Если аллергия на пенициллин можно флемоклав
Внимание! Информация для врачей.
Penicillin and related antibiotic allergy; skin testing; and desensitization
Liza C O’Dowd, MD
INTRODUCTION*—*Penicillin is the most commonly reported medication allergy, although many patients are not truly allergic [1-3]. Large studies, for example, have shown that at least 80 percent of individuals reporting penicillin allergy are able to tolerate treatment and have either been falsely labeled allergic or lost their sensitivity as a result of years of avoidance [4-6]. However, true penicillin allergy is not uncommon and is a leading cause of fatal drug reactions [7].
Adverse drug reactions to all medications combined are the cause of 2 to 5 percent of hospital admissions in the United States and complicate an additional 6 percent of hospitalizations [1,8].
The evaluation and desensitization of patients with suspected penicillin allergies will be reviewed here. The diagnosis and treatment of anaphylaxis is discussed separately. (See «Anaphylaxis in adults»).
EVALUATION OF PATIENTS WITH HISTORY OF PENICILLIN ALLERGY*—*Several types of allergic reactions can occur following the administration of penicillin (show table 1). Overall, 2 to 4 percent of allergic reactions are life-threatening [2,9,10]. Severe forms of drug allergy can occur via several mechanisms and include anaphylaxis (type I), Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug-induced hypersensitivity syndrome with multiorgan involvement (mechanism of the latter three reactions is uncharacterized). Type I reactions, which may present with anaphylaxis, angioedema, bronchospasm, or urticaria (hives) are the focus of this review.
History*—*It is important to verify the history of «allergy» since the patient may incorrectly assume a non-allergic side effect (especially a gastrointestinal side effect) to be allergic in origin.
Risk factors*—*Certain subgroups of patients are at higher risk for developing allergic reactions (of various types) to penicillins and related antibiotics [11-13]. Patients with HIV infection have higher rates of allergy to a variety of antibiotics, including amoxicillin [11]. Patients with cystic fibrosis frequently develop allergies to ticarcillin and piperacillin [12,13]. It is uncertain if these increased rates of reaction reflect the greater exposure to multiple drugs or are related to immunologic abnormalities associated with these diseases.
The development of exanthems in response to penicillins is well-described in patients during acute infectious mononucleosis and cytomegalovirus, although these types of reactions are distinct, as patients are generally able to tolerate the penicillin after recovering from the acute viral infection [14-17]. Non-pruritic, maculopapular rashes without other symptoms are reported in 3 to 7 percent of children taking amoxicillin, and are not considered a contraindication to future use of the causative drug [18,19].
Patients with a history of an allergic reaction to any drug have an increased incidence of reactions to other drugs. It has been estimated that patients with a history of penicillin allergy have a three-fold increased risk of reacting to any medication [20]. This phenomenon was well-illustrated in a review of 969 patients who had allergic reactions to sulfonamide antibiotics and were subsequently treated with nonantibiotic sulfonamides, including loop and thiazide diuretics and sulfonylureas [3]. These patients had an increased incidence of allergic reactions (including asthma, eczema, urticaria, dermatitis, Stevens-Johnson syndrome, and anaphylaxis) to the nonantibiotic sulfonamide (9.9 versus 1.6 percent in controls who had not had an prior allergic reaction to a sulfonamide antibiotic). However, their reaction rate to penicillin was even greater (14 percent). Thus, there was a greater incidence of reactivity to a non-related drug (penicillin) than to a related non-antibiotic sulfonamide, suggesting that the increased reactivity reflects a general predisposition to develop allergic reactions rather than a specific immunologic cross reactivity.
Assessing risk for anaphylaxis*—*Anaphylaxis from penicillin occurs with a frequency of one episode per 5000 to 10,000 courses of drug therapy [21]. Assessment of the risk is based upon a carefully obtained history coupled with skin testing when appropriate and available. Anaphylaxis can be identified by characteristic symptoms (show table 2). A high risk for anaphylaxis is suggested by a history of bronchospasm, angioedema, hypotension, or shock, particularly if these symptoms occurred within 30 minutes of drug administration during the prior year (show table 3). In contrast, people who report isolated maculopapular rashes without urticaria or pruritus are unlikely to have experienced an IgE-mediated reaction [22].
