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},
"code": "D70",
"name": "Агранулоцитоз",
"icd_name": "Агранулоцитоз",
"gender": 0,
"age_min": 0,
"age_max": 94,
"cause": [
3
],
"periodicity": 1,
"slug": "d70_agranulocitoz",
"lead": "Нарушение здоровья, относящееся к группе другие болезни крови и кроветворных органов",
"description": " \r\nАгранулоцитоз – клинико-лабораторный синдром, основное проявление которого состоит в резком снижении или полном отсутствии нейтрофильных гранулоцитов в периферической крови, что сопровождается повышением восприимчивости организма к грибковым и бактериальным инфекциям. \r\n",
"etiology": "<p>К причинам развития агранулоцитоза относят: </p>\r\n<ul>\r\n<li>Ионизирующая радиация и лучевая терапия, химические вещества (бензол), инсектициды. </li>\r\n<li>Лекарственные средства могут вызвать агранулоцитоз в результате прямого угнетения кроветворения (цитостатики, вальпроевая кислота, карбамазепин, бета-лактамные антибиотики), либо действуя как гаптены (препараты золота, антитиреоидные препараты и пр.). </li>\r\n<li>Аутоиммунные заболевания (например, красная волчанка, аутоиммунный тиреоидит). </li>\r\n<li>Вирусные инфекции (вызванные вирусом Эпштейна – Барра, цитомегаловирус, желтая лихорадка, вирусные гепатиты) обычно сопровождаются умеренной нейтропенией, однако в некоторых случаях может развиться агранулоцитоз. </li>\r\n<li>Тяжелые генерализованные инфекции (как бактериальные, так и вирусные). </li>\r\n<li>Исхудание. </li>\r\n<li>Генетические нарушения. </li>\r\n</ul>",
"pathogenesis": "<p>В зависимости от причины возникновения и механизма развития патологии, различают следующие виды агранулоцитоза: </p>\r\n<ol>\r\n<li>Миелотоксический.</li>\r\n<li>Иммунный: аутоиммунный;гаптеновый. </li>\r\n<li>Генуинный.</li>\r\n</ol>\r\n<p>Миелотоксический агранулоцитоз возникает в результате подавляющего воздействия неблагоприятных факторов на красный костный мозг, и представляет собой глубокую депрессию кроветворного ростка, ответственного за продукцию гранулоцитов. </p>\r\n<p>В основе аутоиммунного агранулоцитоза лежит патологическая реакция иммунной системы, сопровождающаяся образованием антител к собственным нейтрофилам. Такая разновидность агранулоцитоза встречается при аутоиммунном тиреоидите, ревматоидном артрите, системной красной волчанке и других коллагенозах. Агранулоцитоз, развивающийся при некоторых инфекционных заболеваниях (гриппе, инфекционном мононуклеозе, малярии, желтой лихорадке, брюшном тифе, вирусном гепатите, полиомиелитеи др.) также имеет иммунный характер. </p>\r\n<p>Гаптеновый агранулоцитоз возникает, когда в иммунных реакциях участвуют гаптены – вещества, сами по себе безвредные, однако при определенных условиях способные провоцировать иммунные реакции, разрушающие гранулоциты. В роли гаптенов чаще всего выступают лекарственные вещества, так что гаптеновый агранулоцитоз рассматривают, как грозное осложнение различных лечебных мероприятий. О генуинном агранулоцитозе говорят в тех случаях, когда причина резкого снижения количества гранулоцитов в крови остается неизвестной. </p>",
"diagnostics": "<p> </p>\r\n<p>Наиболее важным для подтверждения агранулоцитоза является исследование общего анализа крови и пункция костного мозга. Картина периферической крови характеризуется лейкопенией (1-2х109/л), гранулоцитопенией (менее 0,75х109/л) или агранулоцитозом, умеренной анемией, при тяжелых степенях – тромбоцитопенией. При исследовании миелограммы выявляется уменьшение количества миелокариоцитов, снижение числа и нарушение созревания клеток нейтрофильного ростка, наличие большого количества плазматических клеток и мегакариоцитов. Для подтверждения аутоиммунного характера агранулоцитоза производится определение антинейтрофильных антител. </p>\r\n<p>Всем пациентам с агранулоцитозом показано проведение рентгенографии легких, повторные исследования крови на стерильность, исследование биохимического анализа крови, консультация стоматолога и отоларинголога. Дифференцировать агранулоцитоз необходимо от острого лейкоза, гипопластической анемии. Также необходимо исключение ВИЧ-статуса</p>",
