scholarly journals Regulation of megakaryocyte ploidy in vivo in the rat

Blood ◽  
1990 ◽  
Vol 75 (1) ◽  
pp. 74-81 ◽  
Author(s):  
DJ Kuter ◽  
RD Rosenberg
Keyword(s):  
Platelet Count ◽  
Feedback Loop ◽  
Antiplatelet Antibody ◽  
Normal Platelet Count ◽  
Normal Platelet ◽  
Plasma Factor ◽  
Ploidy Changes ◽  
The Relationship ◽  
Made In

Abstract The relationship between the bone marrow (BM) megakaryocyte and the circulating platelet was explored. Incremental changes in platelet count were made in rats by infusion of antiplatelet antibody or by platelet transfusion, and the response of megakaryocytes was measured by flow cytometry. Proportional changes in megakaryocyte ploidy were demonstrated: As the platelet count declined, ploidy increased; as the platelet count increased, ploidy decreased. Even moderate degrees of thrombocytopenia and thrombocytosis (48% and 177% of the normal platelet count) were associated with changes in ploidy. These changes were not the results of the technique used to alter the platelet count because reinfusion of platelets after 3 hours of thrombocytopenia prevented any ploidy change. These studies proved that the circulating platelet and the megakaryocyte constitute a classic feedback loop whose activity can be measured by the degree of ploidization of the megakaryocyte. The minimal duration of thrombocytopenia necessary to promote megakaryocyte ploidy changes was approximately 10 hours. Using a BM culture assay, we identified a plasma factor which induced alterations in megakaryocyte ploidy and whose level is inversely proportional to the platelet count.

scholarly journals Regulation of megakaryocyte ploidy in vivo in the rat

Blood ◽  
1990 ◽  
Vol 75 (1) ◽  
pp. 74-81 ◽  
Author(s):  
DJ Kuter ◽  
RD Rosenberg
Keyword(s):  
Platelet Count ◽  
Feedback Loop ◽  
Antiplatelet Antibody ◽  
Normal Platelet Count ◽  
Normal Platelet ◽  
Plasma Factor ◽  
Ploidy Changes ◽  
The Relationship ◽  
Made In

The relationship between the bone marrow (BM) megakaryocyte and the circulating platelet was explored. Incremental changes in platelet count were made in rats by infusion of antiplatelet antibody or by platelet transfusion, and the response of megakaryocytes was measured by flow cytometry. Proportional changes in megakaryocyte ploidy were demonstrated: As the platelet count declined, ploidy increased; as the platelet count increased, ploidy decreased. Even moderate degrees of thrombocytopenia and thrombocytosis (48% and 177% of the normal platelet count) were associated with changes in ploidy. These changes were not the results of the technique used to alter the platelet count because reinfusion of platelets after 3 hours of thrombocytopenia prevented any ploidy change. These studies proved that the circulating platelet and the megakaryocyte constitute a classic feedback loop whose activity can be measured by the degree of ploidization of the megakaryocyte. The minimal duration of thrombocytopenia necessary to promote megakaryocyte ploidy changes was approximately 10 hours. Using a BM culture assay, we identified a plasma factor which induced alterations in megakaryocyte ploidy and whose level is inversely proportional to the platelet count.

Do Extra-Platelet Sources Contribute to the Plasma Level of Thrombospondin?

1988 ◽  
Vol 59 (02) ◽  
pp. 273-276 ◽  
Author(s):  
J Dawes ◽  
D A Pratt ◽  
M S Dewar ◽  
F E Preston
Keyword(s):  
Platelet Count ◽  
Background Concentration ◽  
Serum Concentrations ◽  
Bone Marrow Depression ◽  
Serial Sampling ◽  
Control Serum ◽  
Platelet Release ◽  
Highly Correlated ◽  
The Relationship

SummaryThrombospondin, a trimeric glycoprotein contained in the platelet α-granules, has been proposed as a marker of in vivo platelet activation. However, it is also synthesised by a range of other cells. The extraplatelet contribution to plasma levels of thrombospondin was therefore estimated by investigating the relationship between plasma thrombospondin levels and platelet count in samples from profoundly thrombocytopenic patients with marrow hypoplasia, using the platelet-specific α-granule protein β-thromboglobulin as control. Serum concentrations of both proteins were highly correlated with platelet count, but while plasma β-thromboglobulin levels and platelet count also correlated, there was no relationship between the number of platelets and thrombospondin concentrations in plasma. Serial sampling of patients recovering from bone marrow depression indicated that the plasma thrombospondin contributed by platelets is superimposed on a background concentration of at least 50 ng/ml probably derived from a non-platelet source, and plasma thrombospondin levels do not simply reflect platelet release.

