Causes of Drug Allergies
Drug Allergies Causes: Book Excerpts
Medications or substances causing Drug Allergies:
The following drugs, medications, substances or toxins are some of the possible
causes of Drug Allergies as a symptom.
This list is incomplete and various other drugs or substances
may cause your symptoms.
Always advise your doctor of any medications or treatments you are using,
including prescription, over-the-counter, supplements, herbal or alternative treatments.
See full list of 88
medications causing Drug Allergies
What causes Drug Allergies?
Causes: Drug Allergies:
Drugs which may cause anaphylactic reactions includes: fentanyl, pethidine, dextrans, anti-inflammatory drugs, antibiotics, chemotherapeutic agents, antiseptics (chlorhexidine gluconate, mercurochrome), solvents (cremophor), diagnostic agents, hormones (ACTH, calcitonin, glucocorticoids), streptokinase, antivenoms, tetanus, human serum albumin, acetyl cysteine, cimetidine, desferoxamine and allergy immunotherapy vaccines.
Related information on causes of Drug Allergies:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Drug Allergies may be found in:
Causes of Drug Allergies: Online Medical Books
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Review excerpts from medical books online, free, without registration,
for more information about the causes of Drug Allergies.
Latex allergy:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Approximately 1% of the population has a latex allergy. Anyone who is in frequent contact with latex-containing products is at risk for developing a latex allergy. (See Products that contain latex, page 358.)The more frequent the exposure, the higher the risk. The populations at highest risk are medical and dental professionals, workers in latex companies, and patients with spina bifida.
Other individuals at risk include:
❑ patients with a history of asthma or other allergies, especially to bananas, avocados, tropical fruits, or chestnuts
❑ patients with a history of multiple intra-abdominal or genitourinary surgeries
❑ patients who require frequent intermittent urinary catheterization.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
anaphylaxis:
Causes
(Handbook of Diseases)
The causes of anaphylactic reaction are ingestion of or other systemic exposure to a sensitizing drug or other substance.
Sensitizing substances
Sensitizing substances include serums (usually horse serum), vaccines, allergen extracts, enzymes (such as l-asparaginase), hormones, penicillin and other antibiotics, sulfonamides, local anesthetics, salicylates, polysaccharides, diagnostic chemicals (sulfobromophthalein, sodium dehydrocholate, and radiographic contrast media), foods (legumes, nuts, berries, seafood, and egg albumin) and sulfite-containing food additives, and insect venom (honeybees, wasps, hornets, yellow jackets, fire ants, mosquitoes, and certain spiders).
A common cause of anaphylaxis is penicillin, which induces anaphylaxis in 1 to 4 of every 10,000 patients treated with it. Penicillin is most likely to induce anaphylaxis after parenteral administration or prolonged therapy and in atopic patients who are allergic to other drugs or foods.
Pathophysiology
An anaphylactic reaction requires previous sensitization or exposure to the specific antigen, resulting in the production of specific immunoglobulin (Ig) E antibodies by plasma cells. This antibody production takes place in the lymph nodes and is enhanced by helper T cells. IgE antibodies then bind to membrane receptors on mast cells (found throughout connective tissue, often near small blood vessels) and basophils.
On reexposure, the antigen binds to adjacent IgE antibodies or cross-linked IgE receptors, activating a series of cellular reactions that trigger degranulation — the release of powerful preformed chemical mediators (such as histamine, prostaglandins, and platelet activating factor) from mast cell stores. IgG or IgM enters into the reaction and activates the release of complement fractions.
This acute phase of the response occurs within minutes of exposure. Because of the systemic nature of the exposure, activation of mast cells is widespread, and the massive release of these powerful mediators near blood vessels leads to vascular collapse by stimulating contraction of certain groups of smooth muscles and by increasing vascular permeability. In turn, increased vascular permeability leads to decreased peripheral resistance and plasma leakage from the circulation to extravascular tissues (which lowers blood volume, causing hypotension, hypovolemic shock, and cardiac dysfunction).
In the later phase of this response (8 to 12 hours later), other mediators are synthesized and released, including chemokines, leukotrienes, and cytokines. These agents mediate the inflammatory response by recruiting eosinophils and lymphocytes. This delayed response may be less dramatic than the acute phase of anaphylaxis, but with a diffuse inflammatory response, further smooth-muscle contraction and edema can occur and progress to grave systemic symptoms.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
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