Anaphylactoid reaction to ethanol.
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Biomedical subjects
Publications and source records attributed to S Ting.
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Resistance to murine listeriosis requires humoral factors which alter production or delivery of monocytes to infective foci. Production of such factors is under genetic control and may be modulated by bacterial components. Two components from Listeria monocytogenes, monocytosis producing activity (MPA) and immunosuppressive activity (ISA) were used to study monocytopoiesis in mice with known abnormalities in microphage-related functions. Listeria-sensitive A/J mice fail to produce or respond to MPA or an endogenous mediator of monocytosis (EF). These studies provided evidence that a second humoral factor, decreases monocytopoiesis. Sera from A/J mice are more active in this respect and MPA treatment increases the amount of inhibitory factor in A/J mice. A polyclonal B cell activator, ISA, which induces suppressor splenic macrophages, suppresses the anti-SRBC response in resistant B10. A mice but not in A/J mice. ISA induced no change in prostaglandin E2 production by spleen cells of either strain. One interpretation of these findings is that A/J mice after stimulation by ISA or MPA, produce a substance which inhibits development of mononuclear phagocytes.
Forty-one subjects with dermographia were studied for a 4-week period. Twenty subjects received ketotifen therapy, the other 21 received chlorpheniramine (H1) for 2 weeks, and then chlorpheniramine plus cimetidine (H1 + H2). Both groups had significant suppression of dermographia and skin wheals caused by dextromethorphan and histamine after 2 weeks. The inhibition by ketotifen of dermographia, histamine wheal, and the dextromethorphan wheal increased from week 2 to week 4. During the first 2 weeks, ketotifen's activity was comparable to chlorpheniramine. Ketotifen's activity increased during the second 2 study weeks to match the additional chlorpheniramine. These results suggest that ketotifen may have additional pharmacologic activities besides H1 antagonism, including possible inhibition of mast cell mediator release. As a consequence, cutaneous vascular hyperresponsiveness may decrease. Ketotifen appears promising as treatment for allergic skin disorders.
Urticaria, after ingesting ethanol, is rare. A 36-year-old Caucasian male developed multiple, generalized, pruritic urticarial lesions 5 to 15 minutes after drinking alcoholic beverages of any type. A blinded challenge with 5 mL of chemically pure 95% ethanol in concentrated grape juice caused urticaria and an elevation of plasma histamine. Pure grape juice alone was unreactive. Prick skin tests with Brewers' yeast, ethanol, acetaldehyde, and acetic acid were negative. Hydroxyzine (25 mg, p.o., q.i.d.), given for three days prior to challenge, inhibited skin response and histamine release. Biopsy of the urticarial lesions caused by ethanol ingestion showed mast cell degranulation. In this subject, ethanol appeared to directly affect mast cell mediator release by non-IgE mechanisms.
The enzymatic isotopic analysis of histamine requires extraction and concentration of [3H]-1-methylhistamine from the reaction mixture. The assay was modified to include enzymatic reaction at 0 degrees C to reduce blank values and direct application of protein-free reaction mixture to a thin-layer chromatography plate for isolating of the product. The analysis was quantitative down to 100 pg/ml of histamine, adequate for monitoring plasma histamine content.
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Ten adult asthmatic subjects were tested for response to inhaled atropine sulfate before and after 3 weeks of inhaled atropine therapy. Four of the ten initial responders no longer responded after the 3 weeks. The mean FEV1 increase was 0.49 L before treatment and 0.30 L after treatment (P = .025). Subsensitivity to the effects of atropine develops, but may be limited to a subset of patients.
By use of a modified heat-suction, skin blister technique, we found that oral hydroxyzine, 25 mg four times a day, inhibits antigen-induced ultrastructural changes of mast cells and in vivo histamine release in the skin of ragweed-sensitive individuals. To our knowledge this is the first demonstration that an orally active antihistamine can inhibit in vivo cutaneous anaphylactic reactions.
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An adolescent, contemplating a military career, was found to have orthostatic proteinuria. A thorough evaluation failed to reveal any renal abnormalities. He was tested on a milk-free diet at the request of the parents. The proteinuria cleared, but recurred on an initial open challenge; it did not recur subsequently on a blinded challenge. This experience suggests that patients with orthostatic proteinuria should be evaluated with an elimination diet trial.
In order to evaluate the effect of Verapamil on human cutaneous anaphylactic responses, ragweed-sensitive individuals were skin tested with ragweed, ragweed plus Verapamil, and Verapamil alone. In addition, using a skin chamber technique, the effect of Verapamil on antigen-induced histamine release in vivo was investigated. The results suggest that Verapamil, applied locally in non-irritant doses, does not affect Type I hypersensitivity skin reactions.
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Beta-adrenergic agonists in metered dose inhalers (MDIs) are used extensively in the treatment of asthma. Previously we reported that 23 of 1450 (1.6%) of our asthmatic patients experienced immediate bronchoconstriction after using MDI-albuterol. In this study we investigated immediate bronchoconstriction after use of MDI-metaproterenol and after placebo-inhaler with "inert ingredients" only. Results suggest that those patients who complained of chest tightness or lack of relief following the use of MDI beta-adrenergic agonists are having true bronchoconstriction. The bronchoconstrictive response is most likely caused by the propellants or the other inert ingredients contained in these MDIs.
Foods as a cause for migraine attacks were evaluated in 43 adults with recurrent migraine. Skin testing, elimination diets, double-blind challenges, and measurements of plasma histamine were performed. Thirteen subjects experienced 66% or greater reduction in headache frequency during a diet trial. Six subjects became headache free. Eleven of 16 skin test-positive patients responded to diet manipulation, while only two of 27 skin test-negatives did (P less than .005). Seven subjects agreed to double-blind challenges. In five of seven, at least one food provoked migraine. Placebo challenges did not provoke migraine. In three subjects, plasma histamine rose during migraine provoking challenges. The relationship between food ingestion and migraine is based in part on allergic mechanism. Tests for IgE-specific food allergy appear helpful in selecting patients likely to benefit from diet therapy.
Five hundred allergy clinic patients were prick skin tested with papain, 1 mg/mL, in addition to usual local aeroallergens. Five of 475 subjects with seasonal allergic disease had positive skin tests to both papain and local pollens. None of the 25 individuals with negative skin test to pollens had skin reactivity to papain. The five subjects with positive skin tests to papain underwent double-blind placebo-papain challenges. All papain challenges were positive. Placebo challenges were negative. Papain-induced symptoms included palatal itching, watering itchy eyes, sneezing, rhinorrhea, abdominal cramps, diarrhea, and diaphoresis. Circulating papain-specific IgE was detected in all the papain-sensitive individuals, but not in control subjects. Confirmed papain sensitivity occurred in 1.05% of allergic subjects. In the papain-sensitive patients, cross-reacting antibodies with chymopapain were found. The small number of non-allergic subjects did not show any papain or chymopapain sensitivity in vitro.
Cromolyn has been shown to inhibit histamine release from mast cells induced by various stimuli in vitro. However, the local effects of cromolyn on codeine-induced wheal and flare skin reactions are not well understood. Intradermal injection of codeine induced prominent whealing in almost all humans. We studied the effect of local cromolyn injection on codeine-induced skin reactions, histamine release, and ultramicroscopic changes in mast cells in 10 volunteers. The finding in this study showed that injection of a 2% cromolyn solution before or together with the codeine injection does not affect the subsequent skin reactions, histamine release and ultramicroscopic changes of mast cells.