Haematological conditions
David M. Luesley, Mark D. Kilby in Obstetrics & Gynaecology, 2016
Platelets are formed from megakaryocytes, which are large multinucleate cells found in the bone marrow. Their differentiation and proliferation is under the control of thrombopoietin. Each megakaryocyte can generate 2000–3000 platelets. Thrombocytopenia in pregnancy is relatively common and there are a number of possible causes. Platelet function disorders are less common but do occur so will be covered briefly.
The transport and exchange systems: respiratory and cardiovascular
Nick Draper, Helen Marshall in Exercise Physiology, 2014
Platelets, or thrombocytes, are formed by budding off from the cytoplasm of megakaryocytes in the red bone marrow. During their development in the bone marrow, megakaryocytes fragment into around 2,500 smaller sub-cellular units. These units are called platelets, each with its own plasma membrane within which it stores a wide range of chemicals including ATP, glycogen and serotonin. There are normally around 250 million platelets found in each millilitre of blood. The primary role of platelets is blood clot formation to stop blood loss following trauma to a blood vessel. Arriving at the site of an injury, plate-lets stick to the side of the wound and create a platelet plug which seals the wound. They are assisted in this role by the blood-borne enzyme, thrombin, which converts the plasma protein fibrinogen to fibrin. Fibrin threads interact with the platelets to create a fibrin mesh which encapsulates the platelets and seal the wound. An illustration of erythrocytes trapped in a fibrin mesh is shown in Figure 6.13.
Retinoids and Concomitant Surgery
Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish in Retinoids in Dermatology, 2019
Systemic isotretinoin use has been found to be associated with thrombocytopenia; however, association of thrombocytopenia and systemic isotretinoin use is a rare occurrence, and only five cases have been reported up to 2016. Rapid recovery of platelet counts was observed 7–9 days after cessation of systemic isotretinoin in four of these cases. In one case, thrombocytopenia lasted 2 months but other clinical conditions apart from isotretinoin use may have contributed to the prolonged thrombocytopenia. It can be concluded that the risk of bleeding due to retinoid-related thrombocytopenia is very low (2). A clinical study reported that isotretinoin lowered platelet counts in 110 patients treated for acne. Platelet counts for all the patients in this study were at least 200,000/microliter, and this is a value which is normal by any standard. According to the results of this study, there is no increased risk of bleeding as a result of thrombocytopenia in patients who are on systemic retinoid therapy (2). Thrombocytosis is an uncommon finding during systemic isotretinoin use. Data about the incidence of this finding are controversial, and no clinical complications of isotretinoin-induced thrombocytosis have been reported in the literature. Platelet counts should drop to normal values 3 weeks following discontinuation of systemic isotretinoin therapy. A clinical study has shown that acne treatment with systemic isotretinoin therapy for a duration of 1 month does not lead to an increase in prothrombin time (PT) or the international normalized ratio (INR); however, the same study showed that systemic retinoid use prolongs activated partial thromboplastin time (APTT) in these patients. APTT alteration was within normal time standards and had no impact on blood coagulation in patients in this study (2). In summary, systemic isotretinoin therapy rarely affects coagulation and creates a very low risk of bleeding during or after a surgical intervention.
Optimized tool for evaluation of platelet function measured by impedance aggregometry
Published in Platelets, 2021
Anna Schultz-Lebahn, Mette Tiedemann Skipper, Anne-Mette Hvas, Ole Halfdan Larsen
Platelet aggregation measured by impedance aggregometry is highly dependent on platelet count. We previously developed a tool to interpret impedance aggregometry based on the strong linear correlation between platelet counts and platelet aggregation at reduced platelet counts. The present study aimed to optimize the tool by expanding the model to include normal platelet counts. We combined data from three previous studies on 266 healthy individuals measuring impedance aggregometry with four agonists (collagen, adenosine diphosphate, thrombin receptor activating peptide-6, and ristocetin). Reduced platelet counts were established in vitro. The investigated platelet counts ranged from 26–425x109/L. A positive linear correlation was found between platelet counts and platelet aggregation across normal and reduced platelet counts (all p-values
The interaction between preoperative platelet count and function and its relationship with postoperative bleeding in cardiac surgery
Published in Platelets, 2017
Marco Ranucci, Ekaterina Baryshnikova
Platelet function tests (PFTs) before cardiac surgery are predictive of postoperative bleeding and can guide a correct timing of surgery in patients under P2Y12 inhibitors. Thrombocytopenia affects PFT and may determine postoperative bleeding. The present study aims to investigate the relationship between platelet count and function, and its role in determining postoperative bleeding in cardiac surgery patients pre-treated with P2Y12 inhibitors. The study includes 589 consecutive cardiac surgery patients, tested before surgery with platelet count and multiple electrode aggregometry (MEA) ADPtest (investigating P2Y12 receptor platelet reactivity) and TRAPtest (investigating the thrombin-dependent platelet reactivity). Platelet function was linearly associated (P = 0.001) with platelet count at the ADPtest and the TRAPtest, demonstrating a positive association in the whole spectrum of platelet count. The ADPtest (P = 0.001) and platelet count (P = 0.001) were negatively associated with postoperative bleeding, whereas the TRAPtest was not. At a multivariable analysis, the ADPtest (P = 0.026) and platelet count (P = 0.006) remained independent predictors of postoperative bleeding. The platelet transfusion rate was 5.7% in patients with ADPtest ≥30 U and platelet count ≥150 000 cells/µL, 14.3% in patients with ADPtest ≥30 U and platelet count
Study of a humanized inhibitory anti-platelet glycoprotein VI phage antibody from a phage antibody library
Published in Hematology, 2016
Qinghong Liu, Chunmei Zhang, Lingjia Yu, Yongyu Shi, Liping Zhang, Jun Peng, Xuebin Ji, Ming Hou
Objective: The aims of the study were to study the effect of anti-platelet glycoprotein (GP) VI auto-antibodies on platelet aggregation and use phage surface display technology to produce anti-platelet GPVI phage antibody fragment, which may be developed to inhibit platelet aggregation in the treatment of cardiovascular disease. Methods: Plasma samples from patients with immune thrombocytopenia (ITP) were screened by monoclonal antibody immobilization of the platelet antigen assay and the platelet aggregation test for anti-platelet GPVI auto-antibody with an inhibitory effect. The humanized anti-platelet GPVI phage antibody was produced by phage surface display technology. The function of the phage antibody fragment against platelet aggregation was examined by the platelet aggregation test. Results: Of 726 ITP patients, 2 (0.27%) patients’ plasma significantly inhibited platelet aggregation induced by collagen-1. After five rounds of selection, enrichment, and purification, a soluble phage antibody fragment was produced, which can inhibit platelet aggregation induced by collagen-1. The results demonstrate that only a few of the screened anti-platelet GPVI auto-antibodies showed an inhibitory effect on platelet aggregation. Discussion: A completely humanized anti-GPVI soluble phage antibody can be produced by phage surface display technology. The antibody was able to specifically block collagen-induced platelet aggregation without influencing the aggregation responses to other agonists. Conclusions: Results of the present study suggest that very few anti-platelet GPVI auto-antibodies inhibit the aggregation function of platelet. The humanized anti-platelet GPVI produced by phage surface display technology is promising to be used to inhibit platelet aggregation in the treatment of cardiovascular disease.
Related Knowledge Centers
- Growth Factor
- Megakaryocyte
- Blood
- Cell Nucleus
- Thrombocytosis
- Thrombocytopenia
- Heparin-Induced Thrombocytopenia