Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THROMBOCYTOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1997

Serum thrombopoietin level is not regulated by transcription but by the total counts of both megakaryocytes and platelets during thrombocytopenia and thrombocytosis.

Thrombopoietin (Tpo) regulates platelet production, but the mechanisms regulating the serum Tpo level and platelet count in circulation have been a subject of debate. Tpo was reported to be expressed mainly in liver and kidney, but we found that Tpo is expressed in all tissues examined: abundantly in liver, kidney, muscle, colon, brain and intestine, and moderately in bone marrow, spleen, lung, stomach, heart, thymus, ovary, and endothelial and leukemic cell lines. The levels of Tpo transcripts in major Tpo producing organs, liver and kidney, and in the platelet production sites bone marrow and spleen, were constant during acute thrombocytopenia induced by anti-platelet monoclonal antibody administration in mice, and during thrombocytosis induced by Tpo injection. Furthermore, we noticed that platelet count is not exactly inversely proportional to serum Tpo level. During acute thrombocytopenia, serum Tpo level transiently increased a few hours after antibody injection, and returned to the basal level just when matured megakaryocytes accumulated in bone marrow and spleen but the platelet count was still low. Matured megakaryocytes in bone marrow and spleen increased when the serum Tpo level decreased, and decreased when platelet count rebounded. Taken together with other observations, we propose here a modified version of Kuter and Rosenberg's theory, that is, Tpo is constitutively expressed in a variety of organs throughout the body, even in acute thrombocytopenia and thrombocytosis, and that the serum Tpo level is not regulated by Tpo gene expression nor only by platelet counts in circulation, but by the total counts of both megakaryocytes in bone marrow and spleen and of platelets in circulation.

Animals↗
PubMed1997

Pregnancy in a patient with essential thrombocytosis.

An insurgent case of pregnancy in a patient in whom essential thrombocytosis was diagnosed five years earlier is described. Pregnancy was confirmed and therapy with platelet aggregation inhibitor was introduced. The pregnancy reached full term notwithstanding a positive result of the "Triple Test" during the 15th week of gestation. A histology exam of the placenta revealed an ischemic lesion. We retain that platelet aggregation inhibitor therapy remains an important aid in eliminating the risk of thrombosis determined by the presence of two conditions that are predisposed to these risks, such as pregnancy and essential thrombocytosis.

Aspirin↗
PubMed1991

Benign familial thrombocytosis.

A 13-year-old girl was found to have a platelet count in excess of 4 million/microliters while being evaluated for a minor bleeding episode. Her father and two sisters also had thrombocytosis. All four affected patients were asymptomatic and had no clinical or laboratory evidence of a myeloproliferative disorder other than an elevated platelet count. This represents the second reported instance of benign familial thrombocytosis.

Adolescent↗
PubMed1997

Allogeneic marrow transplantation for primary myelofibrosis and myelofibrosis secondary to polycythaemia vera or essential thrombocytosis.

Primary myelofibrosis is a clonal haemopoietic disorder, incurable with conventional therapy, and associated with a median survival of 4-5 years. Patients with polycythaemia vera and essential thrombocytosis who progress into a myelofibrotic picture also have a poor prognosis. Between 1980 and 1996, 13 patients with myelofibrosis due to one of these three myeloproliferative disorders (primary myelofibrosis [n=8], essential thrombocytosis [n=3], polycythaemia vera [n=2]) underwent allogeneic marrow transplantation in Seattle. The median age was 40 years (range 18-49). The median time from myeloproliferative diagnosis to transplantation was 39 months (range 5-192). Three patients received preparative regimens containing total body irradiation and 10 received busulphan-cyclophosphamide regimens. Nine patients received marrow from HLA-matched related donors, one from a one antigen mismatched related donor, and three from HLA-matched unrelated donors. The median time to both granulocyte and platelet engraftment was 21 d. Nine patients survive between 1.2 and 7.1 years post-transplant. Two patients relapsed at 1 year post-transplant, both of whom survive in a chronic myeloproliferative state. Four patients died of transplant-related complications between 43 d and 2.2 years post-transplant. At 1 year post-transplant the majority of the disease-free survivors have normal peripheral blood counts and none-to-minimal marrow fibrosis. These preliminary results are encouraging, and suggest that stem cell transplantation can be curative therapy for selected patients with myelofibrosis.

Adolescent↗
PubMed1989

Platelet function and structure in myeloproliferative disease, myelodysplastic syndrome, and secondary thrombocytosis.

