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PubMedDate not supplied

[The epidemiological aspects of tuberculous pleurisy in Romania].

The re-organization of the Tb network in Romania, which took place after 1948, made possible a gradual accumulation of a number of data on the epidemiological surveillance of the territory, including the tuberculous pleurisies. The incidence of tuberculous pleurisies showed a decrease from 30.7/100,000 to 4.2/100,000 between 1958 and 1985, followed by a "stagnation" at 4.3/100,000 for 1986-1989. In 1990, the incidence of Tb pleurisy reached 6.8/100,000. The weight of pleural localization among the respiratory ones was maintained 15%-13% for 1960-1980, with a subsequent diminution up to 7.9% in 1989. By age-groups, the incidence of Tb pleurisy was at its highest level (19.1/100,000) at the age of 20-24 years in 1990 (as well as in 1972, 1980 and 1985). The present time imperative is the improving of the etiological diagnosis of pleurisies by a larger accessibility to the histological (pleural biopsy puncture) and bacteriological investigations.

Adolescent↗

PubMed1992

Endothelin-1 inhibits PAF-induced paw oedema and pleurisy in the mouse.

1. The current study analyses the effects of endothelin-1 (ET-1) on paw oedema and pleurisy induced by platelet activating factor (PAF) and other inflammatory agents in the mouse. 2. Combined subplantar injection of ET-1 (0.5 pmol/paw) did not modify oedema caused by histamine (1 to 100 mumol/paw), 5-hydroxytryptamine (1 to 100 mumol/paw) or bradykinin (1 to 100 nmol/paw) but markedly inhibited the response to PAF (0.95 to 3.8 nmol/paw). The selective action of ET-1 against PAF-induced (1.9 nmol/paw) oedema was dose-dependent, reaching a maximum at 0.5 pmol/paw and lasted up to 2 h. 3. ET-1 (0.5 pmol/paw) also inhibited paw oedema (3-4 h) caused by zymosan (500 micrograms/paw). In contrast, it did not modify either the early (1-4 h) or late (48-72 h) phases of the oedematogenic response to carrageenin (300 micrograms/paw), when given either together with or 24 h after the carrageenin. 4. Intrathoracic injection of PAF (1.9 nmol/cavity) induced pleurisy characterized by an increase in pleural exudate volume, and in accumulation of Evans Blue which was maximal at 30 min and lasted up to 4 h. When injected together with PAF, ET-1 (0.5 pmol/cavity) virtually abolished PAF-induced pleurisy. 5. It is concluded that ET-1 is a potent inhibitor of PAF-induced inflammation in the mouse. Its mechanism of anti-inflammatory action in this species, in contrast to what has been found in other species, does not appear to derive from its potent vasoconstrictor properties as ET-1, at the doses used, failed to affect oedematogenic responses to other inflammatory mediators.

Animals↗

PubMed1975

Monosymptomatic exudative pleurisy in persons exposed to asbestos dust.

Among 25 persons with monosymptomatic exudative pleurisy of unknown etiology there were 11 men who had been exposed to asbestos. Ten of them were investigated during an observation period of 4 to 8 years. The exudate was more or less sanguinolent, had a prolonged course and recurred on the same or opposite side in the majority of cases. Large numbers of eosinophilic cells were present in seven exudates. Clinical symptoms were very discrete. After the disappearance of the exudate, persisting pleural thickening was present in nine patients. Decortication was performed in four of these patients and signs of non-specific chronic pleurisy was found. Asbestos bodies were found in one case and suspected in another. No other etiological signs were observed in any of the 11 men during the period of observation. At the end of the period of observation, radiological signs of mild basal pulmonary fibrosis were found in one patient and signs suggestive of this were present in a further three patients. Six of the men were troubled by dyspnoea. Three of these had reduced physical working capacity owing to respiratory factors. It is concluded that asbestos should be suspected as the causative factor in monosymptomatic exudative pleurisy if other etiological factors can be excluded.

Adult↗

PubMed1976

[Richettsial pericarditis and pleurisy].

The authors report two cases of rickettsial disease due to R. Conori with mainly pericarditis in one case, sero-fibrinous pleurisy in the other. They then recall a few general data concerning this rickettsial disease and the very restricted place that it occupies in the etiology of pericarditis and, even more so, in the case of pleurisy. The conditons of diagnosis, which are mainly serological, are discussed, in particular with regard to pericarditis and tuberculous pleurisy.

Acute Disease↗

PubMed1979

[Isotopic indicators in the diagnosis of malignant pleurisies (author's transl)].

