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Biomedical subjects

J H Dijkman

Publications and source records attributed to J H Dijkman.

At least 91 records · Page 5Linked to original sources
PubMed1990

Ranitidine compared with the dimethylprostaglandin E2 analogue enprostil as adjunct to pancreatic enzyme replacement in adult cystic fibrosis.

In a double-blind cross-over randomized study adjunct therapy with ranitidine (2 x 150 mg) was compared with enprostil (2 x 35 micrograms) in eight adult cystic fibrosis (CF) patients receiving a fixed dose of enteric-coated microsphere capsules of pancreatin (Pancrease). The study consisted of two consecutive 14-day treatment periods. All patients kept a fixed daily fat intake during the last 5 days of each treatment period and performed 72-h faecal collections during the last 3 days of each treatment period. Gastrointestinal complaints were scored at the end of each treatment period. During treatment with ranitidine there was less faecal fat excretion (18.9% versus 25.1%; NS), less faecal weight (263 versus 303 g/day; NS), and a lower gastrointestinal complaints score (5.3 versus 3.1; P less than 0.05) compared with the treatment with enprostil. One patient dropped out during the treatment period with enprostil because of very severe diarrhoea and abdominal discomfort. We conclude from this study that adjunct therapy with ranitidine has significantly less side effects and may give a better reduction of faecal fat excretion and daily faecal weight in CF.

Adult↗
PubMed1990

Tension subcutaneous emphysema. A case report.

A case is presented of severe barotrauma due to thoracoscopy with multiple lung biopsies and consecutive mechanical ventilation for pneumocystis carinii pneumonia. When tension subcutaneous emphysema developed, circulatory collapse occurred. Relief of pressure by a subcutaneous drain reversed the circulatory state.

Drainage↗
PubMed1989

[The Phadiatop test, a new in-vitro test for inhalation allergy].

The Phadiatop test, a new in-vitro test for inhalant allergy, was evaluated in relation to a RAST panel, and in comparison with total IgE. In 248 patients, aged 12-64 years, who had been prescribed pulmonary medication in general practice, the Phadiatop, total IgE (PRIST), and specific IgE (RAST) test were carried out with seven inhalant allergens common in the Netherlands. RAST was considered positive at class greater than or equal to 2 and total IgE elevated at values greater than or equal to 200, greater than or equal to 150, and greater than or equal to 100 kU/l in age groups 12-14, 15-16, and 17-64 years respectively. The result of the Phadiatop test is given as positive or negative. The predictive value of the Phadiatop test for one or more positive RAST results was 100% and its predictive value for all RAST results being negative was 97.1%, while these predictive values for total IgE were 84.7% and 71.2% respectively. It is concluded that the Phadiatop test is a valuable test to confirm or exclude sensitization to common inhalant allergens.

Adolescent↗
PubMed1989

Measurement of specific IgE antibodies in individuals exposed to formaldehyde.

Using an in-vitro test, the presence of formaldehyde-specific IgE antibodies was investigated in sera from four groups of individuals exposed to formaldehyde by different routes and concentrations. Group (A) 28 subjects living or working in rooms or places where formaldehyde-containing construction materials were used; (B) 18 subjects occupationally exposed to relatively high concentrations of formaldehyde; (C) 12 paramedic employees working in a renal dialysis unit where formaldehyde-sterilized dialysers were being used; and (D) 28 subjects undergoing haemodialysis with these formaldehyde-sterilized dialysers. Formaldehyde-specific IgE antibodies could be detected in only one of the 86 serum samples. This particular sample was from a worker occupationally exposed to formaldehyde (group (B], but who did not show any work-related symptoms. In two pools of control sera from unexposed subjects no specific IgE antibodies to formaldehyde were detected. It is concluded that exposure to formaldehyde, even in relatively high concentrations, rarely evokes the production of specific IgE antibodies. The presence of these specific antibodies is not necessarily attended by allergic symptoms. On the other hand, the symptoms supposed to be related to formaldehyde exposure and reported in this study by 24 out of 28 subjects in group (A), and some of the subjects in groups (B) and (C), cannot be attributed to an IgE-mediated sensitization to formaldehyde.