"treatment": "<p> В первую очередь необходимо устранение причинного повреждающего фактора, срочная госпитализация больного агранулоцитозом, желательно в гематологическое отделение, и помещение его в стерильные условия. </p>\r\n<p>Необходим тщательный уход за кожей и слизистыми оболочками. Подкожные и внутримышечные инъекции следует заменить внутривенными, чтобы предотвратить развитие абсцессов. </p>\r\n<p>Назначаются антибиотики широкого спектра действия, по показаниям — противогрибковые и противовирусные препараты, иммуноглобулин. Могут применяться также препараты гранулоцитарного колониестимулирующего фактора (КСФ). При некротической энтеропатии больному следует проводить парентеральное питание. </p>\r\n<p>При аутоиммунном агранулоцитозе производится угнетение аутоиммунной агрессии, больному показаны глюкокортикоиды в высоких дозах до нормализации числа гранулоцитов в крови с последующей постепенной отменой гормонов. При гаптеновом агранулоцитозе введение глюкокортикоидов не эффективно. </p>\r\n<p>При лечении цитостатического агранулоцитоза средствами выбора являются препараты рекомбинантных гемопоэтических факторов роста. </p>",
"prevention": "<p>Чтобы не допустить развитие агранулоцитоза, следует избегать контакта с фактором, способным вызвать заболевание. Во время приема цитостатиков необходим тщательный контроль показателей гемограммы (картины крови). </p>\r\n<p>Большой проблемой является профилактика повторных гаптеновых агранулоцитозов. При гаптеновых агранулоцитозах - 80% смертельных исходов, и прогноз ухудшается при повторном применении вызвавшего нейтропению лекарства. Установить, какой препарат является гаптеном, нелегко, поэтому нужно навсегда исключать из употребления все препараты, которые применялись перед появлением агранулоцитоза. </p>",
"clinical_picture": "<p>Клиническая картина во многом напоминает симптомы цитостатической болезни и проявляется в виде поражения организма различными инфекциями в результате снижения эффективности иммунного ответа. Характерны (особенно при лекарственном агранулоцитозе) острое начало и быстрое нарастание клинических симптомов. Иногда возникновению основных признаков агранулоцитоза предшествует короткий скрытый период, характеризующийся слабостью, недомоганием, головными болями. Возникает лихорадка, афтозный стоматит, ангина, озноб, боль в суставах. Развиваются язвенно-некротические поражения слизистой оболочки полости рта в виде изъязвлений, покрытых сероватым налётом, некротических бляшек и язв с грязно-серым налётом на миндалинах (агранулоцитарная ангина). </p>\r\n<p>Процесс распространяется на нёбные дужки, язычок, твёрдое нёбо, дёсны и порой сопровождается незначительным увеличением регионарных лимфатических узлов, чаще всего шейных и подчелюстных. Данные изменения могут быть также на слизистой оболочке желудочно-кишечного тракта, лёгких, печени, мочевого пузыря, половых органов. </p>\r\n<p>При гаптеновом агранулоцитозе развитие болезни бурное. После приёма препаратов, вызвавших агранулоцитоз, возникает нарастающая слабость, боль в горле, повышение температуры тела до 39—40 °С, появляется и нарастает гнилостный запах изо рта (глоточно-ротовая форма). Нередко развиваются стоматит, ларингоспазм и асфиксия по причине скопления некротических плёнок и отёка гортани. К ошибке в диагностике может привести тот факт, что начальные проявления кишечно-некротической энтеропатии и поражение слизистых оболочек ротовой полости опережают появление лабораторных показателей агранулоцитоза. </p>",
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"code": "D70",
