Causes of Immune disorders
Immune disorders Causes: Book Excerpts
Immune disorders as a symptom:
Conditions listing Immune disorders
as a symptom may also be potential underlying causes of Immune disorders.
Our database lists the following as having
Immune disorders as a symptom of that condition:
Medical news summaries relating to Immune disorders:
The following medical news items are relevant to causes of Immune disorders:
Related information on causes of Immune disorders:
As with all medical conditions,
there may be many causal factors.
Further relevant information on causes of Immune disorders may be found in:
Causes of Immune disorders: Online Medical Books
16 MEDICAL BOOKS ONLINE!
Review excerpts from medical books online, free, without registration,
for more information about the causes of Immune disorders.
Common variable immunodeficiency:
Causes
(Professional Guide to Diseases (Eighth Edition))
The cause of common variable immunodeficiency is unknown. Most patients have a normal circulating B-cell count but defective synthesis or release of immunoglobulins. Many also exhibit progressive deterioration of T-cell (cell-mediated) immunity revealed by delayed hypersensitivity skin testing.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Allergic purpuras:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
The most common identifiable cause of allergic purpura is probably an autoimmune reaction directed against vascular walls, triggered by a bacterial infection (particularly streptococcal infection). Typically, upper respiratory tract infection occurs 1 to 3 weeks before the onset of symptoms. Other possible causes include allergic reactions to some drugs and vaccines, to insect bites, and to some foods (such as wheat, eggs, milk, and chocolate).
Allergic purpura affects more males than females and is most prevalent in children ages 3 to 7. The prognosis is more favorable for children than adults.
» READ BOOK EXCERPT ONLINE »
Source: Professional Guide to Diseases (Eighth Edition), 2005
Allergic rhinitis:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Hay fever reflects an immunoglobulin (Ig) E-mediated type I hypersensitivity response to an environmental antigen (allergen) in a genetically susceptible individual. In most cases, it’s induced by windborne pollens: in the spring by tree pollens (oak, elm, maple, alder, birch, and cottonwood), in the summer by grass pollens (sheep sorrel and English plantain), and in the fall by weed pollens (ragweed). Occasionally, hay fever is induced by allergy to fungal spores. In addition to individual sensitivity and geographical differences in plant population, the amount of pollen in the air can be a factor in determining whether symptoms develop. Hot, dry, windy days have more pollen than cool, damp, rainy days.
In perennial allergic rhinitis, inhaled allergens provoke antigen responses that produce recurring symptoms year-round. The allergens trigger antibody production and histamine release, producing itching, swelling, and mucus. The major perennial allergens and irritants include dust mites, feather pillows, mold, cigarette smoke, upholstery, and animal dander. Seasonal pollen allergy may exacerbate signs and symptoms of perennial rhinitis.
Allergic rhinitis is the most common atopic allergic reaction, affecting more than 20 million Americans. It’s most prevalent in young children and adolescents but can occur in all age groups.
» 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
Common variable immunodeficiency:
Causes
(Handbook of Diseases)
Exactly what causes common variable immunodeficiency is unknown. Most patients have a normal circulating B-cell count but defective synthesis or release of immunoglobulins. Many also exhibit progressive deterioration of T-cell (cell-mediated) immunity, which is revealed by delayed hypersensitivity skin testing.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Allergic purpura:
Causes
(Handbook of Diseases)
The most common identifiable cause of allergic purpura is probably an autoimmune reaction directed against vascular walls, triggered by a bacterial infection (particularly streptococcal infection). Typically, an upper respiratory tract infection occurs 1 to 3 weeks before the onset of symptoms. Other possible causes include allergic reactions to some drugs and vaccines, allergic reactions to insect bites, and allergic reactions to some foods (such as wheat, eggs, milk, and chocolate).
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Chronic fatigue and immune dysfunction syndrome:
Causes
(Handbook of Diseases)
Although the cause of CFIDS is unknown, researchers suspect that it may be found in human herpesvirus 6 or in other herpesviruses, enteroviruses, or retroviruses. Rising levels of antibodies to EBV, once thought to implicate EBV infection as the cause of CFIDS, are now considered a result of this disease.
CFIDS may be associated with a reaction to viral illness that’s complicated by dysfunctional immune response and by other factors that may include sex, age, genetic disposition, prior illness, stress, and environment.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Allergic rhinitis:
Causes
(Handbook of Diseases)
Hay fever reflects an immunoglobulin (Ig) E–mediated, type I hypersensitivity response to an environmental antigen (allergen) in a genetically susceptible individual. In most cases, it’s induced by wind-borne pollens: in spring, by tree pollens (oak, elm, maple, alder, birch, cottonwood); in summer, by grass pollens (crabgrass, bluegrass, fescue, and ryegrass); and in fall, by weed pollens (ragweed). Occasionally, hay fever is induced by allergy to fungal spores.
With perennial allergic rhinitis, inhaled allergens provoke antigen responses that produce recurring symptoms year-round.
The major perennial allergens and irritants include dust mites, feather pillows, mold, cigarette smoke, upholstery, and animal dander. Seasonal pollen allergy may exacerbate symptoms of perennial rhinitis.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
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