Glycemia and Immune Responses

The intensity of experimental and clinical immune responses was correlated with the degree of glycemia of the reacting subject. Hyperglycemias resulting from overdosage with sugars, cortisol, adrenaline, or from diabetes inhibit the anaphylactoid reactions; anaphylaxis, and the tuberculin reaction; but potentiate infections. Hypoglycemias resulting from fasting, insulin and adrenalectomy potentiate the anaphylactoid reactions, anaphylaxis, and the tuberculin reaction; but inhibit infections. The hypothesis is proposed that hyperglycemia inhibits certain antigen-antibody combinations; this results in an inhibition of hypersensitivity, but an aggravation of infection.     

Adverse reactions to acetylcysteine and effects of overdose.

Since the introduction in 1979 of intravenous acetylcysteine (Parvolex) as an antidote for overdosage of paracetamol the National Poisons Information Service and the manufacturer have been notified of 38 adverse reactions that were anaphylactoid in nature and 19 accidental overdoses. The most common feature of the anaphylactoid reaction to normal dosage was rash; other features reported included angioedema, hypotension, and bronchospasm; all the patients recovered. The features associated with an overdose of acetylcysteine were similar but more severe; two patients died, but the extent to which the overdose of acetylcysteine may have been implicated was not clear in either case.     

ALLERGIC REACTIONS TO “KISSING BUG” BITES

In addition to local allergic skin reactions to the bite of the kissing bug, Triatoma protracta, the systemic reactions can vary from a mild urticarial reaction to a severe anaphylactoid reaction consisting of shock, generalized angioneurotic edema and laryngeal edema. The diagnosis can be established by the clinical history, the finding of an engorged kissing bug, the presence of typical local and systemic signs, and finally, a positive reaction to a skin test with an extract of the bug.     

Adverse reactions to drugs in general practice.

Of 817 patients in a general-practice survey of adverse reactions to drugs, 41% were thought to have "certainly" or "probably" had a reaction to the drug prescribed. Adverse effects on the gastrointestinal and central nervous systems were the most frequently reported, and 90% of reactions had occurred by the fourth day of treatment. More patients given drugs acting on the central nervous system and antihistamines reported reactions than those in other categories. A higher incidence of adverse drug effects is shown in this general-practice survey than in other, mainly hospital-based, surveys. Further intensive surveillance for adverse effects of drugs is recommended to provide additional information on the burden of drug-induced disease in the community.     

Dextran anaphylactoid reaction in Sprague-Dawley CFY rats.

From a closed colony of randomly-bred Sprague-Dawley CFY rats about 23% failed to respond to intravenous dextran with the characteristic generalized anaphylactoid reaction, but still exhibited an inflammatory response when dextran was given into the foot pad. Brother-sister mating of rats showing the most expressed generalized reaction (reactor rats) yielded good responder offsprings, while the non-reactors had descendants completely unresponsive to systemic dextran. Brother-sister mating of selected non-reactor rats led to a gradual decrease in dextran paw oedema in the subsequent generations, and after the third mating, a complete local non-reactivity developed. In these rats the intradermal injection of dextran failed to increase vascular permeability, while the inflammatory response evoked by histamine, 5-HT, bradykinin, and compound 48/80 remained unchanged as compared to that of the reactor animals. These result show that the anaphylactoid reaction in Sprague-Dawley CFY rats is under genetic control.     

Underlying immunopathology as a cause of adverse responses to two intravenous anaesthetic agents.

A patient who had shown some evidence of immunological sensitivity underwent several operations under general anaesthesia for otitis media without ill effect. On his second exposure to Althesin, however, he suffered a severe reaction. Facial angioneurotic oedema was accompanied by peripheral vasodilatation and sweating, and C3 conversion was observed in his plasma. Subsequent anaesthetics produced no reactions until four years later, when thiopentone and suxamethonium were given. This reaction was much milder, but C3 conversion again occurred. Although the clinical signs indicated an anaphylactoid reaction, the laboratory findings suggested that this patient had an underlying immunopathological condition involving complement activation, which could be triggered by any intravenous agent that activated complement. The judgment that a reaction to a particular drug is anaphylactic cannot be made on the basis of clinical signs alone. Simple laboratory analysis will show whether the reaction is due to an underlying immunopathological condition that may be triggered by any of several drugs.     

Neuropeptides as central integrators of autonomic nerve activity: effects of TRH, SRIF, VIP and bombesin on gastric and adrenal nerves

The nerve activity of the gastric ramus of the splanchnic (sympathetic) nerve, gastric ramus of the vagus, adrenal ramus of the splanchnic nerve and the superior laryngeal nerve (laryngeal ramus of vagus) were assessed before and after i.c.v. injection of neuropeptides in the rat. TRH stimulated the vagal branch but attenuated the sympathetic outflow to the stomach. In contrast, the sympathetic outflow to the adrenal was enhanced by TRH. SRIF suppressed the activity of all the nerves studied. VIP did not affect the sympathetic outflow to the stomach while suppressing the gastric branch of the vagus. The adrenal sympathetic branch as well as the superior laryngeal nerve was stimulated by VIP. Bombesin suppressed both vagal and sympathetic outflow to the stomach but markedly stimulated the laryngeal branch of the vagus. The adrenal sympathetic nerve was either stimulated or attenuated slightly by bombesin. These results indicate that centrally administered neuropeptides produce reactions specific for each nerve.     