"name": "Агранулоцитоз",
"icd_name": "Агранулоцитоз",
"gender": 0,
"age_min": 0,
"age_max": 94,
"cause": [
3
],
"periodicity": 1,
"slug": "d70_agranulocitoz",
"lead": "Нарушение здоровья, относящееся к группе другие болезни крови и кроветворных органов",
"description": " \r\nАгранулоцитоз – клинико-лабораторный синдром, основное проявление которого состоит в резком снижении или полном отсутствии нейтрофильных гранулоцитов в периферической крови, что сопровождается повышением восприимчивости организма к грибковым и бактериальным инфекциям. \r\n",
"etiology": "<p>К причинам развития агранулоцитоза относят: </p>\r\n<ul>\r\n<li>Ионизирующая радиация и лучевая терапия, химические вещества (бензол), инсектициды. </li>\r\n<li>Лекарственные средства могут вызвать агранулоцитоз в результате прямого угнетения кроветворения (цитостатики, вальпроевая кислота, карбамазепин, бета-лактамные антибиотики), либо действуя как гаптены (препараты золота, антитиреоидные препараты и пр.). </li>\r\n<li>Аутоиммунные заболевания (например, красная волчанка, аутоиммунный тиреоидит). </li>\r\n<li>Вирусные инфекции (вызванные вирусом Эпштейна – Барра, цитомегаловирус, желтая лихорадка, вирусные гепатиты) обычно сопровождаются умеренной нейтропенией, однако в некоторых случаях может развиться агранулоцитоз. </li>\r\n<li>Тяжелые генерализованные инфекции (как бактериальные, так и вирусные). </li>\r\n<li>Исхудание. </li>\r\n<li>Генетические нарушения. </li>\r\n</ul>",
"pathogenesis": "<p>В зависимости от причины возникновения и механизма развития патологии, различают следующие виды агранулоцитоза: </p>\r\n<ol>\r\n<li>Миелотоксический.</li>\r\n<li>Иммунный: аутоиммунный;гаптеновый. </li>\r\n<li>Генуинный.</li>\r\n</ol>\r\n<p>Миелотоксический агранулоцитоз возникает в результате подавляющего воздействия неблагоприятных факторов на красный костный мозг, и представляет собой глубокую депрессию кроветворного ростка, ответственного за продукцию гранулоцитов. </p>\r\n<p>В основе аутоиммунного агранулоцитоза лежит патологическая реакция иммунной системы, сопровождающаяся образованием антител к собственным нейтрофилам. Такая разновидность агранулоцитоза встречается при аутоиммунном тиреоидите, ревматоидном артрите, системной красной волчанке и других коллагенозах. Агранулоцитоз, развивающийся при некоторых инфекционных заболеваниях (гриппе, инфекционном мононуклеозе, малярии, желтой лихорадке, брюшном тифе, вирусном гепатите, полиомиелитеи др.) также имеет иммунный характер. </p>\r\n<p>Гаптеновый агранулоцитоз возникает, когда в иммунных реакциях участвуют гаптены – вещества, сами по себе безвредные, однако при определенных условиях способные провоцировать иммунные реакции, разрушающие гранулоциты. В роли гаптенов чаще всего выступают лекарственные вещества, так что гаптеновый агранулоцитоз рассматривают, как грозное осложнение различных лечебных мероприятий. О генуинном агранулоцитозе говорят в тех случаях, когда причина резкого снижения количества гранулоцитов в крови остается неизвестной. </p>",
"diagnostics": "<p> </p>\r\n<p>Наиболее важным для подтверждения агранулоцитоза является исследование общего анализа крови и пункция костного мозга. Картина периферической крови характеризуется лейкопенией (1-2х109/л), гранулоцитопенией (менее 0,75х109/л) или агранулоцитозом, умеренной анемией, при тяжелых степенях – тромбоцитопенией. При исследовании миелограммы выявляется уменьшение количества миелокариоцитов, снижение числа и нарушение созревания клеток нейтрофильного ростка, наличие большого количества плазматических клеток и мегакариоцитов. Для подтверждения аутоиммунного характера агранулоцитоза производится определение антинейтрофильных антител. </p>\r\n<p>Всем пациентам с агранулоцитозом показано проведение рентгенографии легких, повторные исследования крови на стерильность, исследование биохимического анализа крови, консультация стоматолога и отоларинголога. Дифференцировать агранулоцитоз необходимо от острого лейкоза, гипопластической анемии. Также необходимо исключение ВИЧ-статуса</p>",