Air Pollutants↗
PubMed1989

The effect of inhaled budesonide on the maximal degree of airway narrowing to leukotriene D4 and methacholine in normal subjects in vivo.

In normal humans in vivo, maximal airway narrowing to LTD4 is more severe than to methacholine. Moreover, LTD4 heightens the maximal response to methacholine for several days. To investigate whether or not this is due to inflammatory changes in the airway wall, we studied the effects of the corticosteroid budesonide on the dose-response curves to inhaled LTD4 and to methacholine. In a two-period, double-blind, placebo-controlled design, budesonide (400 micrograms twice a day) or placebo was inhaled by eight normal subjects on six consecutive days, with a 3-wk washout. Complete dose-response curves to LTD4 (0.36 to 43 nmol) were performed on Day 5, and to methacholine (1.28 to 655 mumol) on Days 4 and 6 of each period using a validated method. The response was measured by FEV1 and standardized partial expiratory flow-volume curves (V40p), and was expressed as the percent fall from baseline. A maximal response plateau was considered if more than two doses fell within a 5% response range. All subjects reached plateaus to methacholine and to LTD4. Budesonide reduced the maximal response to LTD4 (mean difference with placebo, 7.9% fall for FEV1, and 8.4% fall for V40p; p less than 0.05). During placebo the maximal response to methacholine 24 h after LTD4 was higher than 24 h before (mean change, 2.7% fall in FEV1 and 5.5% fall in V40p; p less than 0.05), but not during budesonide (mean change, -2.5% fall in FEV1 and -0.1% fall in V40p; p greater than 0.2), the changes being significantly different between the two periods (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1989

Antileukoprotease-containing bronchiolar cells. Relationship with morphologic disease of small airways and parenchyma.

Twenty-seven surgically removed lungs and lobes were studied to assess the relation between the abundance of bronchiolar epithelial cells containing antileukoprotease (ALP) (ALP-pos/mm) and the degree of small airways disease (SADscore) and emphysema (destructive index = DI, and number of normal alveolar attachments on membranous bronchioles = normal AA/min). Between subjects, ALPpos/mm correlated with SADscore in membranous bronchioles (rs = 0.75; p less than 0.001) and with normal AA/mm (rs = -0.38; p = 0.05). Evaluation within each subject revealed significant correlations of ALPpos/mm with SADscore in membranous as well as in respiratory bronchioles (p less than 0.001), and also with normal AA/mm (p = 0.005). In membranous and in respiratory bronchioles, ALPpos/mm correlated significantly with the ALP concentration in homogenized tissue, as measured by ELISA (rs = 0.55 and 0.57, respectively; p less than 0.01). It is concluded that disease in small airways and destruction of their alveolar attachments are associated with a rise of the number of ALP-containing epithelial cells. We hypothesize that this cellular increase is part of the general defense against inflammatory and destructive processes in distal human airways, leading to higher levels of proteinase inhibitor in order to minimize tissue damage.

Bronchi↗
PubMed1989

Antileukoprotease is associated with elastin fibers in the extracellular matrix of the human lung. An immunoelectron microscopic study.

Human lung antileukoprotease (ALP) is a potent inhibitor of neutrophil elastase that is locally produced by submucosal bronchial glands and by secretory cells in the bronchiolar epithelium. In a recent light microscopic investigation, ALP was detected in the connective tissue matrix of the lung. The present immunoelectron microscopic study was performed in order to extend our knowledge about the exact localization of ALP in the extracellular matrix of the lung. Both elastin and ALP were detected in central and peripheral human lung specimens using specific antibodies in a two-step, gold-labeling procedure. ALP could be demonstrated in the parenchymal matrix of the alveolar walls exclusively in association with the amorphous elastin fibers. In addition, the subepithelial connective tissue of the bronchial wall also showed a clear labeling for ALP, which was present exclusively over the elastin fibers. The results of this study strongly suggest that ALP play a modulating role in destructive pulmonary diseases such as emphysema in which degradation of elastin fibers by elastase is thought to occur.

