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Background: Several studies showed a close link between metabolic syndrome (MetS), type 2 diabetes (T2DM) and cerebrovascular diseases. There is considerable debate regarding the role of uric acid (UA) as a risk factor in these conditions. Objective: The aim of this narrative review is to discuss the links between UA, MetS, T2DM and cerebrovascular disease. Methods: An extensive review has been conducted based on the scientific literature published in English, and indexed in MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and Google Scholar from January to May 2019. Additional relevant studies published after the initial review were also considered during the period of June 2019-October 2019, during which this manuscript was written. The Mesh Terms considered were: uric acid, antioxidant, oxidant, metabolic syndrome, diabetes, cerebrovascular diseases, stroke, haemorrhagic stroke, neurocognitive disorders, and their combinations. Results: the literature review shows a dose-dependent inflammatory action of UA, which occurs with serum concentrations >4 mg/dl (>0.24 mmol/l), representing one of the contributors of the chronic inflammatory process that underlies metabolic and cerebrovascular diseases. Conclusion: UA, which is associated with arterial hypertension and cardiovascular diseases, represents one of the indicators of oxidative homeostasis. Increasing concentrations represent a status of active inflammation which is observed with metabolic and cerebrovascular diseases.

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The presence of metabolic syndrome does not seem to provide hyperuricemia. By contrast, higher serum uric acid level may predict the risk of metabolic syndrome. Moreover, our results suggest that uric acid cannot be considered a risk factor for early atherosclerosis, at least when assessed using carotid ultrasound.

Recent findings on the antioxidant effects of pretreatment with α-lipoic acid (α-LA) on the crush injury of rat sciatic nerve confirm the possible usefulness of α-LA administration in humans with peripheral nerve injuries. We discussed this issue in relation with our recent results in which the combined employment of α-LA and γ-linolenic acid with a rehabilitation program for six weeks reduced sensory symptoms and neuropathic pain in patients with compressive radiculopathy syndrome from disc-nerve root conflict in comparison with patients submitted to rehabilitation program alone for six weeks.