Rhabdomyolysis is a syndrome involving the destruction of skeletal muscle fibers, resulting in the release of intracellular contents, inflammation, and significant damage to organs such as the kidneys. The release of inflammatory cytokines, as IL-1β, potentiates the immune system's, causing muscle and kidney damage and severe acute anemia.

To describe scientific evidence on elevated IL-1β levels associated with the progression of severe anemia in rhabdomyolysis.

This is an integrative literature review conducted in the PubMed and SciELO databases, covering the years 2010 to 2025. Articles published in English and Portuguese were included, using the descriptors: "IL-1β", "anemia", "rhabdomyolysis", "erythropoietin", and "inflammatory cytokines".

The analyzed studies suggest that the massive release of intracellular constituents during rhabdomyolysis triggers a significant inflammatory response, IL-1β playing a prominent role. This cytokine exerts a direct inhibitory effect on renal erythropoietin production, which is essential for erythropoiesis. In the presence of tissue hypoxia and anemia, continuous inflammatory signaling impedes the compensatory response of the bone marrow. Therefore, there’s a clinical worsening that, in severe and untreated cases, can lead to chronic kidney injury, aplasia, the need for hemodialysis, and even death. However, the exacerbated expression of IL-1β increases oxidative stress, aggravating damage to erythropoiesis, which results in a reduction in the number of circulating erythrocytes and intensifies symptomatology in rhabdomyolysis.

Although rhabdomyolysis can affect any individual due to strenuous activities or dietary factors, it’s observed that some individuals have a greater predisposition to elevated IL-1β levels. This predisposition may be associated with genetic factors, pre-existing conditions, or individual specificities that influence the inflammatory response.

In addition to increasing the inflammatory response and affecting the immune system, IL-1β directly impacts hematological processes, generating a cycle that worsens the clinical condition, especially anemia, inflammation, and damage renal function. Strategies aimed at reducing inflammation and restoring blood cell production can significantly improve the clinical prognosis of these patients, reducing morbidity and mortality related to the condition.