"treatment": "<p> В первую очередь необходимо устранение причинного повреждающего фактора, срочная госпитализация больного агранулоцитозом, желательно в гематологическое отделение, и помещение его в стерильные условия. </p>\r\n<p>Необходим тщательный уход за кожей и слизистыми оболочками. Подкожные и внутримышечные инъекции следует заменить внутривенными, чтобы предотвратить развитие абсцессов. </p>\r\n<p>Назначаются антибиотики широкого спектра действия, по показаниям — противогрибковые и противовирусные препараты, иммуноглобулин. Могут применяться также препараты гранулоцитарного колониестимулирующего фактора (КСФ). При некротической энтеропатии больному следует проводить парентеральное питание. </p>\r\n<p>При аутоиммунном агранулоцитозе производится угнетение аутоиммунной агрессии, больному показаны глюкокортикоиды в высоких дозах до нормализации числа гранулоцитов в крови с последующей постепенной отменой гормонов. При гаптеновом агранулоцитозе введение глюкокортикоидов не эффективно. </p>\r\n<p>При лечении цитостатического агранулоцитоза средствами выбора являются препараты рекомбинантных гемопоэтических факторов роста. </p>",
"prevention": "<p>Чтобы не допустить развитие агранулоцитоза, следует избегать контакта с фактором, способным вызвать заболевание. Во время приема цитостатиков необходим тщательный контроль показателей гемограммы (картины крови). </p>\r\n<p>Большой проблемой является профилактика повторных гаптеновых агранулоцитозов. При гаптеновых агранулоцитозах - 80% смертельных исходов, и прогноз ухудшается при повторном применении вызвавшего нейтропению лекарства. Установить, какой препарат является гаптеном, нелегко, поэтому нужно навсегда исключать из употребления все препараты, которые применялись перед появлением агранулоцитоза. </p>",
"clinical_picture": "<p>Клиническая картина во многом напоминает симптомы цитостатической болезни и проявляется в виде поражения организма различными инфекциями в результате снижения эффективности иммунного ответа. Характерны (особенно при лекарственном агранулоцитозе) острое начало и быстрое нарастание клинических симптомов. Иногда возникновению основных признаков агранулоцитоза предшествует короткий скрытый период, характеризующийся слабостью, недомоганием, головными болями. Возникает лихорадка, афтозный стоматит, ангина, озноб, боль в суставах. Развиваются язвенно-некротические поражения слизистой оболочки полости рта в виде изъязвлений, покрытых сероватым налётом, некротических бляшек и язв с грязно-серым налётом на миндалинах (агранулоцитарная ангина). </p>\r\n<p>Процесс распространяется на нёбные дужки, язычок, твёрдое нёбо, дёсны и порой сопровождается незначительным увеличением регионарных лимфатических узлов, чаще всего шейных и подчелюстных. Данные изменения могут быть также на слизистой оболочке желудочно-кишечного тракта, лёгких, печени, мочевого пузыря, половых органов. </p>\r\n<p>При гаптеновом агранулоцитозе развитие болезни бурное. После приёма препаратов, вызвавших агранулоцитоз, возникает нарастающая слабость, боль в горле, повышение температуры тела до 39—40 °С, появляется и нарастает гнилостный запах изо рта (глоточно-ротовая форма). Нередко развиваются стоматит, ларингоспазм и асфиксия по причине скопления некротических плёнок и отёка гортани. К ошибке в диагностике может привести тот факт, что начальные проявления кишечно-некротической энтеропатии и поражение слизистых оболочек ротовой полости опережают появление лабораторных показателей агранулоцитоза. </p>",
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"name": "Контактный дерматит неуточненный",