Adult↗
PubMed1989

Tissue distribution of antileukoprotease and lysozyme in humans.

We studied the distribution of the proteinase inhibitor antileukoprotease (ALP) and lysozyme (LSZ) in normal human tissues by use of an immunohistochemical technique. ALP could be demonstrated in a variety of healthy tissues, generated by secretory cells in lacrimal, respiratory, proximal digestive, and genital glands, but not in the urinary tract, endocrine glands, or the hematological system. In lung, part of the non-ciliated cell population in membranous bronchiolar epithelium, as well as in respiratory bronchioles, stained positively for the inhibitor. The distribution of ALP and LSZ was parallel in most but not all of the tissues examined. The distribution of ALP around most of the external orifices of the human body is discussed in relation to its possible local physiological role in defense against inflammatory reactions. The widespread parallel distribution of LSZ, a bacteriolytic agent, suggests a complementary role to ALP in local defense.

Adult↗
PubMed1989

[Thoracoscopy in the immunosuppressed patient].

The article reports on diagnostic thoracoscopy in 65 patients suffering from pulmonary complications in immunosuppression. The high sensitivity of 98% and the relatively low rate of complications assign to thoracoscopy a place between transbronchial peripheral and surgical open lung biopsy.

Biopsy↗
PubMed1988

Interactions among stimulated human polymorphonuclear leucocytes, released elastase and bronchial antileucoprotease.

1. We investigated the effect of stimulated human polymorphonuclear leucocytes (PMN's) on both the antitrypsin and anti-elastase activity of bronchial antileucoprotease (ALP). 2. Incubation of ALP with stimulated human PMN's resulted in a rapid loss of anti-elastase activity which paralleled that of the antitrypsin activity, suggesting that both inhibitor activities are represented by the same active site. 3. The myeloperoxidase-oxidizing system was found to be responsible for the inactivation of ALP. 4. The oxidized inhibitor was unable to form stable complexes with PMN elastase but was resistant to breakdown by proteolytic enzymes from stimulated PMN's. 5. It was observed that stimulated cells are capable of releasing elastase which shows full activity in the presence of a large molar excess of ALP. 6. We conclude from this study that stimulated PMN's are able to inactivate ALP by which released elastase is able to express enzymatic activity in spite of the presence of this low-molecular-weight inhibitor. Thus, inactivation of ALP by triggered PMN's may contribute to destructive processes in which elastase is thought to be a mediator.

Chromatography, Gel↗
PubMed1988

Quantity of anti-leucoprotease relative to alpha 1-proteinase inhibitor in peripheral airspaces of the human lung.

1. Peripheral airspaces were selectively lavaged using balloon-tipped catheters of 2 mm diameter. 2. Molar anti-leucoprotease/alpha 1-proteinase inhibitor ratios as determined in these lavage fluids by enzyme immunoassays ranged from 0.02 to 0.14 (mean 0.08). 3. These data indicate that peripheral airspaces contain minor amounts of anti-leucoprotease relative to alpha 1-proteinase inhibitor. This observation does not necessarily mean that anti-leucoprotease is of minor importance in protecting the lung interstitium.

Acute-Phase Proteins↗
PubMed1988

Antileucoprotease in the developing fetal lung.

