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PubMed1979

A study on acid glycosaminoglycans in pleural diseases.

1. Pleural fluid contained protein-bound hyaluronic acid, protein-bound chondroitin sulfate, hyaluronic acid, chondroitin sulfate, undersulfated chondroitin sulfate and dermatan sulfate. The composition of acid glycosaminoglycans in pleural fluid seems to reflect the rate of biosynthesis and degradation of these polysaccharides at some sites which are closely related to the pleural cavity. 2. A possibility was suggested that hyaluronic acid was synthesized in pleural tissue and was excreted shortly thereafter into the surroundings, as evidenced by experiments with rabbit pleural tissue. 3. In human, hyaluronic acid, chondroitin sulfate, dermatan sulfate and heparan sulfate were found in thickened pleurae caused by lung cancer, in those caused by asbestosis and also in tumor tissues of pleural mesothelioma. The molecular size of hyaluronic acid from pleural mesothelioma was found to be larger than that from human unbilical cord. 4. Quantification and histochemical study of acid glycosaminoglycans demonstrated that the quantity of hyaluronic acid in tissue specimens of mesothelioma by far exceeded that in non-mesothelioma cases (statistically significant). 5. Thus a possibility was suggested that histochemical investigation together with microquantitation of hyaluronic acid in pleural tissue may prove to be an efficient means of differential diagnosis of pleural mesothelioma. 6. Definite conclusion on the relationship between the fluctuation with time in quantity of acid glycosaminoglycans of the effusions and etiology of pleurisy awaits further investigations.

Adult↗
PubMed1979

Comparison of the diagnostic values of biopsies of the pleura and cytologic evaluation of pleural fluids.

Results of a comparison of the diagnostic efficacy of percutaneous needle biopsy of the parietal pleura with that of cytologic examination of pleural fluid sediment obtained concurrently from 166 patients with benign or cancerous pleural disorders are reported. Of 44 patients with confirmatory evidence of cancer involving the pleural surfaces, 43 had positive cytologic findings, whereas pleural biopsies were diagnostic in only 16 cases. Of a total of 122 patients with benign pleural diseases, cytology provided the diagnosis in two cases of eosinophilic pleurisy, and pleural biopsy contributed the diagnosis in four of ten cases of tuberculosis. The data indicate that percutaneous needle biopsy of the parietal pleura is less efficacious in the diagnosis of malignant pleural disease than is cytologic evaluation of the fluid sediment, whereas in the diagnosis of tuberculous pleurisy, pleural biopsy proved superior.

Adult↗
PubMed1979

Pleural effusion: laboratory tests in 300 cases.

The cause of pleural effusion was studied in 300 consecutive patients by clinical examination and laboratory tests. The three most common causes were found to be cancer 117 cases (metastatic 65, bronchogenic 34, mesothelioma 10, lymphoma 7, other 1); tuberculous infection 53; and bacterial infection 38. The cause was not found in 62 patients. Cancer diagnosis was established by cytological examination of pleural fluid (63), closed pleural biopsy (37), and open pleural biopsy (11). Tuberculosis was diagnosed by culture of pleural fluid (12), closed pleural biopsy (38), and open pleural biopsy (3). In cases of empyema 12 Gram-positive and two Gram-negative cocci and two anaerobes were identified. The various causes and the usefulness of the different investigative procedures are discussed, and the data evaluated in the light of current knowledge about mechanisms of transfer through the pleural space.

Empyema↗
PubMed1977

Acid glycosaminoglycans (mucopolysaccharides) in the differential diagnosis of pleural effusion.

Pleural fluid glycosaminoglycans (GAG) in 64 patients with various diseases were isolated by anion-exchange chromatography after proteolysis, and characterised by spectrophotometric, electrophoretic and enzymatic techniques. GAG concentrations ranged from 7 to 1178 microng hexuronate/ml pleural fluid. The highest values (1178, 161 and 160 micron/ml) were found in patients with diffuse mesothelioma. Over 90% of the pleural fluid GAG consisted of hyaluronic acid (HA) in these patients. In other types of pleural effusion the relative HA content varied from 42 to 70% of the total GAG. Determination of pleural fluid HA consequently appears extremely valuable in the diagnosis of the form of mesothelioma producing HA. The mean GAG concentration of pleural fluid was significantly higher in tuberculous pleurisy than in hydrothorax (P less than 0.01), secondary malignant pleural effusion (P less than 0.0005) and idiopathic pleurisy (Pless than 0.03). It was impossible to demonstrate definite correlations between GAG and protein, and GAG and glucose concentrations of pleural fluid.

Diagnosis, Differential↗
PubMed1979

Decreased heat-labile opsonic activity and complement levels associated with evidence of C3 breakdown products in infected pleural effusions.

