Allergy

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Allergy
From Wikipedia, the free encyclopedia

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Allergy
Classification and external resources

Hives are a common allergic symptom.

An allergy is a hypersensitivity disorder of the immune system.[1] Allergic reactions occur when a person's immune system reacts to normally harmless substances in the environment. A substance that causes a reaction is called an allergen. These reactions are acquired, predictable,

and rapid. Allergy is one of four forms of hypersensitivity and is formally called type I (or immediate) hypersensitivity. Allergic reactions are distinctive because of excessive activation of certain white blood cells called mast cells and basophils by a type of antibody called Immunoglobulin E (IgE). This reaction results in an inflammatory response which can range from uncomfortable to dangerous. Mild allergies like hay fever are very common in the human population and cause symptoms such as red eyes, itchiness, and runny nose, eczema, hives, hay fever, or an asthma attack. Allergies can play a major role in conditions such as asthma. In some people, severe allergies to environmental or dietary allergens or to medication may result in life-threatening reactions called anaphylaxis. Food allergies, and reactions to the venom of stinging insects such as wasps and bees are often associated with these severe reactions.[2] A variety of tests exist to diagnose allergic conditions. These include placing possible allergens on the skin and looking for a reaction such as swelling. Blood tests can also be done to look for an allergen-specific IgE. Treatments for allergies include avoiding known allergens, use of medications such as antihistamines that specifically prevent allergic reactions, steroids that modify the immune system in general, and medications such as decongestants that reduce the symptoms. Many of these medications are taken by mouth, though epinephrine, which is used to treat anaphylactic reactions, is injected. Immunotherapy uses injected allergens to desensitize the body's response.
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5.3 Other

[edit] Signs and symptoms
Common symptoms Affected organ Symptom swelling of the nasal mucosa Nose (allergic rhinitis) Sinuses allergic sinusitis redness and itching of the Eyes conjunctiva (allergic conjunctivitis) Sneezing, coughing, bronchoconstriction, wheezing and dyspnea, sometimes outright Airways attacks of asthma, in severe cases the airway constricts due to swelling known as laryngeal edema Ears feeling of fullness, possibly pain,

and impaired hearing due to the lack of eustachian tube drainage. rashes, such as eczema and hives Skin (urticaria) Gastrointestinal abdominal pain, bloating, tract vomiting, diarrhea

Many allergens such as dust or pollen are airborne particles. In these cases, symptoms arise in areas in contact with air, such as eyes, nose, and lungs. For instance, allergic rhinitis, also known as hay fever, causes irritation of the nose, sneezing, itching, and redness of the eyes.[3] Inhaled allergens can also lead to asthmatic symptoms, caused by narrowing of the airways (bronchoconstriction) and increased production of mucus in the lungs, shortness of breath (dyspnea), coughing and wheezing.[4] Aside from these ambient allergens, allergic reactions can result from foods, insect stings, and reactions to medications like aspirin and antibiotics such as penicillin. Symptoms of food allergy include abdominal pain, bloating, vomiting, diarrhea, itchy skin, and swelling of the skin during hives. Food allergies rarely cause respiratory (asthmatic) reactions, or rhinitis.[5] Insect stings, antibiotics, and certain medicines produce a systemic allergic response that is also called anaphylaxis; multiple organ systems can be affected, including the digestive system, the respiratory system, and the circulatory system.[6][7][8] Depending on the rate of severity, it can cause cutaneous reactions, bronchoconstriction, edema, hypotension, coma, and even death. This type of reaction can be triggered suddenly, or the onset can be delayed. The severity of this type of allergic response often requires injections of epinephrine, sometimes through a device known as the EpiPen or Twinject auto-injector. The nature of anaphylaxis is such that the reaction can seem to be subsiding, but may recur throughout a prolonged period of time.[8] Substances that come into contact with the skin, such as latex, are also common causes of allergic reactions, known as contact dermatitis or eczema.[9] Skin allergies frequently cause rashes, or swelling and inflammation within the skin, in what is known as a "wheal and flare" reaction characteristic of hives and angioedema.[10]

[edit] Cause
Risk factors for allergy can be placed in two general categories, namely host and environmental factors.[11] Host factors include heredity, gender, race, and age, with heredity being by far the most significant. However, there have been recent increases in the incidence of allergic disorders that cannot be explained by genetic factors alone. Four major environmental candidates are alterations in exposure to infectious diseases during early childhood, environmental pollution, allergen levels, and dietary changes.[12]

[edit] Foods
One of the most common food allergies is a sensitivity to peanuts. Peanut allergies may be extremely severe, but can sometimes be outgrown by children school-age.[13] Tree nuts, including pecans, pistachios, pine nuts, and walnuts, are another common allergen. Sufferers

may be sensitive to one, or many, tree nuts.[14] Also seeds, including sesame seeds and poppy seeds, contain oils where protein is present, which may elicit an allergic reaction.[14] Egg allergies affect one to two percent of children but are outgrown by about two-thirds of children by the age of 5.[15] The sensitivity is usually to proteins in the white rather than the yolk.[14] Milk, from cows, goats, or sheep, is another common allergy-causing food, and many sufferers are also unable to tolerate dairy products such as cheese. Lactose intolerance, a common reaction to milk, is not in fact a form of allergy. A small portion of children with a milk allergy, roughly ten percent, will have a reaction to beef. Beef contains a small amount of protein that is present in cow's milk.[16] Other foods containing allergenic proteins include soy, wheat, fish, shellfish, fruits, vegetables, spices, synthetic and natural colors, chicken, and chemical additives.[citation needed]

[edit] Non-food proteins
Latex can trigger an IgE-mediated cutaneous, respiratory, and systemic reaction. The prevalence of latex allergy in the general population is believed to be less than one percent. In a hospital study, one in 800 surgical patients (0.125 percent) report latex sensitivity, although the sensitivity among healthcare workers is higher, between seven and ten percent. Researchers attribute this higher level to the exposure of healthcare workers to areas with significant airborne latex allergens, such as operating rooms, intensive-care units, and dental suites. These latex-rich environments may sensitize healthcare workers who regularly inhale allergenic proteins.[17] The most prevalent response to latex is an allergic contact dermatitis, a delayed hypersensitive reaction appearing as dry, crusted lesions. This reaction usually lasts 48 to 96 hours. Sweating or rubbing the area under the glove aggravates the lesions, possibly leading to ulcerations.[17] Anaphylactic reactions occur most often in sensitive patients, who have been exposed to the surgeon's latex gloves during abdominal surgery, but other mucosal exposures, such as dental procedures, can also produce systemic reactions.[17] Latex and banana sensitivity may cross-react; furthermore, patients with latex allergy may also have sensitivities to avocado, kiwifruit, and chestnut.[18] These patients often have perioral itching and local urticaria. Only occasionally have these food-induced allergies induced systemic responses. Researchers suspect that the cross-reactivity of latex with banana, avocado, kiwifruit, and chestnut occurs because latex proteins are structurally homologous with some plant proteins.[17]

[edit] Toxins interacting with proteins
Another non-food protein reaction, urushiol-induced contact dermatitis, originates after contact with poison ivy, eastern poison oak, western poison oak, or poison sumac. Urushiol, which is not itself a protein, acts as a hapten and chemically reacts with, binds to, and changes the shape of integral membrane proteins on exposed skin cells. The immune system does not recognize the

affected cells as normal parts of the body, causing a T-cell-mediated immune response.[19] Of these poisonous plants, sumac is the most virulent.[20] The resulting dermatological response to the reaction between urushiol and membrane proteins includes redness, swelling, papules, vesicles, blisters, and streaking.[21] Estimates vary on the percentage of the population that will have an immune system response. Approximately 25 percent of the population will have a strong allergic response to urushiol. In general, approximately 80 percent to 90 percent of adults will develop a rash if they are exposed to .0050 milligrams (7.7×10−5 gr) of purified urushiol, but some people are so sensitive that it takes only a molecular trace on the skin to initiate an allergic reaction.[22]