Platelet function and morphologic characteristics were evaluated in 43 patients with myeloproliferative disease (MPD), 5 patients with myelodysplastic syndrome (MDS), and 7 patients with secondary thrombocytosis (ST). Platelet Factor IV (PF4) and B-thromboglobulin (BTG) showed slight elevation in ST but significant elevation in all MPDs. They were either normal or slightly elevated in MDS. Defective platelet aggregation with one or more inducers was seen in 62% of all patients. An epinephrine-induced defect was the most consistent aggregation abnormality. Hyperaggregation and spontaneous aggregation were seen in 15% of patients. Of the eight patients who showed increased bleeding tendency, all eight showed defective aggregation with two or more inducers, five showed decreased surface activation response, as well as decreased or abnormal granules and dense tubular disarray in the transmission electron microscope (TEM) study. Seven patients had clinical evidence of recurrent arterial and venous thromboses. Five of these patients showed hyperaggregation response to adenosine diphosphate and collagen and abnormal Wu and Hoak platelet aggregate ratio. Four patients showed spontaneous aggregation on aggregometer. Surface activation response was significantly increased in five patients, and an increase in platelet granules by TEM study was seen in four patients. Primary thrombocythemia could be differentiated from secondary thrombocytosis (ST) by the presence of abnormal aggregation response and significantly increased PF4 and BTG in the former, and greatly elevated plasma fibrinogen and Factor VIII, as part of acute phase reactant response, in the latter.

Aged↗
PubMedDate not supplied

Effect of anagrelide on platelet count and function in patients with thrombocytosis and myeloproliferative disorders.

BACKGROUND: Anagrelide is a quinazolin compound developed initially as an inhibitor of platelet aggregation. Since "in vivo" studies demonstrated that it was responsible for thrombocytopenia in humans, anagrelide has been used recently in a small number of patients with thrombocytosis and myeloproliferative disorders. Platelet count was well controlled in the large majority of patients, and only minimal side effects were observed. PATIENTS: Eight patients (5 with essential thrombocythemia, 2 with chronic granulocytic leukemia, and 1 with idiopathic myelofibrosis) received anagrelide (induction dose 4 mg/die; mean maintenance dose 2 mg/die; mean observation time 26 weeks). Complete blood counts were determined 4 times during the first month, and subsequently every month. "In vivo" and "ex vivo" platelet function was studied before anagrelide and after 4 and 10 days of therapy. RESULTS: Platelet count was reduced and maintained below 500 x 10(9)/L in 5 of 8 patients. Headache, palpitation/tachycardia, gastrointestinal symptoms and a decrease in hemoglobin were the side effects. Anagrelide did not modify the leukocyte count or "in vivo"/"ex vivo" platelet function. CONCLUSIONS: Anagrelide may control thrombocytosis in patients with myeloproliferative disorders, even when traditional drugs have failed. When required, anti-aggregating drugs may be associated with anagrelide, since it has no effect on platelet function.

Adult↗
PubMedDate not supplied

Reticular erythematous mucinosis (REM) with telangiectasias associated with essential thrombocytosis and lung carcinoma.

The cutaneous mucinoses are a heterogeneous group of diseases in which mucin accumulates in the skin. Reticular erythematous mucinosis (REM) is an infrequent variant. We present a 48-year-old man with essential thrombocytosis and REM lesions with atypical telangiectasias on his chest, who developed a non-small cell lung carcinoma. We discuss the unusual clinical finding of telangiectasias over REM lesions and the association with essential thrombocytosis and lung carcinoma.

Biopsy, Needle↗
PubMedDate not supplied

[Spontaneous acute subdural hematoma and primary thrombocytosis in infants. Clinical case].

Acute subdural hematoma in infancy and childhood is relatively rare, causes being both traumatic and atraumatic. This is a case of an infant with spontaneous acute hemorrhage, convulsion and transient idiopathic platelets elevation. A search in the literature revealed it is one of few cases of Primary Thrombocytosis of the infancy up to date described. The association between thrombocytosis and central nervous system disease is remarked.

Hematoma, Subdural↗
PubMed1978

Deep venous thrombosis and postsplenectomy thrombocytosis.

Eighty-six patients undergoing elective splenectomy have been investigated preoperatively and postoperatively by serial platelet counts and leg scanning using iodine 125-labeled fibrinogen. The presence of deep leg vein thromboses detected by labeled fibrinogen was confirmed by dye phlebography. In only five patients (6%) did deep venous thrombosis develop. In none of these five patients did an elevation in platelet count to 600,000/cu mm develop before or at the time of development of the thrombosis. None of 21 other patients who did have a rise in platelet count greater than 1,000,000/cu mm had evidenced of venous thrombosis. These data do not substantiate the need for routine prophylactic antithrombotic therapy in patients in whom postsplenectomy thrombocytosis develops.

