Bronchial hyperreactivity in rhinitis.
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Biomedical subjects
Publications and source records attributed to W J Stevens.
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IgG and IgE containing circulating immune complexes (CIC), total serum IgE and parasite related IgE were determined in monoinfected patients with Schistosoma mansoni or S.haematobium and in patients with a mixed infection. IgE- and IgG-CIC and total serum IgE were significantly higher in the mixed infection group. There is considerable cross-reactivity between the crude S.haematobium and S.mansoni antigen preparations. The level of IgE-CIC is correlated to the levels of total serum IgE and parasite related IgE respectively. Furthermore IgE-CIC levels were related to the intensity of infection. Twelve out of 21 patients suffering from a monoinfection were reinvestigated 1-4 months after specific chemotherapy. Parasitological cure is followed by a significant decrease of total serum IgE and IgE-CIC, whereas parasite related IgE did not change significantly. The importance of the disappearance of IgE-CIC is discussed.
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A simple method for rapid determination of IgG containing circulating immune complexes by commercially available reagents was developed. In this method, serum is incubated with 2.5% polyethyleneglycol. After washing, the precipitate is incubated with radioactively labeled protein A, which binds to IgG in the immune complex. After a further washing, the radioactivity bound is measured. Artificially formed complexes of heat-aggregated human IgG are diluted and a reference curve is constructed. This method is compared to the solid phase C1q-binding method. Our method is slightly more sensitive than the C1q-binding method.
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A standardized bronchial histamine challenge was performed in 423 patients presenting with 1) asthma, 2) rhinitis, 3) asthma and rhinitis 4) rhinitis with cough or 5) chronic cough alone. Each group was further subdivided into allergic and non-allergic subjects. Twenty healthy subjects served as a control group. Mean histamine thresholds (dose causing 15% decrease in FEV1) of all patient groups differed significantly from controls. There were also significant differences between groups: bronchial responsiveness was higher in allergic than in non-allergic subjects and more marked in asthmatics than in patients with rhinitis or cough. In contrast no differences in bronchial responsiveness to housedust mite or grass pollen could be demonstrated between different groups of allergic patients with asthma and/or rhinitis. Moreover correlations between thresholds for histamine and for these allergens were not significant. This lack of correlation suggests that separate mechanisms are responsible for non-specific and specific bronchial hyperresponsiveness. The presence of asthma in an allergic individual is essentially determined by a high degree of non-specific bronchial hyperresponsiveness.
Postoperative infection and cancer metastasis suppose weakened immunological resistance. Immunoevaluation is difficult for technical reasons and for individual variability. Proposed tests are hematology, cytochemistry, immunoglobulin and complement assays, membrane and cytoplasmic fluorescence, rosettes, lymphocyte transformation tests, skin tests, tests for granulocyte and monocyte function. Material and methods should be well standardized. Frozen serum and lymphocytes are peremptory for cellular and humoral evaluation during the different phases of anesthesia.
In a family with partial or total adenine phosphoribosyl transferase (APRT) deficiency, T and B cell function was evaluated by counting rosette-forming cells, by investigating lymphocyte transformation to phytohaemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM), by assaying serum immunoglobulins and determining lymphocyte membrane immunoglobulins by immunofluorescence. Delayed cutaneous hypersensitivity was also assayed. The absence of gross immunological deficiency in the homozygotes, as well as in the heterozygotes, suggests that the APRT-mediated pathway of purine metabolism is relatively unimportant for lymphocyte function.
A case of human thallotoxicosis caused by the taking of a homoeopathic preparation is reported. This preparation was taken accidentally by a patient who rapidly developed symptoms of thallotoxicosis. Treatment with Prussian blue resulted in rapid and total recorvery.
