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PubMed2002

Measurement of spleen volume by ultrasound scanning in patients with thrombocytosis: a prospective study.

Spleen size was assessed in 73 patients with thrombocytosis and in 15 healthy subjects, comparing palpation with ultrasonography (US) measurement of longitudinal diameter and volume. Intraobserver and interobserver variability for volume on US, checked in 12 patients, was very low. Correlation between spleen volume measured by US and that measured by computed tomography was excellent. Splenomegaly was detected by palpation in 25% of patients, by US assessment of longitudinal diameter in 33%, and by US assessment of volume in 52%. After diagnostic work-up, 54 patients had a diagnosis of essential thrombocythemia (ET), 4 of idiopathic myelofibrosis (IMF), and 15 of secondary thrombocytosis (ST). Spleen volume in patients with ST was in the normal range (138 +/- 47 mL) and was significantly lower than that in patients with ET or IMF (370 +/- 210 mL; P <.001). Thus, US-measured volume was the most sensitive method for identifying nonpalpable splenomegaly in patients with primary myeloproliferative diseases, and it may help in distinguishing these diseases from reactive disorders.

Adolescent↗
PubMed2002

Increased soluble and platelet-associated CD40 ligand in essential thrombocythemia and reactive thrombocytosis.

CD40 ligand (CD40L) is expressed on activated CD4(+) T lymphocytes and at the activated platelet surface. A circulating soluble form of CD40L (sCD40L) is generated by the way of a proteolytic cleavage. We measured sCD40L in the plasma of either healthy subjects; patients with inflammatory disorders and low, normal, or high platelet count (reactive thrombocytosis); or patients with essential thrombocythemia (ET). A tight correlation was found between the platelet count and plasma sCD40L. ET patients had the highest levels of sCD40L. Platelet-associated CD40L was increased in ET and reactive thrombocytosis, conditions associated with increased platelet regeneration. Platelet-associated CD40L was released upon platelet activation. In conclusion, platelets appear as a reservoir of CD40L that may be a major contributor to circulating sCD40L. Platelet-associated CD40L may be a potential marker of platelet regeneration.

Adult↗
PubMed1993

Pulmonary hypertension secondary to thrombocytosis in a patient with myeloid metaplasia.

A 72-year-old physician with myeloid metaplasia developed marked thrombocytosis, pulmonary hypertension, and right heart failure following splenectomy. No cause for the pulmonary hypertension could be found. The pulmonary hypertension and right heart failure returned to normal when hydroxyurea therapy corrected the thrombocythemia. It is concluded that thrombocytosis may cause pulmonary hypertension, mediated by pulmonary capillary obstruction from cellular components, involving platelet aggregation, microthrombosis, and stasis, and possible vasoconstrictor effects.

Aged↗
PubMed1979

Thrombocytosis in chronic eosinophilic pneumonia.

Thrombocytosis has not yet been described in chronic eosinophilic pneumonia. A typical patient with chronic eosinophilic pneumonia is described. The patient's thrombocyte count was up to 900,000 per cu mm, which returned to normal under steroid therapy. Thrombocytosis may be associated with chronic inflammation and should not require further investigations such as lung biopsy, in an otherwise usual case of chronic eosinophilic pneumonia.

Adult↗
PubMed2005

Iron deficiency anemia with marked thrombocytosis complicated by central retinal vein occlusion.

We report a case of severe iron deficiency anemia with marked thrombocytosis that was complicated by central retinal vein occlusion. Platelet count was over one million per microliter and an increased number of megakaryocytes was observed in the bone marrow at the time of diagnosis of iron deficiency anemia, features that resemble those of essential thrombocythemia. However, the platelet count rapidly declined with the administration of ferrous fumarate. Accordingly, central retinal vein occlusion was improved and has not recurred. In this case, significant thrombocytosis caused by iron deficiency anemia may have been involved in the development of central retinal vein occlusion.

Adult↗
PubMed1986

Platelet alpha-granule release in chronic myeloproliferative disorders with thrombocytosis.

