Lujun Shao, Yue Li, Cheng Xu, Li Wang, Huiyu Tai
Recorded LOCP cancer status was associated with a distinct inflammatory and hematological profile, mainly higher CRP and lower hemoglobin. Longitudinal, site-specific datasets with richer behavioral and tumor-level information are needed before these markers can be interpreted as predictive or etiological indicators.
Malnutrition, sarcopenia and frailty are common in advanced liver disease and predict poorer survival, encouraging simple blood-based indices when formal assessment is impractical. The most widely used, the Prognostic Nutritional Index (PNI), combines serum albumin and the peripheral lymphocyte count; yet both have been reported to be strongly influenced by systemic inflammation as well as by nutrition, and the index is seldom benchmarked against a disease-specific reference or against albumin alone. We evaluated whether the PNI provides clinically useful prognostic information for short-term mortality in critically ill patients with liver disease, using three independent cohorts: a North American intensive-care primary cohort (n = 3,653), a multicentre external-validation cohort (n = 922) and a single-center Chinese cohort in which hepatitis B was the leading cause of liver disease (n = 453). In each cohort we quantified discrimination of 28-day or in-hospital mortality, compared the PNI with serum albumin alone and with the Model for End-Stage Liver Disease (MELD), and tested whether it improved discrimination or reclassification beyond MELD. The PNI discriminated death only marginally better than chance (area under the curve 0.52-0.56) and no better than albumin alone, so its lymphocyte component added no independent signal; the weak per-standard-deviation association seen in the primary cohort was not significant in either validation cohort. MELD discriminated substantially better everywhere (0.67-0.70). The conventional PNI threshold classified 89-97% of patients as abnormal and was uninformative. Across three case-mixes the PNI behaved as a weak, non-specific prognostic discriminator, adding nothing to MELD, MELD-Na or MELD 3.0; in an exploratory paired subgroup, re-measurement on days 3-7 did not improve discrimination. This is consistent with its components tracking systemic inflammation and chronic physiologic reserve-an axis largely orthogonal to the acute organ failure that drives short-term mortality. Separating the index into its components and testing incremental value provides the comparative evidence this literature has lacked. The PNI was assessed as a discriminator of short-term mortality, not as a measure of nutritional status: nutritional risk is better identified with instruments validated for that purpose, and mortality risk with MELD.