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"code": "Q96",
"name": "Синдром Тернера",
"icd_name": "Синдром Тернера",
"gender": 0,
"age_min": 0,
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"slug": "q96_sindrom_ternera",
"lead": "Нарушение здоровья, относящееся к группе хромосомные аномалии, не классифицированные в других рубриках",
"description": "Синдром Шерешевского - Тернера - это хромосомное заболевание, для которого характерно либо полное отсутствие одной хромосомы, либо наличие дефекта в одной из Х - хромосом. ",
"etiology": "<p>Чёткой связи возникновения синдрома Тёрнера с возрастом и какими-либо заболеваниями родителей не выявлено. Однако беременности обычно осложняются токсикозом, угрозой выкидыша, а роды часто бывают преждевременными и патологическими. Особенности беременностей и родов, заканчивающихся рождением ребёнка с синдромом Тёрнера, — следствие хромосомной патологии плода. Нарушение формирования половых желёз при синдроме Тёрнера обусловлено отсутствием или структурными дефектами одной половой хромосомы (X-хромосомы). </p>",
"pathogenesis": "<p>Основной механизм появления синдрома — нарушения передачи Х хромосомы во время формирования зародыша после зачатия. В большинстве случаев регистрируется полная утрата одной из половых хромосом, реже встречается частичная потеря коротких или длинных плеч либо нарушения формы (уменьшенные размеры, кольцевое строение). Чаще всего страдает наследственный материал, переданный от отца. </p>\r\n<p>У больных встречаются следующие кариотипы: </p>\r\n<ul>\r\n<li>моносомия (кариотип 45 ХО) — наблюдается у 60% пациентов; </li>\r\n<li>кольцевидная Х хромосома (46 ХRХ), делеции плеч (46 ХХр, 46 ХХq) — представлены в 20% случаев; </li>\r\n<li>мозаичное строение клеток, где часть содержат полноценный набор хромосом, а часть — аномальный (46 ХХ и 45 Х0) — выявляется у оставшихся 20%. </li>\r\n</ul>\r\n<p>В результате отсутствия или деформации половой хромосомы у девочек нарушается процесс созревания яичников, отмечается задержка или полное отсутствие полового созревания и, как следствие, развитие бесплодия. Хромосомный дисбаланс, наблюдающийся при синдроме Шерешевского - Тернера, приводит также к возникновению различных аномалий соматического развития (развития тела). </p>\r\n<p> </p>",
"diagnostics": "<p>Для установки правильного диагноза необходимо проведение следующих мероприятий: </p>\r\n<ul>\r\n<li>осмотр врача для выявления внешних признаков заболевания; </li>\r\n<li>анализ крови на уровень половых гормонов; </li>\r\n<li>исследование хромосомного набора в клетках, взятых с внутренней поверхности щеки; </li>\r\n<li>ультразвуковое исследование органов малого таза проводится для определения размеров матки и яичников, которые обычно значительно уменьшены; </li>\r\n<li>ультразвуковое исследование сердца для выявления пороков его развития; </li>\r\n<li>рентгенографическое исследование кистей, позвоночника, локтевых суставов для выявления их деформации и плотности костной ткани; </li>\r\n<li>ультразвуковое исследование почек для выявления аномалий развития. </li>\r\n</ul>",
"treatment": "<p> </p>\r\n<p>На первом этапе терапия заключается в стимуляции роста тела анаболическими стероидами и другими анаболическими препаратами. Лечение следует проводить минимальными эффективными дозами анаболических стероидов с перерывами при регулярном гинекологическом контроле. Главным видом терапии больных является эстрогенизация (назначение женских половых гормонов), которую следует проводить с 14—16 лет. Лечение приводит к феминизации телосложения, развитию женских вторичных половых признаков, улучшает трофику (питание) половых путей, уменьшает повышенную активность гипоталамо-гипофизарной системы. Лечение следует проводить в течение всего детородного возраста больных. </p>\r\n<p>Если с помощью гормональной терапии удаётся вырастить до нормальных размеров матку, то беременность у таких больных возможна с помощью ЭКО с донорской яйцеклеткой. Случаи, где сохранились свои яйцеклетки, единичны. </p>\r\n<p>В последнее время для увеличения показателей окончательного роста проводится терапия соматотропином. </p>",