Adult↗
PubMed1988

Controlled and uncontrolled thrombocytosis. Its clinical role in essential thrombocythemia.

Only two of 19 patients with spontaneously evolving essential thrombocythemia remained asymptomatic in a 421 patient-month observation. The rest of the patients showed hemorrhagic diathesis (four patients), nonspecific neurological semiology (two patients), and occlusive vascular illness in cerebral, myocardic, arterial, and often multiple locations (total, 12 patients). Peripheral neuropathy was found in five of 10 patients studied. In this series the incidence of cerebral ischemia in the uncontrolled condition was 180 times higher than the epidemiologic expectancy in a population not affected by the disorder. Of 35 ischemic attacks, 22 occurred when the platelet count was more than than 1000 X 10(9)/l, 13 when the count ranged from 650 to 990 X 10(9)/l, and none occurred at counts of less than 650 X 10(9)/l. In contrast, therapeutic control of the thrombocytosis caused all complications to disappear. These findings point out the danger of the natural course of the illness and justify active therapy. At the same time they call into question some of the most commonly used criteria in the diagnosis of essential thrombocythemia.

Adult↗
PubMed1985

The incidence of thrombotic and hemorrhagic disorders in association with extreme thrombocytosis: an analysis of 129 cases.

We have presented a retrospective study of 129 patients with platelet counts of 1,000 X 10(9)/L or more--72 with myeloproliferative disorders (MPD), and 57 with reactive thrombocytosis (RT)--in an effort to determine the incidence of thrombohemorrhagic complications. Thrombotic disorders occurred with approximately equal frequency in the two groups, being found in three patients (4%) with MPD and three (5%) with RT when the platelet count was over 1,000 X 10(9)/L and in 11% of the patients in each group when the platelet count was less than 1,000 X 10(9)/L. In contrast, bleeding manifestations were more common in MPD, where 36% of patients were affected on one or more occasions versus only 4% of those with RT. However, bleeding was generally not severe, with only six patients requiring transfusions, and three of these patients had been receiving aspirin or corticosteroids when they developed severe gastrointestinal bleeding.

Aged↗
PubMed1978

Thrombocytosis and platelet aggregates in the circulation of adjuvant arthritic rats.

A marked increase in platelet count was observed in adjuvant-induced polyarthritic rats. Elevation of platelet count was still significant 3 months after onset of disease. Increased number and larger size of platelets reflect an increase in the rate of platelet production. By means of the platelet-count ratio technique, circulating platelet aggregates were demonstrated in rats with severe arthritis. Aspirin treatment prevented thrombocytosis and formation of platelet aggregates.

Animals↗
PubMed1984

Platelet membrane fatty acids in thrombocytosis due to myeloproliferative disorders.

The fatty acid composition of platelet membranes has been analysed in patients with thrombocytosis due to myeloproliferative disorders, who had not taken any drugs. A significant increase in palmitic and oleic acid, together with a decrease in stearic, linoleic and arachidonic acids was observed. The fatty acid pattern of platelet membranes was also analysed in patients during treatment with ASA (acetylsalicylic acid). ASA ingestion completely normalizes the platelet content of palmitic acid and partially that of stearic and arachidonic acid, whereas it has no effect on the level of linoleic acid and raises that of oleic acid. The altered pattern of fatty acids observed in patients may interfere with platelet function by decreasing membrane fluidity. Treatment of patients with ASA seems to act on platelet membranes by partially normalizing the fatty acid composition.

Adult↗
PubMed2005

Thrombocytosis and toxocariasis: report of two pediatric cases.

We report two cases of visceral larva migrans (VLM) syndrome by Toxocara in children. The biological presentation was unusual and characterized by persistent secondary thrombocytosis (>1,000 x 10(9)/L) mimicking an essential thrombocythemia and variable hypereosinophilia syndrome. Both children had non-specific symptoms including abdominal pain, skin rash, and fever. The diagnosis was confirmed by serology. The children were treated with either thiabendazole or albendazole, resulting in normalization of eosinophil and platelet counts.

Bone Marrow Examination↗
PubMed1991

Treatment of thrombocytosis in chronic myeloproliferative disorders with interferon alfa-2b.

