- 1Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
- 2Department of General Practice, Fuyang Hospital Affiliated to Anhui Medical University, Anhui, China
- 3Department of Endocrinology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China
Purpose: The purpose of study was to describe the association between ferritin and all-cause mortality of cases with stroke.
Methods: Clinical data derived from
Multiparameter Intelligent Monitoring in Intensive Care were analyzed.
The primary endpoint was 30-day mortality. The potential prognostic
roles of Ferritin L were analyzed by Cox proportional hazard models. The
independent prognostic roles of Ferritin L in the cases were analyzed
by smooth curve fitting.
Results: Concerning 30-day mortality, the HR (95% CI) for a high Ferritin (≥373) was 1.925 (1.298, 2.854; p = 0.00113),
compared to a low ferritin (< 373). After adjusting for multiple
confounders, the HR (95% CI) for a high Ferritin (≥373) was 1.782
(1.126, 2.820; p = 0.01367), compared to a low Ferritin (<
373). A non-linear association between Ferritin and 30-day mortality was
found. Using recursive algorithm and two-piecewise linear regression
model, inflection point (IP) was calculated, which was 2,204. On the
left side of the IP, there was a positive relationship between Ferritin
and 30-day mortality, and the effect size, 95% CI and p value were 1.0006 (1.0004, 1.0009) p < 0.0001, respectively. On the right of the IP, the effect size, 95% CI and p value were 1.0000 (1.0000, 1.0000) and 0.3107, respectively.
Conclusion: Ferritin was associated with increased
risk of stroke; it is important to further examine the association if
the increased uric acid would increase the outcome of stroke in a
longitudinal study. The non-linear relationship between Ferritin and
all-cause mortality of stroke was observed. Ferritin was a risk factor
for the outcome of stroke when ferritin was <2204.
1 Introduction
Stroke, a neurological deficit originating from
cerebrovascular causes, disrupts blood supply to part of the brain,
potentially inducing irreversible damage to deprived neural tissues and
consequently triggering substantial morbidity and mortality worldwide (1–3).
With various subtypes, including ischemic and hemorrhagic strokes, each
presenting unique pathophysiology, risk factors, and outcomes, stroke
management demands rigorous attention to detail, a comprehension of its
multifaceted nature, and often, a patient-centric approach to care (4).
While acute phase interventions, both medical and/or surgical, followed
by rehabilitative strategies, remain fundamental to stroke management, a
prudent understanding and investigation of potential prognostic markers
are pivotal to interpret, forecast, and possibly enhance patient
outcomes (3–5).
Ferritin, a cellular protein that binds and sequesters
iron, is traditionally recognized as an indicator of iron stores within
the body (6, 7).
Elevated serum ferritin levels, aside from implications in iron
metabolism disorders, have also been acknowledged as an acute-phase
reactant, often elevating in situations of systemic inflammation,
cellular injury, and specific disease states (8).
Within cardiovascular diseases, elevated ferritin levels have been
associated with adverse outcomes, highlighting its potential utility as a
prognostic marker (9).
Furthermore, emerging data insinuate that ferritin, through its
involvement in iron metabolism and its capacity to induce oxidative
stress, might participate in the pathophysiological cascade following
ischemic cell death and in propagating secondary injury mechanisms
post-stroke. Nevertheless, the explicit association between ferritin
levels and outcomes in stroke patients warrants further elucidation.
While stroke instigates a complex interplay of inflammatory, oxidative,
and neurodegenerative processes, defining the role of ferritin—both as a
marker and a participant in this cascade—requires meticulous
investigation (10, 11).
Given the pathophysiological complexity and heterogeneity among stroke
patients, it is imperative to discern whether ferritin levels maintain a
consistent, independent association with outcomes or simply reflect the
inflammatory and oxidative processes that prevail following cerebral
ischemia or hemorrhage (12, 13).
This study commences an exploration into the association
between serum ferritin levels and all-cause mortality in stroke
patients, delving into the complexities of stroke subtypes and
coexisting variables that could potentially influence this relationship.
By unraveling these associations, we aim to enhance our understanding
of stroke pathophysiology, potentially facilitating the development of
novel prognostic and therapeutic strategies aimed at mitigating the
profound impact of this formidable neurological challenge. In this
study, we utilized real-world data obtained from the latest
Multiparameter Intelligent Monitoring in Intensive Care (MIMIC) database
to assess the association between ferritin and stroke patient outcomes,
adjusting for various potential confounders.
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