Biomedical subjects
Publications and source records attributed to U Wahn.
Cat allergen 1, the major allergen from cats, has been demonstrated to be present in surface washing and in saliva. With the use of an immunohistologic technique with monospecific anti-CA 1, we demonstrated two different sources of the protein, mucous salivary glands and hair roots, where it originates from sebaceous glands.
Two purified allergens from Dermatophagoides pteronyssinus, Dp 42 (identical to P1) and Dp X were studied for their ability to induce histamine release from washed leukocytes and to bind to IgE antibodies from the serum of 27 mite-sensitive children. Almost all patients were demonstrated to be sensitive to both proteins by both assays. Dp 42 was found to have the highest allergenic activity, releasing histamine from leukocytes at a median concentration 10 times lower than for Dp X. There was a positive correlation between basophil sensitivity to both proteins and allergen specific serum IgE concentrations.
We compared allergen-induced histamine release (HRA) from actively sensitized human leukocytes and RAST inhibition (RI) for their capacity to measure the activity of allergen extracts. Four different grass pollen preparations were investigated for their allergenic activities by employing leukocytes and sera from 13 patients sensitive to grass pollen allergens. We could demonstrate that both test systems detect differences in allergenic activities of the preparations with similar accuracy and reproducibility. HRA is more sensitive than RI but shows greater variability of the results. Pooling of sera from individual patients diminishes individual sensitivities in RI. By this means the precision of RI is further increased. As reagents for RI can be standardized and stored under stable conditions, RI can be performed at different times and different laboratories under identical conditions. For these reasons, RI seems to be more suitable for routine standardization of allergen extracts than HRA.
Thirty-one children with seasonal hay fever, sensitive to rye grass by skin test, RAST, and leukocyte histamine release, received preseasonal hyposensitization with a rye grass pollen extract either subcutaneously (cumulative dose 40,000 PNU) or orally (cumulative dose 400,000 PNU). While there was a significant (p less than 0.005) increase in specific serum IgG-antibodies and a decrease (p less than 0.005) of leukocyte sensitivity in the subcutaneously treated group, oral treatment with an aqueous pollen extract could not be demonstrated to be immunologically effective.
A boy with inoperable mediastinal echinococcosis is reported, who developed anaphylactic reactions during chemotherapy with mebendazole. IgE-mediated hypersensitivity was demonstrated by elevated echinococcus-specific serum IgE-antibody concentrations, by allergen-induced histamine release from washed leukocytes, and by passive sensitization of nonsensitized leukocytes with the patient's serum. During hyposensitization with echinococcus antigen no further anaphylactic symptoms were observed over a two years period. There was a decrease in allergen-specific serum IgE-concentrations and in basophil sensitivity to echinococcus antigen. The indication for hyposensitization in echinococcosis is discussed.
Disodium chromoglycate, an antiasthmatic drug, which is effective in inhibiting mediator release from bronchial mast cells, failed to inhibit allergen-induced histamine release in vitro from actively sensitised basophils of grass pollen sensitive children and adults. In contrast, ketotifen, a drug that has been demonstrated in a number of placebo controlled studies to be of lower efficacy in vivo, inhibits histamine release. Our data support the concept that human basophils and mast cells respond differently to antianaphylactic drugs.
Forty children allergic to grass pollen were divided into two groups, and matched by their serum IgE antibody concentrations to grasses. For two preseasonal treatment periods one group received immunotherapy with an alum adsorbed grass pollen extract, while the second group was treated orally with an aqueous extract of the same allergens. The patients' postseasonal self evaluation as well as the mean symptom scores calculated from symptom diaries indicate, that oral treatment is significantly less effective in controlling seasonal allergic symptoms than subcutaneous immunotherapy. During oral treatment neither an increase of specific serum IgG antibodies, nor a suppression of the seasonal increase in specific serum IgE antibodies could be demonstrated.
In order to determine the allergenic activity of five purified horse allergens, 22 children allergic to horses according to history, skin test, and leukocyte histamine release were evaluated. Washed leukocytes from all patients were tested for allergen-induced histamine release utilizing four epidermal horse allergens (Ags 6, 9, 11, and 15) and horse serum albumin. Crossed radioimmunoelectrophoresis was carried out with a standard horse dander extract and serum from each patient. The results showed considerable variation in the individual allergoprints. Ag 11 had the highest mean allergenic activity. Sensitivity to horse serum albumin was demonstrated three times. Our data show that the amount of serum IgE antibodies bound by horse allergens correlates significantly with the capacity of the allergens to induce histamine release from washed leukocytes.
Explore the source record for details and available documents.
