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PubMed1990

Thrombocytosis in malignant pleural mesothelioma.

The prevalence of thrombocytosis (defined as a platelet count above 400,000/mm3 in at least two examinations) and the prevalence of thromboembolism were retrospectively investigated in a series of 41 patients with malignant pleural mesothelioma and in 40 subjects with non small cell lung carcinoma. All the patients were examined at necropsy. The mesothelioma patients showed a higher prevalence of thrombocytosis (56.8% vs 24.2%; p less than 0.01). However, the prevalences of thromboembolism were similar in the two groups of patients (36.6% and 32.5% respectively). Among those with mesothelioma the prevalence of thrombocytosis varied widely from one histological type to another (76.9% in mixed type, 57.1% in the epithelial, and 30% in the sarcomatous type), the difference between mixed and sarcomatous being statistically significant (p less than 0.01). Moreover, the mesothelioma patients of under 70 years had thrombocytosis more often than those over 70 (80% vs 29.4%; p less than 0.01).

Aged↗
PubMed2002

Low-molecular-weight heparins and thrombocytosis.

BACKGROUND: A possible association between low-molecular-weight heparins (LMWHs) and thrombocytosis was suspected from spontaneous reports to the French Pharmacovigilance System. This association is not mentioned in LMWH's summary of product characteristics. METHODS: All case records in the French Pharmacovigilance database were reanalyzed for relevance and causality, and the case/noncase approach was used including reports of thrombocytosis as cases and all other reports as noncases. RESULTS: Fifty-one patients treated with LMWHs had platelet counts >500 x 10(3)/mm(3). All patients were asymptomatic, and 1 had a positive rechallenge. There were 143 cases of thrombocytosis among the 174 213 reports in the database, with 61 of 4644 involving LMWHs. The calculated relative reporting ratio is 27.5 (p < 0.0001; 95% CI 19.5 to 38.9). CONCLUSIONS: There is a highly significant association of thrombocytosis reported with LMWH treatment.

Adolescent↗
PubMed2006

Reactive thrombocytosis associated with enoxaparin.

A 42-year-old man was hospitalized for a closed head injury caused by a bicycle accident. On hospital day 8, he developed thrombocytosis. Eleven days later, his platelet count reached 1005 x 10(3)/mm(3). A review of his drug therapy indicated enoxaparin as a potential reversible cause of reactive thrombocytosis. Enoxaparin was discontinued, and the patient's platelet count declined, eventually normalizing 6 days later. At that time, enoxaparin was restarted; this resulted in an increase in his platelet count that peaked 8 days later at 920 x 10(3)/mm(3). After each occurrence of thrombocytosis, enoxaparin was switched to unfractionated heparin in combination with sequential compression devices for deep vein thrombosis prophylaxis. No complications secondary to thrombocytosis were noted. Our patient's experience suggests that unfractionated heparin may be substituted for enoxaparin if this adverse effect is suspected.

Accidents↗
PubMedDate not supplied

Mechanism of thrombocytosis in hepatoblastoma: a case report.

Although thrombocytosis has long been recognized as a common finding in children with hepatoblastoma, its mechanism is still unknown. In this study, to confirm the role of thrombopoietin (Tpo) in the thrombocytosis in hepatoblastoma, the expression of Tpo mRNA in tumor cells was examined and the serum Tpo level was analyzed during the course of the disease. A 1-year, 6-month-old girl was diagnosed as having advanced hepatoblastoma. At diagnosis, she had marked thrombocytosis with 1220 x 10(9)/microL. After resection of the tumor and after four courses of chemotherapy, the level of alpha-fetoprotein normalized but the platelet count remained high. However, after the fifth course of chemotherapy, the platelet count decreased and normalized within 3 months. By enzyme-linked immunosorbent assay, the serum Tpo level was not high at diagnosis, whereas high Tpo levels were observed after chemotherapy. By polymerase chain reaction, Tpo mRNA was detected in both normal liver and tumor tissues, but the level of expression was not different between them. Therefore, in hepatoblastoma the serum Tpo level is not correlated with a high platelet count, and there is no difference in Tpo expression between normal liver and tumor tissues. Other unknown factors and their production sites to induce thrombocytosis should be examined in further studies.

Female↗
PubMed1992

Incidence of thrombocytosis in lymphomas.

Reactive thrombocytosis due to malignancies and in particular those related to lymphomas have not yet been extensively evaluated. We report data on thrombocytosis recognized in 18 out of 101 patients with lymphomas diagnosed in our department over the last 3 years. All showed high platelet counts at the time of diagnosis. The incidence of thrombocytosis seems to be more frequent in males (21.2%) than in females (14.8%) and a slightly higher frequency was found in Hodgkin's disease (21.4%) than in non Hodgkin's lymphomas (16.4%). The incidence of thrombocytosis in lymphomas seems to be similar to that seen in other malignancies and because of this we conclude that a high platelet count cannot be used to distinguish malignancies.