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"lead": "Нарушение здоровья, относящееся к группе дерматит и экзема",
"description": "Контактный дерматит — воспалительная реакция кожи, возникающая в ответ на прямое воздействие раздражающих веществ (щелочей, кислот, моющих средств, растворителей, хлорной извести и т. п.). Симптомы заболевания зависят от силы и характера воздействия. \r\n",
"etiology": "<p>Главной причиной, вызывающей дерматит любого вида, является соприкосновение кожи с любыми раздражителями из окружающей среды. </p>\r\n<p>Вещества, наиболее часто вызывающие контактный дерматит: </p>\r\n<ul>\r\n<li>никель – металл, широко применяемый для изготовления монет, украшений, пряжек, посуды, а также зубных протезов; </li>\r\n<li>латекс – используется для изготовления презервативов, резиновых перчаток, детских пустышек, сосок и игрушек; </li>\r\n<li>лекарственные кремы и мази, в состав которых входят антибиотики, гормоны; </li>\r\n<li>косметические средства, предназначенные для ухода за кожей, и декоративная косметика; </li>\r\n<li>бытовая химия (стиральные порошки, средства для мыться посуды и др.); </li>\r\n<li>синтетические материалы, используемые для изготовления одежды; </li>\r\n<li>различные вещества, такие как краски, клей, чернила и др. </li>\r\n</ul>",
"pathogenesis": "<p>Простой контактный дерматит обусловлен прямым повреждением клеток верхнего слоя кожи - эпидермиса. Из поврежденных клеток высвобождаются различные биологически активны вещества (медиаторы воспаления и факторы хемотаксиса), вызывающие расширение сосудов (эритема), выход жидкости в дерму и эпидермис (отек и волдырь) и клеточную инфильтрацию. Наблюдается внеклеточный и внутриклеточный отек эпидермиса. </p>\r\n<p>Простой контактный дерматит, вызванный однократным воздействием едкого вещества, например сильной кислоты или щелочи, на кожу, называют химическим ожогом . При химическом ожоге воспаление развивается в течение нескольких минут и часов. Белее легкая форма простого контактного дерматита возникает при многократном воздействии слабого раздражающего вещества, например мыла или моющего средства, и проявляется через несколько недель или месяцев после первого контакта с этим веществом. У больных атопическими заболеваниями , особенно диффузным нейродермитом , кожа более чувствительна к действию раздражающих веществ. </p>",
"diagnostics": "<p>Диагноз ставится на основании дерматологической симптоматики. Проводятся аппликационные кожные пробы (не ранее 2 недель после купирования симптомов дерматита), гистологическое исследование кожного покрова.</p>",
"treatment": "<p> </p>\r\n<p>Лечение заболевания необходимо начинать с исключения контакта кожи с аллергеном. Если развитие контактного дерматита связано с профессиональной деятельностью пациента, то необходимо постоянное использование защитных средств (перчатки, маски, защитные костюмы). </p>\r\n<p>Больным, у которых выявлена аллергическая реакция на никель, рекомендуется соблюдение диеты, ограничивающей продукты, содержащие это вещество (геркулес, греча, пшено, соя, чечевица, томаты, семечки, шоколад, какао). </p>\r\n<p>Больным рекомендуется в течение нескольких дней принимать антигистаминные средства. </p>\r\n<p>При выраженном воспалительном процессе на пораженном участке кожи пациентам назначается местное применение мазей, кремов или лосьонов, содержащих кортикостероиды. Гормональные мази наносятся на чистую кожу 1–2 раза в день тонким слоем. Длительность курса лечения обычно не превышает 2 недель. </p>\r\n<p>При обширных поражениях, а также тяжелых реакциях организма на контакт с аллергеном, врач может назначить системные кортикостероидные препараты для приема внутрь</p>",