IgE-mediated penicillin allergy can be lost over time if a patient has successfully avoided exposure, with a minority of patients still being reactive after 20 years of avoidance. Thus, the time that has elapsed since the patient’s last reaction is also used to assess risk.
Our approach to the patient with a possible IgE-mediated penicillin allergy is summarized in the figure (show figure 1). Patients should ideally undergo a penicillin skin test (if available) if they have a history of penicillin or other beta-lactam allergy and require a beta-lactam antibiotic to treat a serious infection for which no other alternative antibiotic is appropriate [9,23]. (See «Penicillin skin testing» below).
At the moment, however, the supplies of commercially available PPL (the major determinant skin test reagent) have been withdrawn from the market within the United States and it is not clear when or if they will be re-introduced. If a reliable source of PPL is not available, skin testing will not reliably identify patients with allergic reactivity to penicillin, and should not be undertaken. In that case, a careful assessment of the patient’s history of reactions to penicillin or its derivatives must be used to assess risk.
PENICILLIN SKIN TESTING*—*Skin testing is the most reliable method of determining if a patient with a previous history of a penicillin allergy is at risk for an immediate hypersensitivity reaction upon rechallenge. Skin testing provides information about IgE-mediated, type 1 reactions only, and has no role in the evaluation of other types of reactions, such as Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), other exfoliative dermatitides, erythema multiforme, hepatitis, or nephritis.
In vivo, penicillin and its metabolites function as haptens, or small molecular weight molecules that adhere to proteins to form hapten-protein complexes that are antigenic. When penicillin G is added to a solution of protein or human serum, the beta-lactam ring of the drug spontaneously opens and binds to proteins to form a benzylpenicilloyl determinant. Approximately 95 percent of the administered penicillin undergoes this process; this altered form is called benzylpenicilloyl or the «major determinant». Other metabolic products of penicillin metabolism include penicilloate and penilloate; these are called the «minor determinants» [9]. Many patients who are allergic to penicillin have formed IgE molecules to these metabolite-protein complexes, rather than to the parent drug. Therefore, skin testing must include reagents that will allow detection of these antibodies.
Reagents and technique*—*Skin testing for penicillin should ideally be performed with penicillin G and the major and minor determinants.
Although benzylpenicilloyl complexed to protein (the major determinant) was previously produced commercially as benzylpenicilloyl polysine (PPL or PrePen), it is currently unavailable.
IgE antibodies to minor determinants are generally responsible for anaphylactic reactions and can predict the likelihood of a more severe reaction. IgE antibodies to major determinants of penicillin in general mediate urticarial drug reactions in addition to anaphylactic reactions [9,24].
Skin testing usually takes between one and four hours to complete and should be performed by an allergist/immunologist. Prick/puncture testing is performed initially. If prick testing is negative, then intradermal testing is performed.
A positive skin test is defined by the development of a wheal and flare reaction to either antigenic determinant that is equal or larger in size to that associated with the histamine control, with the histamine control normally producing a wheal of at least three mm in diameter. (See «Overview of skin testing for allergic disease»).
Testing is complete when the patient either has a positive reaction to any reagent or completes the testing protocol. In most centers, testing is followed by the administration of a single dose of oral penicillin and a period of observation to confirm that the drug is tolerated.
Источник
Здравствуйте.
Обращаюсь за консультацией.
Такая ситуация с одной моей родственницей (ей 21 год):
Пре-амбула: ДМС, 5-6 месяцев назад держалась температура от 37 до 38: очень полно обследовали в 122 МСЧ и больнице им. Боткина (СПб). Ничего не нашли, выписали с диагнозом «хронический тонзиллит».
Развитие:
В воскресенье вечером заболела подмышка, температура 37,5.