The distribution of antileucoprotease in the lungs of 25 fetuses of 9-40 weeks' gestation was studied with monoclonal antibodies and an indirect immunoperoxidase technique. Antileucoprotease was detected from 16 weeks in submucosal glands and collecting ducts in the trachea and main and lobar bronchi: it was also found in the surface epithelium of the trachea at 20 weeks, in main and lobar bronchi at 20 weeks, and in smaller bronchi at 20-25 weeks. Non-ciliated cells containing antileucoprotease were observed in the bronchiolar epithelium at 36 and 40 weeks. The results of this study indicate that antileucoprotease is available from birth. It may therefore form part of the first line of defence of the lung.

Cell Differentiation↗
PubMed1988

Antileukoprotease, its role in the human lung.

The number of antileukoprotease-containing epithelial cells in the bronchioles of 27 surgically removed lungs shows a close positive correlation with inflammation of the small airways (bronchioles) and an inverse correlation with the number of undamaged alveolar walls surrounding the bronchioles. So, more antileukoprotease-producing cells are present when bronchioles and adjacent alveoli are more diseased. These results suggest that antileukoprotease-producing cells constitute part of the inflammatory response in and around bronchioles, serving to minimize local tissue destruction. The increased production of this potent elastase-inhibitor, however, seems insufficient to prevent tissue damage. We investigated in vitro whether antileukoprotease might be inactivated by stimulated polymorphonuclear leukocytes (PMN's). The antitryptic and antielastolytic capacities of antileukoprotease were rapidly destroyed by myeloperoxidase-derived oxidants from stimulated PMN's. It was observed that elastase, released by stimulated PMN's, retains full activity when cell stimulation was performed in the presence of a molar excess of antileukoprotease. These results indicate that inactivation of antileukoprotease by stimulated PMN's might be a factor which plays a role in elastase-mediated destruction of lung tissue.

Chromatography, Gel↗
PubMed1988

The combined effects of histamine and methacholine on the maximal degree of airway narrowing in normal humans in vivo.

In normal subjects in vivo the dose-response curve to inhaled nonsensitizing stimuli reaches a plateau at mild degrees of airway narrowing. We investigated whether the limitation of the response is due to non-optimal smooth muscle activation, by administering high doses of histamine and methacholine together. In fifteen normal subjects a complete dose-response curve to methacholine was recorded by a tidal breathing method on three randomized days. On a separate day a complete histamine inhalation test was carried out. Each methacholine test was directly followed by double blind inhalation of the highest dose of either histamine or methacholine, or a dose of saline. The response was measured by flows from partial flow-volume curves (V 40p), and was expressed in % fall from baseline. Twelve subjects reached a maximal response plateau to methacholine which was reproducible. The addition of saline or extra methacholine did not change the response from its methacholine plateau value. Histamine caused a small increase in the response on top of the methacholine plateau (+ 9.0% fall; p less than 0.001). However, the response to the combined histamine and methacholine was not significantly larger than the maximal response to histamine alone. We conclude that there is no interaction between histamine and methacholine on the maximal degree of airway narrowing. This suggests that the plateau of the dose-response curve in normal subjects in vivo is due to other factors than limited smooth muscle activation.

Adult↗
PubMed1987

Elastase inhibitors in sputum from bronchitic patients with and without alpha 1-proteinase inhibitor deficiency: partial characterization of a hitherto unquantified inhibitor of neutrophil elastase.

