Platelet activation by ADP is increased in selected patients with anterior ischemic optic neuropathy or retinal vein occlusion

Kuhli-Hattenbach, Claudia; Hellstern, Peter; Kohnen, Thomas; Hattenbach, Lars‐Olof

doi:10.1080/09537104.2016.1276548

Cited by 14 publications

(16 citation statements)

References 27 publications

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“…They found significantly greater platelet aggregation of ADP among NAION and RVO patients compared with healthy controls. 19 MPV values were evaluated in RVO patients and retinal artery occlusion patients and were found to be high in both diseases. Therefore, the authors stated that larger platelets may contribute to the pathogenesis of retinal vascular occlusion.…”

Section: Discussionmentioning

confidence: 99%

Central retinal vein occlusion associated with platelet activation

Çıtırık

2019

Ophthalmol Eye Dis

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Purpose:The aim of this article is to determine and compare the platelet activation by three main platelet activation parameters: mean platelet volume, platelet distribution width, and plateletcrit in patients with central retinal vein occlusion and control subjects.Methods:This study included 30 patients with nonischemic central retinal vein occlusion and 30 control subjects. The levels of mean platelet volume, platelet distribution width, and plateletcrit were measured in all groups.Results:The mean serum level of mean platelet volume was 10.01 ± 0.89 fl in central retinal vein occlusion group and 8.74 ± 1.45 fl in control group. The mean serum level of platelet distribution width was 14.31 ± 1.49% and 11.65 ± 1.81% in central retinal vein occlusion group and control group, respectively. Mean serum plateletcrit value was 0.27 ± 0.07% in central retinal vein occlusion group and 0.23 ± 0.07% in control group. Mean platelet volume, platelet distribution width, and plateletcrit levels were significantly higher in central retinal vein occlusion patients than controls ( p < 0.05).Conclusion:Subclinical platelet activation reflected by mean platelet volume, platelet distribution width, and plateletcrit may have an impact on the genesis of vessel occlusion in central retinal vein occlusion. The results may be important for the clinical management of patients with central retinal vein occlusion.

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Section: Discussionmentioning

confidence: 99%

Central retinal vein occlusion associated with platelet activation

Çıtırık

2019

Ophthalmol Eye Dis

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“…A TUBB1 mutation screening study in patients with hypothyroidism and altered MPV and/or a history of thrombotic disease would be of great interest. Therefore, patients bearing a TUBB1 mutation with cardiovascular risk factors could be monitored and the question arises whether antiplatelet drugs might be effective as prophylaxis (Kuhli‐Hattenbach et al , ). Conversely, thyroid function and morphology assessment could be suggested in patients with congenital macrothrombocytopaenia.…”

Section: Discussionmentioning

confidence: 99%

TUBB 1 mutations cause thyroid dysgenesis associated with abnormal platelet physiology

et al. 2018

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The genetic causes of congenital hypothyroidism due to thyroid dysgenesis (TD) remain largely unknown. We identified three novel TUBB1 gene mutations that co‐segregated with TD in three distinct families leading to 1.1% of TUBB1 mutations in TD study cohort. TUBB1 (Tubulin, Beta 1 Class VI) encodes for a member of the β‐tubulin protein family. TUBB1 gene is expressed in the developing and adult thyroid in humans and mice. All three TUBB1 mutations lead to non‐functional α/β‐tubulin dimers that cannot be incorporated into microtubules. In mice, Tubb1 knock‐out disrupted microtubule integrity by preventing β1‐tubulin incorporation and impaired thyroid migration and thyroid hormone secretion. In addition, TUBB1 mutations caused the formation of macroplatelets and hyperaggregation of human platelets after stimulation by low doses of agonists. Our data highlight unexpected roles for β1‐tubulin in thyroid development and in platelet physiology. Finally, these findings expand the spectrum of the rare paediatric diseases related to mutations in tubulin‐coding genes and provide new insights into the genetic background and mechanisms involved in congenital hypothyroidism and thyroid dysgenesis.

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“…First, we examined the effect of night-shift work on the rates of SPA and platelet aggregation induced by a low-dose agonist. SPA and small aggregate formation in low concentrations of ADP or epinephrine have been reported to be elevated in patients with arterial or venous thrombotic diseases such as anterior ischemic optic neuropathy, retinal vein occlusion 26) , or acute coronary syndrome 27 , 28) due to platelet hypersensitivity resulting from platelet stimulation. Thus, rates of SPA and platelet aggregation induced by a low-dose agonist can be used to document platelet sensitivity to platelet stimuli ex vivo .…”

Section: Discussionmentioning

confidence: 99%

The impact of night‐shift work on platelet function in healthy medical staff

Nakao

Yasumoto

Tokuoka

et al. 2018

Journal of Occupational Health

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Objectives: Rotating shift work has been reported to increase the risk of cardiovascular diseases. Vascular endothelial dysfunction and platelet activation are among the leading causes of thrombus formation in patients with myocardial infarction or stroke. Endothelial function has been shown to be impaired immediately after night-shift work; however, it is not known whether platelets are also activated. The aim of this study was to investigate the acute impact of night-shift work on platelet function. Methods: This observational study included 11 healthy medical staff members (seven women, median age 32 years). We examined each subject's platelet aggregation rates and the serum concentrations of eicosanoid mediators after night-shift work and on day-shift work without preceding night-shift work (baseline). Results: Platelet aggregation did not differ from baseline levels after night-shift work. However, serum cyclooxygenase (COX)-metabolized eicosanoid mediators, particularly thromboxane (Tx) B2 (a stable metabolite of TxA2 and the most important marker of platelet activation), were significantly higher after the night-shift than at baseline (median 65.3 vs 180.4 ng/ml). Conclusions: Although platelet aggregation did not increase, there was an increase in serum COX-metabolized eicosanoid mediators such as TxB2 in healthy medical staff after night-shift work. This platelet hypersensitivity may be one of the mechanisms underlying the significant association between night-shift work and adverse cardiovascular outcomes.

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Platelet activation by ADP is increased in selected patients with anterior ischemic optic neuropathy or retinal vein occlusion

Cited by 14 publications

References 27 publications

Central retinal vein occlusion associated with platelet activation

Central retinal vein occlusion associated with platelet activation

TUBB 1 mutations cause thyroid dysgenesis associated with abnormal platelet physiology

The impact of night‐shift work on platelet function in healthy medical staff

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