[edit] Genetic basis
Allergic diseases are strongly familial: identical twins are likely to have the same allergic diseases about 70% of the time; the same allergy occurs about 40% of the time in non-identical twins.[23] Allergic parents are more likely to have allergic children,[24] and their allergies are likely to be more severe than those from non-allergic parents. Some allergies, however, are not consistent along genealogies; parents who are allergic to peanuts may have children who are allergic to ragweed. It seems that the likelihood of developing allergies is inherited and related to an irregularity in the immune system, but the specific allergen is not.[24] The risk of allergic sensitization and the development of allergies varies with age, with young children most at risk.[25] Several studies have shown that IgE levels are highest in childhood and fall rapidly between the ages of 10 and 30 years.[25] The peak prevalence of hay fever is highest in children and young adults and the incidence of asthma is highest in children under 10.[26] Overall, boys have a higher risk of developing allergy than girls,[24] although for some diseases, namely asthma in young adults, females are more likely to be affected.[27] Sex differences tend to decrease in adulthood.[24] Ethnicity may play a role in some allergies; however, racial factors have been difficult to separate from environmental influences and changes due to migration.[24] It has been suggested that different genetic loci are responsible for asthma, to be specific, in people of European, Hispanic, Asian, and African origins.[28]

[edit] Hygiene hypothesis
Main article: Hygiene hypothesis Allergic diseases are caused by inappropriate immunological responses to harmless antigens driven by a TH2-mediated immune response. Many bacteria and viruses elicit a TH1-mediated immune response, which down-regulates TH2 responses. The first proposed mechanism of action of the hygiene hypothesis stated that insufficient stimulation of the TH1 arm of the immune system lead to an overactive TH2 arm, which in turn led to allergic disease.[29] In other words, individuals living in too sterile an environment are not exposed to enough pathogens to keep the immune system busy. Since our bodies evolved to deal with a certain level of such pathogens, when it is not exposed to this level, the immune system will attack harmless antigens and thus normally benign microbial objects — like pollen — will trigger an immune response.[30]

The hygiene hypothesis was developed to explain the observation that hay fever and eczema, both allergic diseases, were less common in children from larger families, which were, it is presumed, exposed to more infectious agents through their siblings, than in children from families with only one child. The hygiene hypothesis has been extensively investigated by immunologists and epidemiologists and has become an important theoretical framework for the study of allergic disorders. It is used to explain the increase in allergic diseases that have been seen since industrialization, and the higher incidence of allergic diseases in more developed countries. The hygiene hypothesis has now expanded to include exposure to symbiotic bacteria and parasites as important modulators of immune system development, along with infectious agents. Epidemiological data support the hygiene hypothesis. Studies have shown that various immunological and autoimmune diseases are much less common in the developing world than the industrialized world and that immigrants to the industrialized world from the developing world increasingly develop immunological disorders in relation to the length of time since arrival in the industrialized world.[31] Longitudinal studies in the third world demonstrate an increase in immunological disorders as a country grows more affluent and, it is presumed, cleaner.[32] The use of antibiotics in the first year of life has been linked to asthma and other allergic diseases.[33] The use of antibacterial cleaning products has also been associated with higher incidence of asthma, as has birth by Caesarean section rather than vaginal birth.[34][35]

[edit] Other environmental factors
International differences have been associated with the number of individuals within a population that suffer from allergy. Allergic diseases are more common in industrialized countries than in countries that are more traditional or agricultural, and there is a higher rate of allergic disease in urban populations versus rural populations, although these differences are becoming less defined.[36] Exposure to allergens, especially in early life, is an important risk factor for allergy. Alterations in exposure to microorganisms is another plausible explanation, at present, for the increase in atopic allergy.[12] Endotoxin exposure reduces release of inflammatory cytokines such as TNF-α, IFNγ, interleukin-10, and interleukin-12 from white blood cells (leukocytes) that circulate in the blood.[37] Certain microbe-sensing proteins, known as Toll-like receptors, found on the surface of cells in the body are also thought to be involved in these processes.[38] Gutworms and similar parasites are present in untreated drinking water in developing countries, and were present in the water of developed countries until the routine chlorination and purification of drinking water supplies.[39] Recent research has shown that some common parasites, such as intestinal worms (e.g., hookworms), secrete chemicals into the gut wall (and, hence, the bloodstream) that suppress the immune system and prevent the body from attacking the parasite.[40] This gives rise to a new slant on the hygiene hypothesis theory — that coevolution of man and parasites has led to an immune system that functions correctly only in the presence of the parasites. Without them, the immune system becomes unbalanced and oversensitive.[41] In particular, research suggests that allergies may coincide with the delayed establishment of gut flora in infants.[42] However, the research to support this theory is

conflicting, with some studies performed in China and Ethiopia showing an increase in allergy in people infected with intestinal worms.[36] Clinical trials have been initiated to test the effectiveness of certain worms in treating some allergies.[43] It may be that the term 'parasite' could turn out to be inappropriate, and in fact a hitherto unsuspected symbiosis is at work.[43] For more information on this topic, see Helminthic therapy.

[edit] Pathophysiology

This is a summary diagram that explains how allergy develops.

Tissues affected in allergic inflammation.

[edit] Acute response

Degranulation process in allergy. Second exposure to allergen.1 - antigen; 2 - IgE antibody; 3 FcεRI receptor; 4 - preformed mediators (histamine, proteases, chemokines, heparine); 5 granules; 6 - mast cell; 7 - newly formed mediators (prostaglandins, leukotrienes, thromboxanes, PAF)

In the early stages of allergy, a type I hypersensitivity reaction against an allergen encountered for the first time and presented by a professional Antigen-Presenting Cell causes a response in a type of immune cell called a TH2 lymphocyte, which belongs to a subset of T cells that produce a cytokine called interleukin-4 (IL-4). These TH2 cells interact with other lymphocytes called B cells, whose role is production of antibodies. Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a kind of Fc receptor called FcεRI) on the surface of other kinds of immune cells called mast cells and basophils, which are both involved in the acute inflammatory response. The IgE-coated cells, at this stage are sensitized to the allergen.[12] If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils. Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complex interacts with the same allergenic molecule, and activates the sensitized cell. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth muscle contraction. This results in rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on the individual, allergen, and mode of introduction, the symptoms can be systemwide (classical anaphylaxis), or localized to particular body systems; asthma is localized to the respiratory system and eczema is localized to the dermis.[12]

[edit] Late-phase response
After the chemical mediators of the acute response subside, late phase responses can often occur. This is due to the migration of other leukocytes such as neutrophils, lymphocytes, eosinophils and macrophages to the initial site. The reaction is usually seen 2–24 hours after the original reaction.[44] Cytokines from mast cells may also play a role in the persistence of long-term effects. Late phase responses seen in asthma are slightly different from those seen in other allergic responses, although they are still caused by release of mediators from eosinophils, and are still dependent on activity of TH2 cells.[45]

[edit] Diagnosis
An allergy testing machine being operated in the diagnostic immunology lab at Lackland Air Force Base Before a diagnosis of allergic disease can be confirmed, the other possible causes of the presenting symptoms should be carefully considered.[46] Vasomotor rhinitis, for example, is one of many maladies that shares symptoms with allergic rhinitis, underscoring the need for professional differential diagnosis.[47] Once a diagnosis of asthma, rhinitis, anaphylaxis, or other allergic disease has been made, there are several methods for discovering the causative agent of that allergy.

