuloma component is frequently missing and the existence of borderline states, notably with periarteritis nodosa, is unquestionable. Corticosteroids and immunodepressants have transformed the prognosis of the Churg-Strauss syndrome, while its physiopathological mechanism remains mysterious.

Churg-Strauss Syndrome↗
PubMed1989

A circulating suppressive factor of platelet cytotoxic functions after rush immunotherapy in Hymenoptera venom hypersensitivity.

A receptor for the Fc fragment of IgE has been described on human blood platelets. This receptor mediated the IgE-dependent stimulation of platelets by the specific allergen in Hymenoptera venom (HV) hypersensitivity. This platelet reactivity was abolished after rush desensitization. To understand the mechanism of such a down-regulation, we studied the effects of sera recovered from patients treated by HV rush desensitization on platelets of untreated HV sensitive patients. The present data describe the presence of a circulating factor able to suppress, in a dose-dependent manner, platelet stimulation by the specific allergen. This circulating factor was not allergen specific, not depleted by IgE or IgG antibody immunoadsorption, and was found at higher concentrations in the sera of patients receiving monthly high dosages of HV (200 micrograms maintenance dose). The physicochemical characterization showed that this circulating factor had a m.w. of 20,000 to 25,000, an isoelectric point of 4.2, was heat and acid stable, and sensitive to trypsin, but not to neuraminidase. These characteristics were similar to a newly described lymphokine, platelet activity suppressive lymphokine, suggesting the intervention of such a lymphokine in HV rush desensitization.

Bee Venoms↗
PubMed1989

From subclinical alveolitis to granulomatosis. Sequential evaluation of pulmonary involvement in extrathoracic sarcoidosis.

Follow-up of patients with subclinical inflammatory alveolitis associated with systemic diseases may represent the best opportunity to study the mechanisms responsible for the development of interstitial lung disease. We report a seven-year sequential pulmonary evaluation of one patient with clinically isolated gastric sarcoidosis, treated by gastrectomy, without evidence of clinical, radiologic or functional lung impairment and with chronic subclinical lymphocyte alveolitis. Five years later, she developed an overt interstitial lung disease characterized by fine crackles, diffuse parenchymal opacities and impaired diffusing capacity, preceded by an expansion of polymorphonuclear neutrophils in the lower respiratory tract, raising the hypothesis that these cells may be implicated in the pathogenesis of pulmonary derangement in sarcoidosis. This observation illustrates the importance of pulmonary follow-up of unaffected patients with systemic diseases and with subclinical inflammatory alveolitis, and the potential predictive value of neutrophil alveolitis in the pulmonary outcome of these patients.

Adult↗
PubMed1989

Clinical and subclinical alveolitis in collagen vascular diseases: contribution of alpha 2-macroglobulin levels in BAL fluid.

The probability that patients with collagen vascular diseases (CVD) will develop fibrosis is unpredictable. Since changes in bronchoalveolar lavage (BAL) cell data can be observed in CVD patients without evidence of lung involvement, we investigated whether the study of soluble components in BAL could help to distinguish CVD patients with lung involvement (n = 15) from those without pulmonary disease (n = 37). Our results demonstrate that the alveolitis observed in patients with overt lung involvement is associated with an increase of BAL alpha 2-macroglobulin (alpha 2-MA). In contrast, the BAL alpha 2-MA levels were found to be normal in CVD patients without evidence of pulmonary disease as well as in CVD patients with overt lung involvement treated with steroids. This was observed even in the presence of high neutrophil or lymphocyte counts in BAL. In conclusion, when neutrophils or lymphocytes accumulate in the lungs of CVD patients without evidence of lung damage, in the majority of patients this cell accumulation is not associated with an increase of BAL soluble components.

Adult↗
PubMed1989

Subclinical alveolar inflammation in rheumatoid arthritis: superoxide anion, neutrophil chemotactic activity and fibronectin generation by alveolar macrophages.

