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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">ophthalmology</journal-id><journal-title-group><journal-title xml:lang="ru">Офтальмология</journal-title><trans-title-group xml:lang="en"><trans-title>Ophthalmology in Russia</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1816-5095</issn><issn pub-type="epub">2500-0845</issn><publisher><publisher-name>Ophthalmology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18008/1816-5095-2016-3-135-143</article-id><article-id custom-type="elpub" pub-id-type="custom">ophthalmology-315</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОБЗОРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS</subject></subj-group></article-categories><title-group><article-title>ЭВОЛЮЦИЯ ПРЕДСТАВЛЕНИЙ О РОЛИ ВГД В ПРОГРЕССИРОВАНИИ ГЛАУКОМЫ (ОБЗОР)</article-title><trans-title-group xml:lang="en"><trans-title>EVOLUTION THE CONCEPTS OF ROLE OF INTRAOCULAR PRESSURE IN GLAUCOMA PROGRESSION (REVIEW)</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Курышева</surname><given-names>Н. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Kurysheva</surname><given-names>N. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p> д.м.н., профессор, руководитель консультативно‑диагностического отдела </p></bio><bio xml:lang="en"><p> MD, Professor, Head of the Diagnostic Department </p></bio><email xlink:type="simple">e-natalia@list.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Шаталова</surname><given-names>Е. О.</given-names></name><name name-style="western" xml:lang="en"><surname>Shatalova</surname><given-names>E. O.</given-names></name></name-alternatives><bio xml:lang="ru"><p>кмн, врач‑офтальмолог</p></bio><bio xml:lang="en"><p>PhD, ophthalmologist</p></bio><email xlink:type="simple">katiamdtenax@yandex.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Центр офтальмологии Федерального медико-биологического агентства России,  Клиническая больница № 86, ул. Гамалеи, 15, Москва, 123098, Российская Федерация</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Ophthalmological Center of the Federal Medical and Biological Agency of Russia, Clinical Hospital No. 86,  Gamalei St. 15, Moscow, 123098, Russian Federation</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Сеть медицинских центров «Клиники доктора Шаталова»,  &#13;
ул. Набережная, 10А, Московская область, г. Орехово-Зуево, 142603, Российская Федерация</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Clinics of Dr. Shatalov Nabereznaya street, 10A, Moscow region,  &#13;
Orechovo-Zuevo, 142603, Russian Federation</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>29</day><month>09</month><year>2016</year></pub-date><volume>13</volume><issue>3</issue><fpage>135</fpage><lpage>143</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Курышева Н.И., Шаталова Е.О., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Курышева Н.И., Шаталова Е.О.</copyright-holder><copyright-holder xml:lang="en">Kurysheva N.I., Shatalova E.O.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.ophthalmojournal.com/opht/article/view/315">https://www.ophthalmojournal.com/opht/article/view/315</self-uri><abstract><sec><title> </title><p> </p></sec><sec><title> </title><p> </p><p>Роль повышенного офтальмотонуса в прогрессировании ГОН была подчеркнута неоднократно. Впервые вопрос о роли повышенного внутриглазного давления (ВГД) как первопричины глаукомы возник в начале 60-х годов прошлого столетия. Однако вскоре эпидемиологические исследования по этому поводу подвергли сомнению роль ВГД как диагностического критерия глаукомы из-за относительно редкого обнаружения заболевания среди лиц с офтальмогипертензией и из-за частого выявления глаукомы при нормальном ВГД. Многоцентровые исследования, предпринятые с целью выяснить необходимость гипотензивной терапии в лечении глаукомы, показали важность снижения ВГД: было установлено, что снижение ВГД на 1 мм рт. ст. уменьшает риск развития глаукомы на 10-19%. Кроме того, оказалось, что скорость прогрессирования глаукомы весьма вариабельна и зависит не только от формы глаукомы, но и от других факторов, например, стадии заболевания и вида терапии. Согласно данным Шведского исследования, ГОН чаще прогрессировала у больных, получавших более агрессивное лечение: аргон-лазерную трабекулопластику и синустрабекулэктомию. Наиболее важным фактором риска прогрессирования ГОН, как показали все исследования, является возраст. По-прежнему, спорными остаются вопросы, касающиеся влияния флуктуаций ВГД, снижения ретробульбарного кровотока, гипотензивного лечения, на прогрессирование глаукомной оптиконейропатии. Несмотря на то, что последнее многоцентровое исследование UKGTS (2014) показало снижение скорости прогрессирования глаукомы у больных, применявших латанопрост, у высокого процента больных, не получавших лечения, отсутствовало прогрессирование заболевания. В связи с этим вопрос о роли ВГД, как главного пускового фактора в патогенезе глаукомы, остается открытым.</p></sec></abstract><trans-abstract xml:lang="en"><p>The role of elevated intraocular pressure (IOP) in the progression of glaucoma optical neuropathy has emphasized repeatedly. The question about the role of elevated IOP as the underlying cause of glaucoma arose in the early 1960s. However, epidemiological studies have questioned the role of IOP as a diagnostic criterion for glaucoma, due to the relatively rare detection the disease among those with ocular hypertension and frequent detection of glaucoma with normal IOP. Multicenter studies determining the role of antihypertensive therapy in the treatment of glaucoma, have shown the importance of reducing IOP: decricing IOP at 1 mm Hg reduced the risk of developing glaucoma on 10-19%. In addition, it was found that the rate of glaucoma progression is very variable. It depends not only on the form of glaucoma, but also on other factors such as the stage of disease and therapy. Swedish study shown normal-tension glaucoma often progressed among the patients with more aggressive treatment such as argon laser trabeculoplasty or trabeculectomies. According to the study’s data, age is the most important risk factor for the progression of normal-tension glaucoma. Such questions as fluctuations in IOP, reduction of retrobulbar blood flow, antihypertensive treatment on the progression of glaucoma are still discussed. Despite the fact that the latter UKGTS multicenter study (2014) showed a decrease in the rate of progression of glaucoma in patients treated with latanoprost, a high percentage of non-treated patients didn’t have disease’s progression. In this regard, the role of IOP as main starting factor in glaucoma pathogenesis is still open.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>ВГД</kwd><kwd>многоцентровые исследования</kwd><kwd>офтальмогипертензия</kwd><kwd>глаукома нормального давления</kwd><kwd>САП</kwd><kwd>прогрессирование ПОУГ</kwd></kwd-group><kwd-group xml:lang="en"><kwd>IOP</kwd><kwd>multicenter study</kwd><kwd>ocular hypertension</kwd><kwd>glaucoma normal pressure</kwd><kwd>perimetry</kwd><kwd>progression of POAG</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Strömberg U. Ocular hypertension. Frequency, course and relation to other disorders occurring in glaucoma, as seen from mass survey of all inhabitants over forty years of age in a Swedish town. Acta Ophthlmol Suppl. 1962; Suppl 69:1 75.</mixed-citation><mixed-citation xml:lang="en">Strömberg U. Ocular hypertension. 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