Reactions To Drugs Are Allergic

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 Everyone reacts to medications differently.

One person may develop a rash while


taking a certain medication, while another person on the same drug may have no
adverse reaction. Does that mean the person with the rash has an allergy to that
drug?

All medications have the potential to cause side effects, but only about 5 to 10% of
adverse reactions to drugs are allergic.

Whether allergic or not, reactions to medications can range from mild to life-
threatening.
It is important to take all medications exactly as your physician prescribes. Call
your doctor if you have side effects that concern you, or you suspect a drug allergy
has occurred. If your symptoms are severe, seek medical help immediately.

Allergic Reactions
Allergy symptoms are the result of a chain reaction that starts in the immune
system. Your immune system controls how your body defends itself. For instance, if
you have an allergy to a particular medication, your immune system identifies
that drug as an invader or allergen. Your immune system may react to medications
in several ways

Most allergic reactions occur within hours to two weeks after taking the
medication and most people react to medications to which they have been exposed
in the past. This process is called "sensitization." However, rashes may develop up
to six weeks after starting certain types of medications.

. Common types of allergy are:

Type I: Immediate Hypersensitivity (Anaphylactic Reaction) These allergic reactions are


systemic or localized, as in allergic dermatitis (e.g., hives, wheal and erythema reactions). ...
 Type II: Cytotoxic Reaction (Antibody-dependent) ...
 Type III: Immune Complex Reaction. ...
 Type IV: Cell-Mediated (Delayed Hypersensitivity)

 Type I: Immediate Hypersensitivity (Anaphylactic Reaction)


 The most severe form of immediate allergic reactions is anaphylaxis (an-a-fi-
LAK-sis). Symptoms of anaphylaxis include hives, facial or throat swelling,
wheezing, light-headedness, vomiting and shock.

Most anaphylactic reactions occur within one hour of taking a medication or


receiving an injection of the medication, but sometimes the reaction may
start several hours later. Anaphylaxis can result in death, so it is important to
seek immediate medical attention if you experience these symptoms.
Antibiotics are the most common culprit of anaphylaxis, but more recently,
chemotherapy drugs and monoclonal antibodies have also been shown to
induce anaphylaxis. These allergic reactions are systemic or localized, as in allergic
dermatitis (e.g., hives, wheal and erythema reactions).
 Immune reaction is due to production of antibodies called Immunoglobulin E
(IgE) specific to the drug. These antibodies travel to cells that release
chemicals, triggering an immediate allergic reaction. This reaction causes
symptoms in the nose, lungs, throat, sinuses, ears, lining of the stomach or on
the skin and usually occurs within minutes to a few hours of taking the drug.
The reaction is the result of an antigen cross-linking with membrane-bound IgE
antibody of a mast cell or basophil. Histamine, serotonin, bradykinin, and lipid
mediators (e.g., platelet activating factor, prostaglandins, and leukotrienes) are
released during the anaphylactic reaction. These released substances have the
potential to cause tissue damage.
 Common triggers:

 , it’s very important to know what triggered the reaction. An allergist can review your
medical history and, if necessary, conduct diagnostic tests. The most common triggers
are:
 Food: including peanuts, tree nuts such as walnuts and pecans, fish, shellfish,
cow’s milk and eggs.
 Latex: found in disposable gloves, intravenous tubes, syringes, adhesive tapes
and catheters. Health care workers, children with spina bifida and genitourinary
abnormalities and people who work with natural latex are at higher-risk for latex-
induced anaphylaxis.
 Medication: including penicillin, aspirin and non-steroidal anti-inflammatory drugs
such as ibuprofen, and anesthesia.
 Insect sting: with bees, wasps, hornets, yellow jackets and fire ants being the
most likely to trigger anaphylaxis.

 Type II: Cytotoxic Reaction (Antibody-dependent)