"prevention": "<p>Единственно возможными методами профилактики рождения ребенка с синдромом Шерешевского-Тёрнера могут служить медико-генетическое консультирование и пренатальная диагностика.</p>",
"clinical_picture": "<p>Дети с синдромом Шерешевского-Тёрнера могут рождаться недоношенными, однако даже в случае доношенной беременности росто-весовые показатели ребенка нередко снижены (масса тела 2500—2800 г, длина 42-48 см). </p>\r\n<p>При рождении у ребенка обнаруживаются типичные признаки синдрома Шерешевского-Тёрнера: короткая шея со складками кожи по бокам, врожденные пороки сердца, лимфостаз, отечность стоп и кистей и др. В период новорожденности таким детям свойственно нарушение сосания, моторное беспокойство, частые срыгивания фонтаном. В раннем возрасте дети с синдромом Шерешевского-Тёрнера отличаются отставанием в физическом развитии, задержкой речевого развития, частыми повторными средними отитами, приводящими к кондуктивной тугоухости. </p>\r\n<p>К моменту пубертатного периода рост больных составляет 130-145 см. Кроме низкорослости, типичный внешний вид характеризуется короткой шеей с крыловидными складками, «лицом сфинкса», низкой границей роста волос, маленькой челюстью, деформацией ушных раковин, широкой грудной клеткой. Изменения костно-суставной системы у больных с синдромом Шерешевского-Тёрнера могут быть представлены врожденной дисплазией тазобедренных суставов, сколиозом. Ранее развитие остеопророза вследствие дефицита эстрогенов обусловливает высокую частоту переломов костей запястий, позвоночника, шейки бедра. Нарушения черепно-лицевого скелета включают маленькую челюсть, высокое готическое нёбо, аномалии прикуса. </p>\r\n<p>Наиболее частыми сердечно-сосудистыми пороками, сопровождающими синдром Шерешевского-Тёрнера, служат дефект межпредсердной перегородки, открытый артериальный проток, коарктация аорты, аневризма аорты. </p>\r\n<p>Со стороны мочевыделительной системы у больных может отмечаться наличие подковообразной почки, удвоение лоханок, стеноз почечных артерий, приводящий к артериальной гипертензии. </p>\r\n<p>Нарушения развития зрительной системы при синдроме Шерешевского-Тёрнера в большинстве случаев представлены опущением века, косоглазием, близорукостью, дальтонизмом. </p>\r\n<p>Интеллект, как правило, сохранен; в редких случаях отмечается олигофрения. </p>\r\n<p>Ведущим признаком синдрома Шерешевского-Тёрнера является первичный гипогонадизм (половой инфантилизм), который выявляется почти у 100% пациенток. Яичники представлены двухсторонними фиброзными тяжами, не содержащими фолликулов; отмечается гипоплазия матки. Большие половые губы имеют мошонкообразный вид; малые половые губы, клитор и девственная плева недоразвиты. При синдроме Шерешевского-Тёрнера отмечается первичная аменорея, недоразвитие молочных желез, непигментированные втянутые соски, скудное подмышечное и лобковое оволосение. В подавляющем большинстве случаев женщины с синдромом Шерешевского-Тернера страдают бесплодием, однако при мозаичных вариантах возможно зачатие и вынашивание плода. </p>\r\n<p>У мужчин с синдромом Шерешевского-Тёрнера, кроме характерных внешних признаков и соматических пороков, отмечается гипоплазия яичек, двусторонний крипторхизм (неопущение яичка), иногда – отсутствие яичек, низкий уровень тестостерона. </p>",
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"code": "Q96",
"name": "Синдром Тернера",
"icd_name": "Синдром Тернера",
"gender": 0,
"age_min": 0,
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"slug": "q96_sindrom_ternera",
"lead": "Нарушение здоровья, относящееся к группе хромосомные аномалии, не классифицированные в других рубриках",
"description": "Синдром Шерешевского - Тернера - это хромосомное заболевание, для которого характерно либо полное отсутствие одной хромосомы, либо наличие дефекта в одной из Х - хромосом. ",