药物类过敏反应生物标志物探究

药物类过敏反应为非免疫球蛋白E(IgE)介导的急性过敏反应,与Ⅰ型超敏反应临床症状相似,首次接触药物即可发生,在临床药物过敏反应中占有相当大的比例.药物类过敏反应生物标志物可特异性反映药物类过敏反应的发生发展,监测其生物标志物可实现对该不良反应进行可靠的非临床评价和临床诊断,从而降低该不良反应的发生率.本文介绍了药物类过敏反应特点,重点阐述了组胺等几种药物类过敏反应生物标志物的研究现状,希望为药物类过敏反应的非临床评价以及临床诊断提供参考.     

The protective effect of prolil-glycil-proline peptide (PGP) under compound 48/80-induced anaphylactoid reaction in mice

The influence of PGP on compound 48/80-induced anaphylactoid reaction development in mice and on histamine secretion from rat peritoneal mast cells (RPMS) under their activation by compound 48/80 were investigated. Anaphylactoid reaction was caused by intraperitoneal injection of compound 48/80 into mice. The number of animals with manifestations of anaphylactoid reaction symptoms, the severity of these symptoms, the amount of died animals and the time of death were registering during an hour. Mast cells for in vitro investigations were obtained from rats’ peritoneal cavity. Secreted histamine was evaluated from formation of fluorescent product of it’s condensation with ortho-phthalaldehyde. The preventive injection of PGP in mice (15 min before compound 48/80) decreased the mortality rate of animals and intensity of anaphylactoid reaction symptoms. But PGP had no effect on histamine secretion from mast cells under their activation by compound 48/80 in vitro. Results show that there is a component in the mechanism of PGP protective effect under anaphylactoid reaction which is not connected with mast cells stabilization.     

Antioxidant activity levels and oxidative stress as blood markers of allergic response to drugs.

Antioxidant enzymes work together in human blood cells against toxic reactive oxygen species. Although their relationship with several pathophysiologic processes has been stated, not much is known about the connection between antioxidant defence and allergy. This study was designed to determine the enzymatic activities and the oxidative indices in the blood and serum proteins in patients suffering from allergy to drugs. We hypothesize that serum and blood reactions may serve as useful clinical marker for the allergic state. We used enzymatic antioxidant activities, thiobarbituric acid reactive substances, and carbonyl contents of proteins as suitable markers. We determined superoxide dismutases, glutathione peroxidase and catalase activities in each cell type. After antihistaminics plus steroids were given as part of a protocol treatment, enzymatic antioxidant activities, thiobarbituric acid reactive substance levels, and carbonyl contents were used as recovering markers for the disease. We found a relationship between antioxidant enzymatic activities, thiobarbituric acid reactive substance levels, and carbonyl contents for allergic reactions belonging to several type I and type IV allergies, as well as cross-reactive intolerance to nonsteroidal anti-inflammatory drugs and an anaphylactoid reaction to a radiocontrast media. A similar pattern also exists for analogous allergic manifestations and disease-like status.     

Anaphylactic reactions to cinoxacin.

During 1981 to mid-1988 three cases of anaphylactic shock after treatment with the quinolone derivative cinoxacin were reviewed by the Netherlands Centre for Monitoring of Adverse Reactions to Drugs and 17 cases of an anaphylactic type of reaction notified to the World Health Organisation Collaborating Centre for International Drug Monitoring. In five out of six patients for whom data were available the reaction began shortly after taking a single capsule of a second or next course of treatment. Cinoxacin is related to nalidixic acid, and one patient previously treated with that agent subsequently had an anaphylactoid reaction to cinoxacin and later developed a skin reaction to nalidixic acid. There were no deaths, and patients treated as an emergency with plasma expanders or with adrenaline and corticosteroids generally recovered promptly and uneventfully. In view of the potentially fatal consequences of anaphylactic reactions to cinoxacin and other quinolones doctors should take care when prescribing these drugs.     

Anaphylactoid reactions and angioedema during alteplase treatment of acute ischemic stroke

Among 105 patients given recombinant tissue plasminogen activator (rt-PA, alteplase) intravenously for acute stroke, 2 (1.9%) had lingual angioedema, which progressed to a fatal anaphylactoid reaction in 1. The authors review the 2 cases and possible mechanisms responsible. They warn that patients who are taking an angiotensin-converting-enzyme inhibitor may be at increased risk for angioedema with concomitant alteplase therapy.     

Changes in Risk of Immediate Adverse Reactions to Iodinated Contrast Media by Repeated Administrations in Patients with Hepatocellular Carcinoma

Background

To elucidate whether repeated exposures to iodinated contrast media increase the risk of adverse reaction.

