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PubMed1994

Significance of thrombocytosis in patients with epithelial ovarian cancer.

OBJECTIVES: Our objective was to determine the relevance of a preoperative platelet count in ovarian cancer. Special interest was directed to a possible prognostic significance of thrombocytosis in this disease. STUDY DESIGN: Charts of 130 patients with epithelial ovarian cancer were reviewed retrospectively. Survival analyses were performed with the Kaplan-Meier method. Differences in survival were examined according to Mantel and Breslow. Platelet counts were furthermore correlated to other clinical parameters. For this purpose the Spearman rank test and a stepwise logistic regression model were used. Data comparison was accomplished with the Mann-Whitney U test and the chi 2 test. RESULTS: Prevalence of thrombocytosis was 38%. No differences in survival between patients with or without thrombocytosis was found. Volume of ascites and hemoglobin concentrations were independently associated with thrombocytosis (p = 0.002 and p = 0.004, respectively). CONCLUSIONS: Thrombocytosis is not a useful prognostic factor in ovarian cancer. Elevated platelets are predominantly associated with the presence of ascites and marked anemia.

Adult↗
PubMed2001

Early elevation of serum thrombopoietin levels and subsequent thrombocytosis in healthy preterm infants.

To verify pathophysiological mechanisms underlying thrombocytosis in low-birth-weight (LBW) preterm babies, we evaluated kinetic changes in platelet counts and thrombopoietic cytokines including thrombopoietin (TPO), interleukin 6 (IL-6) and IL-11 in 24 uncomplicated preterm infants. Platelet counts in cord blood (CB) (265 +/- 64 x 10(9)/l) were similar to adult levels, increased by d 14 (473 +/- 140 x 10(9)/l), and then remained fairly constant. Thrombocytosis (> 500 x 10(9)/l) was observed in 9/24 (38%) subjects. Mean TPO level in CB was 5.11 +/- 1.51 fmol/ml, peaked at d 2 (7.64 +/- 3.28 fmol/ml), decreased at d 5 (3.93 +/- 1.67 fmol/ml), and thereafter kept fairly constant during the remaining neonatal period. Compared with term infants, mean TPO levels of preterm infants in CB and at d 2 were significantly higher (P < 0.01). There was an inverse correlation between platelet counts and TPO levels (r = 0.45, P < 0.001, n = 88). Preterm neonates with thrombocytosis had significantly higher TPO values in CB than those without thrombocytosis (P < 0.05). There was no significant relationship between platelet counts and IL-6. IL-11 was not detectable. These results suggest that an early elevation of serum TPO levels is related to the subsequent thrombocytosis in LBW preterm infants.

Biomarkers↗
PubMed1986

Essential thrombocytosis with the Philadelphia chromosome (Ph').

Essential thrombocytosis is a myeloproliferative disease not known to have consistent cytogenetic abnormalities. A 46-year-old black woman with essential thrombocytosis and a Philadelphia chromosome is reported. Iron deficiency and tuberculosis were present but when effectively treated did not result in resolution of thrombocytosis. Megakaryocytic hyperplasia of bone marrow, abnormal platelet function studies and a compatible clinical state suggested the diagnosis of essential thrombocytosis. The diagnostic criteria for other myeloproliferative diseases were not met. The Philadelphia chromosome was consistently obtained from bone marrow preparations. We conclude that the Philadelphia chromosome may be found in essential thrombocytosis as well as other, previously reported, myeloproliferative diseases.

Bone Marrow↗
PubMed1990

Thrombocytosis after pneumonia with empyema and other bacterial infections in children.