The tracers that are used in thoracic pathology have an elective tumoural affinity, present such a special reaction towards pleural effusions that we were led to study Bleomycin labelled with Cobalt 57 in 34 cases of pleurisy of various etiologies. The hyperfixation, circumscribed to the effusion in all these cases, presented a double problem : of radiobiological risk and of diagnostic significance. We tried to solve the last problem by means of a precise protocol applied to 16 cases, quantifying comparatively the specific radio-activity of pleural fluid and serum and studying the evolution of the pleural serous gradient, after injection of 2 mCi of labelled Bleomycin in 16 patients with suspected malignant pleurisy. From this limited study, it appeared that the sero-pleural gradient of the tracer, 24 hours after injection, was very high, above 5 and up to 15 in 7 malignant pleurisies out of 8; between 2 and 4 in others. It was sometimes below 5 and less in effusions, non malignant or doubtful. This gradient decreased very rapidly to reach 0 on the fourth day, except in recurring chronic effusions. Pending the confirmation of results, after a prolonged experiment, this protocol appeared valuable for diagnostic and physiopathological reasons.

Adult↗

PubMed1977

[Primary nonspecific chronic pleurisy (author's transl)].

Cytologic examinations of pleural exudate and cyto-histological examination of biopsies taken from the pleura give useful contributions in the differential diagnosis of primary chronic nonspecific pleurisy. In the early stage of disease the cellular findings are characteristic and enable easy differentiation of mesothelioma. Later on in primary chronic nonspecific pleurisy alterations of mesothelial cells can be seen which mimic tumorous cells and may be erroneously taken for mesothelioma cells. Quantity and quality of these alterations of nucleus and cytoplasma of mesothelial cells in primary chronic nonspecific pleurisy can be distinguished from tumor cells of mesothelioma by critical evaluation in the majority of cases.

Biopsy↗

PubMed1992

[A clinical study of tuberculous pleurisy].

Forty-eight cases of tuberculous pleurisy were examined and the following results were obtained. (1) Most of the patients were male, and there was no significant age and underlying diseases. (2) Fever and chest pain were observed mainly in younger patients, and sputum and dyspnea in older patients. (3) All of the cases examined had exudative pleural effusion, and increased ADA activity was frequently observed. (4) Mycobacterium tuberculosis was detected in the sputum of 65%, and also in the pleural effusion of 28% of the patients. The pathological diagnosis of tuberculosis was made by pleural biopsy in 83% of the patients, suggesting that pleural biopsy is very useful in the diagnosis of tuberculosis pleurisy. (5) The prognosis of the patients with tuberculosis pleurisy was good. Steroid therapy was generally ineffective.

Adolescent↗

PubMed1991

Comparison of several new 5-lipoxygenase inhibitors in a rat Arthus pleurisy model.

The 5-lipoxygenase inhibitors WY-50,295 tromethamine, A-64,077, L-663,536 and ICI-207,968 were compared in a reverse passive Arthus reaction-induced pleurisy model of eicosanoid biosynthesis in the rat. When a 1 h pretreatment schedule was employed, all four inhibitors equivalently blocked leukotriene B4 (LTB4) production with ED50 values of 2.0-2.9 mg/kg p.o. Conversely, WY-50,295 tromethamine (225 mg/kg p.o.) and L-663,536 (100 mg/kg p.o.) did not significantly alter thromboxane B2 (TxB2) levels, whereas A-64,077 (50 mg/kg p.o.) and ICI-207,968 (100 mg/kg p.o.) significantly reduced TxB2 by 50 and 72%, respectively. When 3 and 18 h pretreatment schedules were employed, WY-50,295 tromethamine demonstrated a longer duration of action than the other 5-lipoxygenase inhibitors with ED50 values of 1.7 and 6.3 mg/kg p.o., respectively. At doses of 50 and 100 mg/kg p.o., all drugs tested significantly inhibited inflammatory cell influx by 15-27%, albeit in a non-dose-related manner. However, only A-64,077 significantly lowered fluid extravasation by 35%, presumably due to inhibition of cyclooxygenase product formation. These results demonstrate that in this rat reverse passive Arthus pleurisy model, WY-50,295 tromethamine potently and selectively inhibits 5-lipoxygenase in vivo, and possesses a longer duration of action than the other 5-lipoxygenase inhibitors employed.

Animals↗

PubMed1991

Inhibition of leukotriene B4 biosynthesis by disulfiram and A-64077 during carrageenan-induced pleurisy in the rat.

