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Inflammation: the driver of poor outcomes among children with severe acute malnutrition?
Jonathan P Sturgeon1,2, James M Njunge3,4, Claire D Bourke1,2
1Zvitambo Institute for Maternal and Child Health Research, Harare, Zimbabwe.
Insights
Severe acute malnutrition (SAM) is a deadly childhood condition linked to inflammation. Understanding inflammation
Area of Science:
- Pediatric Nutrition
- Immunology
- Global Health
Background:
- Severe acute malnutrition (SAM) causes 10% of deaths in children under 5 in low-income countries.
- SAM is a complex, multisystem disease with significant lean mass loss and organ dysfunction.
- Pathogenic pathways of SAM, particularly concerning infections, are not fully understood.
Approach:
- This review synthesizes current knowledge on SAM pathophysiology.
- It focuses on the role of inflammation in SAM's clinical presentation and outcomes.
- Potential therapeutic targets are explored based on evidence from other inflammatory conditions.
Key Points:
- Children with SAM exhibit heightened intestinal and systemic inflammation.
- Chronic inflammation and immunomodulation contribute to increased infection-related morbidity and mortality.
- Inflammation is central to the pathophysiology of SAM, impacting hospitalization and long-term health.
Conclusions:
- Recognizing inflammation's role is crucial for developing novel therapeutic strategies for SAM.
- Targeting inflammatory pathways may offer a transformational approach to SAM treatment.
- Further research into anti-inflammatory interventions is warranted for SAM management.
Abstract:
Severe acute malnutrition (SAM) is the most life-threatening form of undernutrition and underlies at least 10% of all deaths among children younger than 5 years in low-income countries. SAM is a complex, multisystem disease, with physiological perturbations observed in conjunction with the loss of lean mass, including structural and functional changes in many organ systems. Despite the high mortality burden, predominantly due to infections, the underlying pathogenic pathways remain poorly understood. Intestinal and systemic inflammation is heightened in children with SAM. Chronic inflammation and its consequent immunomodulation may explain the increased morbidity and mortality from infections in children with SAM, both during hospitalization and in the longer term after discharge. Recognition of the role of inflammation in SAM is critical in considering new therapeutic targets in this disease, which has not seen a transformational approach to treatment for several decades. This review highlights the central role of inflammation in the wide-ranging pathophysiology of SAM, as well as identifying potential interventions that have biological plausibility based on evidence from other inflammatory syndromes.
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