Platelet alpha-granule release in 22 patients affected by chronic myeloproliferative disorders with thrombocytosis and seven subjects with thrombocytosis secondary to splenectomy were studied. We found elevated beta-thromboglobulin (BTG) and platelet factor 4 (PF4) plasma levels in all patients. Intraplatelet content of BTG and PF4 was decreased in patients with idiopathic thrombocythaemia (IT) and idiopathic myelofibrosis (IMF). The BTG and PF4 results were also expressed as the ratio plasma BTG and PF4: whole blood platelet count. In patients with IT, BTG: whole blood platelet count ratio was low, conversely, the same ratio was high in patients with IMF. In conclusion, our results suggest the presence of an abnormal, BTG-deficient clone in IT and a peripheral platelet activation in IMF.

Beta-Globulins↗
PubMed1999

Thrombocytosis with sideroblastic erythropoiesis: a mixed myeloproliferative myelodysplastic syndrome.

Some patients with haematological neoplasms have features which overlap between a myelodysplastic syndrome and a myeloproliferative disorder. Two such patients are reported, both having sideroblastic erythropoiesis and thrombocytosis and one sequentially developing features of atypical chronic myeloid leukaemia, idiopathic myelofibrosis and acute megakaryoblastic leukaemia. The prevalence of thrombocytosis among cases of refractory anaemia with ring sideroblasts may be as high as 15-20% and has implications for choice of therapy.

Anemia, Sideroblastic↗
PubMed2002

Pseudohyperkalemia occurring in a patient with chronic renal failure and polycythemia vera without severe leukocytosis or thrombocytosis.

Pseudohyperkalemia is defined as a serum potassium concentration 0.4 mEq/l greater than the plasma concentration. The basis of this phenomenon is the release of intracellular potassium from platelets, leukocytes, or erythrocytes, commonly in the setting of extreme leukocytosis (> 10 x 10(4)/microl) or thrombocytosis (> 60 x 10(4)/microl). We report a case of pseudohyperkalemia in a patient with chronic renal failure and polycythemia vera without the finding of severe leukocytosis or thrombocytosis (white blood cell count 1.88 x 10(4)/microl and platelet count 37.9 x 10(4)/microl, respectively). The serum potassium concentration was 8.2 mEq/l, while the plasma potassium level was 6.4 mEq/l in a sample obtained simultaneously. The concentrations of platelet factor IV and beta-thromboglobulin, known to be markers of platelet activation, were greater than 100 ng/ml and 200 ng/ml, respectively, indicating that platelet activation may have been related to the development of pseudohyperkalemia in this patient. These findings suggest that pseudohyperkalemia should be considered when hyperkalemia is seen in a patient with chronic renal failure and myeloproliferative disorders.

Aged↗
PubMed1983

Human leukocyte interferon to control thrombocytosis in chronic myelogenous leukemia.

Nine patients with refractory chronic myelogenous leukemia and severe symptomatic thrombocytosis (greater than or equal to 1 X 10(6) platelets/mm3) were given partially purified human leukocyte interferon-alpha. A significant decline in platelet counts, from a mean (+/- SE) of 1.71 +/- 0.53 X 10(6)/mm3 to a mean of 0.52 +/- 0.24 X 10(6)/mm3 (p less than 0.01), resulted in all patients. Maintenance of low platelet counts was achieved in two patients for more than 143 and 300 days, respectively. Treatment with human leukocyte interferon-alpha was stopped in the remaining patients because of increases in the leukocyte count, toxicity, or both. Our preliminary observations suggest that human leukocyte interferon-alpha may significantly alleviate progressive thrombocytosis in advanced chronic myelogenous leukemia. Further studies of human leukocyte interferon-alpha and chemotherapeutic agents are indicated.

Adult↗
PubMed1999

Thrombocytosis after prophylactic administration of enoxaparin: unexpected findings in a Polish prospective multicenter trial on the efficacy and safety of enoxaparin in the prevention of postoperative thromboembolism.