Heat-labile opsonic activity was measured simultaneously in serum and pleural fluid of patients with transudates, infectious exudates (with positive or negative bacterial culture) and neoplastic exudates, using two different complement-dependent phagocytic tests: the killing of Staphylococcus aureus Wood 46 variant strain (K50 opsonic titers) and the assessment of ingestion rate of endotoxin-coated paraffin particles (Oil Red 0 uptake test). K50 opsonic titers were lower in culture-positive pleural effusions as compared to culture-negative (P < 0.002) or neoplastic effusions (P < 0.002). These results were corroborated by the Oil Red 0 uptake test. The data obtained with the two assays showed a significant correlation (P < 0.001). The hemolytic activity of complement (CH50) as well as the levels of C3 breakdown product, C3d, were measured in the same sera and pleural fluid samples and in an additional group of patients with pleural effusions of the same etiology. Effusions with positive cultures showed lower CH50 values (P < 0.01) and higher C3d values (P < 0.05) when compared to culture-negative pleural fluids. Finally, evidence for immune complexes in pleural effusions and sera was looked for by determination of Clq binding activity. Levels were higher in culture-positive effusions when compared to culture-negative fluids (P = 0.005).K50 opsonic titers showed a positive correlation with CH50 values (P < 0.001) for all fluids tested. Similarly Clq binding activity correlated with C3d levels in effusions of infectious origin (P = 0.05). Recovery experiments using the various bacterial species isolated from culture-positive pleural effusions showed evidence of complement inactivation upon incubation with pooled sera at concentrations of 10(7)-10(8) microorganisms/ml. These results indicate that one important reason for bacterial persistence in empyema may be decreased opsonization secondary to local consumption of complement.

Adult↗
PubMed1979

The pH of sclerosing agents: a determinant of pleural symphysis.

The rate of success in producing pleural symphysis with intrapleural instillation of sclerosing agents has been variable. Differences in the designs of studies probably account for some of the variability, but the reasons for the remainder are not clear. Since a low pH of the pleural fluid is associated with pleural adhesions and loculations, the pH of the commonly used solutions of sclerosing agents was determined, both in their usual concentrations and when diluted with large quantities of exudative pleural fluid. The buffered solution of tetracycline hydrochloride had the most acidic pH (2.0) and showed little change when diluted by pleural fluid. A 0.5 percent solution of sodium hydroxide had the highest pH (13.0). The remainder of the sclerosing solutions showed a range of pH from 4.3 to 8.7. Experimental and clinical experience suggests that tetracycline consistently has the highest rate of success in producing pleural symphysis. It appears that when proper technique is employed, the pH of the solution of the sclerosing agent is an important determinant of the production of pleural symphysis.

Animals↗
PubMed1977

[Asbestosic pleural calcifications and the associated pathology (study of 32 cases)].

The presence of calcified pleural plaques together with asbestos professional exposition is the sign of patent dust inhaling and can be related to asbestos pathology. The observations on a homogeneous group of 32 cases of asbestosic pleural calcifications are analyzed. The frequency of malignant pleural and bronchial tumours (2 pleural mesothelioma, 3 bronchial epithelioma) is classical. That there was no serious pulmonary fibrosis can be attributed to the conditions of dust inhaling. There was a relatively high frequency of pleural effusions, the benignity of which could not always be ascertained. Therefore, besides the convincing facts, the precise study of cases with calcified pleural plaques (pleural antecedents, circumstances of the discovery, evolution) could be a rough way of appreciating the frequency of benign asbestos pleurisies.

Aged↗
PubMed1979

Pleural fluid lysozyme in human disease.

Lysozyme content was measured in the plasma and pleural fluid of 110 patients with pleural effusions of various causes. The concentration of pleural fluid lysozyme was significantly higher (P less than .001) in patients with tuberculous pleurisy than in those with primary pulmonary carcinoma, metastatic carcinoma of the lung, connective tissue disease, nonspecific pleurisy, or congestive heart failure. Tuberculous patients also had a significantly higher (P less than .001) pleural fluid-to-plasma lysozyme ratio than did the other patients. Plasma lysozyme activity did not differ significantly among the various patient groups. Lysozyme was identified immunohistochemically in epithelioid cell granulomas in tuberculosis, in activated macrophages in lymph nodes adjacent to tuberculous lesions, and in granulocytes in pleural empyema. No lysozyme was detected in neoplastic cells in pulmonary carcinoma. The results show that the determination of pleural fluid lysozyme is a simple, fast method for obtaining corroborative information in the differential diagnosis of tuberculous pleurisy.

Adolescent↗
PubMed1978

Fibrinogen, fibrin(ogen) degradation products and fibrinopeptide A in pleural effusions. High turnover of fibrinogen in pleurisy.