Effective management of allergic diseases relies on the ability to make an accurate diagnosis.[48] Allergy testing can help confirm/rule out allergies and consequently reduce adverse reactions and limit unnecessary avoidance and medications.[49][50] Correct diagnosis, counseling and avoidance advice based on valid allergy test results will help reduce the incidence of symptoms, medications and improve quality of life.[49] For assessing the presence of allergen-specific IgE antibodies, you can use two different methods—a skin prick test or an allergy blood test. Both methods are recommended by the NIH guidelines and have similar diagnostic value in terms of sensitivity and specificity.[50][51] A healthcare provider can use the test results to identify the specific allergic triggers that may be contributing to the symptoms. Using this information, along with a physical examination and case history, the doctor can diagnose the cause of the symptoms and tailor treatments that will help the patient feel better. A negative result can help the doctor rule out allergies in order to consider other possible. NIH Guidelines state that: “sIgE tests are useful for identifying foods potentially provoking IgEmediated food-induced allergic reactions, and specified „„cutoff‟‟ levels, defined as 95% predictive values, may be more predictive than skin prick tests of clinical reactivity in certain populations.” It further states, “sIgE tests are very useful for detecting the presence of sIgE antibodies, which indicates the presence of allergic sensitization. Fluorescence-labeled antibody assays have comparable sensitivity to that of skin prick tests, and the absolute levels of sIgE antibodies may directly correlate with the likelihood of clinical reactivity when compared with oral food challenges for the identification of foods provoking IgE mediated FA.”[52] According to NICE Guidelines, skin prick tests and blood tests are equally cost-effective and health economic evidence show that both the IgE antibody test and the skin prick test were cost effective compared with no test.[49] Also, earlier and more accurate diagnoses save cost due to reduced GP consultations, referrals to secondary care, misdiagnosis and emergency admissions.[53] Allergy undergoes dynamic changes over time. Regular allergy testing of relevant allergens provides information on if and how patient management can be changed, in order to improve health and qu

Anaphylactic shock: A widespread and very serious allergic reaction. Symptoms include dizziness, loss of consciousness, labored breathing, swelling of the tongue and breathing tubes, blueness of the skin, low blood pressure, heart failure, and death. Immediate emergency treatment is required for this type of shock, including administration of antivenom in the case of bee or wasp stings.ality of

life. An nual testing is often the practice for determining whether allergy to milk, egg, soy, and wheat have been outgrown and the testing interval is extended to 2 to 3 years for allergy to peanut, tree nuts, fish, and crustacean

What is it?

Anaphylaxis is an extreme allergic reaction to certain foods, insect stings or drugs, which results in rapid chemical changes in the body. The most common triggers are nuts, eggs, shellfish, pollen, dust, latex, certain medications, wasps and bee stings. Top Symptoms

    

Blood vessels dilate, producing red, blotchy skin Air passages become constricted, resulting in breathing difficulties Face and neck may swell Heart, brain and lungs may suffer from a dramatic drop in oxygen supply Casualty may wheeze and gasp for air

Serum Sickness


Author: Hassan M Alissa, MD; Chief Editor: Herbert S Diamond, MD more...

Pathophysiology
Serum sickness is an example of the type III, or immune complex–mediated, hypersensitivity disease. The molecular size, charge, structure, amount, and valence of the antigen involved influence the type of immune complexes formed.[2] After the initial exposure to a foreign antigen in the absence of a preexisting antibody, serum sickness can develop within 1-2 weeks. Upon subsequent exposure, however, serum sickness develops sooner. The disease appears as the antibody formation begins, and the pathogenesis of serum sickness is related to protracted interaction between antigen and antibody in the circulation, with antigen-antibody complex formation in an environment of antigen excess. The immunologic interactions observed in serum sickness occur when antigens capable of remaining in the circulation for long periods incite antibody formation.[3] Typically, serum protein molecules are removed from the circulation by nonimmune processes that are not yet completely understood. Small complexes usually circulate without triggering inflammation, and large complexes are cleared by the reticuloendothelial system. However, intermediate-sized complexes that develop in the context of slight antigen excess may deposit in blood vessel walls and tissues, where they induce vascular and tissue damage resulting from activation of complement and granulocytes.[4] Endothelial cells increase the expression of adhesion molecules, and monocytes and macrophages release proinflammatory cytokines. Subsequently, additional inflammatory cells are recruited, and necrosis of the small vessels develops. Complement activation promotes chemotaxis and adherence of neutrophils to the site of immune complex deposition. This may be facilitated by increased vascular permeability due to release of vasoactive amines from tissue mast cells.[4]

At this point, complement levels fall to half their levels prior to the antibody response.[3] This clinicopathological syndrome usually develops within 1-2 weeks of antigen injection. Free antigen continues to clear from the blood, leading to antibody excess and the formation of large immune complexes, which are quickly removed by circulating macrophages. Finally, the antigen is no longer detectable, and the level of circulating antibodies continues to rise. Clinical recovery is usually apparent after 7-28 days, as intermediate-sized immune complexes are cleared by the reticuloendothelial system. Secondary serum sickness is the result of antigen recognition by presensitized cells of the immune system. It is characterized by a shorter latent period, exaggerated symptoms, and a brief clinical course. Why immune complex disease occurs under certain circumstances is not known. Possible factors may include high levels of immune complexes and a relative deficiency of some complement components leading to a decreased ability to eliminate immune complexes.[1] Not all substances that are recognized as foreign by the immune system elicit an immune response. The antigen must be of characteristic size or have specific antigenic determinants and physiological properties to be an effective stimulator of the immune system. After an appropriate antigen is introduced, an individual's immune system responds by synthesizing antibodies after 4-10 days. The antibody reacts with the antigen, forming soluble circulating immune complexes that may diffuse into the vascular walls, where they may initiate fixation and activation of complement. Complement-containing immune complexes generate an influx of polymorphonuclear leukocytes into the vessel wall, where proteolytic enzymes that can mediate tissue damage are released. Immune complex deposition and the subsequent inflammatory response are responsible for the widespread vasculitic lesions seen in serum sickness.

Rheumatic fever
From Wikipedia, the free encyclopedia

Jump to: navigation, search Rheumatic fever is an inflammatory disease that occurs following a Streptococcus pyogenes infection, such as streptococcal pharyngitis or scarlet fever. Believed to be caused by antibody cross-react