Thrombocytosis is seen in association with many conditions, including infectious diseases. We studied thrombocytosis after severe bacterial infections, particularly pneumonia with empyema in children. A systematic survey of the phenomenon was conducted. Twenty-seven children admitted for pneumonia with empyema were studied. Thrombocytosis (platelet counts greater than 500 x 10(3)/microliters) was present in 92.5%. Platelet counts reached their maximum at 15.1 +/- 3.7 days (range, 7 to 25) and declined to normal after 3 weeks of illness. Compared with a healthy control group, significant thrombocytosis, but of lower incidence, was also noted in children with lobar pneumonia without pleural effusion, bacterial meningitis and osteomyelitis. Platelet functions were examined in seven of the children but no abnormalities were observed. Bone marrow aspiration of three children with pneumonia and empyema showed megakaryocytic hyperplasia. We found no correlation between thrombocytosis, neutrophilia, fever, the clinical course, complications, prognosis or treatment. Neither thromboembolic nor hemorrhagic phenomena were observed.

Bacterial Infections↗
PubMed1991

Elevated serum interleukin-6 levels in patients with reactive thrombocytosis.

Interleukin-6 (IL-6) is known to promote megakaryocytopoiesis in vitro and raise platelet counts in vivo. To determine if there is a relationship between circulating IL-6 and thrombocytosis in man, we measured bioactive IL-6 in the serum of 13 patients with myeloproliferative disorders and 143 patients with reactive thrombocytosis having platelet counts greater than or equal to 600 x 10(9)/l. IL-6 activity was assayed using the IL-6-responsive B9 cell line. Seventy-one controls with normal platelet counts had a mean IL-6 level of 2.19 U/ml +/- 1.08 (SD). None of the 13 patients with myeloproliferative disorders had elevated IL-6 levels (1.56 U/ml +/- 1.2). In contrast, serum IL-6 levels of 143 patients (158 samples) with reactive thrombocytosis were significantly greater than controls (38.3 U/ml +/- 94.6; P less than 0.001), with 83% of the samples showing elevated serum IL-6. No significant correlation was observed between serum IL-6 levels and platelet counts in the reactive thrombocytosis group. We conclude that elevated IL-6 is associated with reactive thrombocytosis, and hypothesize that the increased platelet count in many cases is causally related to elevated IL-6.

Humans↗
PubMed2005

Primary and secondary thrombocytosis in childhood.

This review summarizes current data on the pathomechanisms and clinical aspects of primary and secondary thrombocytosis in childhood. Primary thrombocytosis is extremely rare in childhood, mostly diagnosed at the beginning of the second decade of life. As in adults, the criteria of the Polycythemia Vera Group are appropriate to diagnose primary thrombocytosis. The pathomechansims of non-familial forms are complex and include spontaneous formation of megakaryopoietic progenitors and increased sensitivity to thrombopoietin (Tpo). Familial forms can be caused by mutations in Tpo or Tpo receptor (c-mpl) genes. These mutations result in overexpression of Tpo, sustained intracellular signalling or disturbed regulation of circulating Tpo. Treatment of primary thrombocytosis is not recommended if platelet counts are <1500/nl and bleeding or thrombosis did not occur in patient's history. In severe cases, decision on treatment should weigh potential risks of treatment options (hydroxyurea, anagrelide) against expected benefits for preventing thrombosis or haemorrhage. Secondary thrombocytosis is frequent in children, in particular in the first decade of life. Hepatic Tpo production is stimulated in acute response reaction to a variety of disorders. Thrombosis prophylaxis is not required, even at platelet counts >1000/nl, except for cases with additional prothrombotic risk factors.

Adolescent↗
PubMed1991

Thrombocytosis in adults: analysis of 777 patients.

A total of 777 patients with thrombocytosis, defined as a platelet count of greater than 500 x 10(9)l-1, seen in a University hospital over a 1-year period, were studied prospectively for aetiology. The most frequent causes of thrombocytosis were infection (21.9%), rebound thrombocytosis (19.4%), tissue damage (17.9%), chronic inflammatory disorders (13.1%) and malignancy (5.9%). Thrombocytosis associated with multiple causative factors, occurring simultaneously, was seen in 6.1% of cases. Thrombocytosis of greater than or equal to 1 million x 10(9)l-1 was found most frequently in patients with multiple aetiological factors occurring at the same time, in myeloproliferative disorders, or in postsplenectomy patients.

