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Biomedical subjects

R Patterson

Publications and source records attributed to R Patterson.

At least 19 recordsLinked to original sources

Pulmonary haemorrhage and haemolytic anaemia due to trimellitic anhydride.

Two young men who had been exposed at work to epoxy resin powder containing trimellitic anhydride (TMA) presented with haemolytic anaemia and repeated haemoptyses. They did not return to work at the factory and the symptoms and the anaemia resolved spontaneously. Seven similar cases have lately been presented at meetings, so it seems that TMA, already known to cause respiratory syndromes such as asthma, can also lead to several extrapulmonary toxic effects, including haemoptyses and haemolytic anaemia. Studies on these patients' sera with TMA haptenised protein and cells pointed to an immunological mechanism.

Adolescent

Cytotoxicity of ionophore A23187 for basophils and other human blood cells.

The calcium ionophore A23187(A23) at concentrations exceeding 1 microgram/ml has been shown to be progressively cytotoxic for human blood basophils, neutrophils, lymphocytes, and erythrocytes. Toxicity to basophils was considered to be manifested by the increasing inability of 2-deoxyglucose (2DG) to inhibit histamine release (HR) at increasing concentrations of A23. The toxicity to neutrophils and lymphocytes was demonstrated by decreased lactate production (LP) after incubation with A23 of Ficoll-Hypaque fractions greatly enriched in each respective cell type. Red cells present in dextran-sedimented leukocytes were increasingly susceptible to lysis during washing subsequent to exposure to increasing concentrations of A23. A concentration of 4 microgram A23/ml, which is cytotoxic at 37 degrees C, produced optimal and noncytotoxic HR at 22 degrees C. It was possible to reduce A23 concentrations required for optimal HR by increasing Ca++ from 0.6 to 3 mM.

Anti-Bacterial Agents

The effect of histamine-1 and histamine-2 antagonists on airway responses to histamine in the rhesus monkey.

This study used rhesus monkeys with consistent respiratory responses to aerosolized histamine. Two systems of histamine challenge were evolved to study the effects of histamine antagonists on the histamine-induced respiratory response. One system consisted of administering increasing subreactive concentrations of histamine until an airway response (H) occurred. This threshold histamine dose was repeated (H'). The pulmonary function changes occurring with the H' challenge were less intense than those with H. M, a histamine-2 receptor antagonist, when given before the H' dose was associated with a potentiated H' response compared with the threshold H response. This provides evidence for histamine-2 receptor sites in rhesus monkey airways. A second system used duplicate histamine challenges with a known reactive dose of histamine. In this system, the pulmonary function changes occurring with the repeated challenge (H') were greater than with the first reactive challenge dose (H). This H' response was inhibited partially with diphenhydramine, a histamine-1 receptor antagonist. These two systems of histamine challenge provide an experimental model for evaluating pharmacologic alteration of histamine-induced respiratory responses. There is evidence for the existence of histamine-1 and histamine-2 receptor sites in the airways of the rhesus monkey.

Animals

The immune response of patients with ragweed hay fever treated with polymerized ragweed antigens.

This report describes the immune response of patients with ragweed hay fever treated with polymerized ragweed antigens (PRW). Their IgG antibody responses to crude ragweed extract, antigen E, antigen K, and antigen Ra3 were determined by a solid-phase radioimmunoassay. The results indicate that PRW contains an array of clinically important antigens that are available for immunologic processing and result in an immune response in patients treated with this new form of immunotherapy for ragweed hay fever.

Analysis of Variance

Reduced allergenicity of high molecular weight ragweed polymers.

Polymerized ragweed antigens of different molecular weight ranges were studied to determine if the degree of allergenicity was dependent on molecular size of the polymers. In this study, allergenicity is defined as the ability to elict IgE-mediated skin reactivity. Ragweed antigen treated with glutaraldehyde was fractionated into one preparation with a molecular weight range of 200,000 to 20,000,000 and another with molecular weights less than 200,000. Except for the difference in molecular sizes of the two molecular sizes of the two preparations, all ragweed polymers had been treated in an identical fashion. The low molecular weight fraction had cutaneous endpoint reactivity greater than 10(5) to 10(8) times that of the high molecular weight materials. In these and other studies, immunogenicity defined as the ability to induce an IgG antibody response was retained by the high molecular weight material. The results are consitent with the hypothesis that allergenicity decreases as the molecular weight of the polymerized allergen increases.

Allergens

Allergic bronchopulmonary aspergillosis in pediatric practice.

Twelve cases of allergic bronchopulmonary aspergillosis in the pediatric age group are reported. The average age of diagnosis was 14.5 years with a range from 6 to 18 years. All patients had a history of pulmonary infiltrations or atelectasis or both documented by chest radiographs. Eight patients had bronchograms or tomograms, and seven of them showed proximal bronchiectasis. Total serum IgE concentrations were elevated in all patients. Preciptitating antibodies against Aspergillus fumigatus were positive in all patients at the time of diagnosis, and became negative in some after therapy. The specific IgE or IgG antibody activity agaist Af was elevated in all 12 patients. After prednisone was started the total serum IgE sharply declined to a plateau and remained at this level until a flare of allergic aspergillosis occurred. A flare of allergic aspergillosis is characterized by an increasing total serum IgE concentration followed by pulmonary infiltration. Clinical and roentgenologic improvements were observed after steroid therapy. The importance and methods of early diagnosis in the pediatric population are discussed.

Adolescent

The evaluation of selected parameters of immune function in asthmatics after long-term corticosteroid therapy.