Anti-elastase function in sputum sol-phase from patients with alpha 1-proteinase inhibitor (alpha 1PI) deficiency was compared with sol-phase from patients with cigarette smoke-induced bronchitis and emphysema. Both alpha 1PI (2P less than 0.01) and anti-leucoprotease (ALP) (2P less than 0.01) concentrations were lower in sol-phase from the alpha 1PI-deficient group, although alpha 2-macroglobulin (alpha 2M) levels were similar. There was no difference in alpha 1PI function between the two groups, but the inhibitor was only congruent to 30% active. The absolute neutrophil elastase (NE) inhibitory capacity was similar in both groups (median 185 micrograms of NE inhibited/ml of sputum, range 80-480, for the alpha 1PI-deficient group; median 175, range 80-300, for the bronchitic group). A substantial proportion of NE inhibition in secretions could not be accounted for by the amount of alpha 1PI, ALP and alpha 2M present (median 74.8%, range 43.2-97.4, for alpha 1PI-deficient sol-phase; median 50.0%, range 0-80.8, for bronchitic sol-phase). Gel filtration of sol-phase demonstrated the presence of NE inhibition in the low molecular weight fractions which was markedly sensitive to changes in substrate concentration and ionic strength, in contrast to purified alpha 1PI and ALP. Sputum sol-phase from both groups failed to prevent hydrolysis of elastin-fluorescein or succinyltrialanyl-p-nitroanilide by NE completely during prolonged incubation in the presence of an excess of functional inhibitors. This was more apparent in secretions from subjects with alpha 1PI deficiency and may explain why such patients have a more rapidly progressive form of emphysema.

Adult↗
PubMed1987

Determination of elastase inhibitory activity of alpha 1-proteinase inhibitor and bronchial antileukoprotease: different results using insoluble elastin or synthetic low molecular weight substrates.

We have determined the effect of two elastase-specific synthetic low molecular weight substrates, L-pyroglutamylprolylvaline-paranitroanilide and succinyltrialanyl-paranitroanilide, together with insoluble elastin-fluorescein, on the determination of the neutrophil elastase (NE) inhibitory capacity of purified alpha 1-proteinase inhibitor (alpha 1-PI) and bronchial antileukoprotease (ALP). In addition, the inhibitory capacities of mixtures of alpha 1-proteinase inhibitor, antileukoprotease and alpha 2-macroglobulin prepared in ratios similar to that in lung secretions were determined. Purified inhibitors, alone or in combinations, inhibited about 1 mole neutrophil elastase per mole inhibitor when assessed using synthetic substrates. However, when elastin-fluorescein was used in the assay system, the purified inhibitors showed an inhibitory capacity that was 40-85% of the value obtained using synthetic substrates. Even less inhibition was observed when mixtures of inhibitors were assessed using elastin-fluorescein (23-44% of the value for synthetic substrates). Our data indicate that results of elastase inhibitor activity measurements depend on the type of substrate which has been used.

Blood Proteins↗
PubMed1987

Maximal airway narrowing to inhaled leukotriene D4 in normal subjects. Comparison and interaction with methacholine.

We investigated whether or not leukotriene D4 can influence the maximal degree of airway narrowing in normal humans by comparing the maximal responses to inhaled methacholine and LTD4, and evaluating the interaction between both agonists. In 8 normal subjects, methacholine challenges were performed 24 h before and 24 and 72 h after a LTD4 challenge. Doubling doses of methacholine (1.3 to 655 mumol) or LTD4 (0.007 to 192 nmol) were inhaled by using a recently validated method. The highest dose of LTD4 was followed by the maximal dose of methacholine. The response was measured by FEV1 and volume history standardized partial expiratory flow-volume curves (V40p), and was expressed as percent fall from baseline. All subjects reached a maximal response plateau to both agonists. The maximal response plateau to LTD4 was systematically higher than to methacholine on the preceding day (mean difference, 13.4 and 12.7% fall for FEV1 and V40p, respectively) (p less than 0.01). Addition of methacholine on top of the LTD4 plateau caused a further increase in the response (mean, 6.6 and 4.8% fall, respectively) (p less than 0.005). The maximal responses to methacholine at 24 and 72 h after the LTD4 challenge were higher than at 24 h before (mean difference at 24 h, 4.0 and 8.5% fall for FEV1 and V40p, respectively, and at 72 h 5.7 and 9.3% fall) (p less than 0.05). However, the provocative dose of methacholine causing a 10% fall in FEV1 (PD10) or a 40% fall in V40p (PD40) was not altered by the previous LTD4 challenge test.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