Adolescent↗
PubMed1997

Benign familial microcytic thrombocytosis with autosomal dominant transmission.

Familial thrombocytosis is an extremely rare disorder, so far reported in only a handful of families. In the majority of cases the characteristics were of essential thrombocythemia. Most patients presented with a platelet count above 800,000/mm3, were diagnosed as having a myeloproliferative disease, and some required chemotherapy. We describe a benign form of familial thrombocytosis with autosomal dominant inheritance in five healthy members of three generations of a family, all of whom had moderate thrombocytosis within the range 422,000-662,000/mm3, characterized by low mean platelet volume. A careful medical history and a 5-year follow up of the subjects did not reveal any untoward clinical development. This variant of familial thrombocytosis is therefore of a benign nature. Possible mechanisms linking thrombocytosis with platelet microcytosis in this family are discussed.

Adolescent↗
PubMed2006

Impact of thrombocytosis and C-reactive protein elevation on the prognosis for patients with renal cell carcinoma.

AIM: C-reactive protein (CRP) elevation is reportedly a prognostic factor in patients with renal cell carcinoma (RCC). Thrombocytosis has recently been reported also to be a prognostic factor in RCC and, like CRP, to be related to inflammatory cytokines such as interleukin-6. The aim of this study was to evaluate the importance of both thrombocytosis and CRP elevation in tumor recurrence and prognosis for patients with RCC. METHODS: The clinical records of 178 patients who underwent radical nephrectomy were reviewed. Thrombocytosis was defined as a platelet count >or=350,000/mm(3), and CRP elevation was defined as a CRP level >or=1.0 mg/dL. Disease-free survival and cause-specific survival rates were calculated. Independent predictors for recurrence and prognosis were determined. RESULTS: Patients with thrombocytosis and patients with elevated CRP levels had significantly higher pathological T stage, clinical stage, tumor size, histological grade, and percentage of microvascular invasion than did patients without THC and patients with CRP levels <1.0 mg/dL, respectively. There was a significant correlation between platelet counts and CRP levels. Multivariate analysis showed that distant metastasis, tumor size, grade 3 components, and CRP elevation were independent predictors for prognosis but thrombocytosis was not. In N0M0 RCC patients, tumor size, microvascular invasion, and CRP elevation were independent predictors for recurrence. CRP elevation and tumor size were independent predictors for prognosis. CONCLUSIONS: Platelet count and CRP level are strongly correlated in patients with RCC, but only CRP elevation is an independent predictor for recurrence and prognosis.

C-Reactive Protein↗
PubMed1981

Platelet phospholipids in thrombocytosis due to myeloproliferative disorders.

Platelet phospholipids were analyzed in patients with thrombocytosis due to myeloproliferative disorders and secondary thrombocytosis. A significant increase of phosphatidylcholine together with a decrease of sphingomyelin was observed in each of the 8 patients with primary thrombocythaemia and in each of the 5 patients with excessive thrombocytosis due to primary polycythaemia. The phospholipid pattern of the 3 patients with secondary thrombocytosis did not differ from that of the normal controls. This marked difference in the platelet phospholipids may be helpful in distinguishing secondary thrombocytosis persisting for a prolonged period of time after splenectomy from previously unrecognized primary thrombocythaemia unmasked by splenectomy. The decreased sphingomyelin/lecithin ratio of platelets in primary thrombocythaemia may interfere with platelet function by increasing the fluidity of their membrane.

Blood Platelets↗
PubMed2001

Interleukin-6 stimulates thrombopoiesis through thrombopoietin: role in inflammatory thrombocytosis.