The availability of inhaled beclomethasone diproprionate permitted the discontinuation of continuous, long-term systemic corticosteroid therapy (SCT) in a group of asthmatics who had previously required SCT to control their asthma. Twelve patients had been on SCT for a period of 2-22 years with an average duration of 7 years. To determine whether this previous long-term SCT and the current use of inhaled beclomethasone diproprionate had an effect on leucocyte functions, a variety of studies reflecting T lymphocyte, B lymphocyte and granulocyte function was done. The results were compared with those of twelve asthmatic patients of similar age ranges who had never received steroids. Results showed that the two patient populations could not be differentiated on the basis of phytohaemagglutinin stimulation of lymphocytes, sheep erythrocyte rosette formation, IgG, IgA, IgM and IgE concentrations or granulocyte bactericidal activity. Delayed skin reactivity was present in both groups, with more positive reactions in the non-SCT group. Polymorphonuclear adherence values were slightly lower in the SCT female population using beclomethasone diproprionate. The latter two minor differences may be due to the previous SCT, the use of beclomethasone diproprionate or the limited population of patients studied. We conclude from these studies that the long-term use of SCT at the low doses required for control of asthma resulted in little permanent effect on the variety of lymphocyte and granulocyte functions tested.

Adrenal Cortex Hormones

The management of allergic bronchopulmonary aspergillosis.

Twenty-five patients with allergic bronchopulmonary aspergillosis (ABPA) were observed for periods of 12 months to 10 years (average duration, 2.6 years) after initial therapy with prednisone, which was then tapered and discontinued unless maintained at minimal doses as required for control of asthma. Thirteen patients have had no recurrence, 4 patients did not comply with the initial regimen and could not be considered to be controlled, and 8 patients had 12 recurrent episodes of ABPA characterized by pulmonary infiltrates with no explanation other than ABPA. The exacerbations were closely correlated with sharp increases in total serum IgE, which subsequently decreased after resumption of prednisone therapy. The increase of IgE preceded the pulmonary infiltrates in 7 or 12 exacerbations. The exacerbations, characterized by increased serum IgE and pulmonary infiltrates, may be associated with minimal symptoms. Acute asthma without pulmonary infiltrates was not associated with increased IgE. Four exacerbations occurred during administration of beclomethasone diproprionate used for control of asthma, and therefore, this agent does not appear to prevent or reverse exacerbations of ABPA. Twelve exacerbations occurred in 8 persons, with 2 patients having 4 and 2 recurrences, respectively. This suggests that exacerbations are more likely to occur in certain patients. Serial measurements of total serum IgE appears to be a useful index of disease activity in ABPA. In the 4 patients who did not comply with the prednisone therapy regimen or regular physician visits, patterns of IgE changes, clinical evaluations, and chest roentgenograms were not of use in evaluation of the clinical state or progress of the patient. A treatment regimen is suggested for initial therapy and recurrences of ABPA on the basis of these observations.

Aspergillosis, Allergic Bronchopulmonary

IgA and IgG antibody activities of serum and bronchoalveolar fluid from symptomatic and asymptomatic pigeon breeders.

Serum IgA and IgG antibody activities against pigeon serum were measured in 16 symptomatic pigeon breeders, 20 asymptomatic pigeon breeders, and 3 normal subjects by radioimmunoassay. The IgA and IgG antibody activities against pigeon antigen of the group of patients with disease was significantly greater than those of patients in the asymptomatic and the control group. The overlap of results for the symptomatic and asymptomatic breeders limits the diagnostic value of these individual IgA or IgG antibody determinations. Bronchoalveolar fluid and serum samples from a smaller group of pigeon breeders who underwent lung lavage were available for studies of antibody activity against pigeon serum. Ten asymptomatic and 6 symptomatic breeders were available for study. Both IgG and IgA antibody activities were detected by radioimmunoassay in serum samples and bronchoalveolar fluid. The IgA antibody activity determined by the radioimmunoassay was higher in the respiratory secretions.

Alveolitis, Extrinsic Allergic

Ionophore and arachidonic acid stimulation of airway responses in rhesus monkeys.

Aerosolized doses of the ionophore, A23187, and arachidonic acid individually resulted in no airway response in rhesus monkeys. When these two agents were given simultaneously, by aerosol, an airway response occurred. The pulmonary function abnormalities that occurred qualitatively simulated those of an antigen-induced airway response. This is the first demonstration in our laboratory of two agents which singly will not produce a response but which are reactive when delivered in combination. Other fatty acids did not produce a similar response. The response to A23187 and arachidonic acid occurred only in rhesus monkeys from our colony which had been demonstrated to have airway responses to aerosolized antigen challenge, a response shown previously to be associated with hyperreactive airways to pharmacologic stimuli. The A23187 and arachidonic acid response was inhibited by aerosolized 5,8,11,14-eicosatetraynoic acid, an inhibitor of the cyclooxygenase and lipoxygenase pathways of arachidonic acid metabolism. Further, indomethacin, a prostaglandin synthetase inhibitor of the cyclooxygenase pathway, inhibited the response, although previous studies showed that this drug will potentiate an antigen-induced response in this animal model of asthma. The slow-reacting substance of anaphylaxis antagonist, FPL 55712, did not inhibit the A23187-arachidonic acid response under the conditions of these experiments. The mechanism of the A23187-arachidonic acid airway response in rhesus monkeys may or may not be the same as the antigen-induced response.

5,8,11,14-Eicosatetraynoic Acid

A familial occurrence of allergic bronchopulmonary aspergillosis.

A family was recently studied in which two brothers with identical HLA serotypes had allergic bronchopulmonary aspergillosis. One of the two had a normal bronchogram. A field investigation of the family residence showed that a barn was the probable source of the organism causing disease in these patients. Immunologic characterization of the family members showed a broad spectrum of response to the environmental exposure.

Adolescent