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PubMed1977

[Thrombocytosis and cancer. Apropos of a chronological series of 100 patients].

The authors report a personal chronological series of 100 cancer patients submitted to an analytical study, and noted thrombocytosis in 18% of cases. They attempt to draw up a correlation between the presence of increased platelets, and the site of the primary tumour, its spread, the state of anemia or iron deficiency in these patients. During a general review of the literature, they compare their results with those of various american and german series and report the various pathogenic hypotheses suggested upto date. They emphasise the fact that routine platelet counts may be of great interest in the detection of certain early carcinomas in spite of the generally moderate levels of thrombocytosis observed. They therefore have a place in routine health checks.

Blood Cell Count↗

PubMedDate not supplied

Mild thrombocytosis secondary to iron-deficiency anemia and stroke.

A 45-year-old woman with mild thrombocytosis secondary to iron-deficiency anemia suffered from hemispheric infarction in absence of vascular, cardiac or coagulation pathologies. The modest raise of the platelets count seemed as the sole possible cause for the cerebral infarction. We wish to emphasize the inconstant benignity of mild non essential thrombocytosis at levels less than 1 million/cu.mm.

Anemia, Hypochromic↗

PubMed1990

Thrombocytosis in Henoch-Schonlein syndrome.

To ascertain the frequency of thrombocytosis in Henoch-Schonlein syndrome (HSS) a small retrospective survey was undertaken. Sixty-five per cent of the cases of HSS showed thrombocytosis, which might be related to the severity of the illness.

Humans↗

PubMed1990

[Chronic myelogenous leukemia with marked thrombocytosis--comparison with essential thrombocythemia with Ph1 in its megakaryokinetics].

A case of chronic myelogenous leukemia (CML) with marked thrombocytosis and its megakaryokinetics were reported. Patient was 57-year old woman who had a marked thrombocytosis (1,413 x 10(3)/microliters) and a bone marrow megakaryocytosis. Bone marrow karyotype demonstrated Ph1 chromosome in all cells examined. However, on physical examination, there was no splenomegaly. CBC showed no immature myeloid cells, and neutrophil alkaline phosphatase was elevated. These manifestations were consistent with so called essential thrombocythemia (ET) with Ph1 chromosome reported by Nissenblatt. To know the megakaryokinetics of this case, we examined the number of colony forming unit-megakaryocyte (CFU-M), platelet glycoprotein (PGP) IIb/IIIa positive cells, cytoplasmic area, and DNA content, comparing with those of normal subjects, CML, and ET. We found a marked increase of CFU-M and PGP IIb/IIIa positive cells, but in contrast, decreased DNA content and cytoplasmic area. This pattern of megakaryokinetics was consistent with that of CML. We conclude that ET with Ph1 chromosome may be a variant of CML rather than ET itself.

Adolescent↗

PubMed1985

The effect of different doses of 32P in the treatment of primary thrombocytosis.

We report on a follow up in 23 patients with primary thrombocytosis treated with two different doses of 32phosphorus phosphate (32P). Ten patients with essential thrombocytosis (ET) received 2 mCi and 13 patients with polycythemia vera (PV) received the standard dose of 0.1 mCi/kg b.w. The patients were listed as having a complete response (CR), partial response (PR) or no response (NR) considering platelet count at 3 and 12 months after 32P injection. The results indicate the existence of a clear correlation of the rate of remission with the 32P injected dose. PV patients show, in fact, a percentage of complete remission higher than ET patients. However, the use of higher doses induces more early and long-term complications.

Adult↗

PubMed1987

Evaluation of platelet function in postsplenectomy thrombocytosis.

The usually transient post-splenectomy thrombocytosis has no well defined effect on the development of thromboembolism. We studied 14 patients submitted to splenectomy for different causes: portal vein thrombosis (PVT), idiopathic thrombocytopenia purpura (ITP) and lymphoma. The mean platelet count in PVT patients was significantly higher than in all other subjects. In PVT group we demonstrated various alterations in platelet aggregation curves and a frequent increase of platelet 5-HT levels. In effect, we noted that all the PVT patients showed a myeloproliferative disease (MPD) before the surgical procedure. We therefore conclude that the increased incidence of thromboembolism in the patients who underwent splenectomy is probably caused by a preexisting MPD rather than the post-splenectomy thrombocytosis.

