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HYPERSENSITIVITY
REACTIONS OF A DRUG
T.SAI SWAPNA
II/VI PHARM.D
Y17PHD0827
NIRMALA COLLEGE OF
PHARMACY ,ATMAKUR
HYPERSENSITIVITY
 Hypersensitivity refers to the undesirable reactions
produced by the normal immune system , including allergies
and autoimmunity
 These reactions may cause damaging , uncomfortable or
occasionally fatal
 These reactions require a presensitized state of the host
DRUG HYPERSENSITIVITY;
 It is an immunologically mediated reaction producing
symptoms unrelated to pharmacodynamic actions of the drug
generally occuring with much smaller amounts and have a
different time course of onset and duration
 These reactions account for about 1/6th of all ADR’S
 The most common allergic reactions occurs in skin and
observed 2-3% in hospitalized patients
 Antibiotics and antiepileptics are the drugs most frequently
causing hypersensitivity reactions
 The severity and symptoms depends up on the immune
activation and duration of treatment , sex
TYPES ;
 1. ANAPHYLAXIS
 2. CYTOTOXIC
 3 . IMMUNE COMPLEX
 4 . DELAYED TYPE
TYPES ;
s. no Mechanism Examples
1. IgE mediated hypersensitivity Anaphylaxis , asthma
2. Cytotoxic antibody dependent Haemolytic anaemia
thrombocytopenia
3. Immune complex damage Serum sickness , SLE
4 . Delayed Dermatitis
IGE MEDIATED
 IgE antibodies is ready to react to small amounts of antigens
 Stimulate receptors bound ige antibodies
 The drug causes formation of tissue sensitive ige antibodies
that are fixed to mast cells
 Subsequent exposure of drug activate leucocytes and release of
chemical mediators that cause allergy
CYTOTOXIC ;
 The mediator of these reactions are IgE /IgM membrane
attack complex
 It results when drug binds to RBC and is recognised by IgE
antibodies
 The Ag- Ab reactions trigger the lysis of RBC either by
activating complement system or by action of cytotoxic T cells
or by phagocytosis of macrophages leads to disintegration of
cell
EXAMPLES ;
 Seen in high dose pencillin and cephalosporin
 Quinine induced immune thrombocytopenia
 Heamolytic anemia
IMMUNE COMPLEX ;
 These reactions occurs within 1 – 2 hours of drug
administration
 Soluble antigen antibody forms soluble complexes
deposited on vascular endothelium and activate complement
 Characterized by allergic inflammatory reactions in tissues
CLINICAL FEATURES ;
 Vasculitis
 Sulphamethoxazole , cephalexin , amoxicillin , NSAID’S
and diuretics
DELAYED REACTIONS ;
 These reactions mediated by T cell and macrophages
 Activation of T cell release of cytokines these activate
macrophages and NK cells
 The term delayed because the response occurs after 48 – 72
hours after antigen response
 Pnemonitis , contact dermatitis
PSUEDOALLERGY ;
 Pathogenically poorly determined , alternation in
metabolism of histamines .
 Detection of particular immune mechanism is negative
 The exact mechanism is unknown by which these cause
reactions through IgE / T cells or not
 These reactions mainly occurs when taken of NSAID’S
CLINICAL SYMPTOMS OF
DRUG HYPERSENSITIVITY;
 Urticaria
 Erythema
 Stevens john syndrome
 Epidermal necrosis
DIAGNOSIS ;
 Patient symptomology
 IgE
 Skin testing
 RAST testing
 Antiglobulin test
 ESR , CRP , ANA
 Patch test lymphocyte proliferation assay
TREATMENT ;
 Discontinuation of drug
 Alternative medications
 Additional therapy to manage symptoms caused by drugs
 Systemic corticosteroids and antihistamines may improve
dermatological effects
THANK YOU

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Hypersensitivity reactions of a drug

  • 1. HYPERSENSITIVITY REACTIONS OF A DRUG T.SAI SWAPNA II/VI PHARM.D Y17PHD0827 NIRMALA COLLEGE OF PHARMACY ,ATMAKUR
  • 2.
  • 3. HYPERSENSITIVITY  Hypersensitivity refers to the undesirable reactions produced by the normal immune system , including allergies and autoimmunity  These reactions may cause damaging , uncomfortable or occasionally fatal  These reactions require a presensitized state of the host
  • 4. DRUG HYPERSENSITIVITY;  It is an immunologically mediated reaction producing symptoms unrelated to pharmacodynamic actions of the drug generally occuring with much smaller amounts and have a different time course of onset and duration  These reactions account for about 1/6th of all ADR’S  The most common allergic reactions occurs in skin and observed 2-3% in hospitalized patients
  • 5.  Antibiotics and antiepileptics are the drugs most frequently causing hypersensitivity reactions  The severity and symptoms depends up on the immune activation and duration of treatment , sex
  • 6. TYPES ;  1. ANAPHYLAXIS  2. CYTOTOXIC  3 . IMMUNE COMPLEX  4 . DELAYED TYPE
  • 7. TYPES ; s. no Mechanism Examples 1. IgE mediated hypersensitivity Anaphylaxis , asthma 2. Cytotoxic antibody dependent Haemolytic anaemia thrombocytopenia 3. Immune complex damage Serum sickness , SLE 4 . Delayed Dermatitis
  • 8. IGE MEDIATED  IgE antibodies is ready to react to small amounts of antigens  Stimulate receptors bound ige antibodies  The drug causes formation of tissue sensitive ige antibodies that are fixed to mast cells  Subsequent exposure of drug activate leucocytes and release of chemical mediators that cause allergy
  • 9.
  • 10. CYTOTOXIC ;  The mediator of these reactions are IgE /IgM membrane attack complex  It results when drug binds to RBC and is recognised by IgE antibodies  The Ag- Ab reactions trigger the lysis of RBC either by activating complement system or by action of cytotoxic T cells or by phagocytosis of macrophages leads to disintegration of cell
  • 11. EXAMPLES ;  Seen in high dose pencillin and cephalosporin  Quinine induced immune thrombocytopenia  Heamolytic anemia
  • 12. IMMUNE COMPLEX ;  These reactions occurs within 1 – 2 hours of drug administration  Soluble antigen antibody forms soluble complexes deposited on vascular endothelium and activate complement  Characterized by allergic inflammatory reactions in tissues
  • 13.
  • 14. CLINICAL FEATURES ;  Vasculitis  Sulphamethoxazole , cephalexin , amoxicillin , NSAID’S and diuretics
  • 15. DELAYED REACTIONS ;  These reactions mediated by T cell and macrophages  Activation of T cell release of cytokines these activate macrophages and NK cells  The term delayed because the response occurs after 48 – 72 hours after antigen response  Pnemonitis , contact dermatitis
  • 16. PSUEDOALLERGY ;  Pathogenically poorly determined , alternation in metabolism of histamines .  Detection of particular immune mechanism is negative  The exact mechanism is unknown by which these cause reactions through IgE / T cells or not  These reactions mainly occurs when taken of NSAID’S
  • 17. CLINICAL SYMPTOMS OF DRUG HYPERSENSITIVITY;  Urticaria  Erythema  Stevens john syndrome  Epidermal necrosis
  • 18. DIAGNOSIS ;  Patient symptomology  IgE  Skin testing  RAST testing  Antiglobulin test  ESR , CRP , ANA  Patch test lymphocyte proliferation assay
  • 19. TREATMENT ;  Discontinuation of drug  Alternative medications  Additional therapy to manage symptoms caused by drugs  Systemic corticosteroids and antihistamines may improve dermatological effects