Albumin Therapy in Acute Ischemic Stroke
Summary
The management of acute ischaemic stroke centres on rapid reperfusion and neuroprotection to salvage penumbral tissue. Albumin therapy, traditionally employed to correct hypoalbuminaemia and maintain colloid oncotic pressure, has been repurposed as a multimodal neuroprotective intervention. Human serum albumin (HSA) confers antioxidant and anti‐inflammatory effects, stabilises endothelial function, and reduces blood–brain barrier disruption. In rodent models, high‐dose albumin infusions markedly decrease infarct volume, improve microvascular perfusion and attenuate cerebral oedema. Early‐phase clinical studies established the safety of administering 2 g/kg HSA within six hours of symptom onset, with signals of functional benefit in patients with moderate deficits. Larger randomised trials, while not meeting primary efficacy endpoints, revealed subgroup advantages and highlighted the importance of optimal dosing, timing and patient selection. Safety considerations—principally fluid overload and pulmonary oedema—have been manageable with tailored monitoring. Current investigations are refining albumin derivatives, delivery vehicles and combination regimens with thrombolytic agents to enhance central nervous system bioavailability and therapeutic efficacy.
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Albumin Therapy in Acute Ischemic Stroke publication trend
The graph below shows the total number of articles in albumin therapy in acute ischemic stroke across all publications each year (not limited to Nature Index journals).
Technical terms
Human serum albumin: The principal protein in blood plasma, utilised therapeutically for its colloid oncotic properties and antioxidant capacity.
Neuroprotection: Strategies aimed at preventing neuronal injury or death following ischaemic insult.
Infarct volume: The total volume of brain tissue irreversibly damaged by ischaemia.
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