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The lymphocyte stimulation responses to the mitogens phytohemagglutinin (PHA), concanavalin A (Con A) and pokeweed (PWM) were investigated in 30 hospitalized depressed women undergoing a dexamethasone suppression test (DST). Patients were classified according to DSM-III as having major depression with melancholia, without melancholia, and minor depression. The Hamilton Depression Rating Scale (HDRS) and the State-Trait Anxiety Inventory (STAI) were measured. Patients with major depression showed significantly decreased lymphocyte stimulation induced by PHA, Con A, and PWM as compared to those with minor depression. These differences could not be attributed to age, body weight, weight loss, total number of leukocytes, menopausal status, sleep disturbances, concomitant use of low-dosage benzodiazepines or length of drug-free period before testing. The group mean differences in lymphocyte stimulation counts were not affected by the severity of illness or the severity of state and trait anxiety. There were no significant differences in the lymphocyte responses to PHA, Con A, and PWM between DST non-suppressors and DST suppressors. No significant correlations were established between baseline and post dexamethasone cortisol values and the lymphocyte stimulation counts.
Congenital C1-inhibitor deficiency, or hereditary angioneurotic edema (HAE), is a rare autosomal dominant disease due to alterations in the C1 inhibitor gene that results in a deficiency of antigenic and/or functional C1-INH. Affected patients are heterozygous, and their deficiency is incomplete, many of them having up to 20% of the normal amount of the inhibitor. The disease is characterised by recurrent, circumscribed, non-pitting, and non-pruritic subepithelial swellings of sudden onset, which fade during the course of 48-72 hours, but can persist up to 1 week. Lesions can be solitary or multiple and primarily involve the extremities, larynx, face, and bowel wall. Bradykinin is believed to be the main, but certainly not the sole, mediator responsible for the bouts of edema in HAE. The diagnosis is suggested by family history, the lack of accompanying pruritus or urticaria, the presence of recurrent gastrointestinal attacks of colics, and episodes of laryngeal edema. Diminished C4 concentrations during symptomatic periods are highly suggestive for the diagnosis. Further laboratory diagnosis depends on demonstrating a deficiency of C1-INH antigen (type I) in most kindreds, but some kindreds have an antigenically intact but dysfunctional protein (type II) and require a functional assay to establish the diagnosis. Prophylactic administration of either attenuated androgens or protease inhibitors has proved useful in reducing frequency or severity of attacks. Infusions of a vapour-heated C1-INH concentrate are safe and effective means of both preventing and treating attacks. Nevertheless, this treatment is expensive and this extract is not readily available. It is emphasised that administration of angiotensin converting enzyme inhibitors is contraindicated in patients suffering from protease inhibitor deficiency states.
The stingray is one of the most dangerous fishes for man. The sting is poisonous and causes a painful wound. Fatalities are reported. Most injuries due to stingrays occur in coast regions of the tropics and subtropics. Therefore, physicians in countries with a moderate climate are less informed about the management about these kinds of injuries. The characteristics, treatment and prevention are discussed in connection with a case that occurred in Belgium in a devotee of aquarium fishes.
We have studied the effect of pancreastatin and its C-terminal fragment (33-49) on mitogen-stimulated T lymphocyte proliferation. In a concentration range from 10(-12) to 10(-8) M they exhibit a dose-dependent stimulatory effect on concanavalin A-induced response with the maximal effect at 10(-8) M concentration. They were inactive in response to a B-cell mitogen, lipopolysaccharide, which points to an involvement of T but not B lymphocytes in their response. Pancreastatin can still produce a stimulatory effect when added 18 h after incubation of cultures with concanavalin A and apparently uses a diacylglycerol independent mechanism. When cells were preincubated for 4, 16 or 24 h with pancreastatin or its fragment and then stimulated with concanavalin A, a ten times lower concentration of peptides was needed (10(-9) M) to obtain the maximal response. This suggests that resting cells are more sensitive to pancreastatin and its fragment. Both peptides exhibit a very similar pharmacological profile, indicating that the C-terminal part of the molecule is responsible for the effect on T-cell proliferation.