Pathophysiology

Pathophysiology of rheumatic heart disease Rheumatic fever is a systemic disease affecting the peri-arteriolar connective tissue and can occur after an untreated Group A Beta hemolytic streptococcal pharyngeal infection. It is believed to be caused by antibody cross-reactivity. This cross-reactivity is a Type II hypersensitivity reaction and is termed molecular mimicry. Usually, self reactive B cells remain anergic in the periphery without T cell co-stimulation. During a Streptococcus infection, mature antigen presenting cells such as B cells present the bacterial antigen to CD4-T cells which differentiate into helper T2 cells. Helper T2 cells subsequently activate the B cells to become plasma cells and induce the production of antibodies against the cell wall of Streptococcus. However the antibodies may also react against the myocardium and joints,[10] producing the symptoms of rheumatic fever. Group A streptococcus pyogenes has a cell wall composed of branched polymers which sometimes contain M protein that are highly antigenic. The antibodies which the immune system generates against the M protein may cross react with cardiac myofiber protein myosin,[11] heart muscle glycogen and smooth muscle cells of arteries, inducing cytokine release and tissue destruction. However, the only proven cross reaction is with perivascular connective tissue.[citation needed] This inflammation occurs through direct attachment of complement and Fc receptormediated recruitment of neutrophils and macrophages. Characteristic Aschoff bodies, composed of swollen eosinophilic collagen surrounded by lymphocytes and macrophages can be seen on light microscopy. The larger macrophages may become Aschoff giant cells. Acute rheumatic valvular lesions may also involve a cell-mediated immunity reaction as these lesions predominantly contain T-helper cells and macrophages.[12] In acute rheumatic fever, these lesions can be found in any layer of the heart and is hence called pancarditis. The inflammation may cause a serofibrinous pericardial exudate described as "bread-and-butter" pericarditis, which usually resolves without sequelae. Involvement of the endocardium typically results in fibrinoid necrosis and verrucae formation along the lines of closure of the left-sided heart valves. Warty projections arise from the deposition, while subendothelial lesions may induce irregular thickenings called MacCallum plaques. Chronic rheumatic heart disease is characterized by repeated inflammation with fibrinous resolution. The cardinal anatomic changes of the valve include leaflet thickening, commissural fusion and shortening and thickening of the tendinous cords.[12]

[edit] Prevention

Prevention of recurrence is achieved by eradicating the acute infection and prophylaxis with antibiotics. The American Heart Association recommends that daily or monthly prophylaxis continue long-term, perhaps for life.[13 ivity that can involve the heart, joints, skin, and brain,[1] the illness typically develops two to three weeks after a streptococcal infection. Acute rheumatic fever commonly appears in children between the ages of 6 and 15, with only 20% of first-time attacks occurring in adults.[1] The illness is so named because of its similarity in presentation to rheumatism.[2]

Glomerulonephritis
Glomerulonephritis, also known as glomerular nephritis, abbreviated GN, is a renal disease (usually of both kidneys) characterized by inflammation of the glomeruli, or small blood vessels in the kidneys.[1] It may present with isolated hematuria and/or proteinuria (blood or protein in the urine); or as a nephrotic syndrome, a nephritic syndrome, acute renal failure, or chronic renal failure. They are categorized into several different pathological patterns, which are broadly grouped into non-proliferative or proliferative types. Diagnosing the pattern of GN is important because the outcome and treatment differs in different types. Primary causes are intrinsic to the kidney. Secondary causes are associated with certain infections (bacterial, viral or parasitic pathogens), drugs, systemic disorders (SLE, vasculitis), or diabetes.


[edit] Thin Basement Membrane Disease
Thin basement membrane disease is an autosomal dominant inherited disease characterized by thin glomerular basement membranes on electron microscopy. It is a benign condition that causes persistent microscopic hematuria.

[edit] Non Proliferative
This is characterised by absence of increase in the number of cells (lack of hypercellularity) in the glomeruli. They usually cause nephrotic syndrome. This includes the following types:

[edit] Minimal change GN (also known as Minimal Change Disease)
Main article: Minimal change disease This form of GN causes 78.4% of nephrotic syndrome in children, but only 20% in adults. As the name indicates, there are no changes visible on simple light microscopy, but on electron microscopy there is fusion of podocytes (supportive cells in the glomerulus). Immunohistochemistry staining is negative. Treatment consists of supportive care for the massive fluid accumulation in the patients body (= oedema) and as well as steroids to halt the

disease process (typically Prednisone 1 mg/kg). Over 90% of children respond well to steroids, being essentially cured after 3 months of treatment. Adults have a lower response rate (80%). Failure to respond to steroids ('steroid resistant') or return of the disease when steroids are stopped ('steroid dependent') may require cytotoxic therapy (such as cyclosporin), which is associated with many side-effects.

[edit] Focal Segmental Glomerulosclerosis (FSGS)
Main article: Focal segmental glomerulosclerosis FSGS may be primary or secondary to reflux nephropathy, Alport syndrome, heroin abuse or HIV. FSGS presents as a nephrotic syndrome with varying degrees of impaired renal function (seen as a rising serum creatinine, hypertension). As the name suggests, only certain foci of glomeruli within the kidney are affected, and then only a segment of an individual glomerulus. The pathological lesion is sclerosis (fibrosis) within the glomerulus and hyalinisation of the feeding arterioles, but no increase in the number of cells (hence non-proliferative). The hyaline is an amorphous material, pink, homogeneous, resulting from combination of plasma proteins, increased mesangial matrix and collagen. Staining for antibodies and complement is essentially negative. Steroids are often tried but not shown effective. 50% of people with FSGS continue to have progressive deterioration of kidney function, ending in renal failure.

[edit] Membranous glomerulonephritis
Main article: Membranous glomerulonephritis Membranous glomerulonephritis (MGN), a relatively common type of glomerulonephritis in adults, frequently produces a mixed nephrotic and nephritic picture. Its cause is usually unknown, but may be associated with cancers of the lung and bowel, infection such as hepatitis and malaria, drugs including penicillamine, and connective tissue diseases such as systemic lupus erythematosus. Individuals with cerebral shunts are at risk of developing shunt nephritis, which frequently produces MGN. Microscopically, MGN is characterized by a thickened glomerular basement membrane without a hypercellular glomerulus. Immunofluorescence demonstrates diffuse granular uptake of IgG. The basement membrane may completely surround the granular deposits, forming a "spike and dome" pattern. Tubules also display the symptoms of a typical Type III hypersensitivity reaction, which causes the endothelial cells to proliferate, which can be seen under a light microscope with a PAS stain.[2][3] Prognosis follows the rule of thirds: one-third remain with MGN indefinitely, one-third remit, and one-third progress to end-stage renal failure. As the glomerulonephritis progresses, the tubules of the kidney become infected, leading to atrophy and hyalinisation. The kidney appears to shrink. Treatment with corticosteroids is attempted if the disease progresses.

In extremely rare cases, the disease has been known to run in families, usually passed down through the females. This condition, similarly, is called Familial Membranous Glomerulonephritis. There have only been about nine documented cases in the world.

[edit] Proliferative
This type is characterised by increased number of cells in the glomerulus (hypercellular). Usually present as a nephritic syndrome and usually progress to end-stage renal failure (ESRF) over weeks to years (depending on type).