Thrombotic Thrombocytopenic Purpura: Mechanism for Effectiveness of Plasmapheresis

1979 ◽  
Author(s):  
J. G. Kelton ◽  
P. B. Neame ◽  
I. Walker ◽  
A. G. Turpie ◽  
J. McBride ◽  
...  
Keyword(s):  
Platelet Count ◽  
Thrombotic Thrombocytopenic Purpura ◽  
The Other ◽  
Unknown Etiology ◽  
Normal Range ◽  
Antiplatelet Antibody ◽  
Thrombocytopenic Purpura ◽  
Serious Illness ◽  
Normal Platelet ◽  
Very High

Thrombotic thrombocytopenic purpura (TTP) is a rare but serious illness of unknown etiology. Treatment by plasmapheresis has been reported to be effective but the mechanism for benefit is unknown. We have investigated the effect of plasmapheresis in 2 patients with TTP by quantitating platelet associated IgG (PAIgG) levels prior to and following plasmapheresis. Both patients had very high levels of PAIgG at presentation (90 and A8 fg IgG/platelet respectively, normal 0-5). in both, the PAIgG levels progressively fell to within the normal range and the platelet count rose following plasmapheresis. One patient remained in remission with normal platelet counts and PAIgG levels. The other relapsed after plasmapheresis and the PAIgG level rose prior to the fall in platelet count. Plasmapheresis was repeated and resulted in normalization of both the platelet count and PAIgG level. It is suggested that plasmapheresis removes antiplatelet antibody or immune complexes which may be of etiological importance in this illness.

Cancer incidence in patients with a high normal platelet count: a cohort study using primary care data

2018 ◽  
Vol 35 (6) ◽  
pp. 671-675 ◽  
Author(s):  
Emily Ankus ◽  
Sarah J Price ◽  
Obioha C Ukoumunne ◽  
William Hamilton ◽  
Sarah E R Bailey
Keyword(s):  
Primary Care ◽  
Cohort Study ◽  
Platelet Count ◽  
Cancer Incidence ◽  
Normal Platelet Count ◽  
Normal Platelet ◽  
Primary Care Data

Thrombotic Thrombocytopenic Purpura: Mechanism for Effectiveness of Plasmapheresis

1979 ◽  
Author(s):  
J.G. Kelton ◽  
P.B. Neame ◽  
I. Walker ◽  
A.G. Turpie ◽  
J. McBride ◽  
...  
Keyword(s):  
Platelet Count ◽  
Thrombotic Thrombocytopenic Purpura ◽  
The Other ◽  
Unknown Etiology ◽  
Normal Range ◽  
Antiplatelet Antibody ◽  
Thrombocytopenic Purpura ◽  
Serious Illness ◽  
Normal Platelet ◽  
Very High

Thrombotic thrombocytopenic purpura (TTP) is a rare but serious illness of unknown etiology. Treatment by plasmapheresis has been reported to be effective but the mechanism for benefit is unknown. We have investigated the effect of plasmapheresis in 2 patients with TTP by guantitating platelet associated IgG (PAIgG) levels prior to and following plasmapheresis. Both patients had very high levels of PAIgG at presentation (90 and 48 fg IgG/platelet respectively, normal 0-5). In both, the PAIgG levels progressively fellto within the normal range and the platelet count rose following plasmapheresis. One patient remained in remission with normal platelet counts and PAIgG levels. The other relapsed after plasmapheresis and the PAIgG levelrose prior to the fall in platelet count. Plasmapheresis was repeated and resulted in normalization of both the platelet count and PAIgG level. It is suggested that plasmapheres is removes antiplatelet antibody or immune complexes which may be of etiologicalimportance in this illness.

A PLASMA FACTOR FROM A PATIENT WITH A BLEEDING TENDENCY CAUSES PLATELET SECRETION IN THE ABSENCE OF EXTRACELLULAR CALCIUM

1987 ◽  
Author(s):  
S R Cockbill ◽  
S Heptinstall ◽  
H B Burmester
Keyword(s):  
Protein A ◽  
Ion Exchange Resin ◽  
Bleeding Tendency ◽  
Clotting Factors ◽  
Platelet Suspension ◽  
Normal Platelet ◽  
Plasma Factor ◽  
Extensive Release ◽  
Platelet Secretion

