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Nutrition· 2026Q2· Derleme

Kronik kritik hastalığın metabolik disfonksiyonu: mekanizmalar, klinik sonuçlar ve terapötik perspektifler

Metabolic dysfunction in chronic critical illness: mechanisms, clinical consequences and therapeutic perspectives

Sílvia Castro, Cristina Granja, Joanna Colleen Dionne, Alexandra Binnie

Kısa özet

Kronik kritik hastalıklı (K KH) hastalar, kalıcı metabolik esnek olmama, katabolizmadan anabolizmaya geçişte bozulma, mitokondriyal disfonksiyon, değişmiş otofaji ve azalmış ketogenez sergiler, bu da kas israfına ve iyileşmenin gecikmesine katkıda bulunur.

Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.

Ana noktalar

  • K KH hastaları, kalıcı metabolik esnek olmama ve katabolizmadan anabolizmaya geçişte bozulma gösterir.
  • Mitokondriyal disfonksiyon, değişmiş otofaji ve azalmış ketogenez, K KH'nin özellikleridir.
  • Bu metabolik sorunlar, epigenetik ve immünometabolik değişikliklerle birlikte kas israfına ve bağışıklık disfonksiyonuna yol açar.
  • Mekanizmaya yönelik kanıtların çoğu akut faz veya preklinik çalışmalardan gelmektedir ve K KH hastalarında doğrulanması sınırlıdır.

Yapay zekâ ile başlık ve abstract'tan üretildi; tam metin okunmaz.

Özet (abstract)

Advances in intensive care have improved survival from acute critical illness, leading to a growing population of patients with chronic critical illness (CCI), many of whom require prolonged organ support. This condition is associated with persistent catabolism, inflammation, and poor long-term outcomes. Understanding the metabolic alterations underlying this failure to recover may help identify targets for monitoring and intervention. This review synthesizes current clinical and translational evidence on metabolic dysregulation in CCI and discusses its implications for monitoring, nutritional strategies, and therapeutic interventions. We performed a narrative review informed by a structured search of PubMed/MEDLINE followed by manual reference screening. Preclinical, translational and clinical studies addressing energy metabolism, mitochondrial function, autophagy, ketone metabolism, inflammation and recovery trajectories in critical illness were qualitatively synthesized. Available evidence suggests that patients with CCI exhibit persistent metabolic inflexibility, impaired transition from catabolism to anabolism, mitochondrial dysfunction, altered autophagy, and disturbances in substrate utilization, including reduced ketogenesis. These alterations, together with epigenetic and immunometabolic reprogramming, may contribute to muscle wasting, immune dysfunction, and delayed functional recovery, features consistent with the persistent inflammation, immunosuppression and catabolism syndrome (PICS). Much of the mechanistic evidence, however, derives from preclinical or acute-phase studies, and validation of these findings in patients with CCI remains limited. CCI may represent a state of impaired metabolic and cellular adaptation associated with persistent inflammation, organ dysfunction, and failed recovery from acute critical illness. Improved understanding of these mechanisms may support more individualized metabolic monitoring, nutritional support, and therapeutic strategies. Further prospective and translational studies are required to determine clinical relevance and guide targeted interventions.

Yazarların özeti; kaynağından alınmıştır. Nutrition, 2026 · DOI ↗

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