Hypersensitivity reactions mechanisms

The exact mechanism of action of thiabendazole (Mintezol) is unknown. This drug appears to suppress egg or larval production and tiierefore may interrupt die life cycle of the helminth. Thiabendazole is used to treat threadworm. Thiabendazole may cause hypersensitivity reactions, drowsiness, and dizziness. 

Radiocontrast media (RCM) are highly concentrated solutions of triiodinated benzene derivatives used for performing diagnosis and treatment of vascular disease and enhancement of radiographic contrast [1,2]. However, adverse reactions after RCM administration are common [3]. The frequency and mechanisms of hypersensitivity reactions differ between monomeric and dimeric as well as between ionic and non-ionic types of RCM. Mild immediate reactions have been reported to occur in 3.8-12.7% of patients receiving ionic monomeric RCM and in 0.7-3.1% of patients receiving non-ionic RCM [4-6]. Severe immediate adverse reactions to ionic RCM have been reported in 0.1-0.4% of intravenous procedures, while reactions to nonionic iodinated RCM are less frequent (0.02-0.04%) [4-7]. Fatal hypersensitivity... 

The evidence that immediate hypersensitivity reactions may indeed be caused by an IgE-mediated allergic mechanism is also mainly indirect. However, some data support the concept that a subgroup of reactions may be IgE-mediated ... 

A classic mechanism by which some reactive metabolites are believed to mediate hypersensitivity reactions is by acting as a hapten (i.e., the reactive metabolite binds to... 

Specific immunotherapy (SIT) with aeroallergens directly addresses adaptive mechanism in hypersensitivity reactions. A meta-analysis of SIT studies revealed positive effects of subcutaneous... 

Non-allergic hypersensitivity reaction corresponds with the traditional term food intolerance . It affects about 20% of patients, inducing symptoms similar to those observed during an allergy bout, however, it is triggered by non-immunological mechanisms. 

There are other ways in which endotoxins may act to produce cotton dust induced airway disease. These include 1) an instrinsic toxicity due to lipid A, responsible for both pyro-genicity and tissue damage 2) a hypersensitivity reaction involving anti-lipid A antibodies. Further, changes in mechanical properties of the lung could be explained by the release of histamine or serotonin caused by endotoxins. 

Adverse reactions may include the following Fever porphyria dysuria gout hepatic reaction nausea vomiting anorexia thrombocytopenia and sideroblastic anemia with erythroid hyperplasia vacuolation of erythrocytes increased serum iron concentration adverse effects on blood clotting mechanisms mild arthralgia and myalgia hypersensitivity reactions including rashes, urticaria, pruritus fever acne photosensitivity porphyria dysuria interstitial nephritis. 

Pharmacology Lodoxamide is a mast cell stabilizer that inhibits the in vivo Type I immediate hypersensitivity reaction. Although lodoxamide s precise mechanism of action is unknown, the drug may prevent calcium influx into mast cells upon antigen stimulation. 

Roychowdhury, S. and Svensson, C.K. (2005) Mechanisms of drug-induced delayed-type hypersensitivity reactions in the skin. AAPS Journal,... 

Individualistic adverse reactions to foods can occur through several different types of mechanisms (Taylor and Hefle, 2001). True allergic reactions can include both IgE-mediated immediate hypersensitivity reactions and cell-mediated delayed h)q5ersensitivity reactions (Taylor and Hefle, 2001). However, only IgE-mediafed reactions have been documented to occur with ingestion of molluscan shellfish in sensifive individuals. 

Numerous glucocorticosteroids for topical application are available. Essentially they all suppress the symptoms of inflammatory and hypersensitivity reactions and their mechanism of action is similar. Their indications include seborrhoeic and atopic dermatitis, phototoxic reactions, psoriasis, chronic discoid lupus, hypertrophic lichen planus and alopecia areata. However it has to be kept in mind that the use of corticosteroids for these conditions in most cases only gives symptomatic relieve and that the problem tends to recur on cessation of therapy. Traditionally topical corticosteroid formulations are grouped according to approximate relative efficacy. This efficacy is determined by both the potency of the agent and the concentration in which the corticosteroid is used. 

Both exocytotic and nonexocytotic mechanisms can contribute to adverse drug reactions that involve histamine release. Histamine is only one of several potent physiological mediators that are released from mast cells the other substances can also contribute to the overall immediate hypersensitivity reaction. 

Cardiovascular effects. Hypotension and tachycardia occur in most patients taking clozapine. Cases of potentially fatal myocarditis and dilated cardiomyopathy have been reported in association with clozapine (Kilian et al. 1999). Myocarditis typically occurred within 3 weeks of starting clozapine, but cardiomyopathy may not be apparent for several years. Although rare, treatment-emergent myocarditis and cardiomyopathy occur at a reportedly higher incidence with clozapine than with other antipsychotics (Coulter et al. 2001). The mechanism by which clozapine may cause myocarditis has not been established, but some authors have speculated that clozapine may cause an immunoglobuhn E (IgE)-mediated type 1 hypersensitivity reaction (Kihan et al. 1999) or a hypereosinophilic syndrome (Hagg et al. 2001). 

Most anaphylactoid reactions are due to a direct or chemical release of histamine, and other mediators, from mast cells and basophils. Immune-mediated hypersensitivity reactions have been classified as types I-IV. Type I, involving IgE or IgG antibodies, is the main mechanism involved in most anaphylactic or immediate hypersensitivity reactions to anaesthetic drugs. Type II, also known as antibody-dependent hypersensitivity or cytotoxic reactions are, for example, responsible for ABO-incompatible blood transfusion reactions. Type III, immune complex reactions, include classic serum sickness. Type IV, cellular responses mediated by sensitised lymphocytes, may account for as much as 80% of allergic reactions to local anaesthetic. 

However, although this is the underlying mechanism, there are different outcomes. Thus, hypersensitivity reactions can result in one of four types of immune response ... 

Drugs such as lidocaine and sulfamethoxazole seem to be able to cause hypersensitivity reaction by this mechanism. 

Type IV Reactions Also termed delay-type hypersensitivity reaction, these take 48-72 h to develop and are not antibody-mediated. Antigens are recognized by CD4+ and/or CD8+ cells in the context of MHC class restrictions on APCs. These reactions are T-cell-mediated where activated T cells release cytokines, resulting in the development of granulomas from macrophages. These mechanisms are responsible for symptoms that may include transplant rejection, contact dermatitis, leprosy, tuberculosis and sarcoidosis. 

Possible mechanisms of fenofibrate-induced liver injury include activation of peroxisome proliferation-activator receptors, a hypersensitivity reaction, and immune -mediated injury from cross-reactivity of the drug with autoantigens. The authors referred to six reported cases of hepatic fibrosis attributed to fenofibrate. Raised transaminase activities occur commonly with fenofibrate but are generally transient, reverse on withdrawal, and do not result in long-term injury. Fenofibrate should be withdrawn if higher than normal enzyme activities persist, and a liver biopsy should be considered if liver enzymes do not normalize after withdrawal. 

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