Adult↗

PubMed1989

Interferon alpha-2a to control thrombocytosis in chronic myelogenous leukemia and essential thrombocythemia.

Four patients with chronic myelogenous leukemia and thrombocytosis and one patient with essential thrombocythemia were treated with purified recombinant human interferon alpha-2a (IFN-alpha 2a). Significant decline in platelet counts, from a mean ( +/- SE) of 1.396 +/- 0.265 x 10(6)/mm3 to a mean of 0.396 +/- 0.04 x 10(6)/mm3 (p less than 0.05), was observed in all patients. The platelet count remained normal for 15, 21 and 30 days after discontinuation of IFN-alpha 2a in 3 patients. In 2 patients the platelet count began to rise slowly two weeks after discontinuation of IFN-alpha 2a. Our preliminary observations suggest that purified recombinant human IFN-alpha 2a may effectively control progressive thrombocytosis in advanced chronic myelogenous leukemia and essential thrombocythemia.

Adult↗

PubMed1989

[Clinical evaluation of the control of antiplatelet therapy through platelet aggregation rate on polycythemia vera associated with thrombocytosis and erythromelalgia].

A 60-years-old woman with polycythemia vera with marked thrombocytosis and intolerable erythromelalgia was presented. A single dose of 400 mg aspirin was effective to improve the pain and cyanosis. And we studied the relationship between platelet aggregation rate and symptoms after administration of several antiplatelet drugs. A single dose of 100, 200, 400 and 800 mg aspirin, 25 mg indomethacin (Id), 200 mg OKY-046, and daily dose of 300 and 600 mg dipyridamole (Dp) and 300 mg ticlopidine (Tc) were given. Aspirin, Id and OKY-046 were effective for the improvement of finger pain. The complete inhibition of spontaneous aggregation (SPA) and aggregation by 2.0 micrograms/ml of collagen were well parallel with the improvement of symptoms. But duration of effect of LKY-046 were only 6 hours. Dp and Tc were not effective for the improvement of pain, had no relation with platelet aggregation rate. The concentration level of aspirin in vivo which suppresses the platelet aggregation induced by SPA and 2.0 micrograms/ml of collagen coincided well with the concentration level of this drug which suppresses the same platelet aggregation in vitro. It seems to be useful to suppress the platelet aggregation induced by SPA and 2.0 micrograms/ml of collagen with aspirin and Id for controlling the platelet aggregation induced circulatory disturbance in patient with thrombocytosis.

Aspirin↗

PubMed1989

Thrombocytosis and hyperkalemia revisited.

A major concern of physicians caring for patients is the development of hyperkalemia, a potentially life-threatening event requiring accurate determination of its etiology. After metabolic and iatrogenic causes have been excluded, factitious hyperkalemia must be considered, one cause of which may be the method of laboratory determination. Hyperkalemia associated with thrombocytosis has been previously described but is a fact commonly overlooked in the evaluation of a patient with hyperkalemia. We compared the potassium levels in simultaneous serum and plasma samples from patients with normal and elevated platelet counts, since platelet activation during clot formation is associated with release of potassium. We found consistently higher potassium levels in serum (containing products of activated platelets) than in plasma (containing nonactivated platelets). The greatest discrepancy in potassium levels was in patients with thrombocytosis. This preliminary study suggests that if there is no obvious explanation for an elevated serum potassium the plasma potassium level should be measured, particularly in patients with elevated platelet counts.

False Positive Reactions↗

PubMed1989

[Therapy of thrombocytosis in myeloproliferative syndromes using recombinant interferon-alpha-2a].

In a prospective open study 16 consecutive patients with a myeloproliferative syndrome and thrombocytosis were treated with interferon (IFN) alpha-2a. 4 patients had polycythemia vera, 4 essential thrombocythemia, 3 myeloid metaplasia and 5 chronic granulocytic leukemia. Platelet counts decreased in all treated patients within 2 to 12 weeks from a median value of 1010 x 10(9)/l to 350 x 10(9)/l. No primary or secondary resistance was observed. The initial dose of IFN was 9 m U per day. After correction of the thrombocytosis, it was progressively reduced to a minimum dose of 3 m U per week. Despite the good platelet response to IFN, leukocytosis persisted in 3 patients and polycythemia in a further 3. Side effects and poor compliance required discontinuation of therapy in 6 patients. Special attention is focused on the follow-up in 6 patients who have been treated for more than 15 months.