Bone Marrow↗
PubMed1992

Serum interleukin-6 levels in patients with thrombocytosis.

Interleukin-6 (IL-6) has been shown to increase platelet counts in several animal models and to enhance megakaryocytopoiesis in vitro. In order to investigate the possible relationship between IL-6 and thrombocytosis, serum IL-6 levels in patients with platelet counts > or = 6 x 10(5)/microliters were measured using an IL-6-responsive bioassay. A cohort of healthy volunteers with normal platelet counts was used to establish a control mean serum IL-6 level [2.19 U/ml +/- 1.08 SD (range 0-5.5)]. Patients with primary thrombocytosis had a mean serum IL-6 level not significantly different from controls. In comparison, serum IL-6 levels of patients with reactive thrombocytosis were significantly greater than controls (38.3 U/ml +/- 94.6; range 0-933; P < 0.001). Although no significant correlation was observed between the degree of serum IL-6 elevation and the height of the platelet count in any individual, elevated serum IL-6 was highly correlated with reactive thrombocytosis.

Hematopoiesis↗
PubMed1999

Leucocytosis, thrombocytosis, and plasma osmolality during rest and exercise: an hypothesis.

The mechanism for inducing leucocytosis (increase in white blood cells) and thrombocytosis (increase in platelets) during exercise is unclear. Because plasma osmolality (Osm) may influence T-cell proliferation, Osm and the number of leucocytes (WBC) and platelets in blood were measured periodically during a 90 min rest period, and were compared with those during upright sitting ergometer exercise in six untrained, healthy men who cycled for 70 min at 71% of their maximal oxygen uptake (VO2max). There were 6 experiments in which the subjects drank different fluid formulations (10 ml x kg(-1) of various ionic and osmotic concentrations intermittently during 60 min of the rest period and during the exercise period. Osmolality, and WBC and platelet counts increased significantly (p < 0.05) within the first 10 min of exercise, but the additional 60 min of exercise did not significantly change the leucocytosis or thrombocytosis. There were low but significant correlations between individual values of total WBC and total Osm during exercise (r0.001(2),284 = 0.39) and during rest plus exercise (r0.001(2),499 = 0.43). With combined data from the six experiments, mean Osm correlated highly and significantly with both mean WBC (r0.001(2),6 = 0.95, p < 0.001) and mean platelets (r0.001(2),6 = 0.94, p < 0.01) during the exercise phase. These data indicate that increases in leucocytes, thrombocytes, and osmolality occur primarily within the first 10 min of high-intensity exercise, but neither hypovolemia nor hyperthermia during exercise contributed to the leucocytosis, thrombocytosis, or hyperosmolality. The high correlations between plasma Osm and WBC or platelet counts suggest changes in osmolality may contribute to the mechanism of leucocytosis and thrombocytosis induced by exercise.

Adult↗
PubMed2000

Thrombocytosis as a predictor of malignancy in women with a pelvic mass.

OBJECTIVE: To determine if thrombocytosis (platelets > 350,000/microL) is a predictor of malignancy in women with a pelvic mass. STUDY DESIGN: The charts of 323 patients who presented with a pelvic mass and subsequently underwent an exploratory laparotomy were reviewed for preoperative platelet count and final diagnosis. Thrombocytosis was defined as a platelet count > 350,000/microL. The data were analyzed utilizing the SPSS 6.1 software package (Chicago, Illinois); analysis of variance and chi 2 tests were used for data comparison. RESULTS: The difference in the platelet counts of patients with malignancy and benign tumors was statistically significant (P < .00001). Eighty-seven patients had cancer; of these, 42 (48.3%) had thrombocytosis. Only 31 (13.8%) patients with benign tumors had thrombocytosis. CONCLUSION: High preoperative platelet counts in women presenting with a pelvic mass may predict a final diagnosis of cancer.

Analysis of Variance↗
PubMed1976

Thrombocytosis in patients with celiac sprue.

In 57% of the patients (12 of 25) seen with celiac sprue, as shown by clinical course and small bowel biopsy, peripheral blood thrombocytosis was present (range: 350,000 to 815,000 platelets per mm(3); mean: 546,000 +/- 44,060 SE). After clinical and histological remission, the platelet counts in these patients fell significantly (range: 188,000 to 300,0000 platelets per mm(3); mean 252,750 +/- 13,211 SE). There was no correlation between thrombocytosis and serum iron, folate, or vitamin B12 levels. Celiac sprue joins inflammatory bowel disease among gastrointestinal disorders as a consideration in the differential diagnosis of thrombocytosis. In these patients, thrombocytosis reflected active disease and was not present during remission. Evaluation of peripheral blood platelets may be useful in the assessment of patients with celiac sprue.