[edit] IgA nephropathy (Berger's disease)
Main article: IgA nephropathy
[4]

[edit] General Information IgA nephropathy is the most common type of glomerulonephritis in adults worldwide. It usually presents as macroscopic haematuria (visibly bloody urine). It occasionally presents as a nephrotic syndrome. It often affects young males within days (24-48hrs) after an upper respiratory tract or gastrointestinal infection. Microscopic examination of biopsy specimens shows increased number of mesangial cells with increased matrix (the 'cement' that holds everything together). Immuno-staining is positive for immunoglobulin A deposits within the matrix. Prognosis is variable, 20% progress to ESRF. ACE inhibitors are the mainstay of treatment. [edit] Summary This is a form of GN characterised by IgA deposits in the mesangeial regions and immunocytochemistry is required for definitive diagnosis of the disease. [edit] Presentation 1. Recurrent gross or microscopic hematuria


gross hematuria occurs post-infection of the respiratory (more common), gastrointestinal, or urinary tract

1. mild proteinuria 2. occasionally nephrotic syndrome (although it usually has a nephritic presentation) 3. rarely, presents with crescentic Rapidly progressive GN [edit] Causes

The disease can be primary or secondary to liver and intestinal diseases. It also overlaps with Henoch-Schonlein purpura, a systemic renal disease in children in which similar IgA deposits occur. [edit] Pathology plasma polymeric IgA is increased in IgA Nephropathy, and circulating IgA-containing immune complexes can be found in the blood of some patients. Plasma IgA is usually monomeric and polymeric plasma IgA is broken down in the liver. IgA is normally found in mucus. There are two forms of IgA and only IgA1 causes nephrogenicity. [edit] Histology Characteristic finding: 1. IgA deposition in the mesangium seen by immunofloresence 2. Electron dense deposits in electron microscopy 3. Absence of early complement components May find: 1. 2. 3. 4. 5. normal glomeruli mesangioproliferative GN focal proliferative GN (healing may cause focal segmental sclerosis) overt cresentic glomerulonephritis leukocytes in glomerular capillaries

[edit] Post-infectious
Post-infectious glomerulonephritis can occur after essentially any infection, but classically occurs after infection with Streptococcus pyogenes. It typically occurs 10–14 days after a skin or pharyngeal infection with this bacterium.

Allergic rhinitis
From Wikipedia, the free encyclopedia

Jump to: navigation, search For the play, see Hay Fever.

Allergic rhinitis

Pollen grains from a variety of common plants can cause hay fever.

ICD-10

J30

ICD-9

477

OMIM

607154

DiseasesDB

31140

MedlinePlus

000813

eMedicine

ent/194 med/104, ped/2560

MeSH

D012221

Allergic rhinitis is an allergic inflammation of the nasal airways. It occurs when an allergen, such as pollen, dust or animal dander (particles of shed skin and hair) is inhaled by an individual with a sensitized immune system. In such individuals, the allergen triggers the production of the antibody immunoglobulin E (IgE), which binds to mast cells and basophils containing histamine. ". When caused by pollens of any plants, it is called "pollinosis", and if specifically caused by grass pollens, it is known as "hay fever Ironically, in hay fever, there is neither any fever nor any hay, but since grasses shed their pollens into the air, at about the same time that hay is being cut, the common term hay fever is used. IgE bound to mast cells are stimulated by pollen and dust, causing the release of inflammatory mediators such as histamine (and other chemicals).[1] This usually causes sneezing, itchy and

watery eyes, swelling and inflammation of the nasal passages, and an increase in mucus production. Symptoms vary in severity between individuals. Very sensitive individuals can experience hives or other rashes. Particulate matter in polluted air, and chemicals such as chlorine and detergents, which can normally be tolerated, can greatly aggravate allergic rhinitis. The physician John Bostock first described hay fever in 1819 as a disease. Allergies are common. Heredity and environmental exposures may contribute to a predisposition to allergies. It is roughly estimated that one in three people have an active allergy at any given time and at least three in four people develop an allergic reaction at least once in their lives. In Western countries between 10–25% of people annually are affected by allergic rhinitis.[2] hide

edit Classification
Allergic rhinitis may be seasonal or perennial. Seasonal allergic rhinitis occurs particularly during pollen seasons. It does not usually develop until after 6 years of age. Perennial allergic rhinitis occurs throughout the year. This type of allergic rhinitis is commonly seen in younger children.[3] Allergic rhinitis may also be classified as Mild-Intermittent, Moderate-Severe intermittent, MildPersistent, and Moderate-Severe Persistent. Intermittent is when the symptoms occur <4 days per week or <4 consecutive weeks. Persistent is when symptoms occur >4 days/week and >4 consecutive weeks. The symptoms are considered mild with normal sleep, no impairment of daily activities, no impairment of work or school, and if symptoms are not troublesome. Severe symptoms result in sleep disturbance, impairment of daily activities, and impairment of school or work.[4]

[edit] Signs and symptoms
The characteristic symptoms of allergic rhinitis are: rhinorrhea (excess nasal secretion), itching, and nasal congestion and obstruction.[5] Characteristic physical findings include conjunctival swelling and erythema, eyelid swelling, lower eyelid venous stasis, transverse nasal crease, swollen nasal turbinates, and middle ear effusion.[6] Other physical signs include folds in the skin below the lower eyelid known as Dennie–Morgan folds, and rings under the eyes, known in patients with allergic rhinitis as "allergic shiners". Sufferers might also find that cross-reactivity occurs.[7] For example, someone allergic to birch pollen may also find that they have an allergic reaction to the skin of apples or potatoes.[8] A clear sign of this is the occurrence of an itchy throat after eating an apple or sneezing when peeling potatoes or apples. This occurs because of similarities in the proteins of the pollen and the food.[9] There are many cross-reacting substances.

Some disorders may be associated with allergies: Comorbidities include eczema, asthma and depression

[edit] Allergy testing
Allergy testing may reveal the specific allergens to which an individual is sensitive. Skin testing is the most common method of allergy testing. This may include intradermal, scratch, patch, or other tests. Less commonly, the suspected allergen is dissolved and dropped onto the lower eyelid as a means of testing for allergies. This test should only be done by a physician, never the patient, since it can be harmful if done improperly. In some individuals who cannot undergo skin testing (as determined by the doctor), the RAST blood test may be helpful in determining specific allergen sensitivity. Allergy testing can either show allergies that aren't actually causing symptoms, or miss allergies that do cause symptoms. The intradermal allergy test is more sensitive than the skin prick test but is more often positive in people who do not have symptoms to that allergen.[10] Even if a person has negative skin-prick, intradermal and blood tests for allergies, they may still have allergic rhinitis, from a local allergy in the nose. This is called local allergic rhinitis.[11] Specialized testing is necessary to diagnose local allergic rhinitis.[12]

[edit] Pollen allergies
Allergic rhinitis triggered by the pollens of specific seasonal plants is commonly known as "hay fever", because it is most prevalent during haying season. However, it is possible to suffer from hay fever throughout the year. The pollen which causes hay fever varies between individuals and from region to region; generally speaking, the tiny, hardly visible pollens of wind-pollinated plants are the predominant cause. Pollens of insect-pollinated plants are too large to remain airborne and pose no risk. Examples of plants commonly responsible for hay fever include:


 

Trees: such as pine, birch (Betula), alder (Alnus), cedar, hazel, hornbeam (Carpinus), horse chestnut (Aesculus), willow (Salix), poplar, plane (Platanus), linden/lime (Tilia) and olive (Olea). In northern latitudes birch is considered to be the most important allergenic tree pollen, with an estimated 15–20% of hay fever sufferers sensitive to birch pollen grains. A major antigen in these is a protein called Bet V I. Olive pollen is most predominant in Mediterranean regions. Hay fever in Japan is caused primarily by sugi (Cryptomeria japonica) and hinoki (Chamaecyparis obtusa) tree pollen. Grasses (Family Poaceae): especially ryegrass (Lolium sp.) and timothy (Phleum pratense). An estimated 90% of hay fever sufferers are allergic to grass pollen. Weeds: ragweed (Ambrosia), plantain (Plantago), nettle/parietaria (Urticaceae), mugwort (Artemisia), Fat hen (Chenopodium) and sorrel/dock (Rumex)

[edit] Management

The goal of rhinitis treatment is to prevent or reduce the symptoms caused by the inflammation of affected tissues. Measures which are effective include avoiding the allergen.[5] Intranasal corticosteroids are the preferred treatment if medications are required with other options used only if these are not effective.[5] Mite proof covers, air filters, and withholding certain foods in childhood do not have evidence supporting their use.[5]

[edit] Steroids
Intranasal corticosteroids are used to control symptoms associated with sneezing, rhinorrhea, itching and nasal congestion. It is an excellent choice for perennial rhinitis.[13] Steroid nasal sprays are effective and safe, and may be effective without oral antihistamines. They take several days to act and so need be taken continually for several weeks as their therapeutic effect builds up with time. Systemic steroids such as prednisone are effective at reducing nasal inflammation, but their use is limited by their short duration of effect and the side effects of prolonged steroid therapy.