Adult↗

PubMed1988

[Postinfectious thrombocytosis as an acute phase reaction: the example of Haemophilus influenzae meningitis].

The postinfectious thrombocytosis occurring in 11 children with Haemophilus influenzae meningitis and/or septicaemia shows regular progress. The rise of thrombocyte concentrations starts around the 5th day after onset of antibiotic therapy, reaches values above 500,000/microliter between the 9th and 12th day, and relapses afterwards to normal values, which are reached around the 20th day. The range of thrombocytosis is influenced by the severity and complications (subdural effusions, secondary infection) of the infection as well as by the age of the patient. An inverse course of serum concentrations of C-reactive protein and thrombocyte concentrations points to the influence of this humoral reaction on the thrombocytic acute phase reaction.

Acute-Phase Reaction↗

PubMed1978

Megakaryocytic responses to thrombocytopenia and thrombocytosis in Sl/Sld mice.

Sl/Sld mice maintain normal platelet counts in spite of a reduced number of megakaryocytes, but their megakaryocytes are macrocytic. The present studied were done to analyze platelet turnover in the steady state and thrombocytopoietic responses to perturbations of the platelet count. Platelet production, estimated with 35S incorporation in the steady state, blood volume, and total complement of peripheral platelets were normal. Sl/Sld mice responded to thrombocytopenia with normal degrees of macromegakaryocytosis and production of macrocytic platelets, but rebound thrombocytosis did not occur. Their megakaryocytes were unusually responsive to transfusion-induced thrombocytosis, showing a prompt and substantial reduction in size. Platelet turnover was normal in undisturbed Sl/Sld mice, and feedback regulation occurred. However, increased numbers of platelets were not produced in response to stimulation. The findings are consistent with the possibility that their megakaryocytes are large because of stimulation rather than a direct local effect of the abnormal microenvironment.

Animals↗

PubMed1983

[Cerebrovascular complications of thrombocytosis].

Cerebrovascular complications of thrombocytosis may be the presenting symptoms of the disease (thrombocythemia or secondary thrombocytosis). In the light of 3 recently studied cases, the clinical, pathogenic and therapeutic aspects are emphasized. Early diagnosis is fundamental if the occurrence of permanent neurologic dysfunction is to be avoided.

Aged↗

PubMed1981

Left ventricular mural thrombus in a patient with thrombocytosis and agnogenic myeloid metaplasia.

The two factors responsible for the development of left ventricular mural thrombi are endocardial injury secondary to old or recent anterior myocardial infarction and left ventricular dysfunction. Endothelial damage also is thought to be the initial event in the development of arterial thrombi. However, arterial thrombi may develop in patients with thrombocytosis secondary to myeloproliferative disorders in the absence of endothelial injury. A patient had thrombocytosis secondary to agnogenic myeloid metaplasia and a left ventricular mural thrombus developed in the absence of clinical or laboratory evidence of old or coronary angiogram and left ventricular function. To our knowledge, this is the first such case reported.

Aged↗

PubMed1993

Prevalence of specific thrombotic accidents in patients with thrombocytosis.

The prevalence of specific thrombotic accidents recognized in 260 patients with thrombocytosis are reported. Ninety one were affected by PV, 86 by ET, 20 by MF and 63 by ST. The highest incidence of thrombosis was in the PV group. About half of ET and MF patients experienced a thrombosis. In all the patients thrombosis preferentially affected the cerebrovascular district (17.3% of the cases). Coronary artery disease occurred in PV while peripheral vascular disease was frequent in ET. Portal vein district thrombosis is not rare during the course of all MPD (7.1%). Apparently, deep vein thrombosis occurs in all patients with both primary and secondary thrombocytosis.

Adult↗

PubMed1994

Identification of masked polycythemia vera from patients with idiopathic marked thrombocytosis by endogenous erythroid colony assay.

