Chylothorax in adult age in association with congenital lymphedema.
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Biomedical subjects
Publications and source records attributed to R Pauwels.
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Of 77 patients with bladder carcinoma, 99 tissue specimens--including tissues of patients with recurrent tumors taken after radiotherapy or cytostatics--were subjected to chromosomal analysis. In 42 specimens, recognizable metaphases could be obtained after conventional Giemsa staining and in a smaller number after C- and/or G-banding. All except one had abnormalities of the chromosomes. Short-term cultures for 24-48 hr in RPMI 1640 plus 15% fetal calf serum plus penicillin-streptomycin gave better results than a direct technique (30 min in 0.075 M KCl + 0.1 microgram colcemid/ml at 37 degrees C, followed by fixation). In low stage/grade tumors the number of recognizable metaphases obtained after short-term cultures is lower than in higher stage/grade tissue specimens.
The effect on the allergen-induced immediate and late bronchoconstriction of theophylline and enprofylline (3-propylxanthine), a new xanthine derivative with negligible ability to antagonize adenosine, was studied in nine patients with asthma. The patients were challenged three times at weekly intervals with the same dose of allergen. FEV1 and SGaw were followed up to 6 hours after challenge. The drugs were administered intravenously. Placebo was always administered on the first occasion. Theophylline and enprofylline were administered on test days 2 and 3 with a double-blind, randomized crossover technique. One hour before the allergen challenge, a loading dose was administered during 60 minutes followed by a constant infusion during 6 hours. The loading infusion was 7.2 mg/kg of theophylline and 2.7 mg/kg of enprofylline. The maintenance dose was 74 mg/hr and 71 mg/hr, respectively. Both theophylline and enprofylline caused a minor initial bronchodilatation. Theophylline and enprofylline slightly but significantly attenuated the immediate bronchoconstricting reaction after allergen inhalation. Theophylline and enprofylline had a significant attenuating effect on the late bronchial reaction. The mean plasma level of theophylline was 0, 10.8, 10.5, and 10.5 mg/L at 0, 1, 4, and 7 hours after the start of the loading infusion, respectively. The corresponding mean plasma levels of enprofylline were 0, 2.6, 2.7, and 2.7 mg/L. Theophylline and enprofylline caused headache in one patient. Two patients developed nausea and vomiting during the enprofylline infusion. The present data suggest that adenosine receptor antagonism may not be the main mode of action of xanthines in inhibiting bronchoconstriction after single dose antigen challenge.
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6 years after mantle field irradiation for stage IA Hodgkin's disease, a patient presented with right-sided chylothorax. Even after thorough investigation no etiology for the chylothorax was found. It is suggested that chylothorax can be due to previous radiotherapy.
The present study examines the influence of Freund's complete adjuvant (FCA) injections on sensitized PVG rats with respect to serum levels of IgE and IgG2 alpha antibodies and total IgE (all assessed by radioimmunoassays) and the capacity of serosal mast cells to release histamine on challenge in vitro with 'immunological' secretagogues (specific antigen, anti-IgE, concanavalin A) or with compound 48/80. The rats were immunized with 10 micrograms ovalbumin (OA); alum, Bordetella pertussis vaccine, or silica gel were employed as adjuvants. Treatment with FCA was performed by single intraperitoneal injections 3, 2, or 1 week(s) before or 1 or 2 weeks after sensitization. Tests were conducted 3 weeks after sensitization. The results show that the effect of FCA treatment varied reproducibly with the adjuvant employed for sensitization and with the timing of the FCA administration. FCA treatment could either increase, fail to affect, or decrease total serum IgE and OA-IgG2 alpha antibody levels as well as serosal mast cell responsiveness, whereas OA-IgE antibody responses were decreased or not affected. Moreover, serum levels of OA-IgE and OA-IgG2 alpha antibodies and total IgE were affected by FCA treatment independently of each other. Finally, serosal mast cell responsiveness to a given secretagogue could be influenced by the FCA treatment apparently independently of that to other secretagogues. A salient finding was that effects of FCA treatment on mast cell responsiveness did not necessarily conform to effects on antibody synthesis. Collectively, these data support the opinion that the mechanisms of action of the IgE-promoting adjuvants employed differ and suggest that the expression of serosal mast cell responsiveness to each examined secretagogue can be regulated separately. They also suggest that the serosal mast cell sensitizing capacity of homocytotropic antibodies may not be adequately quantified by immunochemical methods employing reagents prepared against IgE and IgG2 alpha protein.