В ДМС записали на понедельник к хирургу в «Поликлиническом комплексе». Хирург осмотрел, сказал «к терапевту».
Терапевт осмотрел, сказал «будем лечить воспаление лимфатического узла»:
Рецепт:
ФЛЕМОКЛАВ СОЛЮТАБ
ХИЛАК-ФОРТЕ
ЭУБИКОР
Терапевтом на вопрос «есть ли аллергии?» и ответ «на пенициллин — в детстве» была сделана запись на карточке в разделе аллергия: «пенициллин».
В аптеке ФЛЕМОКЛАВ предложили заменить на АМОКСИКЛАВ: действующее вещество тоже: АМОКСИЦИЛЛИН и КАЛИЯ КЛАВУЛАНАТ. Заменили. 2 таблетки в понедельник.
Во вторник утром: сыпь на ладонях, ладони припухли и болят. Терапевт — на выезде. Принимает зав. поликлинической сменой. Говорит «аллергия, бросаем антибиотики. Лечим аллергию»: укол + Рецепт:
ЭРИУС №10
В среду утром: Сильная Припухлость: ладони, стопы, слизистые оболочки и тд. Сыпь: ладони, стопы, слизистые оболочки.
Зав. поликлинической сменой: госпитализация в больницу им. Боткина.
Направление:
аллергия на АМОКСИКЛАВ
ротавирусная инфекция.
Больница им. Боткина:
анализы (ждем результатов),
гормональное лечение аллергии.
Суббота (сегодня): припухлость: ладони, стопы. Сыпь: ладони, стопы, колени, локти, слизистые оболочки. Субъективное состояние: не улучшается с момента кризиса (среда).
ДМС отправляет к врачам в больнице им. Боткина. Врачи мнутся и говорят «давайте разберемся с аллергией, потом будет искать». Только дерматолог вскользь упомянула: «АМОКСИКЛАВ содержит пенициллин».
Я понимаю, аллергию лечить действительно надо. Но хочется узнать причину аллергии (хотя бы предположительную..)
Я не специалист, но Яндекс говорит, что АМОКСИКЛАВ: «Антибиотик широкого спектра действия; содержит полусинтетический пенициллин амоксициллин…».. точно также, как и ФЛЕМОКЛАВ.
Я верю в методы лечения, избранные врачом, но логику врача (терапевта), выписывающего рецепт на ФЛЕМОКЛАВ после ответа «аллергия на пенициллин» я не понимаю!
Помогите, пожалуйста, просто понять:
в чем может быть причина столь сильной и долгой реакции?
АМОКСИКЛАВ — это действительно пенициллино-образный антибиотик? — он мог вызвать эту реакцию? что-то другое?
Я не хочу просто обвинить врача (терапевта). Мне нужен совет, как в этой ситуации грамотно разобраться..
Спасибо,
Павел.
ПС «Подмышка» кстати, почти прошла…
Rodionov
01.12.2007, 15:58
Да, амоксициллин, входящий в состав флемоклава, является антибиотиком пенициллиновой группы и не должен назначаться при аллергии на пенициллин.
Сообщите, пожалуйста:
Ваша родственница может сообщить результаты общего анализа крови?
Шейные, лимфоузлы не увеличены?
Какие были изменения в горле, как оно беспокоило?
если есть аллергия на пенициллин, то амоксициллин тоже может вызвать аллергию. У меня была больная с инфекцией E. faecium, и аллергией на то ли на пенициллин, то ли на новокаин. Сильно не хотелось прибегать к ванкомицину, поэтому сделали прик-тест с амоксициллином. Результат — отр. Дали аугментин. Результат — атопический дерматит. Обошлись антигистаминными.
В данном случае, если вовлечены слизистые, то это может быть Стивенс-Джонсон, а это уже гораздо серьезнее. Опишите элементы сыпи. они как красные пятна спросветлением в центре? Есть ли пузыри? Если в больнице назначитили стероиды, то это единственно верная тактика, и чем выше дозы, тем, имхо, лучше.
