Başkent Üniversitesi Yayınları

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    Burn Cachexia: Diagnosis and Nutrition Support
    (Başkent Üniversitesi, 2023-03) Pratibha Sharma; Rajpal Singh; Shree Prakash Jaiswal; Sunil Chandiwal
    ABSTRACT Abstract Burn cachexia is a condition in which patients with major burns, especially patients with >20% total burn surface, present with significant rapid weight loss, muscle loss, and fat loss. Burn cachexia is also known as wasting syndrome and is characterized by severe weight loss, muscle and fat loss, fatigue, and anorexia. The current definition of burn cachexia includes association of an underlying disease condition characterized with muscle loss and with or without reduction in fat mass. Cachexia is driven by the molecular pathway known as the ubiquitin-proteolytic pathway. Cytokine activity plays a crucial role in the pathogenesis of cachexia; the consequent inflammation is the main cause of cachexia in major burns, and inflammatory cytokines are upregulated by reactive oxygen species that are triggered by nuclear transcription factor NF-κB. Some other well-known pathways are mitochondrial dysfunction and autophagy, endoplasmic reticulum stress, and insulin resistance. Burn cachexia is inflammation that induces protein degradation and increases cell death. Identification of burn-induced cachexia is a difficult challenge and, if untreated, can lead to death. Nutrition support is an extremely important part of burn management with cachexia and requires special attention. In this case report, we share the practical aspects of burn cachexia diagnosis and application of nutrition to prevent mortality. Our case involved a young male patient with electric burn injury who was diagnosed with burn-induced cachexia who had a successful outcome.
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    Impact of Severe Burns on Pancreatic Islets: An Experimental Model in Rats
    (Başkent Üniversitesi, 2022-03) Santiago J. Santelis; Ayse Ebru Abali; Gonca Ozgun; B. Handan Ozdemir; Neslihan Basci Tutuncu; Mehmet Haberal
    ABSTRACT OBJECTIVES: Severe burn victims experience a systemic inflammatory response and a hypermetabolic response that can generate adverse effects on many distant organs and systems. Our aim in this study was to describe the histopathological changes in the pancreatic islets secondary to severe burns in an experimental animal model. MATERIALS & METHODS: Fourteen Wistar albino rats were randomly divided into 2 groups: the sham group and the burn group. A full-thickness burn model was designed to induce a burn of 25% total body surface area. Seven days after burn induction and sham procedure, pancreatectomy was performed. Pancreatic tissues were examined under light microscopy, and islet size and cellularity were calculated. RESULTS: The histopathologic examination was unremarkable, but the mean number of islets per pancreatic tissue was lower in the burn group than in the sham group. We observed a significant difference in the mean number of cells per one islet between the 2 groups, with the cell count higher in the burn group (P < .05). CONCLUSIONS: During the acute phase of burn injury in rats, we observed a decrease in the number of pancreatic islets with remarkable hypercellularity. Further studies are needed to determine the histological and cellular basis of these changes.