PubMed · 11859494
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J Lommi. 1999. [Cardiac cachexia].. https://pubmed.ncbi.nlm.nih.gov/11859494/
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PURPOSE: To develop and internally validate the PANTHEIA-SIRI prognostic model, which integrates log-transformed systemic inflammation response index (SIRI) with clinical predictors, to estimate overall survival (OS) in metastatic pancreatic ductal adenocarcinoma (mPDAC) treated with first-line chemotherapy. METHODS: We used data from the multicenter PANTHEIA-SEOM registry. OS was defined from chemotherapy start. The model was fitted as a Weibull accelerated failure time model in the survival-analysis population with multiple imputation. Predictors were log-transformed baseline SIRI, modeled with restricted cubic splines, ECOG, tumor burden, chemotherapy regimen, and anorexia-cachexia syndrome. Internal validation used a separate, non-overlapping cohort from the same registry; the centers contributing to each cohort are listed in a supplementary annex. TRIPOD was followed. Discrimination was assessed with Harrell´s C-index and calibration with IPCW Brier scores and IPA. RESULTS: The derivation cohort comprised 672 patients with SIRI data (593 analyzed for survival) across 22 Spanish hospitals (2015-2025); 80.1% had died after a median OS of 9.9 months. The imputation-pooled derivation C-index was 0.654 (95% CI, 0.627-0.681); optimism-corrected, 0.629. Internal validation used 62 separate patients from the same registry; 96.8% had died after a median OS of 9.2 months. The validation C-index was 0.603 (95% CI, 0.518-0.687). Calibration was adequate at 6 and 12 months. CONCLUSIONS: The PANTHEIA-SIRI model provides individualized OS estimates in mPDAC with routine clinical predictors. Its open-access calculator ( https://pantheia-siri.shinyapps.io/calc/ ) may support prognostic communication, treatment-intensity selection, and supportive-care planning. Routine clinical implementation will require further validation in larger, fully independent cohorts.
PURPOSE OF REVIEW: The objective is to summarize the findings from recent (June 2001-2002) studies that have examined the potential benefits of exercise training for the treatment of wasting associated with sarcopenia, cancer, chronic renal insufficiency, rheumatoid arthritis, osteoarthritis and HIV. In many clinical conditions, protein wasting and unintentional weight loss are predictors of morbidity and mortality. The pathogenesis of protein wasting in these conditions can be different, but the fundamental mechanism is an imbalance between muscle protein synthetic and proteolytic processes. The muscle proteins most affected and the precise alterations in their synthetic and proteolytic rates that occur in each cachectic condition are still under investigation. RECENT FINDINGS: Regular exercise, or sometimes just a modest increase in physical activity, can mitigate muscle protein wasting. Aerobic exercise training primarily alters mitochondrial and cytosolic proteins (enzyme activities), while progressive resistance exercise training predominantly increases contractile protein mass. Previous studies indicate that resistance exercise acutely increases the muscle protein synthetic rate more than muscle proteolysis such that the muscle amino acid balance is increased for up to 2 days after exercise. Progressive resistance exercise training increases muscle protein synthesis and muscle mass, but attenuates the increment in proteolysis that results from a single bout of resistance exercise. The cellular mechanisms that produce these adaptations are not entirely clear. SUMMARY: In general, patients with wasting conditions who can and will comply with a proper exercise program gain muscle protein mass, strength and endurance, and, in some cases, are more capable of performing the activities of daily living.
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