Interstitial lung disease (ILD) can be detected by pulmonary function testing (PFT) in 30-40% of rheumatoid arthritis (RA) patients. We assessed by bronchoalveolar lavage (BAL) the patterns of alveolitis in 21 RA patients: group 1 comprised 12 patients without evidence of ILD, and group 29 patients with clinical ILD defined by abnormal pulmonary function tests and/or chest X-ray. Cellular characteristics of BAL were studied in both groups. In addition, alveolar macrophages (AM) from patients in group 1 were isolated, and three parameters of cellular activation were studied: superoxide anion, fibronectin and neutrophil chemotactic activity generation. Total cell counts were not increased in group 1 but significantly increased in group 2 compared to controls. In group 1, 5/12 patients had elevated lymphocyte percentage (greater than 18%) suggesting subclinical lymphocyte alveolitis. In contrast, neutrophil alveolitis (greater than 4%) was found in 7/9 patients in group 2, mean percentage 12.9 +/- 4.2, compared with 1.2 +/- 6.4% in controls and 1.9 +/- 0.5% in group 1. These changes were not correlated with disease duration nor rheumatoid factor titres. Marked elevation of lymphocyte percentage was observed in patients with abnormal serum beta-2-microglobulin. Alveolar macrophages from group 1 patients released increased amounts of superoxide anion (7260 +/- 2700 vs controls 850 +/- 120 URL/5.10(5) cells), neutrophil chemotactic activity (21 +/- 4.8 vs controls 8.1 +/- 0.7 cells/HPF), and fibronectin (6.1 +/- 1.6 vs controls 1.3 +/- 0.2 ng.10(6) cells/hour). Whether or not lymphocyte alveolitis and/or AM dysfunction are pathogenic mechanisms of subsequent interstitial lung disease in patients who are still free of symptoms remains to be determined.

Adult↗
PubMed1989

[Pheochromocytoma revealed by pulmonary edema].

We report the case of a young patient of 37 presenting with two attacks of pulmonary oedema which revealed an underlying pheochromocytoma. The diagnosis was suggested by the raised level of vanyl-mandelic acid in the urine and the abdominal CT scan. After an adrenalectomy the outcome was satisfactory. Pheochromocytoma should be considered in the differential diagnosis of the acute respiratory distress syndrome in the adult linked to the action of the circulating catecholamines on the pulmonary capillaries.

Adrenal Gland Neoplasms↗
PubMed1989

[Pulmonary sarcoidosis simulating primary acute interstitial fibrosis at presentation. Clinical, radiologic, functional and bronchoalveolar cytologic study in 3 cases].

Sarcoidosis very rarely progresses towards severe subacute respiratory failure. We report three observations of recent atypical cases of pulmonary sarcoidosis which were proven by open lung biopsy and developed severe diffuse pulmonary granulomatosis in a few weeks with an associated interstitial fibrosis. In these patients there were diffuse crepitant rales, a dramatic reduction in lung function of 30-60% of lung volumes and diffusion capacity accompanied by major hypoxemia (m +/- DS: 63.3 +/- 4.0 mmHg) without hypercapnia. Bronchoalveolar lavage showed an alveolar neutrophil leucocytosis (7.3 +/- 5.5%) without a lymphocytosis (4.3 +/- 11.5%). In the three cases under study, the clinical picture, the radiological and lung function studies, as well as the data from the bronchoalveolar lavage, were more suggestive of an acute diffuse interstitial fibrosis than of sarcoidosis.

Adult↗
PubMed1989

[Treatment of severe hemoptysis with terlipressin. Study of the efficacy and tolerance of this product].

Terlipressin (Glypressin) is a "pro-hormone"; after intravenous injection the glycyl radicals are slowly cleaved by enzymatic action, liberating vasopressin. We have assessed the efficacy of terlipressin in the treatment of severe hemoptysis. The study was performed on 20 patients: in 5 cases there was very copious hemoptysis and in 15 cases there was repeated hemoptysis of lesser volume. The cause was distributed as follows: 6 cases of neoplasms, 5 were sequelae of tuberculosis, bronchial dilatation 2 cases, pneumonia with abscess 2 cases, chronic airflow obstruction (COPD) 2 cases and 3 cases of silicosis. The treatment consisted of a slow intravenous injection of 2 mgm 4 times per day (9 patients), then in 11 patients an injection of 2 mgm at the time of acute episodes followed by 1 mgm every 6 hours. The patients received an average of between 15 and 20 mgm of the product for a treatment lasting over 5 days at the maximum. The results were as follows: total success 12 cases; partial success (a reduction to at least one-third of the initial hemoptysis): 5 cases; failure: 3 cases. The failures were linked in two cases to neoplastic disease and in one case there was an intolerance to the drug which did not allow the treatment to be pursued.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

[Pulmonary hemorrhagic syndromes. Clinical and diagnostic approach].