1. The effect of disulfiram and A-64077 on leukotriene B4 biosynthesis was investigated using human polymorphonuclear leukocyte preparations and an in vivo rat pleurisy assay. 2. Disulfiram inhibited the calcium ionophore-induced release of LTB4 by human leukocytes in vitro with an IC50 of 4.6 +/- 0.3 microM, a value similar to that observed with the 5-lipoxygenase inhibitor A-64077 (IC50 = 1.2 +/- 0.3 microM). These inhibitors were at least 100-fold more potent than diethyldithiocarbamate, the primary metabolite of disulfiram. 3. In a rat pleurisy model, the administration of A-64077 (p.o., 2 hr pretreatment) caused a marked decrease in LTB4 levels measureable after ionophore stimulation at doses of 3 and 10 mg kg (67 and 96% inhibition, respectively). Disulfiram was about a 100-fold less potent, inhibiting LTB4 release by 65% at 300 mg kg (p.o., 6 hr pretreatment). 4. In contrast to A-64077, the inhibitory effect of disulfiram on LTB4 production by isolated leukocytes from the pleural cavity was reduced by the addition of the cell-free pleural exudate, suggesting that protein binding or conversion of disulfiram to inactive species contributes to diminish the potency of the drug. 5. The results indicate that disulfiram, after oral administration in rats, causes an inhibition of leukotriene biosynthesis in the pleural cavity and further illustrate the limited specificity of this drug as an inhibitor of aldehyde dehydrogenase at doses generally used to inhibit this enzyme in vivo.

Aldehyde Dehydrogenase↗

PubMedDate not supplied

[Immunoglobulins in clear-fluid pleurisy (preliminary note)].

The study of IgG, IgM and IgA immunoglobulins in the pleural exsudate and in the serum of 34 patients with pleurisy of various etiologies shows an increase in the level of serum immunoglobulins as compared with the level in the exsudate. The only immunoglobulin fraction showing variations in relation with the etiology of the disease in the IgG fraction, which is increased in inflammatory exsudates, in contrast with those found in pulmonary cancers. Recovery without sequellae of pleurisy supposes the presence (in situ) of an increased amount of IgG. These observations are supported by a good statistical-mathematical correlation (p less than 0,01 and 0,001).

Adult↗

PubMed1976

[Chemotherapy of reactive exudative pleurisy in breast carcinoma].

An analysis is carried out and the results from the treatment of 84 patients with metastasized mammary gland carcinoma and reactive exudative pleurisy are reported. Monochemiotherapy is applied in 61 patients (73%), mainly with cyclphosphamide and combined (poly) chemiotherapy in 23 patients (27%). A favourable effect on the exudative pluerisy is established in 75 per cent of all the patients treated: in 77 per cent of the treated with monochemiotherapy and 70 per cent of the treated with combined (poly) chemiotherapy. Favourable effect on exudative pleurisy was observed in 80 per cent of the patients treated with cyclophosphamide and complete exudation resorption was achieved in 2/3 of them.

Adult↗

PubMed1975

Tuberculosis pleurisy due to Mycobacterium fortuitum in a patient with chronic granulocytic leukemia.

A case of tuberculous pleurisy due to Mycobacterium fortuitum in a 47-year-old woman with chronic granulocytic leukemia is described. The mycobacterial aetiology of the pleurisy was confirmed by pleural biopsy and by positive culture of M. fortuitum in pleural fluid. Antituberculosis chemotherapy with INH, RMP and EMB, combined initially with prednisolone, was successful in spite of total resistance of the strain to the drugs used. A short review of mycobacterioses and of recent literature on the topic, especially on M. fortuitum, is also presented.

Antibiotics, Antitubercular↗

PubMed1991

[Pleural puncture biopsy--a diagnostic method in tuberculous serofibrinous pleurisy in children].

The biopsy of the parietal pleura with a special needle has become an essential diagnosis method in the adult patients with pleural disease of unknown etiology, and might become a complementary paraclinical method for children also. The certitude diagnosis in tuberculous serous fibrinous pleurisy of the child is laid on evidencing Koch's bacillus at the direct examination or in culture, and on fragments of pleural biopsy puncture, in evidencing the lesions. The study is based on the results obtained in the pleural biopsy puncture made on 6 children. The histologic examination of the pleural fragment showed, in 4 cases of 6, the presence of tuberculous lymphoepithelioid nodules, with central caseous necrosis thus granting certitude to the diagnosis. The pleural biopsy puncture permits an early and certain diagnosis in more than 2/3 of the pleurisies of tuberculous etiology.

Biopsy, Needle↗

PubMed1975

Leucocyte migration and lysosomal enzymes release in rat carrageenin pleurisy.