Внимание! Информация для врачей.
Penicillin and related antibiotic allergy; skin testing; and desensitization
Liza C O’Dowd, MD
INTRODUCTION*—*Penicillin is the most commonly reported medication allergy, although many patients are not truly allergic [1-3]. Large studies, for example, have shown that at least 80 percent of individuals reporting penicillin allergy are able to tolerate treatment and have either been falsely labeled allergic or lost their sensitivity as a result of years of avoidance [4-6]. However, true penicillin allergy is not uncommon and is a leading cause of fatal drug reactions [7].
Adverse drug reactions to all medications combined are the cause of 2 to 5 percent of hospital admissions in the United States and complicate an additional 6 percent of hospitalizations [1,8].
The evaluation and desensitization of patients with suspected penicillin allergies will be reviewed here. The diagnosis and treatment of anaphylaxis is discussed separately. (See «Anaphylaxis in adults»).
EVALUATION OF PATIENTS WITH HISTORY OF PENICILLIN ALLERGY*—*Several types of allergic reactions can occur following the administration of penicillin (show table 1). Overall, 2 to 4 percent of allergic reactions are life-threatening [2,9,10]. Severe forms of drug allergy can occur via several mechanisms and include anaphylaxis (type I), Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug-induced hypersensitivity syndrome with multiorgan involvement (mechanism of the latter three reactions is uncharacterized). Type I reactions, which may present with anaphylaxis, angioedema, bronchospasm, or urticaria (hives) are the focus of this review.
History*—*It is important to verify the history of «allergy» since the patient may incorrectly assume a non-allergic side effect (especially a gastrointestinal side effect) to be allergic in origin.
Risk factors*—*Certain subgroups of patients are at higher risk for developing allergic reactions (of various types) to penicillins and related antibiotics [11-13]. Patients with HIV infection have higher rates of allergy to a variety of antibiotics, including amoxicillin [11]. Patients with cystic fibrosis frequently develop allergies to ticarcillin and piperacillin [12,13]. It is uncertain if these increased rates of reaction reflect the greater exposure to multiple drugs or are related to immunologic abnormalities associated with these diseases.
The development of exanthems in response to penicillins is well-described in patients during acute infectious mononucleosis and cytomegalovirus, although these types of reactions are distinct, as patients are generally able to tolerate the penicillin after recovering from the acute viral infection [14-17]. Non-pruritic, maculopapular rashes without other symptoms are reported in 3 to 7 percent of children taking amoxicillin, and are not considered a contraindication to future use of the causative drug [18,19].
Patients with a history of an allergic reaction to any drug have an increased incidence of reactions to other drugs. It has been estimated that patients with a history of penicillin allergy have a three-fold increased risk of reacting to any medication [20]. This phenomenon was well-illustrated in a review of 969 patients who had allergic reactions to sulfonamide antibiotics and were subsequently treated with nonantibiotic sulfonamides, including loop and thiazide diuretics and sulfonylureas [3]. These patients had an increased incidence of allergic reactions (including asthma, eczema, urticaria, dermatitis, Stevens-Johnson syndrome, and anaphylaxis) to the nonantibiotic sulfonamide (9.9 versus 1.6 percent in controls who had not had an prior allergic reaction to a sulfonamide antibiotic). However, their reaction rate to penicillin was even greater (14 percent). Thus, there was a greater incidence of reactivity to a non-related drug (penicillin) than to a related non-antibiotic sulfonamide, suggesting that the increased reactivity reflects a general predisposition to develop allergic reactions rather than a specific immunologic cross reactivity.
Assessing risk for anaphylaxis*—*Anaphylaxis from penicillin occurs with a frequency of one episode per 5000 to 10,000 courses of drug therapy [21]. Assessment of the risk is based upon a carefully obtained history coupled with skin testing when appropriate and available. Anaphylaxis can be identified by characteristic symptoms (show table 2). A high risk for anaphylaxis is suggested by a history of bronchospasm, angioedema, hypotension, or shock, particularly if these symptoms occurred within 30 minutes of drug administration during the prior year (show table 3). In contrast, people who report isolated maculopapular rashes without urticaria or pruritus are unlikely to have experienced an IgE-mediated reaction [22].
