Orbital Hematoma Following Minor Trauma Due to Platelet Aggregation Abnormality

1998 ◽  
Vol 116 (10) ◽  
pp. 1402 ◽  
Author(s):  
Mushtaq A. Khan
Keyword(s):  
Platelet Aggregation ◽  
Minor Trauma ◽  
Orbital Hematoma

Fibrinolytic Activity in Patients with Essential Thrombocythemia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3223-3223
Author(s):  
Bozena Sokolowska ◽  
Aleksandra Nowaczynska ◽  
Katarzyna Wejksza ◽  
Adam Walter-Croneck ◽  
Martyna Kandefer-Szerszen ◽  
...  
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Essential Thrombocythemia ◽  
Fibrinolytic Activity ◽  
Small Sample ◽  
Control Group ◽  
Minor Trauma ◽  
Bleeding Tendency ◽  
Thrombotic Complications ◽  
Platelet Defects

Abstract Essential thrombocythemia (ET) is characterized by bleeding tendency, thrombotic complications and qualitative platelet defects. All those abnormalities are likely to contribute to the excessive mortality rate of this disease. Among many specific morphological, biochemical and metabolic platelet defects, a complete loss of platelet responsiveness to epinephrine is the most frequent in these patients. Since an abnormal platelet fibrinolytic activity was suggested to contribute to bleeding tendency, our initial goal was to see if platelet fibrinolysis activity is impaired in patients with ET. 22 patients were enrolled into the study (17 females, 5 males age 57.2±13.0.). This group included: 6 untreated patients, 9 treated with anagrelide, 4 with hydroxyurea, and 3 treated with a combination of both drugs. 8 thrombotic complications and 2 clinically significant bleeding episodes occurred. The control group consisted of 6 females age 33.3±9.9. Platelet count was 777±333 x109/L and 257±70 x109/L p<0.001, for the ET and the control group, respectively. Platelet activation was studied using flow cytometry to detect CD62P expression on the platelet surface. There was no difference between the control and the ET group. Platelet aggregation was measured using adenosine diphosphate and epinephrine as agonists. While 90% individuals from control group responded to epinephrine, in 45% of patients, a lack of epinephrine-induced platelet aggregation was detected. In this 45% of patients a statistically significantly lower expression of CD62P on CD61 positive cells was observed (mean value 1.90% versus 3.82%). Further, urokinase-type plasminogen activator (uPA) concentration was evaluated in plasma and in platelet lysates. Concentration of uPA was statistically significantly higher in patient plasma as compared to the control group (0.049±0.030 versus 0.029±0.015 ng/ml, p<0.05). Mean uPA concentration measured in platelet lysates was similar in both groups (ET 0.114±0.060ng/109 platelets, control group 0.110±0.042 ng/109 platelets). However, in platelets lysates from three patients, an extremely high uPA concentration was detected (more than 0.194 ng/109 platelets). One of these patients had an episode of hypermenorrhea and the second presented a thigh hematoma after a minor trauma. In both of those patients platelet count was above 600 x 109/L. In addition, in one patient very low uPA activity in platelet lysates was observed (0.030 ng/109 platelets). In this patient’s medical history, two episodes of DVT occurred. To evaluate platelet fibrinolytic activity, uPA activity was assessed by means of casein zymography. Zymograms have show that similar fibrinolytic activity was present both in patients and the control group and the activity of fibrinolytic enzymes was inhibited by AEBSF, an inhibitor of serine proteases. From the data gathered we concluded that uPA concentration is significantly higher in ET patient plasma as compared to the control group. However, platelet fibrinolytic activity, measured as uPA activity and uPA concentration in platelets lysates obtained from ET patients is not impaired as was initially presumed. Because of the small sample size, we could not precisely assess the clinical importance of extremely high or extremely low uPA activity in platelets lysates. All these data need further evaluation in a larger group of patients.

Fine Structure of Platelet Interaction with a New Microcrystalline Collagen Preparation

1974 ◽  
Vol 32 ◽  
pp. 58-59
Author(s):  
W. H. Zucker ◽  
R. G. Mason
Keyword(s):  
Fine Structure ◽  
Platelet Aggregation ◽  
Hydrochloric Acid ◽  
Whole Blood ◽  
Platelet Adhesion ◽  
Hemostatic Agent ◽  
Native Collagen ◽  
Fibrillar Morphology ◽  
Clinical Interest ◽  
New Form

Platelet adhesion initiates platelet aggregation and is an important component of the hemostatic process. Since the development of a new form of collagen as a topical hemostatic agent is of both basic and clinical interest, an ultrastructural and hematologic study of the interaction of platelets with the microcrystalline collagen preparation was undertaken.In this study, whole blood anticoagulated with EDTA was used in order to inhibit aggregation and permit study of platelet adhesion to collagen as an isolated event. The microcrystalline collagen was prepared from bovine dermal corium; milling was with sharp blades. The preparation consists of partial hydrochloric acid amine collagen salts and retains much of the fibrillar morphology of native collagen.

