Refeeding syndrome (RFS) can be a severe and life-threatening complication of anorexia nervosa (AN) associated with electrolyte abnormalities and organ damage, and occurs with the transition from a prolonged catabolic to anabolic state, particularly with an overzealous nutrient supply. There is no unequivocal definition of RFS, although hypophosphatemia is recognized as a crucial factor in its pathogenesis. RFS can be responsible for cardiovascular complications, such as heart failure, left ventricular damage, and arrhythmias, because of different potential mechanisms: electrolyte imbalances, increased retention of sodium and liquids secondary to insulin secretion, and excessive fat emulsion supplementation. We report on the case of a 13-y-old male patient with severe AN in whom a delayed and reversible myocardial dysfunction was documented during cautious nutritional replenishment, even in the absence of serum electrolyte imbalances. Seven days after the inception of integrative enteral nutrition, heart failure was unexpectedly documented as follows: reduction in fraction ejection, presence of mild bilateral perimalleolar edema, and increased n-terminal prohormone of brain natriuretic peptide. A more pronounced water restriction protocol and delayed achievement of goal feeding rate, resulting also in lower sodium intake, were implemented to reduce cardiac overload with a full resolution of the complication in approximately 2 mo. Refeeding patients with AN could be complicated by heart failure despite cautious nutritional replenishment and regardless of electrolyte imbalance, even in a later phase of recovery. Therefore, strict adherence to recommendations for nutritional replenishment and close monitoring of cardiac function should always be considered when refeeding patients with AN.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.nut.2022.111788 | DOI Listing |
N Engl J Med
January 2025
From Duke University School of Medicine, Durham, NC; and Duke Clinical Research Institute, Durham, NC.
Am J Respir Crit Care Med
January 2025
University of Minnesota, Medicine, Minneapolis, Minnesota, United States.
Chronic Obstr Pulm Dis
January 2024
Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
Background: The impact of iron deficiency on COPD morbidity independent of anemia status is unknown. Understanding the association between iron deficiency, anemia status, and risk of hospitalization in COPD may inform an approach to these comorbidities.
Study Design And Methods: Adults ≥40 years from the Johns Hopkins COPD Precision Medicine Center of Excellence data repository with an outpatient iron profile and 1 year of subsequent follow-up time were included in the study.
Proc Natl Acad Sci U S A
February 2025
Department of Molecular Microbiology, Washington University in St. Louis, School of Medicine, St. Louis, MO 63130.
bradyzoites reside in tissue cysts that undergo cycles of expansion, rupture, and release to foster chronic infection. The glycosylated cyst wall acts as a protective barrier, although the processes responsible for formation, remodeling, and turnover are not understood. Herein, we identify a noncanonical chitinase-like enzyme TgCLP1 that localizes to micronemes and is targeted to the cyst wall after secretion.
View Article and Find Full Text PDFPLoS One
January 2025
Precision Laboratory of Vascular Medicine, Shanxi Cardiovascular Hospital Affiliated Shanxi Medical University, Taiyuan, PR China.
Background: Myocardial ischemia-reperfusion injury (MIRI) is an important complication in the treatment of heart failure, and its treatment has not made satisfactory progress. Nitroxyl (HNO) showed protective effects on the heart failure, however, the effect and underlying mechanism of HNO on MIRI remain largely unclear.
Methods: MIRI model in this study was established to induce H9C2 cell injury through hypoxia/reoxygenation (H/R) in vitro.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!