Two bronchoconstrictory agents, serotonin (5 HT) and carbachol, were investigated in different inbred rat strains in order to delineate possible factors influencing the bronchial reactivity. The challenge was given intravenously and a single dose was given to an individual animal. Inbred strains of rats differed significantly from each other in their reactivity to 5 HT and to carbachol. IC rats were good reactors to both 5 HT and carbachol. RA rats were intermediate reactors to both agents. OM/N rats had a good reaction to 5 HT, but showed only a minor bronchoconstriction after carbachol. BN and LE rats were poor reactors to both agents. The strain reactivities to the 2 provocation agents were not related. Breeding studies, using a good reactor, IC, and a poor reactor, DA strain, showed that the bronchial reactivity to 5 HT was inherited with a pattern that fitted with the autosomal recessive way of inheritance, high reactivity being recessive.
The clinical, radiological and histological features of 6 patients with Wegener's granulomatosis are presented. Because of the frequent finding of "atypical" radiographic features on chest X-rays in our patients, we also reviewed the literature.
Four different strains of rats, BDII, E3, LE, and OM/N, each with a low basal serum level of IgE, were examined with respect to anti-IgE- and ConA-induced release of histamine from serosal mast cells and chopped lung tissue. Tests were performed before and three days after i.p. injection of a graded dose of myeloma IgE (IR 162)-containing ascitic fluid. There was a clearcut strain difference in response capacity with respect to ConA- and anti-IgE-induced release of histamine from serosal mast cells before myeloma IgE-injection. Response capacity increased in some but not all strains after myeloma IgE injection; increase in response capacity of serosal mast cells did not correlate to that of chopped lung tissue. Analogous findings were observed when two of the strains, LE and E3, were passively sensitized by i.p. injection with serum containing another myeloma IgE (IR2). These results indicate that differences exist between mast cells of different rat strains, and within strain between mast cells of various tissues in capacity to become sensitized to myeloma IgE.
Responsiveness was compared for cell populations harvested from the peritoneal and pleural cavities of rats with respect to histamine release induced by specific antigen, anti-IgE, and Con A. Cell populations were obtained from Fischer, PVG or Sprague-Dawley (SD) rats, which were either untreated or immunized with 10 micrograms ovalbumin together with 100 mg alum intraperitoneally. Mast cell histamine release was examined with crude cell populations. The results show that differences in response capacity to the various secretagogues employed do exist between pleural and peritoneal cells in Fischer and PVG strains but under the present circumstances apparently not in SD rats. These differences vary in magnitude with the secretagogue employed and (for cells from immunized animals) with the time elapsed between immunization and test. In PVG rats, neither pleural nor peritoneal mast cell histamine release induced by antigen paralleled serum OA-IgE antibody levels. Furthermore, an increase in anti-IgE induced release of histamine from serosal mast cells occurred in parallel with a decrease in total serum IgE levels. These data indicate that the functional differences observed with respect to release properties of the two cell populations are due not only to intrinsic differences in mast cell populations but also to differences in reaginic antibodies sensitizing the cells.
Budesonide is a potent nonhalogenated glucocorticoid consisting of a 1/1 mixture of the two epimers 22R and 22S. The kinetics of these epimers were studied in six healthy male subjects after intravenous administration of 500 micrograms 3H-budesonide. Estimation of the epimer concentrations in plasma was made possible by development of an HPLC method for simultaneous separation and quantification. The plasma t 1/2, distribution volume (V beta), and plasma clearance for epimer 22R were (mean +/- SD) 2.66 +/- 0.57 hr, 425 +/- 100 l, and 117 +/- 40 l/hr. The corresponding values for epimer 22S were 2.71 +/- 0.69 hr, 245 +/- 38 l, and 67 +/- 19 l/hr. Differences in V beta and plasma clearance between the two were significant. The larger V beta noted for epimer 22R may be a result of higher tissue affinity. The high plasma clearance for both epimers should largely reflect their high rate of liver biotransformation.
Pressurized aerosols of sympathomimetic drugs are widely used in the treatment of bronchial asthma. The efficacy of this form of treatment is diminished in a number of patients by difficulties in coordination between the aerosol actuation and the inhalation. In order to improve the intrapulmonary deposition of terbutaline, an extension tube has been adapted to the regular pressurized aerosol device. In a cross-over randomized study we compared the bronchodilatory effect of increasing doses of terbutaline (250, 500 and 750 micrograms at 25-min intervals) either delivered by the regular pressurized aerosol device or by the device with the extension tube. The study was performed on 11 adult patients with reversible airways obstruction. Spirometry, body plethysmography and flow volume curves were performed. The onset of the bronchodilatory effect of a single dose of 250 micrograms terbutaline was more rapid after delivery via the extension tube. The addition of the extension tube caused a significantly higher bronchodilator efficacy of aerosolized terbutaline on the small airways. Our results show that the addition of an extension tube improves the bronchodilator efficacy of terbutaline delivered from a pressurized aerosol.