IgE-mediated penicillin allergy can be lost over time if a patient has successfully avoided exposure, with a minority of patients still being reactive after 20 years of avoidance. Thus, the time that has elapsed since the patient’s last reaction is also used to assess risk.
Our approach to the patient with a possible IgE-mediated penicillin allergy is summarized in the figure (show figure 1). Patients should ideally undergo a penicillin skin test (if available) if they have a history of penicillin or other beta-lactam allergy and require a beta-lactam antibiotic to treat a serious infection for which no other alternative antibiotic is appropriate [9,23]. (See «Penicillin skin testing» below).
At the moment, however, the supplies of commercially available PPL (the major determinant skin test reagent) have been withdrawn from the market within the United States and it is not clear when or if they will be re-introduced. If a reliable source of PPL is not available, skin testing will not reliably identify patients with allergic reactivity to penicillin, and should not be undertaken. In that case, a careful assessment of the patient’s history of reactions to penicillin or its derivatives must be used to assess risk.
PENICILLIN SKIN TESTING*—*Skin testing is the most reliable method of determining if a patient with a previous history of a penicillin allergy is at risk for an immediate hypersensitivity reaction upon rechallenge. Skin testing provides information about IgE-mediated, type 1 reactions only, and has no role in the evaluation of other types of reactions, such as Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), other exfoliative dermatitides, erythema multiforme, hepatitis, or nephritis.
In vivo, penicillin and its metabolites function as haptens, or small molecular weight molecules that adhere to proteins to form hapten-protein complexes that are antigenic. When penicillin G is added to a solution of protein or human serum, the beta-lactam ring of the drug spontaneously opens and binds to proteins to form a benzylpenicilloyl determinant. Approximately 95 percent of the administered penicillin undergoes this process; this altered form is called benzylpenicilloyl or the «major determinant». Other metabolic products of penicillin metabolism include penicilloate and penilloate; these are called the «minor determinants» [9]. Many patients who are allergic to penicillin have formed IgE molecules to these metabolite-protein complexes, rather than to the parent drug. Therefore, skin testing must include reagents that will allow detection of these antibodies.
Reagents and technique*—*Skin testing for penicillin should ideally be performed with penicillin G and the major and minor determinants.
Although benzylpenicilloyl complexed to protein (the major determinant) was previously produced commercially as benzylpenicilloyl polysine (PPL or PrePen), it is currently unavailable.
IgE antibodies to minor determinants are generally responsible for anaphylactic reactions and can predict the likelihood of a more severe reaction. IgE antibodies to major determinants of penicillin in general mediate urticarial drug reactions in addition to anaphylactic reactions [9,24].
Skin testing usually takes between one and four hours to complete and should be performed by an allergist/immunologist. Prick/puncture testing is performed initially. If prick testing is negative, then intradermal testing is performed.
A positive skin test is defined by the development of a wheal and flare reaction to either antigenic determinant that is equal or larger in size to that associated with the histamine control, with the histamine control normally producing a wheal of at least three mm in diameter. (See «Overview of skin testing for allergic disease»).
Testing is complete when the patient either has a positive reaction to any reagent or completes the testing protocol. In most centers, testing is followed by the administration of a single dose of oral penicillin and a period of observation to confirm that the drug is tolerated.
Нормальная статья, но в от у моей пациентки прик был отрицательный, атопический дерматит развился, с зудом, как положено. Кстати, она не принимала пенициллины в течение 10 лет. Так, что ни длительное воздержание от аллергена, ни предварительная проверка, еще не гарантия.
Нормальная статья, но в от у моей пациентки прик был отрицательный, атопический дерматит развился, с зудом, как положено. Кстати, она не принимала пенициллины в течение 10 лет. Так, что ни длительное воздержание от аллергена, ни предварительная проверка, еще не гарантия.