[edit] Other
Other measures that may be used second line include: antihistamines, decongestants, cromolyn, leukotriene receptor antagonists, and nonpharmacologic therapies such as nasal irrigation.[5] Antihistamine drugs can have undesirable side-effects, most notably drowsiness. First generation antihistamine drugs such as diphenhydramine cause drowsiness, but not second- and thirdgeneration antihistamines such as cetirizine and loratadine.[14] Antihistamine drugs can be taken orally to control symptoms such as sneezing, rhinorrhea, itching and conjunctivitis. It is best to take the medication before exposure, especially for seasonal allergic rhinitis. Ophthalmic antihistamines (such as ketotifen) are used for conjunctivitis; intranasal forms are used for sneezing, rhinorrhea and nasal pruritus.[14] Pseudoephedrine is also indicated for vasomotor rhinitis. It is only used when nasal congestion is present and can be used with antihistamines. In the United States, oral decongestants containing pseudoephedrine must be purchased behind the pharmacy counter by law to combat the making of methamphetamin

Immunity (medical)
From Wikipedia, the free encyclopedia

Jump to: navigation, search Immunity is a biological term that describes a state of having sufficient biological defenses to avoid infection, disease, or other unwanted biological invasion. In other words, it is nothing but the capability of the body to resist harmful microbes from entering the body. Immunity involves both specific and non-specific components. The non-specific components act either as barriers or

as eliminators of wide range of pathogens irrespective of antigenic specificity. Other components of the immune system adapt themselves to each new disease encountered and are able to generate pathogen-specific immunity. e.[15]

Drug Allergies/Sensitivities


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Drug Allergies/Sensitivities
Top Home > Library > Health > Children's Health Encyclopedia Definition A drug allergy is an adverse reaction to a medication, often an antibiotic, that is mediated by the body's immune system. A drug sensitivity is an unusual reaction to a drug that does not involve the immune system. Description Adverse reactions to medication may be allergic reactions involving a child's immune system, individual sensitivities to a drug, or side effects of the drug itself. Some children are allergic or sensitive to drugs that are not harmful for most people. Some drugs, such as aspirin and penicillin or related antibiotics, may induce allergic reactions in some children and sensitivities in other children.
Drug Allergies

Drug allergies account for 5–10 percent of all adverse reactions to medications. They occur when the immune system—designed to protect the body from foreign substances such as bacteria and viruses—recognizes a medication as a harmful substance that must be destroyed. Drugs often induce an immune response; however, the symptoms of an allergic reaction occur in only a small number of children. Although most allergic drug reactions have mild symptoms, on rare occasions they can be life-threatening.

Drug allergies are unpredictable. Most drug allergies develop within days or occasionally weeks of beginning a drug treatment. Although it is very unusual to develop an allergy after months of taking a drug, sometimes children develop a drug allergy after having received multiple doses of the drug. Unlike other types of adverse drug reactions, the frequency and severity of allergic reactions to drugs usually are independent of the amount of drug that is administered. Even a very small amount of a drug can trigger an allergic reaction. Many classes of drugs can induce allergic reactions, resulting in a wide variety of symptoms affecting various tissues and organs. The likelihood that a drug will cause an allergic reaction depends in part on the chemical properties of the drug. Larger drug molecules are more likely to cause allergic reactions than smaller drug molecules. Larger drug molecules include the following:
  

insulin antiserum which contains large immune-system proteins called antibodies recombinant proteins produced by genetic engineering

Unlike most other allergens, such as pollen or mold spores, drug molecules often are too small to be detected by the immune system. Smaller drugs such as antibiotics cannot induce an immune response unless they combine with a body cell or a carrier protein in the blood. Furthermore, drug allergies often are caused by the breakdown products or metabolites of the drug rather than by the drug itself. Sometimes the same drug, such as penicillin, can induce different types of allergic reactions. IGE-MEDIATED ALLERGIES. Most allergies, including most drug allergies, occur because of a reaction with an immune system antibody called immunoglobulin E (IgE). The first exposure to the drug sensitizes the child's immune system by inducing specialized white blood cells to produce IgE that recognizes the specific drug. On subsequent exposure to the drug, the drugspecific IgE antibodies bind to the drug on the surfaces of certain cells of the immune system. This binding activates the cells to release histamine and other chemicals that can cause a variety of symptoms. Thus, a child who has no reaction on first exposure to a drug may have a severe reaction with subsequent exposure. Drug-specific IgE antibodies may cross-react with other drugs that have similar chemical properties, thereby triggering an allergic reaction, as is the case in the penicillin family. For example, the antibodies of a child allergic to penicillin may cross-react with the antibiotic amoxicillin or nafcillin. Insect stings and the intravenous injection of certain drugs are the most common causes of anaphylaxis, the most severe and frightening allergic response. Anaphylaxis involves the entire body. Although it is rare, several hundred Americans die of anaphylaxis every year. Anaphylaxis is most common in children who are allergic to penicillins and similar drugs. These drugs cause 97 percent of all deaths from drug allergies.

OTHER TYPES OF DRUG ALLERGIES. Some drug allergies occur via immune system components other than IgE. Cytotoxic/cytolytic drug allergies occur when a drug allergen that is associated with a cell membrane, usually a blood cell, interacts with other types of antibodies— called immunoglobulin G (IgG) or immunoglobulin M (IgM)—along with other immune system factors. These interactions damage or destroy body cells. Immune complex drug allergies occur when a drug combines with antibodies and other immune system components to form complexes in the blood. These complexes can be deposited in blood vessels and on membranes, causing inflammatory reactions that may be either localized or throughout the body. For instance, serum sickness typically causes a rash and joint swelling after the offending drug is administered. T-cell-mediated allergic drug reactions require immune system cells called T-memory cells that are specific for the drug allergen. When exposed to the allergen, the T-cells are activated and cause an inflammatory response. The most common example of this type of reaction is allergic contact dermatitis that causes inflammations of the skin.
Drug Sensitivities

Drug sensitivities (also called idiosyncratic reactions or unusual adverse reactions) do not involve the child's immune system or the release of histamine. However, the symptoms of drug sensitivities can be very similar to the symptoms of a drug allergy. Unlike drug allergies, sensitivities often occur upon first exposure to a drug and do not lead to anaphylaxis. Demographics Anyone can develop an allergy to any drug at any time. It is not clear why some children develop allergies to drugs that are well tolerated by most people. It is estimated that up to 10 percent of all people develop allergies to penicillin or other antibiotics at some point in their lives. Those taking multiple medications or frequent courses of antibiotics appear to be more at risk for developing drug allergies. The most common drug sensitivity is to aspirin. Nearly 1 million Americans, primarily adults, are sensitive to aspirin. However, many medications, including aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Advil, Motrin, and others), can trigger an asthma attack in children. Asthma is a common chronic respiratory condition in children. Attacks occur when the air passages from the lungs to the nose and mouth are narrowed causing difficulty breathing. Aspirin and aspirin-like medications are common triggers for asthma attacks in as many as 30 percent of asthmatic children. Causes and Symptoms
Drug Allergies

Any drug (either prescription or over-the-counter) can evoke an allergic reaction; however, antibiotics, especially penicillin and related drugs, are the most common cause of drug allergies.

