Hypersensitivity reactions
Occur on 2nd or subsequent exposure to an antigen
Abnormal reactions involving different immune mechanisms
4 types
Type 1 (immediate)
Anaphylactic
IgE mediated
IgE synthesised by B lymphocytes on 1st exposure and binds to mast cells (numerous in bronci, gut, capillaries)
On 2nd exposure mast cells degranulate releasing vasoactive substances (histamine, serotonin, heparin, leukotrienes, PLT activating factor)
Type 2 (cytotoxic)
IgE and M with complement cause cytotoxic cell lysis
Haemolysis, thrombocytopenia
Drug induced
Type 3 (immune complex)
Antibody and antigen react producing an immune complex which deposits in small vessels (lungs, glomeruli, joints)
Underlies many autoimmune diseases
Type 4 (delayed)
T-cells and macrophages attack foreign material
Occurs without complement or antibodies
Contact dermatitis
Granuloma formation
Anaphylactoid
Clinically indistinguishable from anaphylactic reactions
Direct release of vasoactive substances from mast cells
Not mediated via an antigen-antibody response
Dose related (why give drugs slowly)
Investigation of hypersensitivity reactions
Tryptase
An enzyme released from degranulating mast cells which activates complement cascade
Investigate reactions by serum for tryptase immediately, 1h and 6-24h
Higher values more likely to be IgE mediated
Radioallergosorbent tests (RAST) now superseded by CAP (antigen coated capsule exposed to patients serum)
Penicillin, sux and latex only – low sensitivity so need skin prick tests too
Skin prick (or intradermal) testing
4-6/52 post event to allow regeneration IgE
Drop applied to forearm and lancet stabbed through it to break skin
-ve control with saline
+ve control with histamine
Undiluted drug – if reaction then repeated with 1 in 10 dilution