Baseline platelet production is dependent on thrombopoietin (TPO). TPO is constitutively produced and primarily regulated by receptor-mediated uptake by platelets. Inflammatory thrombocytosis is thought to be related to increased interleukin-6 (IL-6) levels. To address whether IL-6 might act through TPO to increase platelet counts, TPO was neutralized in vivo in C57BL/10 mice treated with IL-6, and hepatic TPO mRNA expression and TPO plasma levels were studied. Transcriptional regulation of TPO mRNA was studied in the hepatoblastoma cell line HepG2. Furthermore, TPO plasma levels were determined in IL-6-treated cancer patients. It is shown that IL-6-induced thrombocytosis in C57BL/10 mice is accompanied by enhanced hepatic TPO mRNA expression and elevated TPO plasma levels. Administration of IL-6 to cancer patients results in a corresponding increase in TPO plasma levels. IL-6 enhances TPO mRNA transcription in HepG2 cells. IL-6-induced thrombocytosis can be abrogated by neutralization of TPO, suggesting that IL-6 induces thrombocytosis through TPO. A novel pathway of TPO regulation by the inflammatory mediator IL-6 is proposed, indicating that the number of platelets by themselves might not be the sole determinant of circulating TPO levels and thus of thrombopoiesis. This regulatory pathway might be of relevance for the understanding of reactive thrombocytosis.

Animals↗
PubMedDate not supplied

Paraneoplastic thrombocytosis-induced systemic thromboembolism in a cat.

A six-year-old cat presented with clinical signs consistent with distal aortic thromboembolism while clinical signs of cardiovascular disease were absent. Diagnostics, including thoracic radiographs, electrocardiography, and echocardiography revealed no cardiovascular anomalies. Thoracic radiographs revealed multifocal pulmonary lesions consistent with neoplasia. Complete blood cell count demonstrated a marked thrombocytosis, leukopenia, and neutropenia. Histopathology of the pulmonary lesions confirmed multiple bronchoalveolar carcinomas. Myelodysplasia with megakaryocytic hyperplasia and ineffective myelopoiesis was noted on bone-marrow histopathology from multiple sites. The absence of other causes suggested a paraneoplastic thrombocytosis. The diagnosis of paraneoplastic thrombocytosis-induced thromboembolism was made due to the lack of underlying cardiac disease and the presence of a marked thrombocytosis. The presence of thrombocytosis and thromboembolism associated with neoplasia is discussed.

Animals↗
PubMed2003

The rate of progression to polycythemia vera or essential thrombocythemia in patients with erythrocytosis or thrombocytosis.

BACKGROUND: The clinical relevance of mild erythrocytosis (hematocrit > 0.48 in women or > 0.51 in men) or thrombocytosis (platelet count > 400 x 10(9) cells/L) in asymptomatic persons is uncertain. OBJECTIVE: To estimate the frequency of polycythemia vera or essential thrombocythemia in persons with erythrocytosis or thrombocytosis in a general population. DESIGN: Cohort study. SETTING: Vicenza, Italy. PARTICIPANTS: 10 000 community dwellers age 18 to 65 years and enrolled in the Vicenza Thrombophilia and Atherosclerosis project. MEASUREMENTS: Platelet count and hematocrit at baseline in all participants and at second follow-up if baseline results were abnormal. Measurement of erythrocyte sedimentation rate, peripheral arterial saturation, serum erythropoietin level, and leukocyte alkaline phosphatase level; chest radiography; abdominal ultrasonography; and occult fecal blood testing were done in persons with confirmed high hematocrit or platelet counts. Polycythemia vera and essential thrombocythemia were diagnosed according to the Polycythemia Study Group criteria. RESULTS: At baseline examination, 1 person had polycythemia vera, 1 had essential thrombocythemia, 88 had erythrocytosis, and 99 had thrombocytosis. Second examination confirmed erythrocytosis in 40% (95% CI, 29% to 51%) and thrombocytosis in 8% (CI, 4% to 15%) of those with abnormal baseline results. Among persons with confirmed abnormalities, further evaluation revealed 11 with idiopathic erythrocytosis, 2 with polycythemia vera (3/10 000 [CI, 0.6 to 8.7/10 000]), and 3 with essential thrombocythemia (4/10 000 [CI, 1.09 to 10.2/10 000]). After 5 years of follow-up, 1 additional person with a high platelet count developed essential thrombocythemia, and no persons developed hemorrhagic or thrombotic complications. CONCLUSIONS: The prevalences of polycythemia vera and essential thrombocythemia were higher than expected in this general population. However, the risks for developing polycythemia vera, essential thrombocythemia, or associated vascular complications in persons with erythrocytosis or thrombocytosis were low.

