Veronique Vincent

Background: Sarcopenia and malnutrition may contribute to persistent functional vulnerability after lung transplantation, yet their prevalence using actual criteria, relationship and clinical correlates remain incompletely defined. Methods: Ninety-nine adult lung transplant recipients (Ltx) were included in the study during their routine follow-up. Sarcopenia was defined using EWGSOP2 criteria, integrating muscle strength, dual-energy X-ray absorptiometry-derived appendicular lean mass, and physical performance. Malnutrition was assessed using GLIM criteria before transplantation and at follow-up. Clinical, nutritional, biological, body-composition, and pulmonary-function variables were compared according to sarcopenia status. Results: Sarcopenia was identified in 17 recipients (17.2%), including 12 (12.1%) with severe sarcopenia. Malnutrition was frequent before transplantation and persisted at follow-up, affecting 52 of 98 recipients (53.1%) before transplantation and 23 of 99 recipients (23.2%) after transplantation. Sarcopenia was related to underlying diseases leading to transplantation (mainly COPD and ILD) and sarcopenic Ltx were older (66.1 ± 6.7 vs. 57.7 ± 12.6 years; p = 0.05), had greater smoking exposure (38.2 ± 25.6 vs. 22.2 ± 20.2 pack-years; p = 0.02) and prednisone dose (13.5 ± 8.1 vs. 8.9 ± 2.7 mg/day; p = 0.001). Despite a trend towards lower albuminemia (40.5 ± 4.7 vs. 42.1 ± 4.3 g/L; p = 0.07), malnutrition was not associated with sarcopenia status. Lung function improved substantially after transplantation, with mean FEV₁ increasing from 25.7 ± 16.6% to 82.0 ± 25.4% predicted at assessment (p < 0.001); however, FEV₁ at assessment did not differ considering sarcopenia status. Conclusions: In lung transplant recipients, EWGSOP2-defined sarcopenia was common and largely uncaptured by BMI, malnutrition status, routine biomarkers, adiposity indices, or spirometry recovery. Malnutrition was reduced by personalized nutritional support but persisted in many patients, supporting more systematic muscle-health and nutritional assessment to allow reduced post-transplant morbidity.

COVID-19 is a public health issue with a significant mortality rate and potential long-lasting disabling symptoms responsible for the long-COVID syndrome. Mitochondrial dysfunction is a key mechanism but whether peripheral blood mononuclear cell (PBMC) mitochondrial respiration changes might be associated with mortality and/or occurrence and severity of long-COVID syndrome remains to be investigated. We determined mitochondrial respiratory chain oxygen consumption in twenty COVID-19 patients hospitalized in the intensive care unit and analyzed their remaining symptoms at the third year after hospital release. PBMC mitochondrial respiration was decreased in COVID-19 patients compared to the control group (14.13 ± 2.35 vs. 6.21 ± 0.88 pmol/s/10⁶ cell, p = 0.0006 for the OXPHOS state by CII). Considering COVID severity, such a decrease was greater in long-COVID patients and in patients who deceased (4.91 ± 0.75, p = 0.008 and 4.94 ± 1.11 pmol/s/10⁶ cell, p = 0.04, respectively). PBMC markers of inflammation also increased with the severity of COVID (1.0 ± 0.08 vs. 14.45 ± 2.07, p = 0.02 for ISG15 in patients who died) and ISG15 negatively correlated with PBMC mitochondrial respiration (r = −0.67, p = 0.02 for CII). In conclusion, this study shows that the greater the impairment in PBMC mitochondrial respiration in patients hospitalized in the intensive care unit for COVID-19, the greater the mortality rate and the more severe the long-COVID symptoms—three years after hospital discharge. Further, PBMC markers of inflammation also increased with the severity of COVID and ISG15 negatively correlated with PBMC mitochondrial respiration. These results support that PBMC mitochondrial respiration might be a biomarker of COVID severity and further studies investigating whether modulation of PBMC mitochondrial respiration might improve COVID-19 patients’ prognosis.