BACKGROUND: Heparin-related thrombocytopenia is a common complication of heparin administration and therefore platelet count was monitored in our study. METHODS EXPERIMENTAL DESIGN: Prospective multicentre study. SETTING: 14 Departments of General, Thoracic or OrthopaedicSurgery, Poland. PATIENTS: 290 patients--150 general or thoracic surgery patients aged above 40 years, and 140 orthopaedic surgery patients aged between 18 and 60 years. INTERVENTIONS: All patients received 20 mg (general and thoracic surgery) or 40 mg of enoxaparin (orthopaedic surgery) once daily subcutaneously both before surgery and during postoperative immobilisation. MEASURES: Platelet count was evaluated prior to surgery and on the 5th, 7th, 11th and 15th day following the operation. RESULTS: There was neither thrombocytopenia nor heparin-induced thrombosis. Paradoxically, postoperative platelet count in most cases increased slightly but statistically significantly, but in some however, even above 600 G/l, nevertheless in these patients no thrombotic complications occurred. Postoperative thrombocytosis was greater in patients with neoplasms as well as those with excessive perioperative blood loss and transfusions. CONCLUSIONS: As platelet count was not the main topic of our study, the presented data should be regarded only as preliminary. Further investigations to resolve the cause of the observed phenomenon of thrombocytosis are therefore necessary.

Adolescent↗
PubMed2001

Reactive and clonal thrombocytosis: proinflammatory and hematopoietic cytokines and acute phase proteins.

BACKGROUND: We quantitated proinflammatory and thrombopoietic cytokines in reactive thrombocytosis (RT) and clonal thrombocytosis (CT) to identify a cytokine profile that might aid in the distinction of these two disorders. METHODS: Serum levels of cytokines relevant to platelet biology--interleukins 3, 6, 11, and 1beta; thrombopoietin; tumor necrosis factor alpha; and C-reactive protein (CRP)--were measured by enzyme-linked immunosorbent assay in healthy subjects and in patients with CT and RT. RESULTS: Interleukin-6 and CRP levels were higher in RT patients than in controls or CT patients. Interleukin 1beta levels were higher in the RT group than in the CT and control groups. CONCLUSIONS: In RT, IL-6, IL-1beta, and CRP levels are elevated. In both RT and CT, IL-11 is elevated, but thrombopoietin levels are not.

Adult↗
PubMed2001

[Chronic myelogenous leukemia with marked thrombocytosis].

We report a case of chronic myelogenous leukemia (CML) with marked thrombocytosis. The patient was a 68-year-old woman who showed marked thrombocytosis (> 200 x 10(4)/microliter), a slightly increased leukocyte count without any immature myeloid cells in the peripheral blood, and no hepatosplenomegaly. Philadelphia chromosome (Ph) was detected by karyotype analysis and FISH. The bcr-abl transcript was detected by RT-PCR and the break point was located in the major bcr. Treatment with interferon-alpha was effective, reducing the proportion of Ph-positive cells from 56% to 7% within 21 months. Detailed study of atypical cases of CML such as the present one may provide additional information about the disease pathogenesis.

Aged↗
PubMed1975

Heterogeneity of rabbit platelets. IV. Thrombocytosis with absolute megathrombocytosis in phenylhydrazine-induced hemolytic anemia in rabbits.

Intravenous injection of phenylhydrazine into intact rabbits resulted in a thrombocytosis of 1.85 fold and megathrombocytosis (large platelets) of 2.30 fold. Splenectomy markedly impaired this response. The intravenous injection of red blood cell hemolysates gave a response similar to that of phenylhydrazine in both intact and splenectomized animals. Basal data obtained from intact and splenectomized animals; as well as kinetic data obtained following apparent splenic blockade secondary to phenylhydrazine hemolysis revealed the presence of a splenic platelet pool with preferential splenic sequestration of megathrombocytes. It is suggested that the thrombocytosis and absolute megathrombocytosis of hemolysis is due to splenic blockade by red blood cell hemolysate.

Anemia, Hemolytic↗
PubMed2002

Elevated platelet counts and thrombocytosis in erythema nodosum leprosum.

