Low platelet apachidonic acid in young patients with brain infarction

Färkkilä, M.; Rasi, Vesa; Tilvis, Reijo S.; Ikkala, Esko; Viinikka, Lasse; Ylikorkala, O.; Färkkilä, AM; Miettinen, Tatu A.

doi:10.1016/0049-3848(87)90437-3

Cited by 5 publications

(11 citation statements)

References 17 publications

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“…We identified 11 eligible articles [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 ], and their study characteristics are shown in table 1 .…”

Section: Resultsmentioning

confidence: 99%

“…The overall study quality was high in the studies by Yaemsiri et al [ 23 ] and Iso et al [ 24 ] and medium in the studies by Park et al [ 26 ] and Ricci et al [ 27 ]. As to the remaining 7 studies [ 25 , 28 , 29 , 30 , 31 , 32 , 33 ], the overall quality was low. Although 1 case-control study [ 28 ] and 1 cross-sectional study [ 31 ] had moderate reporting quality (STROBE score 16), their temporal information between exposure and outcome, participant characteristics, or study settings were not sufficiently provided.…”

Section: Resultsmentioning

confidence: 99%

“…Although 1 case-control study [ 28 ] and 1 cross-sectional study [ 31 ] had moderate reporting quality (STROBE score 16), their temporal information between exposure and outcome, participant characteristics, or study settings were not sufficiently provided. The remaining 5 articles [ 25 , 29 , 30 , 32 , 33 ] were determined to be of low reporting quality (STROBE score range 5-11). No studies were adjusted for well-known potential confounders except for that of Yaemsiri et al [ 23 ].…”

Section: Resultsmentioning

confidence: 99%

“…All eligible studies measured blood ARA levels as an estimate of exposure. ARA levels in serum [ 23 , 24 , 25 , 30 , 33 ], erythrocyte membranes [ 26 , 27 , 28 ], plasma [ 29 , 31 , 32 ], and/or platelets [ 29 , 32 , 33 ] were analyzed. Our literature search did not identify any articles that evaluated dietary ARA intake and tissue ARA as assessments of exposure.…”

Section: Resultsmentioning

confidence: 99%

“…Our literature search did not identify any articles that evaluated dietary ARA intake and tissue ARA as assessments of exposure. Outcome definition, classification, or diagnostic procedure were mentioned in 3 nested case-control studies [ 23 , 24 , 25 ], 3 case-control studies [ 26 , 27 , 28 ], and 2 cross-sectional studies [ 31 , 32 ].…”

Section: Resultsmentioning

confidence: 99%

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Arachidonic Acid and Cerebral Ischemia Risk: A Systematic Review of Observational Studies

Sakai

Kakutani

Tokuda

et al. 2014

Cerebrovasc Dis Extra

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Background: Arachidonic acid (ARA) is a precursor of various lipid mediators. ARA metabolites such as thromboxane A₂ cause platelet aggregation and vasoconstriction, thus may lead to atherosclerotic disease. It is unclear whether dietary ARA influences the ARA-derived lipid mediator balance and the risk for atherosclerotic diseases, such as cerebral ischemia. Considering the function of ARA in atherosclerosis, it is reasonable to focus on the atherothrombotic type of cerebral ischemia risk. However, no systematic reviews or meta-analyses have been conducted to evaluate the effect of habitual ARA exposure on cerebral ischemia risk. We aimed to systematically evaluate observational studies available on the relationship between ARA exposure and the atherothrombotic type of cerebral ischemia risk in free-living populations. Summary: The PubMed database was searched for articles registered up to June 24, 2014. We designed a PubMed search formula as follows: key words for humans AND brain ischemia AND study designs AND ARA exposure. Thirty-three articles were reviewed against predefined criteria. There were 695 bibliographies assessed from the articles that included both ARA and cerebral ischemia descriptions. Finally, we identified 11 eligible articles and categorized them according to their reporting and methodological quality. We used the Strengthening the Reporting of Observational Studies in Epidemiology Statement (STROBE) checklist to score the reporting quality. The methodological quality was qualitatively assessed based on the following aspects: subject selection, ARA exposure assessment, outcome diagnosis, methods for controlling confounders, and statistical analysis. We did not conduct a meta-analysis due to the heterogeneity among the studies. All eligible studies measured blood ARA levels as an indicator of exposure. Our literature search did not identify any articles that evaluated dietary ARA intake and tissue ARA as assessments of exposure. Seven of the 11 eligible articles were considered to be of low quality. No articles reported a dose-dependent positive association between an increased cerebral ischemia risk and ARA exposure. However, most studies did not assess the risk in each subtype of cerebral ischemia, thus various etiological types of cerebral ischemia risk were involved in their results. Key Messages: We did not find a positive association between ARA exposure and cerebral ischemia risk. Eligible studies reported inconsistent findings: cerebral ischemia risk did not change or significantly decreased. We could not draw any conclusions due to the limited number of eligible high-quality studies. Further evidence from well-designed observational studies is required. Simultaneously, in order to develop effective preventive measures against cerebral ischemia, it is imperative to establish standardized definitions, nomenclatures, classifications, and diagnostic procedures.