We used the methylcellulose-culture technique to determine the utility of the erythroid progenitor growth in vitro from nonadherent T-depleted bone marrow and peripheral blood cells in distinguishing polycythemia vera (PV) from essential thrombocythemia. Thirty patients with PV (group A) and 30 patients who presented with idiopathic marked thrombocytosis with platelet count greater than 1,000 x 10(9)/L and a normal or reduced hemoglobin (Hb) level (group B) were studied at initial presentation. Endogenous (erythropoietin-independent) erythroid colonies (EEC) were found in all patients in group A and 13 in group B. The numbers of EEC were comparable between patients in group A and the 13 patients with EEC in group B, 11 of whom with initial Hb levels ranging between 6.4 g/dL and 12.6 g/dL were found to have PV 2 to 45 months after initial evaluation. The number of EEC did not correlate with the time to the progression of polycythemia, whereas myelosuppression delayed the subsequent development of PV. Of the two patients with EEC in group B who did not develop PV, both received chemotherapy soon after presentation, which might preclude the evidence of polycythemia evolution. None of the other patients in group B who did not form EEC developed PV with a median follow-up of 24 months. This study indicates that the assessment of EEC in bone marrow or blood is helpful in early identification of PV or prediction of polycythemia evolution in patients with marked thrombocytosis in whom polycythemia has been initially masked or anemia is present.

Aged↗

PubMed1996

Constitutive expression of Mpl ligand transcripts during thrombocytopenia or thrombocytosis.

Mpl ligand (thrombopoietin [TPO]) is the physiological regulator of platelet production. In mice, mRNA encoding the Mpl ligand (Mpl-L) is predominantly found by Northern blot analysis in the liver and kidney. To investigate the mode of regulation of the Mpl-L gene, we have developed several experimental models of severe thrombocytopenia differing in their kinetics and an opposite model of chronic thrombocytosis. Northern analysis performed at various times after induction of a thrombocytopenic state demonstrates that, whatever the number of circulating platelets, no change in Mpl-L mRNA level occurs in liver and kidney. By ribonuclease protection assays, we analyzed the ratios between mRNAs coding for the wild-type Mpl-L form and various splice variants encoding inactive or nonsecreted Mpl-L proteins. No modification in levels of these various isoforms was detected confirming the data of a previous report. Because the highest level of Mpl-L bioactivity in sera was observed only in mice with drastically reduced numbers of both platelets and megakaryocytes, these results further suggest that not only platelets, but also megakaryocytes, must be involved in the regulation of the level of circulating Mpl-L. In addition, we show that no downregulation of wild-type Mpl-L mRNA and no change in the ratio of Mpl-L mRNA isoforms were detected in mice in which a chronic thrombocytosis was induced. Together, these different models extend and further confirm that the regulation of Mpl-L does not occur at a transcriptional level or by a modulation in the ratios of Mpl-L mRNA isoforms.

Animals↗

PubMed1996

Refined chromosomal localization of the human thrombopoietin gene to 3q27-q28 and exclusion as the responsible gene for thrombocytosis in patients with rearrangements of 3q21 and 3q26.

Thrombocytosis is a characteristic clinical feature in patients with myelocytic malignancies and chromosomal rearrangements of 3q21 and 3q26, sometimes called the '3q21q26 syndrome'. The function of thrombopoietin (TPO) in megakaryocytopoiesis and thrombopoiesis as well as its chromosomal location, marked TPO as a candidate gene for malignancies with 3q rearrangements combined with dysmegakaryopoiesis. In this study 12 cases with inv(3)(q21q26) or t(3;3)(q21;q26) were analyzed by means of PFGE, but no rearrangements near the TPO locus were detectable. Six YACs containing the TPO locus were isolated and characterized. By dual color in situ hybridization using a YAC from 3q26 containing the EVI1 gene and a YAC from the TPO locus, the localization of the human TPO gene could be refined to 3q27-q28 about 15-20 Mbp telomeric to the 3q26 breakpoints occurring in myeloid malignancies. TPO levels were analyzed in the serum of three patients and were found to be in the normal range. These results confirm the findings of two previous studies that thrombopoietin expression is not the main cause of thrombocytosis in the 3q21q26 syndrome.

Chromosome Breakage↗