Children also frequently (i.e. to these agents more frequently than to other agents) develop allergies to the following:
     

aspirin sulfa-based drugs barbiturates anticonvulsants insulin preparations, particularly those from animal sources dyes that are injected into blood vessels before taking x rays

The symptoms of a drug allergy vary from quite mild to life-threatening anaphylaxis. Unlike other common allergies, drug allergies often affect the entire body. The most common symptoms of a drug allergy are skin conditions including rash, generalized itching, and urticaria (hives; a very itchy rash with red swellings affecting only a small area of skin or the entire body; possibly the early symptom of anaphylaxis). The type of rash depends on the type of allergic response. Less common symptoms of drug allergies include runny nose, sneezing, and congestion. Uncommon but more serious symptoms of a drug allergy include the following:
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nausea, vomiting, diarrhea abdominal pain or cramps fever low blood cell count wheezing and difficulty breathing inflammation of the lungs, kidneys, and joints angioedema (a sudden swelling of the mucous membranes and tissues under the skin, anywhere on the body but especially on the face, eyes, lips, neck, throat, and genitals)

Angioedema occurs within a few minutes of exposure to the drug, often in conjunction with urticaria. Angioedema often is asymmetrical: for example, only one side of the lip may be affected. Swelling of the tongue, mouth, and airways can cause difficulty speaking, swallowing, or breathing. Angioedema can become life-threatening if the swelling affects the larynx (voice box) and the air passages become blocked. Emergency symptoms of a drug allergy include obstruction of the throat from swelling, severe asthma attack, and anaphylaxis. Allergic reactions to drugs are the most common cause of an inflammation of the kidneys called tubulointerstitial nephritis. The allergic reaction and development of this acute condition may occur between five days and five weeks after exposure to penicillin, sulfonamides, diuretics (drugs to increase urination), and aspirin and other NSAIDs. IGE-MEDIATED ALLERGIES. IgE-mediated allergies can be caused by the following:
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penicillin when the allergic reaction is immediate blood factors, including antisera hormones

 

vaccines (usually an allergic reaction to some component of the vaccine such as egg protein, gelatin, or neomycin, an antibiotic) very rarely, local anesthetics such as Novocain

The most common symptom of an IgE-mediated drug allergy is a rash that develops after the child has taken the drug for several days and produced antibodies against it. ANAPHYLAXIS. Anaphylaxis is a violent immune system reaction that can occur when a child who has large amounts of drug-specific IgE antibodies is re-exposed to the drug. The antibodies bind to the drug very rapidly causing an immediate, severe response. Anaphylaxis most often is caused by the following:
   

penicillin and related antibiotics streptomycin tetracycline insulin

Analphylaxis usually begins within one to 15 minutes following exposure to the drug. Only rarely does the reaction begin an hour or more after exposure. Anaphylaxis can progress very rapidly leading to collapse, seizures, and loss of consciousness within one to two minutes. Without treatment, cessation of breathing, anaphylactic shock, and death can occur within 15 minutes. Any drug that has caused anaphylaxis in a child will probably cause it again on subsequent exposure, unless measures are taken to prevent it. Symptoms of anaphylaxis include:
           

urticaria on various parts of the body angioedema intense itching flushing of the skin coughing and sneezing nausea, vomiting, diarrhea abdominal pain or cramping tingling sensations ear throbbing heart palpitations uneasiness or sudden extreme anxiety swollen throat and/or constricted air passages causing a hoarse voice, wheezing, and difficulty breathing, the most characteristic symptom of anaphylaxis

Constriction of the air passages in the bronchial tract and/or throat, accompanied by shock, can cause a drastic drop in blood pressure that may lead to the following:
  

rapid pulse paleness weakness

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dizziness, lightheadedness slurred speech mental confusion unconsciousness

OTHER DRUG ALLERGIES. Cytotoxic/cytolytic-type drug allergies can be caused by the following:
   

penicillin sulfonamides quinidine methyldopa

Cytotoxic/cytolytic-type of drug allergy can result in the following:
  

immune hemolytic anemia due to the destruction of red blood cells thrombocytopenia from the reduction in blood platelets granulocytopenia from a deficiency of a type of white blood cell called a granular leukocyte

Drugs that can cause immune complex reactions, such as serum sickness or drug-induced lupus syndromes, include:
   

hydralazine procainamide isoniazid phenytoin

Serum sickness (a delayed type of drug allergy that may take one to three weeks to develop) can be caused by an allergic reaction to penicillin or related antibiotics. Serum sickness also can be an allergic response to animal proteins present in an injected drug. Serum sickness is characterized by the following:
       

fever aching joints swelling of the lymph nodes rash general body swelling skin lesions nephritis (an inflammation of the kidneys) hepatitis (an inflammation of the liver)

Some drugs, including penicillins and sulfonamides, can cause delayed dermatologic allergic reactions. These are various types of skin reactions, including eczema, that do not occur immediately upon exposure to the drug. These types of allergies are thought to be caused by metabolites formed from the breakdown or further reaction of the drug.

Drug allergies can result in hypersensitivity reactions, which in turn can result in liver disorders. Such damage can be caused by the following:
    

sulfonamides phenothiazines halothane phenytoin isoniazid

Pulmonary hypersensitivity allergic reactions that affect the lungs and result in rashes and fever may be caused by nitrofurantoin and sulfasalazine.
Drug Sensitivities

Children may have drug sensitivities to aspirin; other NSAIDs; opiates such as morphine and codeine; and some antibiotics, including erythromycin and ampicillin. Symptoms of drug sensitivities often are very similar to those of drug allergies and include rashes, urticaria, and angioedema. Anaphylactoid drug reactions are similar to anaphylactic reactions. However, they are caused by a drug sensitivity rather than a drug allergy and can occur upon the first exposure to a drug. Anaphylactoid reactions can occur in response to the following:
    

opiates radiopaque dyes (radiocontrast media) used in x-ray procedures; 2–3% of patients have immediate generalized reactions to these dyes aspirin and other NSAIDs in some people, usually adults polymyxin pentamidine

When to Call the Doctor

A physician should be consulted whenever a child has an allergic reaction or sensitivity to a drug. The parent or caregiver should seek emergency assistance if a child has a severe or rapidly worsening allergic reaction to a drug that includes wheezing, difficulty breathing, or other symptoms of anaphylaxis. Diagnosis It is important to distinguish between an uncomfortable but mild side effect of a drug and an allergic reaction or sensitivity which could be life-threatening. A drug allergy or sensitivity most often is diagnosed by discontinuing the drug and observing whether the symptoms disappear. Following a drug reaction the parent should describe the exact course of the reaction; the type of symptoms, when they occurred, and how long they lasted; and whether the child had previously been exposed to the drug. A previous allergic-type reaction to the medication usually is

considered diagnostic of a drug allergy. A reaction upon a child's first exposure to the drug is probably a drug sensitivity. Further diagnosis of a drug allergy may depend on the following:
         

a complete medical history, including all drugs taken in the past month, when and how the child received certain drugs, and previous drug reactions whether the drug is known to cause allergic reactions a family history of drug allergies the timing of symptom-onset following drug exposure the timing of symptom-disappearance after discontinuing the drug the type of rash involvement of joints, lymph nodes, or liver associated viral infections other concurrent medications the presence of a chronic disease