Materials and Methods

We retrospectively reviewed 1,861 patients with hepatocellular carcinoma who visited authors’ institution, a tertiary referral center, between 2004 and 2008. We analyzed cumulative probability of adverse reactions and risk factors. We categorized all symptoms into hypersensitivity reactions, physiologic reactions, and other reactions, according to the American College of Radiology guidelines, and evaluated each category as an event. We estimated the association between hazard for adverse reactions and the number of cumulative exposures to contrast media. We also evaluated subsequent contrast media injections and adverse reactions.

Results

There were 23,684 contrast media injections in 1,729 patients. One hundred and thirty-two patients were excluded because they were given no contrast media during the study period. Adverse reactions occurred in 196 (0.83%) patients. The cumulative incidence at 10^th, 20^th, and 30^th examination was 7.9%, 15.2%, and 24.1%, respectively. Presence of renal impairment was found to be one of risk factors for adverse reactions. The estimated hazard of overall adverse reaction gradually decreased until around 10^th exposure and rose with subsequent exposures. The estimated hazard of hypersensitivity showed V-shaped change with cumulative number of exposures. The estimated hazard of physiologic reaction had a tendency toward decreasing and that of other reaction had a tendency toward increasing. Second adverse reaction was more severe than the initial in only one among 130 patients receiving subsequent injections.

Conclusion

Repeated exposures to iodinated contrast media increase the risk of adverse reaction.     

Alternate method of calculating the free-energy change accompanying the growth of saccharomyces cerevisiae (Hansen) on three substrates.

A method is described for determining the free energy of formation of the cells of Saccharomyces cerevisiae (Hansen) that are formed as the result of anaerobic growth on glucose, and aerobic growth on glucose and ethanol. The method is based on the direct relationship that exists between the enthalpy changes and the free-energy changes that accompany the oxidation of 1 g cellular material formed during these growth reactions and the degree of reduction of the same material. When the results of these calculations are used together with the free energies of formation of the reactants and of other products of a given growth reaction, it becomes possible to calculate the free-energy change accompanying this reaction. These free-energy changes are in excellent agreement with those calculated by another method based on the hypothesis that the free-energy change accompanying the conversion of the substrate plus other reactants into cellular material plus other products is equal to zero.     

Reactions to Total Dose Infusion of Iron Dextran in Rheumatoid Arthritis

Ten patients with active rheumatoid arthritis were given a total dose infusion of iron dextran for anaemia. One had an immediate anaphylactoid reaction; the other nine had a brief exacerbation of arthralgia and joint dysfunction of up to seven days'' duration. The erythrocyte sedimentation rate rose by an average of 23 mm. in one hour (Westergren), but this often took longer than seven days to settle to the preinfusion level.It is suggested that this response is probably not due to an exacerbation of rheumatoid arthritis but to a delayed hypersensitivity reaction to the dextran portion of the iron dextran complex. This treatment is potentially dangerous in rheumatoid arthritis; we recommend a preliminary test dose and that the infusion be started very slowly under supervision.     

Plasma prostaglandin E2 level in Kawasaki disease

Plasma levels of prostaglandin E2 and prostaglandin F2 alpha were determined in 15 patients in the acute and recovery stages of Kawasaki disease, 10 patients with anaphylactoid purpura, 16 with bacterial and viral infections and 10 healthy children. Plasma levels of prostaglandin E2 were markedly increased in the acute stage of Kawasaki disease, and these levels were decreased in the recovery stage. The prostaglandin F2 alpha/prostaglandin E2 ratio in the acute stage of Kawasaki disease was markedly decreased. Plasma levels of prostaglandin E2 in patients with anaphylactoid purpura, bacterial and viral infections were within the normal range. In Kawasaki disease which is associated with systemic vasculitis with a severe inflammatory reaction, prostaglandin E2 is considered to be more selectively produced and released than prostaglandin F2 alpha, suggesting that prostaglandin E2 plays an important role in the immunological and inflammatory reaction.     

Attempted Passive Immunization of Young Calves Against Eimeria bovis

SYNOPSIS. Two experiments attempted to produce passive immunity against Eimeria bovis coccidiosis in Holstein-Friesian calves. Immune serum concentrated by a freezing technique, or serum globulin obtained by a precipitating technique from immune calves, was injected intravenously or intraperitoneally into young calves. Four calves received concentrated immune serum injected intravenously on the day of oral inoculation with sporulated oocysts and again 7 and 14 days later. Four calves were given intravenous injections with some of the same serum on the 7th and 14th days after inoculation and 4 others were given a single similar injection with the same serum 14 days after inoculation.
Three calves in a second experiment received intraperitoneal injections of serum globulins in increasing amounts every 3 days for 2 weeks. The calves were then orally inoculated with sporulated oocysts one week after the last globulin injection. Some calves receiving immune serum had an anaphylactoid reaction characterized by increased respiration rate, dyspnea, coughing, and salivation; however, all affected calves recovered spontaneously within 2 hours. Calves receiving serum globulin had no reactions.
Coccidiosis developed in all of the calves in spite of the injection of immune serum or globulin presumed to carry the immune factor. There was no detectable difference in the rate of oocyst discharge or in clinical symptoms between treated and control calves; therefore, no evidence of passive immunity was observed.