Changes in peripheral blood platelet counts associated with the onset of symptomatic erythema nodosum leprosum (ENL) were studied by comparing, in each patient, the value obtained on the day thalidomide therapy commenced with the average of the three preceding values. In the 11 patients studied, the mean platelet count rose from 235 to 322 x 10(3)/mm3, p < 0.001. In 3, the platelet count was above the normal limit, qualifying as thrombocytosis, in 7 the rise was appreciable, and in 2 it was negligible. In the 3 patients studied 1-2 weeks after beginning thalidomide, the mean count was 414 x 10(3)/mm3. Counts obtained after 3 or more weeks of thalidomide therapy were within normal limits. This study provided no direct evidence as to the mechanism responsible for the elevated platelet count, but mediation by interleukin-6 (IL-6) was concluded to be an attractive hypothesis, consistent with prior studies of IL-6 in reactive thrombocytosis and of IL-6 in ENL.

Adult↗
PubMedDate not supplied

Essential thrombocytosis: diagnostic and treatment dilemmas.

Essential thrombocytosis is one of the chronic myeloproliferative disorders that includes polycythemia vera, chronic myelogenous leukemia, and agnogenic myeloid metaplasia. Despite established diagnostic criteria and greater than a quarter century of study, there are still several diagnostic and management dilemmas that plague researchers and clinicians alike. We present a case of essential thrombocytosis in a patient with multiple sequelae.

Aspirin↗
PubMedDate not supplied

Neutrophil hypersegmentation and thrombocytosis in children with iron deficiency anemia.

Neutrophil hypersegmentation is an expected peripheral blood smear finding in megaloblastic anemias. But some clinical reports suggest that neutrophil hypersegmentation may also occur in patients with iron deficiency anemia. In this study we searched the presence of neutrophil hypersegmentation and thrombocytosis in patients with iron deficiency anemia but who had normal serum vitamin B12 and folic acid levels. The study comprised 102 patients with iron deficiency anemia and 21 age-matched healthy controls. All routine tests for iron deficiency anemia were done, serum folate and cobalamin levels were measured, and platelets were counted in all patients and controls. Peripheral blood smears were examined for neutrophil hypersegmentation. Hypersegmentation was found in 30.4% of anemic patients and in 9.5% of controls (p < 0.05). The number of platelets was also significantly higher in anemic children (p < 0.05). These results show that neutrophil hypersegmentation may also be seen in patients with iron deficiency anemia, and thrombocytosis is a common laboratory finding in this disorder.

Anemia, Iron-Deficiency↗
PubMedDate not supplied

A case of essential thrombocytosis developing nephrotic syndrome and severe endothelial damage.

We present a 75-year-old Japanese man with essential thrombocytosis presenting nephrotic syndrome. Proteinuria developed soon after the patient was given a diagnosis of essential thrombocytosis and, 4 years later, it increased to a nephrotic range. Renal biopsy revealed one third of the obtained glomeruli totally sclerotic and the other glomeruli showed a marked thickening of the glomerular basement membrane and mild mesangial proliferation. Remarkable widening of the subendothelial space was evident on electron microscopy. Increased expression of platelet derived growth factor receptor beta was detected in the mesangium and interstitium by immunohistochemistry. Abnormal platelet activation in myeloproliferative disease has been shown to contribute in glomerulosclerosis by releasing various growth factors and cytokines including PDGF. Considering his clinical course and the pathological findings, the probable risk factor for developing severe endothelial damage and glomerulosclerosis is due to the persistence of high platelet count and platelet abnormality.

Aged↗
PubMed1990

[Aggregative behavior and calcium content of platelets in thrombocythemia and thrombocytosis].

Patients with thrombocythaemia due to myeloproliferative disorders (n = 21), with secondary thrombocytosis of various origin (n = 16), and a control group of healthy donors (n = 20) were investigated with respect to the aggregation behaviour and the total calcium content of blood platelets. The calcium content was significantly lower in both groups of patients as compared to controls (2 p less than 0.001). In 16 of 21 patients with myeloproliferative disorders platelet rich plasma did not respond to epinephrine (15 mumol/l), a concentration which induced at least weak aggregation in 14 of 16 patients with secondary thrombocytosis and also in healthy subjects. In patients with thrombocythaemia the mean extent of aggregation induced by epinephrine, collagen or adenosin diphosphate was significantly lower as compared to controls (2 p less than 0.001).

Adenosine Diphosphate↗