How to Cite
Abstract
Pustova N.O.
Pathogenetic peculiarities of diabetes mellitus type 2 and psoriasis
Kharkiv National Medical University, Ukraine
Abstract. The article examines some aspects of the pathogenesis of diabetes mellitus (DM) and psoriasis. The author’s analysis of literature data has made it possible to reveal a number of common features of these diseases. It is proved that psoriasis patients incur a much higher risk of developing DM type 2. Against a background of DM type 2 the course of psoriasis is, as a rule, more severe. Disruption of the liver enzyme function, breakdown of adaptive mechanisms and the autoimmune component are the common features of pathogenetic mechanisms in these diseases. In DM type 2, particularly at its initial stages, an abundant insulin secretion by pancreatic cells is observed. It is possible that hypersecretion of this hormone develops a higher expression of STAT3 with a resultant acceleration in keratinocyte proliferation. Taking into account that psoriasis is a dermatosis, characterized by an accelerated and distorted hyperproliferation of epidermal cells, it is possible to suppose that, against a background of coexistent DM type 2, the result of an abundant secretion of endogenous insulin is that this hormone acts as an activator of protein kinase C and STAT3. Further studies of separate links in the pathogenesis of these diseases can create necessary prerequisites for understanding mechanisms in the development of this pathology and result in the development of pathogenetically substantiated methods of treatment.
Key words: diabetes mellitus type 2, psoriasis, autoimmune processes, epidermal hyperproliferation.
Пустовая Н.А.
Патогенетические особенности сахарного диабета 2 типа и псориаза
Харківський національний медичний університет, Україна
Резюме. В статье рассмотрены некоторые вопросы патогенеза сахарного диабета и псориаза. Проведенный анализ литературных данных позволил выявить ряд общих черт, присущих этим заболеваниям. Доказано, что больные псориазом подвержены гораздо большему риску возникновения СД 2 типа. На фоне СД 2 типа псориаз, как правило, протекает более тяжело. Нарушение ферментообразующей функции печени, срыв адаптационных механизмов, аутоиммунный компонент являются общими чертами патогенетических механизмов при этих заболеваниях. При СД 2 типа, особенно на начальных этапах его развития, наблюдается избыточное выделение инсулина клетками поджелудочной железы. Возможно, что в результате гиперсекреции этого гормона развивается повышенная экспрессия STAT3, что ведет к ускоренной пролиферации кератиноцитов. Учитывая, что псориаз является дерматозом, характеризующимся ускоренной извращенной гиперпролиферацией клеток эпидермиса, можно предположить, что на фоне сопутствующего СД 2 типа в результате избыточной секреции эндогенного инсулина этот гормон выступает активатором протеинкиназы С и STAT3. Дальнейшее изучение отдельных звеньев патогенеза этих заболеваний может стать предпосылкой для понимания механизмов возникновения этой патологии и привести к разработке патогенетически обусловленных методов лечения.
Ключевые слова: сахарный диабет 2 типа, псориаз, аутоиммунные процессы, гиперпролиферация эпидермиса.
Пустова Н.О.
Патогенетичні особливості цукрового діабету 2 типу і псоріазу
Харьковский национальный медицинский университет, Украина
Резюме. У статті розглянуті деякі питання патогенезу цукрового діабету та псоріазу. Проведений аналіз літературних даних дозволив виявити ряд спільних рис притаманних цим захворюванням. Доведено, що хворі на псоріаз схильні до виникнення ЦД 2 типу. На тлі ЦД 2 типу псоріаз, як правило, протікає більш важко. Порушення ферментоутворюючої функції печінки, зрив адаптаційних механізмів, аутоімунний компонент є загальними рисами патогенетичних механізмів при цих захворюваннях. При ЦД 2 типу, особливо на початкових етапах його розвитку, спостерігається надлишкове виділення інсуліну клітинами підшлункової залози. Можливо, що в результаті гіперсекреції цього гормону розвивається підвищена експресія STAT3, що веде до прискореної проліферації кератиноцитів. Враховуючи, що псоріаз є дерматозом, що характеризується прискореною збоченою гіперпроліферацією клітин епідермісу, можна припустити, що на тлі супутнього ЦД 2 типу в результаті надмірної секреції ендогенного інсуліну цей гормон виступає активатором протеїнкінази С і STAT3. Подальше вивчення окремих ланок патогенезу цих захворювань може стати передумовою для розуміння механізмів виникнення цієї патології і привести до розробки патогенетично обумовлених методів лікування.
Ключові слова: цукровий діабет 2 типу, псоріаз, аутоімунні процеси, гіперпроліферація епідермісу.
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