PubMed Health⌕ Search

Biomedical subjects

D A Mathison

Publications and source records attributed to D A Mathison.

At least 37 records · Page 2Linked to original sources
PubMed1981

Immunoglobulin E-rheumatoid factor in the serum of patients with rheumatoid arthritis, asthma, and other diseases.

A solid-phase radioimmunoassay was developed to detect immunoglobulin (Ig)E antibodies that bound to human IgG. IgE-rheumatoid factor activity was found in the serum of 18 of 20 patients with seropositive rheumatoid arthritis, 1 of 4 patients with seronegative rheumatoid arthritis, 3 of 32 patients with seronegative rheumatoid arthritis, 3 of 32 patients with asthma, and in 1 patient with hypocomplementemic vasculitis and iodide sensitivity. Immunopathologic implications of IgE-rheumatoid factor are discussed.

Arthritis, Rheumatoid↗
PubMed1981

Purification and characterization of two functionally distinct forms of C1 inhibitor from a patient with angioedema.

A minority of patients with hereditary angioedema (HAE) have normal concentrations of a dysfunctional C1 inhibitor protein (C1INH) in their plasmas. We purified C1INH from the plasmas of one such patient before and during treatment with the anabolic steroid stanozolol. Both the pretreatment plasma and plasma obtained during stanozolol treatment contained varying amounts of two extremely similar C1INH proteins that were functionally distinct. The pretreatment plasma contained primarily (94%) dysfunctional C1INH that did not inactivate or complex with either purified C1s, activated Hageman factor, or kallikrein and small amounts (6%) of functionally normal C1INH. Stanozolol treatment increased the plasma concentrations of both of these proteins as well as the proportion (23%) of functional C1INH in the plasma. The purified dysfunctional and functional C1INHs had identical or nearly identical molecular sizes, charges, amino acid compositions, and amino sugar contents, and could not be distinguished physicochemically from each other or from normal C1INH. From these studies of purified C1INH proteins we concluded that HAE associated with dysfunctional C1INH is due to a defect at the structural locus for one C1INH gene and that both the dysfunctional C1INH gene and the normal C1INH gene products are present in the plasma of the affected subject. Treatment with stanozolol comparably increased the synthesis of both C1INH proteins. The disproportionate rise in the level of the normal C1INH protein is consistent with the view that it is more rapidly catabolized as a consequence of its interaction with the proteases it inactivates.

Adult↗
PubMed1980

Aspirin-sensitive asthma: tolerance to aspirin after positive oral aspirin challenges.

Two aspirin-sensitive asthmatic patients underwent oral aspirin challenges for investigative purposes. Folowoing the expected respiratory reaction to aspirin, the patients became refractory to the further adverse effects of aspirin. Additionally they began taking 325 mg aspirin per day, and after 6 and 8 mo aspirin dosage was increased to 650 mg per day. We have noted an improvement in their rhinitis and asthma during this open drug trial. Furthermore, maintenance systemic corticosteroids have been reduced in one patient and discontinued in the other without a decline in lung function values. If these intitial observations are found in a larger number of aspirin-sensitive asthmatic patients, changes in our understanding of the pathogenesis of rhinosinusitis-asthma-aspirin syndrome would follow, and treatment for such asthmatic patients might be improved.

Administration, Oral↗
PubMed1980

In vitro releasability of histamine and serotonin: studies of atopic patients.