 In a cytotoxic reaction, the antibody reacts directly with the antigen that is bound to
the cell membrane to induce cell lysis through complement activation. These antigens
may be intrinsic or “self” as in autoimmune reactions or extrinsic or “non-self.”
Cytotoxic reactions are mediated by IgG and IgM. Examples of cytotoxic reaction are
the Rh incompatibility of a newborn, blood transfusion reactions, and autoimmune
diseases like Pemphigus Vulgaris, Bullous Pemphigoid, autoimmune hemolytic anemia
and Goodpasture's syndrome to name a few.
 Triggers:
 The most common cause of type II reactions are medications including penicillins,
cephalosporins, hydrochlorothiazide, and methyldopa, which become associated with
red blood cells or platelets leading to anemia and thrombocytopenia.
 Type III: Immune Complex Reaction
 The reaction of antibody with antigen generates immune complex. In most of the
cases, these immune complexes are removed from blood circulation. Some immune
complexes are removed by phagocytic action of phagocytic cells in blood. Most other
immune complexes are first carried by blood to spleen where they are destroyed by
macrophages. Complement system is also needed for removal of immune complexes
from blood to spleen.
 In some cases large amount of immune complexes are formed and deposited on
various body parts and leads to tissue damage resulting in Type III hypersensitivity
reaction.
 If immune complexes are not removed from blood, they accumulate on wall of blood
vessels and on tissue where filtration of blood and plasma occurs such as glomerular
membrane, synovial membrane of joints etc.
 Type III hypersensitivity reaction is characterized by deposition of immune complexes
on various tissues such as wall of blood vessels, glomerular basement membrane of
kidney, synovial membrane of joints and choroid plexus of brain.
 Deposition of immune complexes initiates reaction resulting in damage of surrounding
tissue and cause inflammation.

 Factors that causes deposition of immune complex and increase susceptibility to Type
III hypersensitivity reaction:
1. Persistent infection:
 In persistent infection such as Malaria, large number of immune complexes are
formed and deposited in tissues.
2. Complement deficiency:
 Complement removes immune complexes from blood, but when complement system
is deficient, large amount of immune complexes circulates in blood and deposits in
tissues.
3. Autoimmunity:
 In autoimmune disease, large amount of immune complexes are formed and
deposited in tissues.
4. Genetic defects:
 In certain genetic defects, small and soluble immune complexes are formed that can
not be phagocytosed.
 IgG and IgM bind antigen, forming antigen-antibody (immune) complexes. These
activate complement, which results in PMN chemotaxis and activation. PMNs then
release tissue damaging enzymes. Tissue damage present in autoimmune diseases
(e.g., systemic lupus erythematosus), and chronic infectious diseases (e.g., leprosy) ,
rheumatoid arthritis can be attributed, in part, to immune complex reactions.
 Type IV: Cell-Mediated (Delayed Hypersensitivity)
 The most common immune response to a drug is due to the expansion of T
cells, a type of white blood cell that recognize the drug as foreign. These T
cells orchestrate a delayed immune response that most often affects the skin,
causing itchy rashes, and occurs days to weeks after exposure to the drug.

 Cell-mediated reactions are initiated by T-lymphocytes and mediated by effector T-


cells and macrophages. This response involves the interaction of antigens with the
surface of lymphocytes. Sensitized lymphocytes can produce cytokines, which are
biologically active substances that affect the functions of other cells. This type of
reaction takes 48-72 hours, or longer, after contact with the antigen to fully develop.
Many chronic infectious diseases, including tuberculosis and fungal infections, exhibit
delayed hypersensitivity.
 Evidence suggests that hypersensitivity reactions, particularly Type III and IV, may be
involved in the pathogenesis of periodontal disease.

 There is an extremely long list of substances that have been documented to produce
delayed hypersensitivity. The most common in domestic animals include flea collars,
poison ivy/oak/sumac, rubber products, dichromates (in cement), and nickel
compounds. Also implicated are therapeutic agents such as ethyl aminobenzoate and
neomycin, various dyes and preservatives.

You should seek medical help immediately if you experience any of these. Many
medications can cause these severe delayed reactions including antibiotics,
medications for epilepsy (seizures), depression and gout.

However, not all drug allergic reactions involve a specific immune reaction. Some
people experience flushing, itching or a drop in blood pressure from intravenous
dyes used in x-rays or CT scans. If you take angiotensin converting enzyme (ACE)
inhibitors for high blood pressure, you may develop a cough or facial and tongu e
swelling. In addition, some people are sensitive to aspirin, ibuprofen or other non -
steroidal anti-inflammatory drugs (NSAIDs). One type of aspirin or NSAID sensitivity
may cause a stuffy nose, wheezing and difficulty breathing. This is most common in
adults with asthma and in people with nasal polyps (benign growths). Other
reactions to NSAIDs can result in hives or in rare instances, severe reactions can
result in shock.
A number of factors influence your chances of having an adverse reaction to a
medication. These include: genetics, body chemistry, frequent drug exposure or the
presence of an underlying disease. Also, having an allergy to one drug predisposes
an individual to have an allergy to another unrelated drug. Contrary to popular myth,
a family history of a reaction to a specific drug typically does not increase your
chance of reacting to the same drug.

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