PubMed · 3468596
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L B Casedonte. 1987. When your patient won't eat.. https://pubmed.ncbi.nlm.nih.gov/3468596/
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PURPOSE OF REVIEW: This review will update clinicians and basic scientists who are interested in the clinical relevance and molecular mechanism of uremic cachexia. Recent studies that examine the role of cytokines and hypothalamic neuropeptides are emphasized. RECENT FINDINGS: A current hypothesis of the cause of cachexia in chronic illness is that proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-6, and leptin, act on the central nervous system to alter the release and function of several key neurotransmitters, thereby altering both appetite and metabolic rate. Proinflammatory cytokines also activate the transcription factor nuclear factor-kappaB, resulting in decreased protein synthesis, and activate the ubiquitin-mediated proteolytic system, which is the major system involved in increased protein degradation. SUMMARY: This review highlights the importance of melanocortin signaling in the pathogenesis of uremia-associated cachexia and the potential of peripheral administration of melanocortin-4 receptor antagonists as a novel therapeutic approach.
Appetite loss, nausea and vomiting are most common gastrointestinal distress in patients with advanced cancers. It is worthwhile to relieve these symptoms for improving their quality of life (QOL), an inadequate treatment, on the contrary, will increase their distressing symptoms. To avoid this, it is essential to clarify the cause of illness, especially to find out whether it is due to a complete mechanical gastrointestinal obstruction or not. If it is so, the use of metoclopramide is a contraindication. Practically, the combined use of octreotide acetate, steroids and morphine will be effective to manage a severe gastrointestinal distress such as an obstinately nausea and vomiting.
The authors present the case of a 49-year-old female who presented to the emergency department with a chief complaint of "not eating well." She was found to have a heart murmur, a focal neurological deficit, and large mitral valve vegetation. The patient was later diagnosed with acute Pseudomonal endocarditis with septic emboli to the brain, liver, spleen, and kidneys. A discussion of the patient presentation, diagnostic evaluation, and outcome are reviewed.