The time course of rat carrageenin pleurisy has been studied. The inflammatory reaction is characterized by exudate formation and massive leucocyte emigration into the pleural space both reaching peak values at 24 hours. Moreover betaglucuronidase, acid phosphatase and lactic dehydrogenase have been assayed in the exudate. The activity of lysosomal enzymes parallels the severity of the inflammatory response, while that of cytoplasmic enzyme lactic dehydrogenase resulted unmodified. Treatment of animals with indomethacin, phenylbutazone, aspirin and flufenamic acid inhibited both exudate formation and leucocyte emigration. In contrast none of these drugs was able to reduce lysosomal enzyme release.

Animals↗

PubMed1992

Homologous tachyphylaxis to bradykinin and its interference with allergic pleurisy in actively sensitized rats.

After recovery from a first intraplantar or intrathoracic stimulation with bradykinin, repeated daily provocation with this peptide resulted in a progressive loss of its ability to cause paw or pleural oedema, reaching 0-20% of the control within seven and four consecutive provocations, respectively. The phenomenon was shown to be time reversible, since the unresponsiveness ceased when stimulations were discontinued, and localized, since paw oedema evoked by the peptide was not modified after desensitization of either the contralateral paw or the pleural cavity. Furthermore desensitization to bradykinin did not influence the pleurisy elicited by either histamine (200 micrograms/cavity), 5-hydroxytryptamine (5-HT) (100 microgram/cavity) or platelet-activating factor (PAF) (1 microgram/cavity), suggesting that the desensitization was selective. In contrast, when actively sensitized animals were submitted to bradykinin-induced tachyphylaxis, pleural exudation and leukocyte influx induced by antigen were drastically reduced, strongly implying bradykinin in this process. We demonstrated that repeated daily stimulation with bradykinin cause selective, local and reversible auto-refractoriness, which may be useful as a tool in attempting to evaluate the role of this peptide in inflammation.

Amino Acid Sequence↗

PubMed1992

Suppression by cetirizine of pleurisy triggered by antigen in actively sensitized rats.

The efficacy of cetirizine in comparison with meclizine, another piperazine H1 receptor antagonist, in rat pleurisy caused by allergen or autacoid was investigated. Sensitization was achieved by subcutaneous injection of a mixture of ovalbumin and aluminium hydroxide. Fourteen days later, the animals were challenged with an intrathoracic injection of ovalbumin (12 micrograms/cavity), which caused drastic mast cell degranulation, followed by pleural oedema and leucocyte influx. Cetirizine and meclizine (2.5-30 mg/kg i.p.), 1 h before challenge, inhibited the exudatory response evoked by antigen, under conditions where neutrophil and eosinophil accumulation was affected only by the former. When administered intrathoracically 22 h after allergen, i.e. using a curative approach, cetirizine (15 micrograms/cavity) drastically reduced the pleural eosinophilia noted 24 h post-challenge, indicating that this drug can reverse an already established eosinophilia. Cetirizine (15 mg/kg i.p.) also restored, to about 39% (P < 0.001), the number of uninjured mast cells recovered from the pleural cavity following allergen stimulation. In normal rats, cetirizine (5-15 micrograms/cavity) completely inhibited the pleural exudation elicited by histamine and only partially the exudation caused by 5-hydroxytryptamine or bradykinin, but was quite inactive against platelet-activating factor. We conclude that the pleural exudation triggered by allergen, vasoactive amines or bradykinin is clearly sensitive to cetirizine. In addition, the ability of the drug to interfere with pleural neutrophil or eosinophil mobilization and mast cell degranulation seems not to be associated with its ability to block the histamine H1 receptor.

Animals↗

PubMed1978

Acute pleurisy in sarcoidosis.

A 47-year-old white man with sarcoidosis presented with a six-week history of acute painful pleurisy. On auscultation a loud pleural rub was heard at the left base together with bilateral basal crepitations. The chest radiograph showed hilar enlargement as well as diffuse lung shadowing. A lung biopsy showed the presence of numerous epithelioid and giant-cell granulomata, particularly subpleurally. A patchy interstitial pneumonia was also present. He was given a six-month course of prednisolone, and lung function returned to normal.

Acute Disease↗

PubMed1978

An outbreak of pleural mesothelioma and chronic fibrosing pleurisy in the village of Karain/Urgüp in Anatolia.

The 575 inhabitants of the remote Anatolian village of Karain suffered 11 deaths from pleural mesothelioma in 1975/76 and there were five cases of fibrosing pleurisy. In the previous five years there had been 25 cases of mesothelioma. Calcified pleural plaques were common on survey radiography. Asbestos does not occur in the local soil or rock, nor is it handled in the village, but a few fibres were found in the water. Fibres were also found in the pleural tissue of two of five cases examined. Inhabitants of the neighbouring villages are free of mesothelioma.

Adult↗