hypersensitivity angiitis

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hy·per·sen·si·tiv·i·ty an·gi·i·tis

an inflammatory reaction in a blood vessel, the result of a specific reaction to an antigenic (allergic) substance or other agents to which the individual expresses unusual vascular sensitization.

microscopic polyangiitis

A systemic small-vessel vasculitis that primarily affects the kidneys, skin, and lungs of middle-aged men.

Clinical findings
Fever, malaise, myalgia, weight loss, and autoimmunity, including antineutrophil cytoplasmic antibodies (p-ANCA). Skin lesions occur in 30 to 50%, usually presenting as purpura due to leukocytoclastic vasculitis, less commonly as nodules involving the vessels of the dermis and subcutaneous fat and ulcers. The kidney shows rapidly progressive focal and segmental glomerulonephritis.

Polyarteritis nodosa.


1. a state of altered reactivity in which the body reacts with an exaggerated immune response to a foreign agent; allergy is a synonym for hypersensitivity. anaphylaxis is a form of hypersensitivity.
There are four basic types of hypersensitivity reactions: Type I (called also immediate hypersensitivity) involves cell-fixed antibody, mainly IgE attached to mast cells or basophils. Antigen binding causes the cell to release vasoactive factors. The basis for anaphylaxis and atopy. Type II causes cell destruction (cytotoxicity) by the action of immunoglobulin with complement or cytotoxic cells. Seen in red blood cell transfusion reactions and in alloimmune hemolytic anemia. See also antibody-dependent cellular cytotoxicity. Type III (called also immune-complex or subacute hypersensitivity) causes tissue damage and inflammation by the deposition of antigen-antibody complexes that activate complement and attract polymorphonuclear cells. Type IV (called also delayed hypersensitivity) involves sensitized T lymphocytes that react with cell bound or associated antigen and release lymphokines, causing mononuclear cell accumulation, tissue damage and inflammation, typically manifesting at least 24 hours after exposure to the antigen.
2. a state of increased responsivity to physical stimuli.

hypersensitivity angiitis
variant of polyarteritis nodosa; a disease of small blood vessels in humans; called also leukocytoclastic vasculitis.
antibody-mediated hypersensitivity
types I, II and III hypersensitivity reactions. Called also immediate hypersensitivity.
bacterial hypersensitivity
immune responses to bacteria or bacterial products may contribute to the clinical features of some diseases, e.g. the anemia associated with salmonellosis, arthritis in erysipelas of pigs, intestinal lesions in Johne's disease, or be the principal cause as in staphylococcal hypersensitivity dermatitis in dogs.
contact hypersensitivity
a type IV reaction produced by contact of the skin with a low-molecular-weight chemical substance having the properties of a hapten in a sensitized individual; it includes allergic contact dermatitis.
cutaneous basophil hypersensitivity
a delayed inflammatory response characterized by large numbers of basophils.
cytotoxic hypersensitivity
type II hypersensitivity.
delayed hypersensitivity
type IV reaction. A slowly developing cell-mediated immune response in which T helper 1 lymphocytes respond to specific antigen by releasing cytokines, some of which activate macrophages, as occurs in tuberculin reaction, graft rejection, some autoimmune diseases, etc.
drug hypersensitivity
may be either an immediate (antibody mediated) or delayed type (T lymphocyte mediated) reaction. See also drug eruption.
flea bite hypersensitivity
see flea allergy dermatitis.
food hypersensitivity
hypersensitivity reaction to various dietary constituents has been the suspected cause of allergic dermatitis in most species, but conclusive evidence is often lacking. It may also result in diarrhea.
fungal hypersensitivity
may contribute to the clinical features of cutaneous fungal infections, particularly kerion formation. It is also the basis for skin testing for systemic mycoses, e.g. histoplasmin and coccidioidin.
helminth hypersensitivity
occurs, e.g. the self-cure phenomenon, and the allergic response of a sensitized animal to an invasion, e.g. of lungs, causes massive pulmonary edema.
immediate hypersensitivity
antibody-mediated hypersensitivity, i.e. types I, II and III, characterized by a response that appears within minutes to hours, resulting either from a release of histamine and other mediators of hypersensitivity from IgE-sensitized mast cells, causing increased vascular permeability, edema and smooth muscle contraction (type I), from antibody-mediated lysis of red blood cells (type II), or from immune complex mediated pathology (type III).
immune complex hypersensitivity
type III hypersensitivity (above).
mold hypersensitivity
see acute bovine pulmonary emphysema-edema.
hypersensitivity pneumonitis
see hypersensitivity pneumonitis.
staphylococcal hypersensitivity
see bacterial hypersensitivity (above).
hypersensitivity threshold
a theory that certain levels of allergens may be tolerated by some sensitized individuals without manifestations of disease, but a slight increase in the level precipitates clinical signs.
tuberculin type hypersensitivity
the classical T lymphocyte cell-mediated hypersensitivity associated with mycobacterium infection or immunization with antigens containing Freund's adjuvant.