Sixteen atopic patients with anaphylaxis to food, eczema, asthma and/or rhinitis were investigated for in vitro reactivity of their leukocytes and platelets to various stimuli. Leukocytes from two patients with anaphylaxis to foods had very high spontaneous release of histamine. Compared to non-atopic volunteers without respiratory disease, leukocytes from the other atopic patients showed increased histamine release after stimulation with methacholine in concentrations between 10(-2) and 10(-6) M. Histamine release induced by anti-IgE or anti-kappa chain serum was slightly decreased in atopics compared to controls, and was significantly decreased at low concentrations of anti-IgE (p less than 0.05). There was no significant difference of means for histamine release induced by the calcium ionophore A-23815. The uptake of 3H serotonin from platelet-rich plasma of atopic patients appeared to occur more slowly than in non-atopics. Serotonin release from washed platelets after stimulation with aggregated IgG was significantly lower in the atopic group (p less than 0.01). There was no significant difference in serotonin release induced by thrombin, epinephrine, ionophore or methacholine. Alterations in releasability of mediator containing cells to immunologic and non-immunologic stimuli may play a role in the expression of atopic disease.

Adolescent↗
PubMed1979

Lymphocytes with immunoglobulin E Fc receptors in patients with atopic disorders.

Lymphocytes from normal nonallergic donors and patients with atopic disorders were analyzed for subpopulations bearing Fc receptors for immunoglobulin (Ig)E (Fc(epsilon)) and IgG (Fc(gamma)), surface IgM (sIgM) and IgD (sIgD), and for T cells forming spontaneous rosettes with sheep erythrocytes (E). The patients were divided into three groups according to serum IgE concentrations and systemic corticosteroid treatment. Group I consisted of 12 atopic patients with either normal or moderately increased IgE levels up to 4,000 U/ml. Four patients of group II and three of group III had 10,500-31,000 U/ml and severe atopic dermatitis. Patients of group III, but not I and II, were receiving corticosteroids systemically. The percentage (mean +/-SD) and total number of Fc(epsilon) (+) lymphocytes were 1.2+/-0.5%, 41+/-24/mm(3) in 12 normals; 1.6+/-0.9%, 59+/-43/mm(3) in patients of group I: 7.0+/-2.0%, 187+/-67/mm(3) in group II; and 0.3+/-0.1%, 13+/-5/mm(3) in patients of group III. The increase in group II and decrease in group III of Fc(epsilon) (+) cells were statistically significantly different from the normal persons and patients of group I. In contrast, the patients did not differ significantly from the donors in sIgM(+), sIgD(+), Fc(gamma) (+), and E(+) cell populations. As shown by depletion of sIg(+) cells in four patients with atopic disorders, the great majority of the Fc(epsilon) (+) lymphocytes were B cells. However, two patients with elevated Fc(epsilon) (+) cell numbers had small numbers of mixed E- and Fc(epsilon)-rosetting cells, presumably T cells. Two patients of group II were examined during an acute herpes simplex infection. Both showed an congruent with80% decrease of Fc(epsilon) (+) cells at that time. No apparent correlation between numbers of Fc(epsilon) (+) cells and IgE level existed in patients of group I. Injection of an IgE myeloma protein into two monkeys did not significantly change their percentages of Fc(epsilon) (+) lymphocytes. The data indicate that Fc(epsilon) (+) lymphocytes are increased in patients with markedly elevated serum IgE and severe atopic disease, suggesting that these cells may be involved in the regulation and(or) synthesis of IgE antibody formation.

Adrenal Cortex Hormones↗
PubMed1979

Potassium iodide sensitivity in four patients with hypocomplementemic vasculitis.

During metabolism studies of radiolabeled proteins in 126 participants four patients were suspected of being sensitive to potassium iodide (Kl) because they repeatedly developed urticaria and other symptoms after Kl administration. Two of the four patients suspected of Kl sensitivity and 10 control patients were orally challenged with Kl to document and characterize Kl sensitivity and to evaluate the possible association(s) of Kl sensitivity with urticaria, hypocomplementemia, and vasculitis. The Kl challenges in the two sensitive patients precipitated urticaria, angioedema, polymyalgias, conjunctivitis, and coryza. One of these two patients also developed a severe systemic illness characterized by fever, headache, peritonitis, episcleritis, and pneumonitis. The four sensitive patients were strikingly similar in that they exhibited hypocomplementemia and dermal vasculitis associated with chronic urticaria or systemic lupus erythematosus, suggesting that other patients with similar clinical features may be sensitive to Kl and that Kl may precipitate severe systemic illness in them.