The diagnosis of pulmonary hemorrhage syndromes (PHS) rests on a body of clinical and paraclinical evidence found in all etiologic forms. Usually, the combination of hemoptysis, iron deficiency anemia, and roentgenologic infiltrates is easy to recognize; in more atypical cases, alveolar bleeding can be demonstrated by determination of the Golde score on bronchoalveolar lavage specimens. Whereas clinical features are nearly invariable, etiologies cover a broad spectrum including some glomerular diseases, idiopathic pulmonary hemosiderosis, connective tissue disorders, pulmonary conditions related to compromised immunity, airborne pulmonary aggressions, and some apparently primary vascular disorders. Regardless of the severity of clinical features at presentation, pulmonary hemorrhage syndromes are always a diagnostic and therapeutic emergency.

Bronchoalveolar Lavage Fluid↗
PubMed1988

Activated alveolar macrophages in subclinical pulmonary inflammation in collagen vascular diseases.

A study was initiated to determine whether alveolar macrophages from patients with collagen vascular diseases but free of pulmonary symptoms were spontaneously activated and whether they released various mediators related to the pathogenesis of pulmonary fibrosis. Alveolar macrophages obtained by bronchoalveolar lavage from 32 patients with proved collagen vascular disease but no evidence of lung disease were compared with those from 10 patients with collagen vascular disease with interstitial lung disease (CVD-ILD) and from 10 healthy controls. The total number of alveolar macrophages did not differ between patients with collagen vascular disease and controls but were substantially increased in the CVD-ILD group. Alveolar macrophages from 31 of the 32 patients with collagen vascular disease and from all 10 in the CVD-ILD group had at least one criterion of activation. Neutrophil chemotactic activity was detected in supernatants from alveolar macrophage culture in 23 of the 32 patients with collagen vascular disease and from nine of the 10 in the CVD-ILD group; fibronectin secretion by alveolar macrophages was increased in 12 of the 32 patients with collagen vascular disease and in nine of the 10 in the CVD-ILD group. Furthermore, alveolar macrophages from 20 of the 32 patients with collagen vascular disease and four of the 10 CVD-ILD patients spontaneously released increased amounts of superoxide anion. Thus alveolar macrophages were spontaneously activated in a high proportion of patients with collagen vascular disease.

Adult↗
PubMed1988

Production of an interleukin-1 inhibitory factor by human alveolar macrophages from normals and allergic asthmatic patients.

In order to study the possible role of alveolar macrophages (AMs) in the development of local immune responses, we compared interleukin-1 (IL-1) production by peripheral blood monocytes and AMs from 17 allergic asthmatics and 32 controls. When stimulated by lipopolysaccharide, alveolar macrophages and blood monocytes from controls released IL-1 (127 +/- 74.6 and 178.8 +/- 120 IL-1 units/ml, respectively) in the same amounts as AMs and blood monocytes from allergic asthmatics (148 +/- 47.5 and 160.5 +/- 78.3 IL-1 units/ml, respectively). After stimulation by anti-IgE or the specific allergen, asthmatic blood monocytes released IL-1-like activity (71.8 +/- 46.4 and 45.4 +/- 25.9 IL-1 units/ml, respectively). In contrast, asthmatic AM supernatants contained no detectable IL-1-like activity after stimulation by allergen or anti-IgE. The same pattern was observed with monocytes and AMs from controls after passive cell sensitization with 20% of IgE-rich serum. In a second step, the effect of supernatants of IgE-dependent stimulated AMs was tested on thymocyte proliferation induced by a purified IL-1, permitting the demonstration of an IL-1 inhibitory factor released by the AMs while these supernatants didn't modify the IL-2-dependent proliferation of a CTL-L line. The use of indomethacin and assessment of PGE2 levels in AM supernatants made it possible to discard the role of prostaglandins in this inhibitory effect. Moreover this activity, which is resistant to heat and trypsin treatment, has a molecular mass between 40 and 50 kD and did not correspond to serum proteases, alpha-1-antiproteinase, and arginase.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