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Список исп. литературыСкрыть список Примечания 1Коморбидные связи между депрессией и РА имеют, очевидно, патогенетические основы. Психонейроиммунология накапливает свидетельства существования взаимных обратных связей между психическими, эндокринными и иммунной системами [3, 10, 27, 78, 80, 102]. В настоящее время обсуждается роль таких провоспалительных цитокинов, как, например, интерлейкин-1, фактор некроза опухоли-a (TNF-a), интерферон-g (IFN-g) в этиологии и патофизиологии депрессии. «Цитокиновая» гипотеза депрессии предполагает, что провоспалительные цитокины, действуя как нейромодуляторы, представляют ключевой показатель в посредничестве центральных поведенческих, нейроэндокринных и нейрохимических характеристик депрессивных симптомов. Соматическое заболевание, которое характеризуется хроническим воспалительным процессом, например РА, согласно данной теории будет сопровождаться аналогичными сдвигами. Хронический либо острый дистресс приводит к дизрегуляции в системе цитокинов, что в свою очередь может инициировать дизрегуляцию гипоталамо-гипофизарно-надпочечниковой и гипофизарно-гипоталамо-тиреоидной осей. Такие закономерности установлены не только при депрессии, но и при РА [22]. Центральные эффекты провоспалительных цитокинов влияют на основные симптомы депрессии, однако данная проблема требует более глубокого изучения [78]. 2Так, нарушения семейного функционирования отмечено у 39% пациентов с РА [8]. При этом депрессия, боль и возраст у больных РА – факторы, снижающие сексуальное влечение и удовлетворение [1, 6]. Литература 1. Abdel-Nasser AM, Ali EI. Determinants of sexual disability and dissatisfaction in female patients with rheumatoid arthritis. Clin Rheumatol 2006; 25: 822–30. 2. Ang DC, Choi H, Kroenke K, Wolfe F. Comorbid depression is an independent risk factor for mortality in patients with rheumatoid arthritis. J Rheumatol 2005; 32: 1013–9. 3. 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