A woman with a history of bruising and bleeding but with a normal platelet count and normal clotting factors, had platelets that appeared grey when stained and viewed under the microscope. Unlike the grey-platelet syndrome, the abnormality was only evident when the blood had been collected into EDTA andnot when citrate or heparin was used as anticoagulant. When we examined the EDTA-blood further we found that large quantities of beta-thromboglobulin andserotonin (5HT) were present in the plasma with only small quantities in the platelets. Hie reverse was the case for blood collected into citrate or heparin. LDH (a cytoplasmic marker) levels in EDTA-plasma were not raised.Platelet-rich plasma (PRP) was prepared from blood collected into heparin and labelled with ^-4C-5HT. Incubating the PRP with EDTA (4mM) or EGTA (3mM, sufficient to chelate all the plasma calcium but not the magnesium) caused extensive release of 14C-5HT from the platelets. When Ca++ was removed by passing the PRP through an ion-exchange resin, extensive 14C-5HT release also occurred. Hie release reaction induced by exposing the platelets to a low-Ca++ environment could be prevented by agents that increase cAMP levels.In a series of cross-over experiments, we discovered that the platelet secretion that occurred on removing Ca++ was caused by a plasma factor. Platelets from a healthy donor which had been labelled with 14C-5HT were resuspended in the patient's heparinised plasma. Incubating the platelet suspension with EGTA resulted in extensive release of 14C-5HT. Heparinised plasma from the patient was also passed through a column of Protein A-Sepharose to remove the immunoglobulin fraction. EGTA-challengof control platelets resuspended in the eluted plasma did not cause any release of 14C-5HT, suggesting that the plasma factor responsible may be an immunoglobulin.We have yet to discover whether this new abnormality (that on initial investigation could be confused with the grey-platelet syndrome) has any relevance to the in vivo bleeding situation in the patient in whom it was discovered.

scholarly journals Phospholipid Accumulation in Histiocytes of Splenic Pulp Associated with Thrombocytopenic Purpura

Blood ◽  
1961 ◽  
Vol 18 (1) ◽  
pp. 73-88 ◽  
Author(s):  
SIDNEY L. SALTZSTEIN
Keyword(s):  
Bone Marrow ◽  
Platelet Count ◽  
Idiopathic Thrombocytopenic Purpura ◽  
Lipid Accumulation ◽  
Thrombocytopenic Purpura ◽  
Normal Platelet Count ◽  
Normal Platelet

Abstract Accumulation of a lipid, histochemically a phospholipid, in the histiocytes of the splenic pulp was observed in seven patients with thrombocytopenic purpura. Six had classical idiopathic thrombocytopenic purpura with abundant megakaryocytes in the bone marrow. Splenectomy resulted in clinical and hematologic remissions in four of these six, continued thrombocytopenia in the fifth, and in the continued requirement of corticosteroid to maintain a reasonably normal platelet count in the sixth. The seventh patient, who died shortly after splenectomy, had marked hypoplasia of megakaryocytes. Similar lipid accumulation was not seen in more than 700 other spleens, removed for a variety of reasons, reviewed in this study. Platelet phagocytosis has been suggested as a source of the lipid.

Idiopathic, asymptomatic thrombocytopenia in Cavalier King Charles spaniels: 11 cases (1983-1993)

1997 ◽  
Vol 33 (5) ◽  
pp. 411-415 ◽  
Author(s):  
LE Smedile ◽  
DM Houston ◽  
SM Taylor ◽  
K Post ◽  
GP Searcy
Keyword(s):  
Platelet Count ◽  
Data Base ◽  
Medical Records ◽  
Immunosuppressive Drugs ◽  
Medical Data ◽  
Giant Platelets ◽  
Normal Platelet Count ◽  
Normal Platelet ◽  
Purdue University

The medical records of 11 Cavalier King Charles spaniels with idiopathic, asymptomatic thrombocytopenia and large-to-giant platelets were identified from a 10-year retrospective search using the Veterinary Medical Data Base at Purdue University. Eight of the dogs had been treated with various immunosuppressive drugs. Six of the treated dogs remained thrombocytopenic, one was not reevaluated, and one developed a normal platelet count. The underlying etiology of idiopathic, asymptomatic thrombocytopenia in Cavalier King Charles spaniels has not been identified, but this condition could represent a congenital macrothrombocytopenic disorder.