"prevention": "<p>Профилактика этого заболевания заключается только в исключении контакта кожи с веществами, вызывающими аллергическую реакцию. При случайном попадании на кожу известного раздражителя необходимо немедленно тщательно смыть его под проточной водой с мылом. </p>\r\n<p>При аллергии на бытовую химию (стиральные порошки, средства для ухода за домом) следует использовать специальные гипоаллергенные средства, но даже при их применении необходимо использовать защитные перчатки. Одежду следует выбирать из натуральных материалов. Рекомендуется отдавать предпочтение украшениям из благородных металлов (золото и серебро). </p>",
"clinical_picture": "<p>В зависимости от характера вещества, воздействующего на кожу, и индивидуальных особенностей проницаемости эпидермиса может развиться один из трех вариантов острого контактного дерматита: эритематозный, буллезный или некротический. </p>\r\n<p>Эритематозный дерматит проявляется покраснением и отеком контактировавшего с раздражителем участка кожи. Болезненность и зуд выражены слабо. Возможна сухость кожи и появление на ней трещин. </p>\r\n<p>Буллезный вариант простого контактного дерматита представлен пузырями различного размера, заполненными прозрачной жидкостью. Пузыри появляются на гиперемированном фоне и лопаются с образованием эрозий. Характерна болезненность, чувство жара или жжения. </p>\r\n<p>Некротический дерматит возникает при воздействии едких веществ (кислот или щелочей) и характеризуется образованием изъязвлений, поверхность которых покрыта струпом. Выражен болевой синдром. После того, как происходит заживление язв, на коже остаются рубцы. </p>\r\n<p>Хроническая форма простого контактного дерматита развивается при многократном воздействии слабого раздражителя. Наиболее часто поражается кожа рук. Заболевание, как правило, связано с использованием средств бытовой химии или профессиональной деятельностью. Хронический дерматит характеризуется усилением рисунка кожи, застойной гиперемией (покраснением), инфильтрацией, сухостью кожи и гиперкератозом (утолщением кожи). В некоторых случаях наблюдаются атрофические процессы в коже. Субъективные ощущения слабо выражены и мало беспокоят больного. </p>",
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"etiology": "<p>Главной причиной, вызывающей дерматит любого вида, является соприкосновение кожи с любыми раздражителями из окружающей среды. </p>\r\n<p>Вещества, наиболее часто вызывающие контактный дерматит: </p>\r\n<ul>\r\n<li>никель – металл, широко применяемый для изготовления монет, украшений, пряжек, посуды, а также зубных протезов; </li>\r\n<li>латекс – используется для изготовления презервативов, резиновых перчаток, детских пустышек, сосок и игрушек; </li>\r\n<li>лекарственные кремы и мази, в состав которых входят антибиотики, гормоны; </li>\r\n<li>косметические средства, предназначенные для ухода за кожей, и декоративная косметика; </li>\r\n<li>бытовая химия (стиральные порошки, средства для мыться посуды и др.); </li>\r\n<li>синтетические материалы, используемые для изготовления одежды; </li>\r\n<li>различные вещества, такие как краски, клей, чернила и др. </li>\r\n</ul>",
"pathogenesis": "<p>Простой контактный дерматит обусловлен прямым повреждением клеток верхнего слоя кожи - эпидермиса. Из поврежденных клеток высвобождаются различные биологически активны вещества (медиаторы воспаления и факторы хемотаксиса), вызывающие расширение сосудов (эритема), выход жидкости в дерму и эпидермис (отек и волдырь) и клеточную инфильтрацию. Наблюдается внеклеточный и внутриклеточный отек эпидермиса. </p>\r\n<p>Простой контактный дерматит, вызванный однократным воздействием едкого вещества, например сильной кислоты или щелочи, на кожу, называют химическим ожогом . При химическом ожоге воспаление развивается в течение нескольких минут и часов. Белее легкая форма простого контактного дерматита возникает при многократном воздействии слабого раздражающего вещества, например мыла или моющего средства, и проявляется через несколько недель или месяцев после первого контакта с этим веществом. У больных атопическими заболеваниями , особенно диффузным нейродермитом , кожа более чувствительна к действию раздражающих веществ. </p>",