Fibrinogen, fibrin(ogen) degradation products (FDP) and fibrinopeptide A (FPA) were analysed in pleural fluids from 20 consecutive patients with major effusions of various aetiology. FPA is a short-lived polypeptide which is split off from fibrinogen, whereafter fibrin is formed. FDP are formed through lysis of fibrin or fibrinogen. In 18 patients no fibrinogen could be detected in pleural fluid, whereas two (both having malignant tumours) had detectable but low concentrations. High FPA concentrations, interpreted as reflecting very recent fibrin formation, were found in all pleural fluids except for one case of empyema and one transudate. Plasma concentrations were low in most cases. The same pattern was found with regard to FDP, i.e. exudates showed high concentrations, whereas plasma concentrations were low. The only patient with a transudate showed absence of fibrinogen and low concentrations of FDP and FPA. We interpret our findings as indicative of a high rate of fibrin formation and degradation in pleural exudates and have not found any differences between various types of pleural exudates. Consequently, the findings may illustrate the close association between the coagulation system and inflammatory reactions which may be common to most pleural diseases.

Adult↗
PubMed1976

Experimental immunotherapy of neoplastic pleural effusion with oil-attached BCG cell-wall skeleton in mice.

An experimental model for neoplastic pleural effusion was made using a transplantable pleural fibrosarcoma MC-106 in ddO mice, and a local immunotherapy of neoplastic pleural effusion with oil-attached BCG cell-wall skeleton was attempted. Viable cells (3 X 10(5)) of MC-106 were injected into the right pleural cavity of the mice on day 0 with a tuberculin syringe which was joined to a two-way tap attached to a capillary manometer. All of the mice in the control group, which received intrapleurally saline solution 24 hr after the injection of tumor cells, died within 24 days and the mean survival time was 16.9 +/- 3.4 (SD) days. Macroscopically massive blooded pleural effusion in both pleural cavities and multiple tumor nodules on the surface of parietal and visceral pleura were observed. On the other hand, the mice which received intrapleurally 100 mug of oil-attached BCG cell-wall skeleton 24 hr after the injection of tumor cells survived much longer. About 50% of the mice remained alive and were killed on day 95. They revealed histologically no malignant lesion of the pleura except for residual changes of inflammatory reactions.

Animals↗
PubMedDate not supplied

[Study of simultaneous dosage of carcino-embryonic antigen (C.E.A.) and beta 2-microglobulin in serum and pleural liquid (author's transl)].

Simultaneous dosage of carcino-embryonic antigen and beta 2-microglobulin was studied in serum and pleural liquid. Among the 20 patients with non-neoplasic infections, the carcino-embryonic antigen was not increased in the serum and only once at a border-line level in the pleura. The level of beta 2-microglobulin seems to be related to the number of lymphocytes in the pleural liquid (increase in 45% of the cases compared to 20% in the serum). Among the 31 cancer patients, carcino-embryonic antigen is increased in the serum of 36% of the cases and in the pleura of 48%. In 5 observations, the pleural levels were considerably increased compared with serum levels, suggesting the existence of a pleural metastasis. The beta 2-microglobulin is elevated in only 26% of the cases in the pleural liquid and in 13% in the serum. At the present state of knowledge, it therefore seems unnecessary to continue investigations concerning the beta 2-microglobulin. On the contrary, the pleural dosage of carcinoembryonic antigen could contribute to the diagnosis.

Beta-Globulins↗
PubMed1978

Effect of pleural effusion on high-dose methotrexate kinetics.

The kinetics of methotrexate were followed in a patient given two 6-hr infusions of 400 mg/kg in the presence and absence of a pleural effusion. Although the decline in serum concentrations during the first 30 hr after the infusion was similar for the two treatment courses, the half-life beginning 30 hr after the infusion was 6.7 hr without the pleural effusion and 14.4 hr with the pleural effusion. Comparison of the intercompartment distribution rate constants indicated slower movement of the drug back into the central compartment from the peripheral compartment when a pleural effusion was present. Pleural fluid methotrexate concentrations were consistently higher than serum concentrations. These data indicate that the increased risk of toxicity following high-dose methotrexate in patients with pleural effusions is due to changes in methotrexate kinetics resulting in delayed excretion.

Child↗
PubMed1977

Pleural effusions.

Many different conditions result in the accumulation of pleural fluid. A diagnostic thoracentesis should be performed on all patients with pleural effusion from whom pleural fluid can be easily obtained. Empirically we have found that when the pleural effusion is more than 10 mm thick on the lateral decubitus roentgenogram, pleural fluid is easily obtained. At least 30 cc fluid should be obtained and distributed to the various laboratories as outlined in Table 2. The results of these tests will show whether the fluid is a transudate or an exudate. If the fluid is a transudate, no further diagnostic procedures need be directed towards the pleura. If the fluid is an exudate, the diagnosis will frequently be made by these original tests and therapy for the pleural disease can be instituted. If the diagnosis has not been made, the results of these tests should lead to a rational diagnostic attack.

Amylases↗