Так эксфолиативный дерматит может быть побочным эффектом амоксициллина, а не аллергической реакцией :ai:
А что аллергические реакции не относятся к побочным эффектам (adverse events)?
А что аллергические реакции не относятся к побочным эффектам (adverse events)?Относятся. Но не все побочные эффекты являются аллергическими. Так высыпания, обусловленные назначением амоксициллина при инфекционном мононуклеозе, не являются аллергической реакцией.
А что аллергические реакции не относятся к побочным эффектам (adverse events)?
Стоп, аллергия — это реакция первого типа. Медикаментозные сыпи — не все реакции первого типа :ab:
to riltsov
С этим трудно не согласиться. В таком случае высыпания не являются аллергическими. Ждем анализа крови.
to Dr
действительно не все 1-го типа. Но аллергия — это реакции всех 4-х типов по jeley-coombs. первый тип — это анафилаксия. Лайел и Стивенс-Джонсон это ракции цитотоксические (какие конкретно АЗКЦ или ГЗТ великие умы еще не решили на скольео я знаю), но все равно это аллергия
вообще не люблю ругаться по поводу терминологии. тем более всяких тонкостей (типа как это называть? эксфолиативный дерматит, токсический эпидермальный некролиз или синдром Лайела). как ни назови патогенез, клиника и лечение от этого ведь не поменяются. правда?
to Dr
действительно не все 1-го типа. Но аллергия — это реакции всех 4-х типов по jeley-coombs. первый тип — это анафилаксия. Лайел и Стивенс-Джонсон это ракции цитотоксические (какие конкретно АЗКЦ или ГЗТ великие умы еще не решили на скольео я знаю), но все равно это аллергия
Действительно, тонкости терминологии иногда спорная штука :az: В основном-то аллергией называют «Тип I — реакции гиперчувствительности немедленного типа, вызываемые антителами класса IgE», а остальные 4 типа реакций гиперчувствительности — согласно смыслу, поскольку аллергией их назвать все же трудно :ai:
как аллерголог аллергологу позволю заметить еще раз, что allergy != anaphylaxis
как аллерголог аллергологу позволю заметить еще раз, что allergy != anaphylaxis
Вы же упоминали классификацию Джела-Кумбса? Где же там слово «аллергия», в какой части упоминается?
Type 1 — immediate (or atopic, or anaphylactic)
Type 1 hypersensitivity is an allergic reaction provoked by reexposure to a specific type of antigen referred to as an allergen.[2] Exposure may be by ingestion, inhalation, injection, or direct contact. The difference between a normal immune response and a type I hypersensitive response is that plasma cells secrete IgE. This class of antibodies binds to Fc receptors on the surface of tissue mast cells and blood basophils. Mast cells and basophils coated by IgE are «sensitized.» Later exposure to the same allergen, cross-links the bound IgE on sensitized cells resulting in degranulation and the secretion of pharmacologically active mediators such as histamine, leukotriene, and prostaglandin that act on the surrounding tissues. The principal effects of these products are vasodilation and smooth-muscle contraction.
The reaction may be either local or systemic. Symptoms vary from mild irritation to sudden death from anaphylactic shock. Treatment usually involves epinephrine, antihistamines, and corticosteroids. If the entire body gets involved, then anaphylaxis can take place; an acute, systemic reaction that can prove fatal.
Some examples:
Allergic asthma
Allergic conjunctivitis
Allergic rhinitis («hay fever»)
Anaphylaxis
Angioedema
Urticaria (hives)
Eosinophilia
Penicillin
Cephalosporin
[edit] Type 2 — antibody-dependent
In type 2 hypersensitivity, the antibodies produced by the immune response bind to antigens on the patient’s own cell surfaces. The antigens recognized in this way may either be intrinsic («self» antigen, innately part of the patient’s cells) or extrinsic (absorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognised by macrophages or dendritic cells which act as antigen presenting cells, this causes a B cell response where antibodies are produced against the foreign antigen.