Adolescent↗
PubMed2000

Etiology and incidence of thrombotic and hemorrhagic disorders in Thai patients with extreme thrombocytosis.

A retrospective study of 126 patients with extreme thrombocytosis (defined as a platelet count > or = 1,000 x 10(9)/L) was performed during a five-year period (June 1994-June 1999). The aim of this study was to determine the etiology and to evaluate the clinical consequences of extreme thrombocytosis. Seventy patients (55.5%) had reactive thrombocytosis (RT) with an age range of 43 +/- 2.2 years, 56 (44.5%) had chronic myeloproliferative disorders (MPD) with an age range of 53 +/- 2.4 years. Underlying causes of RT were malignancy (25/70 or 35.7%), infection (16/70 or 22.9%), postsplenectomized beta-thalassemia/Hb E (11/70 or 15.7%), inflammation (12/70 or 17.1%), iron deficiency anemia (6/70 or 8.6%). Duration post splenectomy in our beta-thalassemia/Hb E patients ranged from 4 months to 21 years, with a median of 10 years. Subtypes of our MPD cases were chronic myeloid leukemia (30/56 or 53.6%), essential thrombocytosis (18/56 or 32.1%), polycythemia vera (4/56 or 7.1%), agnogenic myeloid metaplasia (3/56 or 5.4%) and unclassified MPD (1/56 or 1.8%). Bleeding and thrombotic tendency were respectively noted in 7 (12.5%) and 2 (3.6%) of MPD patients. Two patients of the MPD group (3.6%) experienced both bleeding and thrombotic episodes. One patient (1.4%) of the RT group developed vasculitis-associated thrombosis. However, none of the patients in the RT group had bleeding complications. Extreme thrombocytosis was not a rare condition in a university hospital population, and bleeding and/or thrombotic complication was more common in the MPD group.

Adult↗
PubMed2000

Thrombocytosis in temporal arteritis rising platelet counts: a red flag for giant cell arteritis.

OBJECTIVES: To determine whether early recognition and detection of thrombocytosis in patients with giant cell arteritis can help secure an earlier diagnosis, and whether it can help differentiate cases of arteritic optic neuropathy from other forms of optic neuropathy. METHODS: Medical and ophthalmologic records from 1993 to 1998 of the authors' patients with biopsy-proven temporal arteritis versus the authors' patients with nonarteritic anterior ischemic optic neuropathy and idiopathic demyelinating optic neuritis were prospectively collected. Past and present blood analyses were collected, and platelet counts were compared between patients with giant cell arteritis and control populations. This was done to determine whether thrombocytosis could help with the diagnosis and differentiation of these different disease states. RESULTS: There was a significant difference in the frequency of thrombocytosis in patients with giant cell arteritis (13 out of 19 patients), with or without arteritic ischemic optic neuropathy, as compared with those with nonarteritic anterior ischemic optic neuropathy (zero out of 30 patients), idiopathic optic neuritis (zero out of 26 patients), and healthy age-matched controls (one out of 22 control subjects). This difference was especially helpful in patients whose sedimentation rates were within the normal range (adjusting for age). Also noted was the finding that the rise in the platelet counts was not acute, but rather it was a slow gradual increase for approximately 12 months before the onset of significant systemic or visual symptoms. CONCLUSION: Thrombocytosis should be considered an important marker in patients being referred for evaluation of ischemic optic neuropathy, diplopia, amaurosis fugax, headache, or even generalized malaise. Westegren sedimentation rates <50 mm/hr are often erroneously viewed as nondiagnostic or equivocal in the elderly and just followed. An over-the-phone review of patients' sedimentation rates, complete blood counts, and platelet counts can lead to expedited evaluation and treatment of patients who may be at high risk of visual loss from temporal arteritis. Thrombocytosis should lower a physician's threshold to acutely treat patients for possible arteritic ischemic optic neuropathy until the disease is definitely ruled out.

