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Лечение девочек с задержкой полового развития

Лечение при ЗПР должно быть направлено на устранение фонового заболевания, явившегося причиной отсутствия или позднего появления признаков полового созревания. Независимо от характера заболевания можно назначить замес­тительную гормональную терапию эстрогенами, а в дальнейшем терапию эстроген-гестагенными препаратами в циклическом режиме. При жела-

нии иметь детей пациентке с гонадотропным ги-погонадизмом, обусловленным поражением гипоталамо-гипофизарной системы, для индуци­рования овуляции назначают инъекции ХГ в ком­бинации с менопаузальным гонадотропином (МГ). При гипоталамическом гипогонадизме мо­жет быть назначена также пульсирующая тера­пия гонадотропином в цирхоральном режиме (Claman u. Seibel, 1990; Filicori et al, 1994; Gindoff и. Jewelewicz, 1985).

У девушек, как правило, вначале проводят за­местительную эстрогенную терапию. Ее назнача­ют с костного возраста 11—12 лет конъютирован­ными эстрогенными препаратами, начиная с дозы 0,3 мг/сут (в качестве альтернативы можно назна­чить эстрадиола валерат в дозе 0,2 мг/сут) в тече­ние 6 мес. В течение следующих 6 мес дозу конъ-югированных эстрогенов можно повысить до 0,6 мг/сут (дозу эстрадиола валерата — до 0,5 мг/сут). При проведении терапии в циклическом режиме эстрогены назначают с 1-го по 25-й день, а геста-гены — с 14-го по 25-й. Из гестагенов обычно ис­пользуют дидрогестерон (10 мг/сут), медроксип-рогестерона ацетат (2,5—5 мг/сут) или хлормади-нона ацетат (2 мг/сут). На второй год терапии дозу конъюгированных эстрогенов можно повысить до 0,9—1,25 мг/сут (эстрадиола валерата до 1—1,5 мг/сут). На третий год лечения дозу эстрогенов доводят до конечной, а именно: конъюгированных эстроге­нов до 1,25 мг/сут, эстрадиола валерата до 2 мг/сут (Stolecke, 1998). При сочетанной гипота­ламо-гипофизарной недостаточности заместитель­ную эстроген-гестагенную терапию комбинируют с назначением других гормонов: гидрокортизона, L-тироксина и гормона роста.

4.5. Заключение

Несмотря на прогресс, достигнутый в диаг­ностике и лечении преждевременного полового развития у девочек и гипогонадизма у девушек, мы еще далеки от возможности ранней диагно­стики этих состояний и восстановления нару­шенных физиологических механизмов у этих пациенток.

Препараты — антагонисты гонадолиберина за­медленного действия представляют собой класс веществ, которые благодаря отсутствию у них стимулирующего эффекта гонадолиберина, обыч­но проявляющегося в начале терапии этим гор­моном, могут заменить агонисты гонадолибери­на в лечении девочек с преждевременным поло-

вым развитием. В ближайшие годы мы надеемся оптимизировать временные особенности схемы терапии (завершение лечения агонистами гона-долиберина), а также усовершенствовать методы дифференциальной диагностики гипогонадотроп-ного гипогонадизма и конституциональной ЗПР.

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