"etiology": "<p>Чёткой связи возникновения синдрома Тёрнера с возрастом и какими-либо заболеваниями родителей не выявлено. Однако беременности обычно осложняются токсикозом, угрозой выкидыша, а роды часто бывают преждевременными и патологическими. Особенности беременностей и родов, заканчивающихся рождением ребёнка с синдромом Тёрнера, — следствие хромосомной патологии плода. Нарушение формирования половых желёз при синдроме Тёрнера обусловлено отсутствием или структурными дефектами одной половой хромосомы (X-хромосомы). </p>",
"pathogenesis": "<p>Основной механизм появления синдрома — нарушения передачи Х хромосомы во время формирования зародыша после зачатия. В большинстве случаев регистрируется полная утрата одной из половых хромосом, реже встречается частичная потеря коротких или длинных плеч либо нарушения формы (уменьшенные размеры, кольцевое строение). Чаще всего страдает наследственный материал, переданный от отца. </p>\r\n<p>У больных встречаются следующие кариотипы: </p>\r\n<ul>\r\n<li>моносомия (кариотип 45 ХО) — наблюдается у 60% пациентов; </li>\r\n<li>кольцевидная Х хромосома (46 ХRХ), делеции плеч (46 ХХр, 46 ХХq) — представлены в 20% случаев; </li>\r\n<li>мозаичное строение клеток, где часть содержат полноценный набор хромосом, а часть — аномальный (46 ХХ и 45 Х0) — выявляется у оставшихся 20%. </li>\r\n</ul>\r\n<p>В результате отсутствия или деформации половой хромосомы у девочек нарушается процесс созревания яичников, отмечается задержка или полное отсутствие полового созревания и, как следствие, развитие бесплодия. Хромосомный дисбаланс, наблюдающийся при синдроме Шерешевского - Тернера, приводит также к возникновению различных аномалий соматического развития (развития тела). </p>\r\n<p> </p>",
"diagnostics": "<p>Для установки правильного диагноза необходимо проведение следующих мероприятий: </p>\r\n<ul>\r\n<li>осмотр врача для выявления внешних признаков заболевания; </li>\r\n<li>анализ крови на уровень половых гормонов; </li>\r\n<li>исследование хромосомного набора в клетках, взятых с внутренней поверхности щеки; </li>\r\n<li>ультразвуковое исследование органов малого таза проводится для определения размеров матки и яичников, которые обычно значительно уменьшены; </li>\r\n<li>ультразвуковое исследование сердца для выявления пороков его развития; </li>\r\n<li>рентгенографическое исследование кистей, позвоночника, локтевых суставов для выявления их деформации и плотности костной ткани; </li>\r\n<li>ультразвуковое исследование почек для выявления аномалий развития. </li>\r\n</ul>",
"treatment": "<p> </p>\r\n<p>На первом этапе терапия заключается в стимуляции роста тела анаболическими стероидами и другими анаболическими препаратами. Лечение следует проводить минимальными эффективными дозами анаболических стероидов с перерывами при регулярном гинекологическом контроле. Главным видом терапии больных является эстрогенизация (назначение женских половых гормонов), которую следует проводить с 14—16 лет. Лечение приводит к феминизации телосложения, развитию женских вторичных половых признаков, улучшает трофику (питание) половых путей, уменьшает повышенную активность гипоталамо-гипофизарной системы. Лечение следует проводить в течение всего детородного возраста больных. </p>\r\n<p>Если с помощью гормональной терапии удаётся вырастить до нормальных размеров матку, то беременность у таких больных возможна с помощью ЭКО с донорской яйцеклеткой. Случаи, где сохранились свои яйцеклетки, единичны. </p>\r\n<p>В последнее время для увеличения показателей окончательного роста проводится терапия соматотропином. </p>",
"prevention": "<p>Единственно возможными методами профилактики рождения ребенка с синдромом Шерешевского-Тёрнера могут служить медико-генетическое консультирование и пренатальная диагностика.</p>",