Aged↗
PubMed2000

Thrombocytosis--report of a case.

Thrombocytosis is a common clinical condition. Drugs used for thrombocytosis are hydroxy urea, alkylating agents and interferon alpha. We are reporting a case of chronic myeloid leukemia with thrombocytosis who did not respond to hydroxy urea but was controlled with the addition of a new drug anagrelide. Anagrelide is a platelet reducing agent with no serious side effects. It may be the main weapon against thrombocytosis associated with chronic myeloid leukaemia (CML) and essential thrombocytosis in the coming years.

Aged↗
PubMed2002

[Major thrombocytosis associated with severe anemia in children. Diagnosis of 9 cases].

Major thrombocytosis associated with severe anemia is uncommon in pediatrics. We report 9 consecutive cases observed in Albert Royer Children Hospital of Dakar. They were 7 boys and 2 girls 4 to 15 years old (mean age = 10 years). Six patients had a history of geophagia and 3 presented recent emission of worms by the stools. Anemia was clinically well tolerated in all cases. In initial blood count platelet levels varied from 800 10(3) to 1180 10(3)/mm3 (mean = 1032 10(3)/mm3), while hemoglobin level varied from 3.4 to 7.4 g/dl (mean = 4.9 g/dl). Anemia was microcytic, hypochromic and associated with low serum iron level in all patients. We considered the diagnosis of reactive thrombocytosis induced by iron deficient anemia in all cases. Platelet count and red cell indices were progressively normalised with iron treatment and no complication of thrombocytosis was observed. Considering published data, iron deficiency is one of the most frequent causes of reactive thrombocytosis in children. The physiopathologic mechanism, still unknown, could involve cytokines of thrombopoiesis. Reactive thrombocytosis induced by iron deficiency or other factors have usually a benign course and need no specific treatment other than that of the etiology.

Adolescent↗
PubMed1992

[An infantile case of cerebral infarction associated with thrombocytosis].

Cerebral infarction in children is often caused by intracranial vascular disorder, cardiac disease, head injury, or infection, and is rarely induced by blood disease. In this paper, we describe an infantile case of cerebral infarction associated with thrombocytosis. A female infant of eight months of age developed left hemiparesis after a slight head injury. Her CT and MRI demonstrated a cerebral infarction located from the right internal capsule to the right corona radiata. Laboratory findings revealed iron-deficiency anemia and thrombocytosis with a platelet count 107.5 x 10(4)/mm3. Although she had no disorder that had caused iron deficiency, serum Fe value of the patient was low with a count of 18 micrograms/dl. Her bone marrow was normal except for a slight increase in the number of megakaryocytes. One month later, her anemia was improved by means of oral iron replacement. However, her platelet count remained at more than 100 x 10(4)/mm3 as it had been before. Her condition of left-sided hemiparesis gradually improved by a program of rehabilitation, and did not recur after aspirin administration. Although the main cause of her thrombocytosis that led to a transient cerebrovascular accident is obscure, it is postulated that her iron deficiency anemia induced secondary thrombocytosis, or else the patient had essential thrombocytosis.

Anemia, Hypochromic↗