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“…We identified 11 eligible articles [ 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 ], and their study characteristics are shown in table 1 .…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

See 3 more Smart Citations

Arachidonic Acid and Cerebral Ischemia Risk: A Systematic Review of Observational Studies

Sakai

Kakutani

Tokuda

et al. 2014

Cerebrovasc Dis Extra

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Platelet count and mean volume in acute stroke: a systematic review and meta-analysis

Sadeghi

Sándor

Zsóri³

et al. 2019

Platelets

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Changes of mean platelet volume (MPV) and platelet count (PC) could be a marker or a predictor of acute stroke (AS). We conducted a systematic review and meta-analysis of the published literature on the reporting of MPV and PC in AS. Studies were included in accordance with Patient Population or Problem, Intervention, Comparison, Outcomes, and Setting framework. The PRISMA strategy was used to report findings. Risk of bias was assessed with the Newcastle-Ottawa Scale. We included 34 eligible articles retrieved from the literature. PC was significantly lower in AS patients [standardized mean difference (SMD) = − 0.30, (95% CI: − 0.49 to − 0.11), N = 2492, P = .002] compared with controls (N = 3615). The MPV was significantly higher [SMD = 0.52 (95% CI: 0.28-0.76), N = 2739, P < .001] compared with controls (N = 3810). Subgroup analyses showed significantly lower PC in both ischemic stroke (Difference SMD = −0.18, 95% CI: −0.35-0.01) and hemorrhagic stroke (−0.94, −1.62 to −0.25), but only samples by citrate anticoagulant showed significantly lower result for patients compared to controls (−0.36, −0.68 to −0.04). Ischemic stroke patients had higher MPV (0.57, 0.31-0.83), and samples by Ethylenediaminetetraacetic acid (EDTA) anticoagulant showed significantly higher result for patients compared to controls (0.86, 0.55--1.17). PC and MPV appeared to be significantly different between patients with AS and control populations. MPV was significantly higher in ischemic stroke and PC was significantly lower in both ischemic and hemorrhagic strokes. These characteristics might be related to AS and associated with it. It is advisable to pay attention to elapsed time between phlebotomy and hematology analysis, anticoagulant and hemocytometer types in AS. Systematic review registration: This meta-analysis is registered on the International Prospective Register of Systematic Reviews (PROSPERO) under registration number CRD42017067864 (https:// www.crd.york.ac.uk/prospero/display_record.php?RecordID=67864).

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Incomplete global cerebral ischemia alters platelet biology in neonatal and adult sheep

Littleton-Kearney

Hurn

Kickler

et al. 1998

American Journal of Physiology-Heart and Circulatory Physiology

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Platelets are implicated as etiologic agents in cerebral ischemia and as modulators of neural injury following an ischemic insult. We examined the effects of severe, transient global ischemia on platelet aggregation during 45-min ischemia and 30-, 60-, and 120-min reperfusion in adult and neonatal lambs. We also examined postischemic platelet deposition in brain and other tissues (120-min reperfusion) using indium-111-labeled platelets. Ischemic cerebral blood flow fell to 5 ± 1 and 5 ± 2 ml ⋅ min−1 ⋅ 100 g−1 in lambs and sheep, respectively. During ischemia, platelet counts fell to 47.5 ± 5.1% of control ( P < 0.05) in lambs and 59 ± 4.9% of control in sheep ( P < 0.05). Ischemia depressed platelet aggregation response ( P < 0.01) to 4 μg collagen in lambs and sheep (20.4 ± 29.2 and 26 ± 44.7% of control, respectively). Marked platelet deposition occurred in brain and spleen in sheep, whereas significant platelet entrapment occurred only in brain in lambs. Our findings suggest that ischemia causes platelet activation and deposition in brain and noncerebral tissues.

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Low platelet apachidonic acid in young patients with brain infarction

Cited by 5 publications

References 17 publications

Arachidonic Acid and Cerebral Ischemia Risk: A Systematic Review of Observational Studies

Arachidonic Acid and Cerebral Ischemia Risk: A Systematic Review of Observational Studies

Platelet count and mean volume in acute stroke: a systematic review and meta-analysis

Incomplete global cerebral ischemia alters platelet biology in neonatal and adult sheep

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