"clinical_picture": "<p>Дети с синдромом Шерешевского-Тёрнера могут рождаться недоношенными, однако даже в случае доношенной беременности росто-весовые показатели ребенка нередко снижены (масса тела 2500—2800 г, длина 42-48 см). </p>\r\n<p>При рождении у ребенка обнаруживаются типичные признаки синдрома Шерешевского-Тёрнера: короткая шея со складками кожи по бокам, врожденные пороки сердца, лимфостаз, отечность стоп и кистей и др. В период новорожденности таким детям свойственно нарушение сосания, моторное беспокойство, частые срыгивания фонтаном. В раннем возрасте дети с синдромом Шерешевского-Тёрнера отличаются отставанием в физическом развитии, задержкой речевого развития, частыми повторными средними отитами, приводящими к кондуктивной тугоухости. </p>\r\n<p>К моменту пубертатного периода рост больных составляет 130-145 см. Кроме низкорослости, типичный внешний вид характеризуется короткой шеей с крыловидными складками, «лицом сфинкса», низкой границей роста волос, маленькой челюстью, деформацией ушных раковин, широкой грудной клеткой. Изменения костно-суставной системы у больных с синдромом Шерешевского-Тёрнера могут быть представлены врожденной дисплазией тазобедренных суставов, сколиозом. Ранее развитие остеопророза вследствие дефицита эстрогенов обусловливает высокую частоту переломов костей запястий, позвоночника, шейки бедра. Нарушения черепно-лицевого скелета включают маленькую челюсть, высокое готическое нёбо, аномалии прикуса. </p>\r\n<p>Наиболее частыми сердечно-сосудистыми пороками, сопровождающими синдром Шерешевского-Тёрнера, служат дефект межпредсердной перегородки, открытый артериальный проток, коарктация аорты, аневризма аорты. </p>\r\n<p>Со стороны мочевыделительной системы у больных может отмечаться наличие подковообразной почки, удвоение лоханок, стеноз почечных артерий, приводящий к артериальной гипертензии. </p>\r\n<p>Нарушения развития зрительной системы при синдроме Шерешевского-Тёрнера в большинстве случаев представлены опущением века, косоглазием, близорукостью, дальтонизмом. </p>\r\n<p>Интеллект, как правило, сохранен; в редких случаях отмечается олигофрения. </p>\r\n<p>Ведущим признаком синдрома Шерешевского-Тёрнера является первичный гипогонадизм (половой инфантилизм), который выявляется почти у 100% пациенток. Яичники представлены двухсторонними фиброзными тяжами, не содержащими фолликулов; отмечается гипоплазия матки. Большие половые губы имеют мошонкообразный вид; малые половые губы, клитор и девственная плева недоразвиты. При синдроме Шерешевского-Тёрнера отмечается первичная аменорея, недоразвитие молочных желез, непигментированные втянутые соски, скудное подмышечное и лобковое оволосение. В подавляющем большинстве случаев женщины с синдромом Шерешевского-Тернера страдают бесплодием, однако при мозаичных вариантах возможно зачатие и вынашивание плода. </p>\r\n<p>У мужчин с синдромом Шерешевского-Тёрнера, кроме характерных внешних признаков и соматических пороков, отмечается гипоплазия яичек, двусторонний крипторхизм (неопущение яичка), иногда – отсутствие яичек, низкий уровень тестостерона. </p>",
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"code": "C46",
"name": "Саркома Капоши",
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"lead": "Нарушение здоровья, относящееся к группе злокачественные новообразования мезотелиальной и мягких тканей",
"description": "Саркома Капоши – множественные злокачественные образования на коже с поражением ее сосудов. Чаще всего заболевание поражает мужчин. Саркома Капоши проявляется как беспорядочное новообразование сосудов и пролиферация (разрастание) веретенообразных клеток сосудов. \r\n\r\n ",
"etiology": "<p>Саркома Капоши занимает первое место среди злокачественных новообразований, поражающих больных ВИЧ-инфекцией, достигая цифр 40—60 %. </p>\r\n<p>Вирус герпеса 8-го типа обнаруживается практически у 100 % пациентов, страдающих саркомой Капоши. </p>\r\n<p>К группам риска по развитию саркомы Капоши относятся: </p>\r\n<ul>\r\n<li>ВИЧ-инфицированные мужчины; </li>\r\n<li>пожилые мужчины средиземноморского происхождения; </li>\r\n<li>лица из экваториальной Африки; </li>\r\n<li>лица с пересаженными органами (реципиенты). </li>\r\n</ul>",