Thirty-six patients with chronic myeloproliferative disorders (CMPD) with thrombocytosis (essential thrombocythaemia 19 patients, chronic megakaryocytic granulocytic myelosis five, polycythaemia vera six, chronic myelogenous leukaemia six) were treated with interferon alfa-2b to reduce the platelet count. The pre-treatment platelet count was in the range 450-700 x 10(9)/L in eight patients, 700-1000 x 10(9)/L in eight and above 1000 x 10(9)/L in 20. In the induction phase of treatment 22 patients were treated with interferon alfa-2b 3 million units (MU) daily subcutaneously for 2 months or until the platelet count returned to normal, if earlier. Fourteen patients received 5 MU interferon alfa-2b daily in the same way. In the maintenance phase the doses were reduced to 3 MU and 5 MU thrice weekly, respectively. Complete response (CR), defined as a reduction of platelet count to below 450 x 10(9)/L, was achieved in 78% of patients (within 2 months of induction in 64%). The platelet depleting effect was dose dependent: CR in 2 months in 52% on 3 MU interferon alfa-2b versus 75% on 5 MU. Reduction of interferon dose was followed by an increase in platelet count in 39% of patients. The white cell count fell by 50% in Philadelphia-negative CMPD. Side effects were common, though generally mild, but led to withdrawal of treatment in six patients. Three patients suffered cerebrovascular events during treatment and one shortly thereafter.

Adult↗
PubMed1988

[Thrombocyte function in essential thrombocythemia and reactive thrombocytosis].

Blood of 16 patients with essential thrombocythemia (ET), 9 patients with reactive thrombocytosis (RT) and 13 healthy persons was used for platelet aggregation studies. When the aggregation was induced with adenosine diphosphate (0.01 microM), collagen (0.1 micrograms/ml) or platelet activating factor (PAF 0.5 microM) the plasma of the patients with ET showed significantly decreased aggregation (35%-44% of the value for the control groups). Independent of inhibitors of platelet aggregation, thrombin (0.05 U/ml) caused similar aggregation in healthy controls and patients with ET; patients with RT showed an increase aggregation. Adrenalin-induced aggregation discriminated best between patients with ET and controls. Adrenalin in concentrations ranging from 0.01 micrograms/ml to 100 micrograms/ml caused comparable dose-related amounts of aggregation in healthy controls and patients with RT. Over the whole concentration range, patients with ET showed significantly decreased aggregation (28%-34% of the value for the control groups). This difference proved to be independent of the influence of inhibitors of platelet aggregation. Though concentrations of alpha1-acid glycoprotein never reached inhibitory levels in the plasma of patients with ET (n = 12) they were significantly higher compared with those in normal plasma (n = 12). Fibrinogen concentrations in plasma of ET-patients (n = 12) were in the normal range. Cellular adenosine 3'-5'-cyclic monophosphate concentrations in ET (n = 10) are comparable with normal values (n = 5). The significance of the results for diagnosis and better pathophysiological understanding of ET is discussed.

Blood Platelets↗
PubMed1990

Megakaryocyte precursors (pro- and megakaryoblasts) in bone marrow tissue from patients with reactive thrombocytosis, polycythemia vera and primary (essential) thrombocythemia. An immunomorphometric study.

To determine the number of megakaryocyte precursors (pro- and megakaryoblasts), an immunomorphometric study was performed on paraffin-embedded trephine biopsies of the bone marrow using a monoclonal antibody against platelet glycoprotein IIIa. Eighteen control specimens from patients with no evidence of any hematological disorder and a normal platelet count were selected and assessed together with the same number of specimens from patients with reactive thrombocytosis, polycythemia vera rubra (P. vera) or primary (essential) thrombocythemia (PTH). A strikingly proportionate increase in early megakaryocytes occurred in all patients enrolled in this study, compared with the controls. Moreover, there were no significant correlations between counts for precursors or total megakaryocytes per square millimeter of bone marrow with the corresponding values for platelets. This indicates that despite an orderly increase in immature forms in the bone marrow, the number of platelets circulating in the blood is influenced by other additional factors, such as the expanded platelet pool in the enlarged spleen. The non-disproportionate expansion of megakaryocyte precursors extends previous findings on progenitor cells of this lineage in vitro, particularly in PTH. Histological evaluation of the bone marrow of patients with P. vera and PTH indicated that megakaryopoiesis proceeded to the production of appropriate mature forms with no obvious excess of very small or blastic elements.

Antibodies, Monoclonal↗