Hypersensitivity states

During induction, it is attempted to induce a hypersensitive state in the test animals by exposing them to a high concentration of the test substance. This requires a certain severity of provocation, and a certain period of time (one to several weeks). 

Following the induction, it is tested whether a hypersensitive state now exists in the test animals this test is the challenge. For challenge, a low concentration of the test substance is used. 

Induction period The length of time (at least 1 week) following a sensitization during which period a hypersensitive state is developed by the animal. 

Allergic reaction A reaction to a foreign agent giving rise to a hypersensitive state, mediated via an immunological mechanism and resulting in a particular series of responses. 

Incompatible chemical substances Chemical substances that may cause dangerous reactions from direct contact with one another Induction period The length of time (at least 1 week) following a sensitization during which a hypersensitive state is developed by the animal Inflammation Response of the body tissues to injury typical signs are swelling, redness, and pain... 

IgG protects body fluids, IgA protects body surfaces, IgM protects the bloodstream, IgD has no known antibody function and IgE is found in allergy and hypersensitive states."... 

Woolf CJ, Thompson 8W (1991) The induction and maintenance of central sensitization is dependent on V-methyl-D-aspartic acid receptor activation implications for the treatment of postinjury pain hypersensitivity states. Pain 44 293-299 Wu ZZ, Guan BC, Li ZW, Yang Q, Liu CJ, Chen JG (2004) 8ustained potentiation by substance P of NMDA-activated current in rat primary sensory neurons. Brain Res 1010 117-126 Yamada K, Akasu T (1996) 8ubstance P suppresses GABAA receptor function via protein kinase C in primary sensory neurones of bullfrogs. J Physiol 496(Part 2) 439 49... 

Eisen HN (1959) Hypersensitivity to simple chemicals. In Lawrence HS (ed) Cellular and humoral aspects of hypersensitivity states. Hoeber, New York Eisen HN, Siskind GW (1964) Variations in affinities of antibodies during the immune response. Biochemistry 3 996-1008... 

Weiner LM, Rosenblatt M, Howes HA (1963) The detection of humoral antibodies directed against salicylates in hypersensitivity states. J Immunol 90 788-792 Weisburger JH, Weisburger EK (1973) Biochemical formation and pharmacological, toxicological, and pathological properties of hydroxylamines and hydroxamic acids. Pharmacol Rev 25 1-66... 

Etiology Although the cause is still controversial (23), NCS is beheved to occur in persons who have a predisposition to the condition as a result of excessive peripheral venous pooling that causes a sudden drop in peripheral venous return (24). There is growing evidence that serotonin plays a key role in CNS regulation of both heart rate and blood pressure (25). In the reflex syncopes, there is thought to be disturbances in the production of serotonin as well as postsynaptic receptor density centrally, which leads to a hypersensitive state, with excessive responses to fluctuations in sensory input on a peripheral level. This results in a cardiac hypercontractile state, which activates mech-anoreceptors that normally only respond to stretch. The increase in afferent neural traffic to the brain mimics the conditions seen in hypertension and provokes an apparent paradoxical reflex bradycardia and a drop in peripheral vascular resistance (26). 

Hypersensitivity vasculitis induced by drags is another manifestation of a type III response. Drags involved include some p-lactams, particularly, amoxicillin and cephalexin, cotrimoxazole, NSAIDs, monoclonal antibodies, and chemotherapeutic drags such as tamoxifen and erlotinib. A proportion of small-vessel vasculitis patients have anti-neutrophil cytoplasmic antibodies. Although there is evidence of a pathogenic role for these antibodies and they are used as a diagnostic marker, operative mechanisms underlying this hypersensitivity state are still far from established. 

L. Thomas, In Cellular and Humoral Aspects of the Hypersensitive States H. S. Lawrence, Ed., Hoeber-Harper, New York, 1959, pp. 529-532. 

Katzberg RW Acute reactions to urographic contrast medium incidence, clinical characteristics, and relationship to history of hypersensitivity states - a commentary. AJR Am J Roentgenol 2008 190 1431-1432. 

Immunologic Skin testing of 26 patients clinically diagnosed with immediate (type I) hypersensitivity to infliximab found seven positives (30%) and six of these had infliximab-reactive serum IgE antibo es. One skin test-positive patient had no detectable IgE antibodies to the mAb [155 ]. After multiple infusions with infliximab, a 61-year-old woman with Crohn s disease experienced an acute anaphylactic reaction immediately after the start of an infusion. Although anti-infliximab IgE antibodies were not detected, the concentration of anti-infliximab IgG was high and this remained the case 1 year after the mAb was discontinued. Substitution of adalimumab for infliximab 1 week after the anaphylactic reaction was tolerated until the 12th day when the patient displayed a delayed, type IV hypersensitivity reaction mediated by IgG antibodies specific for adalimumab [ISb ]. In addition to types I and IV hypersensitivities to infliximab, other immune-mediated reactions representing the other hypersensitivity states also occur to infliximab. This is illustrated by a recent report of a case of a 27-year-old woman of infliximab-induced systemic lupus erythematosus [157 ], an autoimmune connective tissue disease which is both a type II and a type III hypersensitivity response. 

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