Allergy Tests

Skin prick tests or intra dermal tests to demonstrate IgE allergies are standardized for very few medications. Penicillin testing is standardized and can be used in extreme situations. Incremental drug challenge tests are also available for several drugs. These tests differ from tests for IgE antibodies but are still useful for demonstrating drug sensitivities. They must be done cautiously as patients are likely to have reactions during the challenge. The allergist injects a tiny amount of the drug under the skin. If the child is allergic to the drug, swelling and itching occur at the site of injection within 15 to 20 minutes. Skin tests can be used to test for only a few drug allergies, for example, for penicillin and closely related antibiotics. Incremental challenge tests are performed for insulin, streptokinase, chymopapain, and antiserum. Patch tests may be used to test for allergies to drugs that are applied to the skin such as topical antibiotics. A patch containing a small amount of the drug is applied to the skin to test for a localized reaction. Desensitization is a test in which the allergist gives the child a tiny dose of the drug—as little as 0.001 or 0.00001 of the usual dose—in its usual form—orally, topically, or by injection. Gradually the dose is increased, and the child's reaction of observed. This procedure is done only in life-threatening situations, however, and only under close observation. Treatment
Mild Allergies/Sensitivities

Drug allergies and sensitivities most often are treated by discontinuing the medication and replacing it with an alternative one. Mild symptoms usually disappear within a few days after discontinuation of the drug. Hives usually disappear within a few hours. Itchy rashes and hives

may be treated with over-the-counter products such as oral antihistamines. Occasionally topical corticosteroid drugs are applied to the skin. Angioedema can take hours or days to subside; however, the swelling can be reduced with a corticosteroid or antihistamine.
Severe Reactions

Severe immediate reactions occurring within one hour of drug administration, accelerated reactions occurring one to 72 hours after drug exposure, and late reactions (including rash, serum sickness, or fever) that develop more than 72 hours after drug exposure are all treated as follows:
  

discontinuation of all nonessential suspect drugs antihistamines for hives and rashes oral corticosteroids for inflammation

Severe angioedema requires an immediate injection of epinephrine (a form of adrenaline) and further observation in a hospital. Anaphylaxis requires an immediate injection of epinephrine into a thigh muscle. Epinephrine opens the air passageways and improves blood circulation. Intravenous fluids and injections of antihistamines or corticosteroids such as hydrocortisone also are administered. Cardiopulmonary resuscitation (CPR) and intubation may be necessary. An asthma attack that is triggered by aspirin or other medications can be relieved by quick-relief or rescue medications. These include:
  

epinephrine short-acting bronchodilators such as albuterol, proventil, ventolin, or xopenex prednisone for all moderate to severe reactions

Desensitization

Desensitization or immunotherapy sometimes is used by an allergy/immunology specialist to treat drug allergies to insulin, penicillin, or other antibiotics. Small amounts of the drug are injected or swallowed over a period of hours or a few days or in slowly increasing doses, to reduce sensitivity. Once antibiotic desensitization has been achieved, the full course of antibiotic treatment is followed. The procedure must be repeated if the drug has been discontinued for more than 72 hours. Sometimes desensitization is used for non-IgE-mediated drug reactions. Desensitization may take up to a month for the following:
    

aspirin alloprinol gold sulfamethoxazole sulfasalazine

Prognosis Mild symptoms of a drug allergy usually disappear without treatment within a few days of discontinuing the drug. Although children may lose their sensitivity to penicillin, if the reaction was urticarial or anaphylaxis, they are not re-challenged with the drug for safety reasons (i.e. it is not possible to predict who has lost sensitivity). In rare cases drug allergies may cause severe asthma attacks, anaphylaxis, or death. Prevention Drug allergies are unpredictable because they occur after a child has been exposed to the drug one or more times. The major prevention for known drug allergies and sensitivities is to avoid those drugs and to inform all physicians, hospital personnel, and dentists of the allergies or sensitivities before treatment. In the case of a serious drug allergy, the child should wear a medical alert necklace or bracelet or carry a card (Medic-Alert and others) at all times to alert emergency medical personnel. Children with allergies or sensitivities to aspirin should avoid all aspirin-containing drugs. Such children usually can tolerate acetaminophen and non-acetylated salicylates such as sodium salicylate and salsalate. If a child is allergic to a drug for which there is no substitute, sometimes the dosage can be reduced to prevent an allergic reaction. If the allergy is mild and the drug cannot be discontinued, the physician may decide to pretreat the allergy, with an antihistamine such as diphenhydramine or a corticosteroid such as prednisone, before the drug is administered to reduce or eliminate the allergic reaction. The physician also may "treat through" the allergy by prescribing antihistamines and corticosteroids during drug administration. Some disorders cannot be diagnosed without the use of radiopaque dyes. Special dyes that reduce the risk of an anaphylactoid reaction can be used. Children at risk for reaction to such dyes may be premedicated with anti-histamines and corticosteroids alone or in combination with beta-adrenergic agents before the dye is injected. Premedications include the following:
  

prednisone diphenhydramine ephedrine

Parental Concerns When a child is given a new medication or starts a new course of treatment with a previous medication, parents should watch closely for symptoms of a drug allergy or sensitivity. If a child suffers a mild to moderate allergic reaction or sensitivity to a drug, the parent should take the following steps:


stay calm and reassure the child; anxiety can worsen the symptoms

 

apply calamine lotion and cold cloths for an itchy rash; do not use medicated lotions observe the child for signs of increasing distress

If a child shows signs of a severe allergic reaction or sensitivity, the parent or caregiver should:
      

inject allergy medication if it is available check the child's air passage, breathing, and circulation call 911 or other emergency assistance if the child is having difficulty breathing, becomes very weak, or loses consciousness begin rescue breathing or CPR if necessary calm and reassure the child inject emergency allergy medicine if available; do not give oral medication if the child is having difficulty breathing prevent shock by laying the child flat, elevating the feet, and covering the child with a coat or blanket

In the case of a severe allergic reaction, a parent should not:
  

assume that any pretreatment with allergy medication will protect the child place a pillow under the child's head if the child is having trouble breathing since this could block the air passage give the child anything by mouth

Resources
Books

Honsinger, Richard W., and George R. Green. Handbook ofDrug Allergy. Philadelphia: Lippincott Williams & Wilkins, 2004.
Periodicals

Honsinger, Richard W. "Drug Allergy." Annals of Allergy,Asthma, and Immunology 93, no. 2 (August 2004): 111. Roberts, Shauna S. "Drug Allergy FAQ." Diabetes Forecast 57, no. 4 (April 2004): 21–2.
Organizations

American Academy of Allergy, Asthma, & Immunology. 555 East Wells Street, Suite 1100, Milwaukee, WI 53202–3823. Web site: www.aaaai.org. American College of Allergy, Asthma & Immunology. 85 West Algonquin Road, Suite 550, Arlington Heights, IL 60005. Web site: www.acaai.org. Asthma and Allergy Foundation of America. 1233 20th Street NW, Suite 402, Washington, D.C. 20036. Web site: www.aafa.org.

National Institute of Allergy and Infectious Diseases. 6610 Rockledge Drive, MSC 6612, Bethesda, MD 20892–6612. Web site: www.niaid.nih.gov.
Web Sites

"Drug Reactions." The Allergy Report. Available online at www.aaaai.org/ar/working_vol3/051.asp (accessed December 27, 2004). Shepherd, Gillian. "Allergic Reactions to Drugs." Allergy & Asthma Advocate, Spring 2001. Available online at www.aaaai.org/patients/advocate/2001/spring/reactions.stm (accessed December 27, 2004). [Article by: Margaret Alic, Ph.D.]

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