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Rats of the Brown Norway (BN)2, Fischer, PVG and Sprague Dawley (SD) strains were immunized intraperitoneally with graded doses of ovalbumin (OA) together with either alum or Silica gel. At specified times after immunization, in vitro histamine release from serosal mast cells and from chopped lung and tracheal tissue was determined after challenge with OA. The development of the capacity to respond in these tests seemed to vary within strain independently for mast cells, lung, and tracheal tissue with immunization dose of antigen and nature of adjuvant. These variations were not closely correlated to observed variations in serum levels of OA-IgE antibody or ratio OA-IgE to total IgE as determined by radioimmunoassay. Furthermore, variations between strains in response capacity did not correlate to inter strain variation in median serum OA-IgE antibody level. These results do not clearly conform to the possibility that one single class of IgE mediates anaphylactic reactivity of various tissues of the rat.
Bordetella pertussis organisms, with or without a small dose of alumhydroxide, enhance in rats the production of IgE antibodies to an unrelated antigen, even if this antigen has been administered 6 weeks beforehand. This non-specific enhancement of IgE antibodies is accompanied by a substantial rise in total serum IgE and by the production of IgE antibodies to B. pertussis. The effect of B. pertussis on IgE synthesis is dose-dependent. No effect of B. pertussis on IgE production can be observed in nude rats.
PVG rats given injections of 1 microgram ovalbumin (OA) together with 10 mg Silica gel failed to provide serosal mast cells or lung tissue with the capacity to release histamine on in vitro challenge with the antigen. However, if such animals were injected i.p. with 100 mg of alum (without any further antigen addition) 3-9 weeks after the primary antigen injection, their mast cells and lung tissue showed a clear-cut capacity to respond in vitro, when examined 1 week after the alum injection. Injection of only 15 mg alum did not induce such a response capacity. The fading of the reactivity induced by an alum injection could be prevented by a repeated injection of the adjuvant alone. Pretreatment of the rats with cyclophosphamide (33 mg/kg) 2 days before the primary antigen injection did not affect the response capacity induced by a booster injection 3 weeks later. S.c. injection of alum also precipitated response capacity in animals primed by i.p. injection of antigen and Silica gel. The anaphylactic response capacity induced by injection(s) of alum was generally accompanied by increased levels of OA-IgE and especially OA-IgG2a antibody; however, a clear-cut correlation between either serosal mast cell or lung tissue response capacity and serum OA-IgE or IgG2a antibody titer could not be demonstrated. These data show that in primed animals, which do not express allergic response capacity, such a capacity can be induced by injecting adjuvant alone, even several weeks after the primary antigen injection.
SD rats were sensitized by an i.p. injection of 1 microgram or 10 micrograms ovalbumin (OA) together with 10 mg Silica gel. At the indicated time after sensitization, allergic response capacity of the animals was estimated by measuring changes in intratracheal pressure induced by an i.v. injection of 0.3 mg OA (low challenge dose) or 5 mg OA (high challenge dose). Animals given 1 microgram OA in Silica gel showed no response capacity at 14, 35 or 47-48 days after sensitization. Animals injected with 10 micrograms OA showed a clear-cut response with a peak at 14 days; at 7 weeks after immunization the response capacity had faded almost completely. Specific OA-IgE antibody and total IgE serum levels were examined by radioimmunoassay. A slight increase in OA-IgE antibody was recorded in animals injected 14 days before test with 10 micrograms ovalbumin and Silica gel; animals given 1 microgram OA and Silica showed no OA-IgE antibody. Five weeks after sensitization, some animals of each group were injected i.p. with 100 mg alum, B. pertussis vaccine (2 ml of Perthydral), or saline, all injections being made without any further antigen addition. 12-13 days after such an injection, alum-treated animals showed high response capacity at bronchial anaphylactic tests and high OA-IgE antibody levels but comparably low levels of total IgE. Animals injected with B. pertussis, on the other hand, showed low response capacity (bronchial anaphylactic tests and OA-IgE antibody levels) but high total IgE-antibody levels. The bronchial anaphylactic response in the B. pertussis-injected animals but not the alum-injected animals was significantly correlated to serum IgG2a antibody levels. These results show that injection of alum or B. pertussis vaccine without antigen can precipitate/enhance anaphylactic response capacity and production of specific and non-specific IgE and IgG2a.
Two directional selections of rats for a high or a low IgM serum levels have been carried out. The criterium of selection was the individual merit of each rat in having a high or a low IgM level when they were 3 months old. All animals were kept together, in order to avoid external influence on the IgM synthesis. The founding population was a mixed nucleus of rats, obtained by breeding of 13 different strains of inbred or outbred rats for two generations. Two lines, one with a high IgM serum level and another with a low IgM serum level, have been separated. At generation 10, they differed from each other by a coefficient of approximately four. These IgM serum levels were not due to differences in IgM catabolism of the two lines since both lines had similar IgM half-lives. Analyses of the data obtained show that, for IgM synthesis, the coefficient of heritability varies between 0.30 to 0.40, and the number of 'independent loci' controlling IgM synthesis ranges from 11 to 14.