Sarcopenia, characterized by the progressive loss of skeletal muscle mass and strength, represents a significant clinical concern among patients undergoing gastric cancer surgery. Postoperative individuals are particularly vulnerable due to gastrointestinal dysfunction, reduced nutrient intake, systemic inflammation, and treatment-induced metabolic stress. This condition is associated with higher complication rates, delayed recovery, chemotherapy intolerance, and decreased survival, underscoring the importance of early detection and effective nutritional management. This narrative review integrates and synthesizes recent evidence from clinical and experimental studies that explore the pathophysiology, diagnosis, and nutritional management of sarcopenia in gastric cancer. The review emphasizes key nutritional risk factors, assessment tools, and intervention strategies applicable to both preoperative and postoperative care. Validated methods such as SARC-F (strength, assistance with walking, rise from a chair, climb stairs, and falls), dual-energy X-ray absorptiometry, and computed tomography imaging play central roles in identifying muscle loss and functional decline. Evidence suggests that protein-enriched diets, branched-chain amino acids, omega-3 fatty acids, and micronutrients such as vitamin D and antioxidants help preserve muscle mass and improve recovery outcomes. Exercise and rehabilitation further enhance these benefits by synergistically promoting muscle protein synthesis and function. Moreover, emerging technologies—including artificial intelligence–assisted nutritional monitoring, nutrigenomics, and biomarker-based personalization—represent promising directions for individualized care. Sarcopenia in gastric cancer is a modifiable and clinically significant condition. Integrating personalized nutrition with structured rehabilitation can markedly enhance functional recovery, treatment tolerance, and quality of life. Future research should aim to develop precision-based nutritional algorithms and standardized diagnostic frameworks to optimize outcomes in this high-risk population.

Profound weight loss with painful symmetrical peripheral neuropathy in diabetic patients was first described as diabetic neuropathic cachexia more than 4 decades ago. It is a distinct type of diabetic peripheral neuropathy that occurs in the absence of other microvascular and autonomic complications of diabetes. The mechanism and precipitating cause are unknown. It was reported to have good prognosis with spontaneous recovery within months to 2 years. However, it was frequently missed by clinicians because the profound weight loss is the most outstanding complaint, rather than the pain, numbness, or weakness. This often leads to extensive investigation to exclude more sinister causes of weight loss, particularly malignancy. We report a case of a young woman with well-controlled diabetes who presented with profound unintentional weight loss (26 kg), symmetrical debilitating thigh pain, and clinical signs of peripheral neuropathy. As the disease entity may mimic an inflammatory demyelinating cause of neuropathy, she was treated with a trial of intravenous immunoglobulin, which failed to give any significant benefit. However, she recovered after 6 months without any specific treatment, other than an antidepressant for the neuropathic pain and ongoing rehabilitation.

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