Adult↗
PubMed1978

Radiographic contrast media studies in high-risk patients.

Patients with prior anaphylactoid reactions (AR) to radiographic contrast media (RCM) are at increased risk for another reaction upon repeat exposure to RCM. One hundred one patients, who had prior AR to RCM, who gave informed consent, and who had an essential need for a repeat RCM study, were pretreated with prednisone, 50 mg orally every 6 hours for 3 doses ending one hour prior to RCM study, and diphenhydramine, 50 mg intramuscularly, one hour prior to RCM study. The repeat RCM study was then carried out using standard procedures with resuscitation equipment readily available. Ninety-six patients had no reaction. Five of the 101 (4.95%) developed AR. These AR consisted only of mild urticaria or pruritus. No significant or life-threatening reactions occurred. Pretreatment decreases the risk in this population of patients and is recommended as standard prophylaxis for patients requiring RCM who have had a previous AR.

Adult↗
PubMed1977

Hypocomplementemia in chronic idiopathic urticaria.

A discrete evoking factor or presumed pathophysiologic mechanism is not recognized in the majority of patients with chronic urticaria or angioedema. Two cases are reported in which chronic urticaria was the main manifestation of an immune cutaneous vasculitis associated with hypocomplementemia attributable to classic and alternative mechanisms of complement activation. Among 72 consecutive patients evaluated for chronic urticaria, 10 additional patients with idiopathic urticaria were found to have hypocomplementemia. Of these, two had evidence of classic and alternative mechanisms of complement activation, five had evidence of only classic pathway activation, and three evidence of predominately or exclusively alternative pathway activation. Circulating immune complexes were found in the majority of patients with classic pathway activation. Hypocomplementemia may provide clues to pathophysiologic mechanisms operative in some patients with chronic urticaria.

Adult↗
PubMed1975

Transtracheal aspiration studies in asthmatic patients in relapse with "infective" asthma and in subjects without respiratory disease.

Exacerbations of bronchial asthma that cannot be accounted for by allergic reactions have sometimes been called "infective" asthma. The validity of this designation was tested by study of transtracheal aspirates (TTA) obtained from 27 asthmatic patients in relapse who had findings suggestive of respiratory infection and 12 subjects without respiratory disease. Aspirates were cultured for aerobic and anaerobic bacteria, Mycobacteria, fungi, Mycoplasma, and viruses. A comparable variety of bacterial and fungal growth in small numbers was obtained from a majority of both groups. Microbial growth did not correlate with the presence of symptoms or signs compatible with infection. Aspirates from asthmatics with chronic bronchitis, immediate hypersensitivity to aeroallergens, or aspirin intolerance yielded no greater growth than did aspirates from asthmatics without these characteristics. In only one asthmatic was there suggestion that overt infection of the lower respiratory tract contributed to exacerbation of asthma. These results do not lend support to the empiric use of antibiotics in the management of unexplained asthmatic relapse.

Adolescent↗
PubMed1975

Provoking factors in bronchial asthma.

Asthmatic patients were identified as having asthma on the basis of lung function studies (76%), objective physical findings of asthma (11%), or a strong history of asthma (13%). Each of the 234 patients so identified was assigned to an asthma subgroup determined by careful clinical assessment of the major provoking factor or factors for his asthmatic episodes; minor provoking factors were also identified. Only 20% of the patients had asthmatic episodes provoked by a single factor. Most asthmatics had at least one major and one or more minor provoking factor(s). Reagin-mediated mechanisms constituted the major provoking factor in 25% of patients and were a minor provoking factor in an additional 20% of the patients. Thus, in only 45% of the patients, were reaginic mechanisms responsible for some part of their asthmatic episodes.

Adolescent↗