ADAMTS-13 Levels Do Not Predict Outcome in Thrombotic Thrombocytopenic Purpura: Protein S Levels Are Maintained during Plasma Exchange with Solvent Detergent Treated Plasma.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2895-2895
Author(s):  
Gail A. Rock ◽  
David Anderson ◽  
Barrett Benny ◽  
David Barth ◽  
William Clark ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Enzyme Activity ◽  
Platelet Count ◽  
Plasma Exchange ◽  
Protein S ◽  
Inhibitor Activity ◽  
Thrombocytopenic Purpura ◽  
Normal Platelet Count ◽  
Normal Platelet ◽  
Alternative Solutions

Abstract Introduction The ultimate therapy for TTP is not yet defined. While approximately 85% of patients respond to plasma exchange with FFP, the use of alternative solutions such as cryosupernatant plasma, which is deficient in the high molecular weight forms of vWF. has not been proven by appropriate randomized prospective sample trials. However, it is intellectually appealing. Additionally, the use of the ADAMTS 13 level either to predict disease or outcome has not been resolved. Methods Cryosupernatant plasma (CSP) was compared to solvent detergent treated plasma (SDP) over one cycle (nine days) of plasma exchange (PE) and subsequent procedures as required. Throughout treatment, ADAMTS 13 and protein S levels were followed. Results At the primary end point of one month, 3 of 35 of the CSP and 1 of 27 of the SDP patients died. The average platelet count was 184 × 109 per litre for CSP and 209 × 109 per litre for SDP. While vWF and FVIII were elevated in all patients at entry, no unusually large vWF multimers were seen at any time. At entry 9 patients had ≤ 0–10% ADAMTS 13 and 14 of 62 had normal levels with the rest in between. At presentation only 9 patients had 100% inhibitor activity with no inhibitor in 18 patients. Of the four patients who died, two who received CSP, had 100% enzyme activity at presentation whereas one had no ADAMTS-13 and another had 10%. All 4 patients died within 10 days. Fifteen patients with less than 10% enzyme activity had >1.5 vWF. However, elevated (>3u/mL) vWF was seen in the presence of normal ADAMTS-13 levels. Six months after remission, and in the presence of a normal platelet count, ADAMTS13 remained low in 5 patients and normal in 15.Protein S levels in 41/62 patients studied showed little variation during therapy with values on day 3 and 5, similar to those seen on entry. Conclusion In idiopathic TTP, ADAMTS 13 levels do not correlate with disease, and are not predictive of outcome. While protein S levels in the SDP were lower than those found in FFP, this did not appear to have clinical significance.

Preoperative thrombocytosis as a predictor of unfavorable survival in resectable non-small cell lung cancer.

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. e18531-e18531
Author(s):  
Jiwen Wang ◽  
Min Luo ◽  
Hanmo Wu ◽  
Liming Sheng ◽  
Dan Su ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Platelet Count ◽  
Small Cell Lung Cancer ◽  
Disease Progression ◽  
Early Stage ◽  
Small Cell ◽  
Small Cell Lung ◽  
Platelet Counts ◽  
Normal Platelet Count ◽  
Normal Platelet

e18531 Background: Activated platelet is thought to promote cancer cells growth and metastasis, playing an important role in progression of cancer. However, the association between platelet counts and prognosis of patient with non small cell lung cancer (NSCLC) had not been fully elucidated. The aim of this study is to investigate the prognostic value of platelet counts in resectable NSCLC. Methods: A total of 636 primary NSCLC patients who had curatively resected surgery in Zhejiang Cancer Hospital from November 2006 to January 2011 were retrospectively analyzed. Preoperative platelet counts and clinicopathological factors were collected from the medical record database. Patients were followed up for disease progression free survival (PDS) and overall survival (OS) until January 20, 2013. The association between platelet counts and patients’ outcome were evaluated. Results: In all patients, 13.8% (88/636) had increased platelet count (>300 × 109/L), referred to as thrombocytosis. The proportion of thrombocytosis was significantly higher in male, squamous-cell carcinoma and stage III than that in female, other histological types and early stage NSCLC. Moreover, thrombocytosis was associated with significantly shortened survival. Multivariate Cox analysis showed patient with thrombocytosis not only had a 1.66 time elevated risk for disease progression (95% CI, 1.14-2.41, p=0.009), but also had and a 1.47 time risk for death (95% CI, 1.04-2.08, P=0.029), compared with that in those having normal platelet count. More interestingly, the risk for replase was increased to 3.19 times (95% CI, 1.41-7.23, p=0.006) in stage I NSCLC with thrombocytosis than that in patients with normal platelet count after stratified analysis by stage. Conclusions: Preoperative platelet count is an independent prognostic predictor in operable NSCLC, especially in early stage I NSCLC. Platelet count may serve as a useful indicator and potential target for personalized treatment with antiplatelet reagent.

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