"diagnostics": "<p>Диагноз ставится на основании дерматологической симптоматики. Проводятся аппликационные кожные пробы (не ранее 2 недель после купирования симптомов дерматита), гистологическое исследование кожного покрова.</p>",
"treatment": "<p> </p>\r\n<p>Лечение заболевания необходимо начинать с исключения контакта кожи с аллергеном. Если развитие контактного дерматита связано с профессиональной деятельностью пациента, то необходимо постоянное использование защитных средств (перчатки, маски, защитные костюмы). </p>\r\n<p>Больным, у которых выявлена аллергическая реакция на никель, рекомендуется соблюдение диеты, ограничивающей продукты, содержащие это вещество (геркулес, греча, пшено, соя, чечевица, томаты, семечки, шоколад, какао). </p>\r\n<p>Больным рекомендуется в течение нескольких дней принимать антигистаминные средства. </p>\r\n<p>При выраженном воспалительном процессе на пораженном участке кожи пациентам назначается местное применение мазей, кремов или лосьонов, содержащих кортикостероиды. Гормональные мази наносятся на чистую кожу 1–2 раза в день тонким слоем. Длительность курса лечения обычно не превышает 2 недель. </p>\r\n<p>При обширных поражениях, а также тяжелых реакциях организма на контакт с аллергеном, врач может назначить системные кортикостероидные препараты для приема внутрь</p>",
"prevention": "<p>Профилактика этого заболевания заключается только в исключении контакта кожи с веществами, вызывающими аллергическую реакцию. При случайном попадании на кожу известного раздражителя необходимо немедленно тщательно смыть его под проточной водой с мылом. </p>\r\n<p>При аллергии на бытовую химию (стиральные порошки, средства для ухода за домом) следует использовать специальные гипоаллергенные средства, но даже при их применении необходимо использовать защитные перчатки. Одежду следует выбирать из натуральных материалов. Рекомендуется отдавать предпочтение украшениям из благородных металлов (золото и серебро). </p>",
"clinical_picture": "<p>В зависимости от характера вещества, воздействующего на кожу, и индивидуальных особенностей проницаемости эпидермиса может развиться один из трех вариантов острого контактного дерматита: эритематозный, буллезный или некротический. </p>\r\n<p>Эритематозный дерматит проявляется покраснением и отеком контактировавшего с раздражителем участка кожи. Болезненность и зуд выражены слабо. Возможна сухость кожи и появление на ней трещин. </p>\r\n<p>Буллезный вариант простого контактного дерматита представлен пузырями различного размера, заполненными прозрачной жидкостью. Пузыри появляются на гиперемированном фоне и лопаются с образованием эрозий. Характерна болезненность, чувство жара или жжения. </p>\r\n<p>Некротический дерматит возникает при воздействии едких веществ (кислот или щелочей) и характеризуется образованием изъязвлений, поверхность которых покрыта струпом. Выражен болевой синдром. После того, как происходит заживление язв, на коже остаются рубцы. </p>\r\n<p>Хроническая форма простого контактного дерматита развивается при многократном воздействии слабого раздражителя. Наиболее часто поражается кожа рук. Заболевание, как правило, связано с использованием средств бытовой химии или профессиональной деятельностью. Хронический дерматит характеризуется усилением рисунка кожи, застойной гиперемией (покраснением), инфильтрацией, сухостью кожи и гиперкератозом (утолщением кожи). В некоторых случаях наблюдаются атрофические процессы в коже. Субъективные ощущения слабо выражены и мало беспокоят больного. </p>",
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}
]
}