Adverse reactions to food, i.e. food allergy and intolerance have gained considerable attention. This overview focuses on the diagnosis and management of IgE-mediated food allergy that is believed to be responsible for most immediate-type food-induced hypersensitivity reactions. Clinically, these reactions are characterised by a variety of signs and symptoms that occur within minutes or hours after consumption of the offending food. Reactions may be limited or more generalised with involvement of the skin, nose, eyes, and/or lungs. In more severe cases, cardiovascular symptoms including hypotension, shock, cardiac dysrhythmias and death can occur. In food-allergic individuals, IgE is produced against naturally occurring food components, primarily glycoproteins that usually retain their allergenicity after heating and/or proteolysis. While adults tend to be allergic to fish, crustaceans, peanuts and tree nuts, children tend to be allergic to cow's milk, egg white, wheat and soy more frequently. "Emerging" food allergens include tropical fruits, sesame seeds, psyllium, spices and condiments. These allergies frequently represent a cross-allergy to an allergen derived from another source, e.g. pollens or natural rubber latex. The evaluation of IgE-mediated food allergy relies on a careful history, physical examination, appropriate skin testing or in vitro testing with food extracts, and/or double blind, placebo-controlled food challenges. Avoidance remains the mainstay of therapy. However, allergens may be "hidden" and labelling can be non-precise or misleading, thereby severely hampering prevention. Patients with severe allergies should keep at hand an emergency kit with adrenaline, an antihistamine and an injectable rapid onset-of-action corticosteroid. At present there is no evidence to support the use of immunotherapy, except for research purposes. Production of "hypoallergenic" food is hampered by incomplete methods for assessing the allergenic potential of such novel foods.
In the past 2 decades, IgE-mediated NRL allergy has become a well-defined condition with recognised risk groups, established diagnostic tools, and adequate prevention strategies (1-3). Furthermore, molecular biology and biochemical techniques have significantly improved our knowledge of the proteins responsible to cause the disease. Clinical manifestations will not be addressed in this review, nor will broad preventive strategies be proposed; these have been discussed elsewhere (4, 5). After a brief introduction this review will focus on specific issues: (1) How do we estimate the prevalence of NRL allergy and who is at risk for clinical sensitisation? (2) What specific allergens cause NRL allergy? How does sensitisation for these allergens occur? Are all patients sensitised for the same allergens? Threshold allergen exposure levels. (4) What is the latex-fruit syndrome? What is the clinical relevance of a positive plant food specific IgE quantification in patients with NRL allergy? (5) How do we diagnose NRL allergy? What are the strengths and weaknesses of currently available diagnostic tools? (7) How do we manage NRL allergy? What is the role of medication and immunotherapy in the treatment of NRL allergy? How do we select an appropriate non-NRL alternative for NRL gloves? Which regulatory provisions have been implemented?
OBJECTIVE: The aim of this study was to evaluate the relative frequencies of sensitisation to four common inhalant allergens in two atopic populations suffering from asthma and/or rhinitis. One had been studied in the period of 1975 till 1979, and a second population was evaluated between 1992 and 1995. DATA SOURCES: At both time periods patients with inhalant allergy and visiting our outpatient clinic were included. Quantification of IgE to Dermatophagoides pteronyssinus, birch, timothy grass, and mugwort was performed via the Phadebas RAST technique (Pharmacia, Brussels, Belgium). RESULTS: In patients suffering from respiratory allergy the frequency of birch pollen sensitisation significantly increased from 13% in the period 1975-1979 to 34% in the period 1992-1995. In contrast, the frequency of house dust mite, timothy grass pollen, and mugwort pollen sensitisation remained almost unchanged. The increase was not associated with an increase in the birch pollen count. CONCLUSION: Birch pollen hypersensitivity has almost tripled among atopic subjects during the last 2 decades. The exact mechanisms for this increase remain to be evaluated.