An example here is the reaction to penicillin where the drug can bind to red blood cells causing them to be recognised as different, B cell proliferation will take place and antibodies to the drug are produced. IgG and IgM antibodies bind to these antigens to form complexes that activate the classical pathway of complement activation for eliminating cells presenting foreign antigens (which are usually, but not in this case, pathogens). That is, mediators of acute inflammation are generated at the site and membrane attack complexes cause cell lysis and death. The reaction takes hours to a day.
Another form of type 2 hypersensitivity is called antibody-dependent cell-mediated cytotoxicity (ADCC). Here, cells exhibiting the foreign antigen are tagged with antibodies (IgG or IgM). These tagged cells are then recognised by natural killer (NK) cells and macrophages (recognised via IgG bound (via the Fc region) to the effector cell surface receptor, CD16 (FcγRIII)), which in turn kill these tagged cells.
Some examples:
Autoimmune hemolytic anemia
Goodpasture’s syndrome
Pemphigus
Pernicious anemia (if autoimmune)
Immune thrombocytopenia
Transfusion reactions
Hashimoto’s thyroiditis
Graves disease (see type V below)
Myasthenia gravis (see type V below)
Rheumatic fever
Hemolytic disease of the newborn (erythroblastosis fetalis)
Acute transplant rejection
[edit] Type 3 — immune complex
Type 3 hypersensitivity occurs when antigens and antibodies are present in roughly equal amounts, causing extensive cross-linking. Large immune complexes that cannot be cleared are deposited in vessel walls and induce an inflammatory response. The reaction can take hours, days, or even weeks to develop.
Some clinical examples:
Rheumatoid arthritis
Immune complex glomerulonephritis
Serum sickness
Subacute bacterial endocarditis
Symptoms of malaria
Systemic lupus erythematosus
Arthus reaction
Farmer’s lung (Arthus-type reaction)
[edit] Type 4 — cell-mediated (delayed-type hypersensitivity, DTH)
See also: Cell mediated immunity
Type 4 hypersensitivity is often called delayed type as the reaction takes two to three days to develop. Unlike the other types, it is not antibody mediated but rather is a type of cell-mediated response.
CD8+ cytotoxic T cells and CD4+ helper T cells recognise antigen in a complex with either type 1 or 2 major histocompatibility complex. The antigen-presenting cells in this case are macrophages which secrete IL-12, which stimulates the proliferation of further CD4+ T cells. CD4+ T cells secrete IL-2 and interferon gamma, further inducing the release of other Type 1 cytokines, thus mediating the immune response. Activated CD8+ T cells destroy target cells on contact while activated macrophages produce hydrolytic enzymes and, on presentation with certain intracellular pathogens, transform into multinucleated giant cells.
ихнее hypersensitivity по-нашенски аллергия. И снова путаница в терминологии гиперчевствительность это аллергия или это еще что-нибудь? Я считаю эти понятия эквивалентными. Посему 4 типа гиперчувствительности есть 4 типа аллергических реакций, и 1-й из них анафилаксия. Англоязычные источники считают, что immediate type hypersensitivity == anaphylaxis, отечественные же относят к немедленному типу аллергических реакций первые 3, к замедленному — 4-й. Спор по этому поводу совршенно бессмыслен. Если же учесть, что оригинальная классификация Джела-Кумбса включала еще и 5-й тип — стимулирующие реакции, позже отнесенный ко 2-му (цитотоксические), то все окончательно запутывается.
С одним можно безусловно согласиться, аллергологи лечат 1-й тип, остальные же отданы в основном в ведение ревматологов.
Кстати при 4-м типе (ГЗТ) роль CD8+ cytolytic T cells довольно невелика, т.к. при наиболее частом варианте, гранулематозном, главную роль играют CD4+ T DTH cells. А CD8+ cytolytic T cells главным образом учааствуют отсроченных реакциях отторжения трансплантата.
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