The blister of porphyria cutanea tarda: A Scanning and Transmission Electron Microscopic study

1986 ◽  
Vol 44 ◽  
pp. 334-335
Author(s):  
Veronika Burmeister ◽  
R. Swaminathan
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Basement Membrane ◽  
Middle Age ◽  
Porphyria Cutanea Tarda ◽  
Minor Trauma ◽  
Electron Microscopic ◽  
Transmission Electron Microscopic Study ◽  
Transmission Electron ◽  
Transmission Electron Microscopic

Porphyria cutanea tarda (PCT) is a disorder of porphyrin metabolism which occurs most often during middle age. The disease is characterized by excessive production of uroporphyrin which causes photosensitivity and skin eruptions on hands and arms, due to minor trauma and exposure to sunlight. The pathology of the blister is well known, being subepidermal with epidermodermal separation, it is not always absolutely clear, whether the basal lamina is attached to the epidermis or the dermis. The purpose of our investigation was to study the attachment of the basement membrane in the blister by comparing scanning with transmission electron microscopy.

Inflammatory process and virgin olive oil phenols: modulation of platelet aggregation and metalloprotease-9 expression in monocytes

Planta Medica ◽  
2008 ◽  
Vol 74 (09) ◽  
Author(s):  
M Dell'Agli ◽  
R Fagnani ◽  
G Galli ◽  
O Maschi ◽  
E de Fabiani ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Olive Oil ◽  
Inflammatory Process ◽  
Virgin Olive Oil

Platelet Activation and Aggregation Induced by Recombinant von Willebrand Factors Reproducing Four Type 2B von Willebrand Disease Missense Mutations

1998 ◽  
Vol 79 (01) ◽  
pp. 211-216 ◽  
Author(s):  
Lysiane Hilbert ◽  
Claudine Mazurier ◽  
Christophe de Romeuf
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Von Willebrand Disease ◽  
Platelet Glycoprotein ◽  
Missense Mutations ◽  
Inhibit Platelet Aggregation ◽  
Wild Type ◽  
A1 Domain ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryType 2B of von Willebrand disease (vWD) refers to qualitative variants with increased affinity of von Willebrand factor (vWF) for platelet glycoprotein Ib (GPIb). All the mutations responsible for type 2B vWD have been located in the A1 domain of vWF. In this study, various recombinant von Willebrand factors (rvWF) reproducing four type 2B vWD missense mutations were compared to wild-type rvWF (WT-rvWF) for their spontaneous binding to platelets and their capacity to induce platelet activation and aggregation. Our data show that the multimeric pattern of each mutated rvWF is similar to that of WT-rvWF but the extent of spontaneous binding and the capacity to induce platelet activation and aggregation are more important for the R543Q and V553M mutations than for the L697V and A698V mutations. Both the binding of mutated rvWFs to platelets and platelet aggregation induced by type 2B rvWFs are inhibited by monoclonal anti-GPIb and anti-vWF antibodies, inhibitors of vWF binding to platelets in the presence of ristocetin, as well as by aurin tricarboxylic acid. On the other hand, EDTA and a monoclonal antibody directed against GPIIb/IIIa only inhibit platelet aggregation. Furthermore, the incubation of type 2B rvWFs with platelets, under stirring conditions, results in the decrease in high molecular weight vWF multimers in solution, the extent of which appears correlated with that of plasma vWF from type 2B vWD patients harboring the corresponding missense mutation. This study supports that the binding of different mutated type 2B vWFs onto platelet GPIb induces various degrees of platelet activation and aggregation and thus suggests that the phenotypic heterogeneity of type 2B vWD may be related to the nature and/or location of the causative point mutation.

Difference of [Ca2+]i Movements in Platelets Stimulated by Thrombin and TRAP: the Involvement of αIIbβ3-Mediated TXA2 Synthesis

1998 ◽  
Vol 79 (06) ◽  
pp. 1184-1190 ◽  
Author(s):  
Yoshiaki Tomiyama ◽  
Shigenori Honda ◽  
Kayoko Senzaki ◽  
Akito Tanaka ◽  
Mitsuru Okubo ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Fibrinogen Binding ◽  
Adp Release ◽  
The Difference ◽  
Txa2 Receptor Antagonist ◽  
High Level ◽  
Inhibition Studies ◽  
Peak Increase ◽  
Second Peak ◽  
Assay Conditions

SummaryThis study investigated the difference of [Ca2+]i movement in platelets in response to thrombin and TRAP. The involvement of αIIbβ3 in this signaling was also studied. Stimulation of platelets with thrombin at 0.03 U/ml caused platelet aggregation and a two-peak increase in [Ca2+]i. The second peak of [Ca2+]i, but not the first peak was abolished by the inhibition of platelet aggregation with αIIbβ3 antagonists or by scavenging endogenous ADP with apyrase. A cyclooxygenase inhibitor, aspirin, and a TXA2 receptor antagonist, BM13505, also abolished the second peak of [Ca2+]i but not the first peak, although these regents did not inhibit aggregation. Under the same assay conditions, measurement of TXB2 demonstrated that αIIbβ3 antagonists and aspirin almost completely inhibited the production of TXB2. In contrast to thrombin-stimulation, TRAP caused only a single peak of [Ca2+]i even in the presence of platelet aggregation, and a high level of [Ca2+]i increase was needed for the induction of platelet aggregation. The inhibition of aggregation with αIIbβ3 antagonists had no effect on [Ca2+]i change and TXB2 production induced by TRAP. Inhibition studies using anti-GPIb antibodies suggested that GPIb may be involved in the thrombin response, but not in the TRAP. Our findings suggest that low dose thrombin causes a different [Ca2+]i response and TXA2 producing signal from TRAP. Endogenous ADP release and fibrinogen binding to αIIbβ3 are responsible for the synthesis of TXA2 which results in the induction of the second peak of [Ca2+]i in low thrombin- but not TRAP-stimulated platelets.

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