In vivo and in vitro allergenic activities of allergen and allergoid preparations from partially purified timothy pollen extract were measured in three different systems. In heterologous PCA titration, the allergen preparation was found to be 32 times more allergenic than the allergoid preparation. By intravenous chaled that treatment of allergen preparations with formaldehyde led to a preparation with the properties of an allergoid. In addition, it was found that the carbohydrate fraction of the refined allergen preparation of timothy a reduction in blood pressure. Thus, the allergen preparation was at least 50 times more potent in inducing systemic anaphylaxis in sensitized rats than the allergoid preparation. In the histamine release assay of grass-sensitive human leukocytes, approximately 1,000 times more allergoid protein than allergen protein was required to achieve 30% histamine release. Although to different degrees, in all three test systems in could be demonstrated that treatment of allergen preparations with formaldehyde led to a preparation with the properties of an allergoid. In addition, it was found that the carbohydrate fraction of the refined allergen preparation of timothy pollen decreased the blood pressure even in nonsensitized animals. The effect of this carbohydrate fraction on blood pressure was immediate but short-lived and immunologically nonspecific.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Sixty children with idiopathic nephrotic syndrome (NS) and 30 unselected controls were studied for IgE mediated hypersensitivity by skin-test, total serum IgE and specific IgE antibodies to various allergens. In 42 patients the NS was steroid-responsive and associated with minimal glomerular changes (MC); in 18 patients it was steroid-resistant and associated with focal-segmental glomerulosclerosis (FSS). A history of allergy was found in 17% of MC, 6% of FSS and 10% of control children. Neither serum IgE concentration nor the incidence of allergen specific IgE antibodies were significantly different between the 3 groups. In the presence of steroid-dependency the prevalence of atopy appeared to be higher. However, our data do not support the hypothesis that for the pathogenesis of NS IgE mediated hypersensitivity plays a general role.
The clinical and immunologic response to immunotherapy with laboratory animal allergens was evaluated. There were 23 patients; 11 had received immunotherapy with 12 different extracts (five mouse, six rat, one rabbit), and 12 were matched untreated patients. As a group, nine of 23 had seasonal hay fever. Among the treated patients nine of 11 subjectively improved with immunotherapy. Blocking antibody titers were determined by serum inhibition of allergen-induced histamine release. Treated patients had mean blocking antibody levels of G30 = 59.3 +/- 38.7. In the untreated patients the antibody level was low (G30 = 4.6 +/- 3.6). The difference between the two groups was highly significant (t test p less than 0.001). The blocking antibody level correlates with both the final weekly allergen dose and also the cumulative allergen dose received during immunotherapy. When pretreatment sera were available a temporal rise in blocking antibody was demonstrated during immunotherapy. In patients allergic to several laboratory animals and treated with one allergen, the blocking antibody response was predominantly specific to the allergen used in immunotherapy. This indicates a lack of cross-reactivity in the IgG response to the major animal allergens. When immunotherapy was discontinued in four patients there was a dramatic decrease in the blocking titer, and after 24 mo the levels were the same as those of untreated patients.
This study evaluated the capacity of rat serum albumin and of its proteolytic fragments to activate human basophils for IgE-mediated histamine release. The leukocytes from 8 out of 33 patients allergic to rats released histamine with rat serum albumin. Two proteolytic fragments of rat serum albumin, each constituting half of the molecule, were used to study the IgE-reactive antigenic sites. These fragments released histamine with the cells of some of the donors, thus demonstrating the presence of at least 2 antigenic determinants on each fragment for a total minimum of 4 sites on the intact rat serum albumin molecule. Most of the allergenic activity, however, was not recovered in the 2 fragments (total recovery mean = 6.4%, range between 0.1 and 31%). This loss could be due to cleavage of the rat albumin molecule in the middle of the third domain with loss of antigenic sites and/or due to minor conformational changes in the fragments as compared with the intact molecule. There was up to a 500-fold difference in the percent of activity recovered in the fragments when tested on cells from different patients. Therefore, there is no single immunodominant site on the molecule equally important for all patients. The cells of all 8 patients also reacted with mouse serum albumin but only 2 with bovine serum albumin. At least 1 determinant on mouse and rat serum albumin is cross-reactive with IgE.
Four new cases with congenital homozygous factor VII deficiency are described. Factor VII levels were reduced to less than 1%, 3%, 8% and 10%, respectively. The incidence and severity of bleeding symptoms were well correlated with the measured factor VII activity. In the severe case of factor VII deficiency (less than 1%) a home treatment program was started because of severe recurrent hemarthroses. This entailed transfusions of 20 U/kg body weight prothrombin complex or factor VII concentrate in case of acute bleeding approximately every three weeks. These transfusions have been carried out successfully without any problems. In contradiction, two brothers with hypoproconvertinemia (factor VII 8% and 10% respectively) reached an age of more than 70 years. Despite replacement therapy postoperative bleeding followed one appendectomy, whereas no postoperative bleeding followed patients requiring Achilles tendon lengthening and an above knee amputation and only slight bleeding followed a tonsillectomy. Based on our experience we suggest that in patients with factor VII deficiency of less than 10%, when undergoing surgery, should be maintained a minimal factor VII activity of 10--15% during the first three postoperative days.
Evaluating plasma levels of cortisol and corticosterone after ACTH-stimulation, and the urinary metabolites tetrahydrocortisone and tetrahydrocortisol in asthmatic children it could be demonstrated, that in most cases there was no suppression of adrenal function following treatment over 6 to 18 months with a daily dose of 200 to 300 microgram beclomethasone dipropionate. Since in a few patients suppression was found, an ACTH stimulation after a six months treatment is recommended.