"pathogenesis": "<p>Патогенез, также как и причины появления саркомы, до конца не изучен. Основной версией патогенеза начальной стадии считается образование раковых клеток из из эндотелия кровеносных или лимфососудов. </p>\r\n<p>На сегодняшний день ученым удалось выделить цитокины, оказывающие стимулирующее действие на клеточные структуры саркомы Капоши. К ним относят: фактор роста фибробластов, интерлейкин 6, трансформирующий фактор роста. В возникновении опухоли у больных СПИДом большое значение отводят онкостатину. </p>\r\n<p>Саркома Капоши является не совсем обычной злокачественной опухолью. Слабая митотическая активность, зависимость процесса от иммунного статуса пациента, возможность обратного развития очагов опухоли, отсутствие клеточной атипии и гистологическое выявление признаков воспаления подтверждают предположение о том, что в начале своего возникновения саркома Капоши скорее представляет собой реактивный процесс, нежели истинную саркому. </p>",
"diagnostics": "<p>Диагностика саркомы Капоши основана на ее типичных клинических проявлениях и данных биопсииобразований. </p>\r\n<p>Гистологическое исследование выявляет в коже множественные новообразованные сосуды и пролиферацию веретенообразных клеток — молодых фибробластов. Наличие гемосидерина и экстравазатов (геморрагических экссудатов) позволяет отличить саркому Капоши от фибросаркомы. </p>\r\n<p>Пациентам проводят иммуннологические исследования крови и анализ на ВИЧ т вирус герпеса 8 типа. </p>\r\n<p>Для выявления поражений внутренних органов при саркоме Капоши применяют УЗИ брюшной полости и сердца, гастроскопию, рентгенографию легких, сцинтиграфию скелета, КТ почек, МРТ надпочечников и т. п. </p>",
"treatment": "<p>Важным моментом в лечении саркомы Капоши является терапия основного заболевания для повышения иммунного статуса организма. </p>\r\n<p>Системное лечение саркомы Капоши обычно назначается пациентам с благоприятным иммунологическим фоном при бессимптомном течении болезни. Оно состоит в интенсивной полихимиотерапии. </p>\r\n<p>В лечении классической и эпидемической формы саркомы Капоши успешно применяются интерфероны: α-2a, α-2b и β. Они препятствуют пролиферации фибробластов и способны инициировать разрушение (апоптоз) опухолевых клеток. </p>\r\n<p>Местное лечение саркомы Капоши включает криотерапию, инъекции химиотерапевтических препаратов и интерферона в опухоль, аппликации динитрохлорбензола и мази проспидия хлорида, др. методы. При наличие болезненных и крупных очагов поражения, а также для лучшего косметического эффекта проводится локальное облучение. </p>",
"prevention": "<p>Основной мерой профилактики заболевания является своевременное и правильное лечение иммунодефицитных состояний. Так, применение антиретровирусных препаратов у ВИЧ-инфицированных больных позволяет длительное время поддерживать нормальную функцию иммунной системы, тем самым предотвращая появление саркомы Капоши.</p>",
"clinical_picture": "<p>Симптомы саркомы Капоши: </p>\r\n<ul>\r\n<li>сформировавшаяся опухоль на коже или слизистой рта имеет тёмный цвет. Если на неё надавить, то она не будет бледнеть; </li>\r\n<li>для опухолей характерна симметричность поражения;</li>\r\n<li>сформированная саркома Капоши имеет чёткую форму и лишь немного возвышается над кожей; </li>\r\n<li>на ранних стадиях развития, сформированные на слизистой рта или коже пятна, имеют небольшие размеры и гладкую поверхность. По мере своего роста они начинают немного шелушиться. На поздних стадиях центр опухоли западает и может изъязвляться; </li>\r\n<li>такого симптома, как боль, при саркоме Капоши обычно не наблюдается. Иногда в месте локализации ракового образования отмечается жжение или зуд; </li>\r\n<li>часто при поражении слизистой рта в патологический процесс вовлекается небо и лимфоузлы, расположенные ближе всего к саркоме. </li>\r\n</ul>\r\n<p>При поражении слизистой рта наблюдается появление следующих симптомов: </p>\r\n<ul>\r\n<li>болевые ощущения во рту; </li>\r\n<li>затруднение приёма пищи, если саркома локализуется ближе к горлу во рту; </li>\r\n<li>некоторое затруднение дыхания. Особенно ярко данный симптом проявляется, если образование сформировалось не только во рту, но и на слизистой верхних воздухоносных путей. </li>\r\n</ul>",
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}
]
}
