druginducedurticaria

1. DRUG-INDUCED URTICARIA

2. Drug-induced urticaria is sometimes called as URTICARIA
MEDICAMENTOSA.
Who gets drug-induced urticaria?
• Acute drug-induced urticaria
• Chronic drug-induced urticaria

3. What causes drug-induced urticaria?
Immune
mechanisms
Type I
(IgE dependent)
Type III
(immune complex-
Non-
immunological m
echanisms
pseudo-allergic
dependent on the
system)
direct release of mast
cell mediators and
the complement syste

4. Drugs that are known to cause
urticaria

5. • Angiotensin-converting enzyme inhibitors (ACEIs)*
• Antibiotics: penicillins*, cephalosporins*, macrolides
macrolides
(erythromycin), aminoglycosides, tetracyclines*, sulphonamide
s, vancomycin, fluoroquinolones
• Anticoagulants: low molecular weight heparin, protamine sulfate
• Hydralazine
• Mannitol
• Muscle relaxants: atracurium, vecuronium, succinylcholine,
curare
• NSAIDS*: ibuprofen, naproxen, diclofenac
• Opioids: morphine*, codeine*, meperidine, fentanyl
• Paracetamol
• Polypeptide hormones: insulin, corticotrophin, vasopressin
• Progesterone
• Quinidine
• Radiographic contrast agents*
• Salicylates* including aspirin
• Sorbitol complexes
• Corticosteroids
• Thrombolytics: alteplase, urokinase
• Vaccines

6. •Acute urticaria
• <6 weeks
•Chronic urticaria
•>6 weeks, with daily
episodic weals.
Contact urticaria
•localised to the site
application(ocassion
generalised)
What are the clinical features of drug-
induced urticaria?

7. What are the complications of drug-induced
urticaria?
• hypotension, dyspnoea, and anaphylaxis.
• Persistent urticaria can have a substantial impact on the quality of life.

8. How is drug-induced urticaria diagnosed?
• comprehensive clinical history.
• can be confirmed by prick
testing, immunoglobulin E tests, and oral
provocation tests.
• Other investigations can include haematology,
tryptase, complement (C3/C4,
C3d), leukocyte histamine release, and urinary
tryptase.

9. The first thing to do ??

10. How is drug-induced urticaria treated?
General measures
• The causative drug should be stopped when possible.
• If due to a type 1 (IgE-mediated) allergy, the urticaria clears within
• Non-essential medications should be avoided if they may be
• Cooling the affected area with a fan, ice pack, or soothing
moisturising lotion may provide relief.

11. PHARMACOLOGICAL MEASURES

12. The international EAACI/GA²LEN/EuroGuiDerm/APAAACI
guideline
Standard dose of
second gen H1
antihistaminics
• If no improvement is seen, increase the dose
upto 4-fold.
Add Omalizumab
150-300mg sc
every 4 weeks
• Increase dose and shorten interval
600mg every 2 weeks
• If no improvement within 6
months
Add ciclosporin
5 mg/kg/day
• A short course of
glucocorticosteroids may be
considered for acute
exacerbations.

13. Treating refractory urticaria
• a four- to five-day course of oral prednisone or prednisolone (systemic corticosteroids)
might be added in severe acute urticaria, particularly if there is angioedema.
• However, systemic corticosteroids do not speed up the resolution of symptoms.
• Steroids are best avoided for long-term therapy due to their adverse effects and the risk of
rebound when they are discontinued.
• Intramuscular adrenaline (epinephrine) is reserved for cases with life-
threatening anaphylaxis or swelling of the throat.

14. What is the outcome for drug-induced
urticaria?
• another attack — possibly worse — if re-exposed.
• Patients should be advised to inform their healthcare providers
about their adverse reaction to the causative drug.
• Sensitised patients cross-react with another drug of the same
class.
• Substitution with a drug from another class should be considered if
the clinical need emerges.

15. URTICARIA DUE TO ANTIHISTAMINES
• an autoimmune/autoreactive
mechanism that could be
present in the pathogenesis of
chronic urticaria.
paradoxical
exacerbation of
chronic urticaria by
H1antihistamines.
• the skin reaction has only
occurred following the
administration of antihistamines
during a challenge
acute
urticaria/angioedema
after the intake of
antihistamines

16. • Two hypotheses have been proposed to explain the paradoxical acute urticarial
exacerbation induced by H1 antihistamines.
1) the antihistamines may shift the H1 histamine receptor from the inactive to the active
state,
2) the direct activation may occur due to cross-reactivity, involving unclear mechanisms,
between the different metabolites of the drugs.

17. • Antihistamine induced urticaria is mostly non-IgE medicated because prick test and
basophil activation tests are negative.
• It may be due to cross reactivity of its metabolites
• After provocation test with fexofenadine, cetrizine, hydroxyzine- there is increased levels of
histamine and leukotriene B4.

18. OMALIZUMAB
• humanised monoclonal antibody
• binds to circulating immunoglobulin E (IgE)
reduces the release
of inflammatory mediators from mast
cells and basophils.
• subcutaneous injection in a dose of two 150-mg injections, once every 4 weeks.

21. HISTAGLOBULIN
• a lyophilised preparation of histamine coupled with
Human Normal immunoglobulin.
• Administered subcutaneously
• induces production of antibody against the histamine-
immunoglobulin complex
binds and inactivates histamine released during
episodes of urticaria.

22. THANKYOU