Adult↗
PubMed1992

Evidence that stem cell factor is involved in the rebound thrombocytosis that follows 5-fluorouracil treatment.

The mechanisms responsible for 5-fluorouracil (5FU)-induced rebound thrombocytosis are not completely understood. SI/SI(d) mice, which do not undergo rebound thrombocytosis in response to 5FU, provide a genetic approach to the study of this phenomenon. Recent reports by several groups that the SI locus encodes a protein known variably as stem cell factor (SCF), mast cell growth factor, or kit ligand, suggests the possibility that the lack of wild-type SCF in SI/SI(d) mice is responsible for their defective response to 5FU-induced thrombocytopenia. It is shown in this report that SCF-treated SI/SI(d) mice are as capable as their wild-type littermates in undergoing rebound thrombocytosis. W/Wv mice, mutated at the locus encoding the SCF receptor, also do not undergo rebound thrombocytosis, but are not responsive to SCF treatment. In normal mice, it is shown by RNA solution hybridization that SCF mRNA expression is increased during the 5FU-induced platelet nadir period. It is also shown by autoradiography that maturing megakaryocytes express SCF receptors, and that in vivo administration of SCF significantly raises the numbers of megakaryocytes, as well as circulating platelet counts. Taken together, these data indicate that SCF may be an important regulator of platelet production under both normal and physiologically disturbed situations.

Animals↗
PubMed1992

Thrombocytosis in patients with tumors producing colony-stimulating factor.

We investigated the cause of thrombocytosis in 14 patients with tumors producing colony-stimulating factor (CSF). Of the 14 patients, 10 had tumors producing granulocyte-CSF (G-CSF) and 4 had tumors producing granulocyte-macrophage--CSF (GM-CSF). Thrombocytosis of greater than 400 x 10(9)/L was noted in 8 of 10 patients with G-CSF-producing tumors and all 4 patients with GM-CSF-producing tumors. Median peak platelet counts were, respectively, 511 x 10(9)/L (range, 384 to 694 x 10(9)/L) and 579 x 10(9)/L (range, 526 to 910 x 10(9)/L) in patients with tumors producing G-CSF and GM-CSF. In most patients, thrombocytosis declined towards the terminal stage. High interleukin-1 (IL-1) and IL-6 levels were found in addition to CSFs in the plasma or culture supernatants of tumor cells obtained from most patients. In patients with GM-CSF-producing tumors, these specimens had megakaryocyte-CSF (Meg-CSF) activity, which was abolished by anti-GM-CSF antibody. These specimens also had megakaryocyte potentiating (Meg-Pot) activity attributable to both GM-CSF and IL-6. In patients with G-CSF-producing tumors, only Meg-Pot activity due to IL-6 was detected. These results indicate that the thrombocytosis in GM-CSF-producing tumors was caused by both the Meg-CSF activity of GM-CSF and the Meg-Pot activity of IL-6 plus GM-CSF, while that in G-CSF-producing tumors was due to the Meg-Pot activity of IL-6.

Adult↗
PubMed1991

Bone marrow and peripheral blood findings in patients with extreme thrombocytosis. A report of 63 cases.

Sixty-three bone marrow (BM) and peripheral blood specimens from patients with platelet counts of 1000 x 10(9)/L or greater were examined in an attempt to determine if any BM or peripheral blood findings could be used reliably to distinguish primary thrombocythemia from other myeloproliferative disorders and extreme examples of reactive thrombocytosis. Our results indicated that the BM findings in primary thrombocythemia were quite similar to those in polycythemia vera and chronic granulocytic leukemia with associated extreme thrombocytosis. However, statistically significant differences between the BM findings in myeloproliferative disorders and extreme reactive thrombocytosis were found in the numbers of megakaryocytes, presence or absence of megakaryocyte clusters, stainable iron, cellularity, and reticulin content. We concluded that BM examination is a useful procedure as an aid in determining the cause of extreme thrombocytosis.

Bone Marrow↗
PubMedDate not supplied

[Thrombocytosis and primary bronchial carcinoma. Study about 164 patients with bronchial carcinoma (author's transl)].

This paper is relating the study of 164 patients with primary and proved bronchial carcinoma. A thrombocytosis superior to 400,000/mm3 was observed in 36.6 p. cent of cases. But no statistic relation was found between the histological type of tumor, a biological inflammatory state, the existence of metastasis and thrombocytosis. However thrombocytosis was more frequently observed among anaemic and hyposideremic patients. No significantly changes of paO2 and paCO2 were noted in patients with thrombocytosis. The systematic platelet count could be of an interest in the interpretation of some thoracic radiography.

Anemia↗
PubMed1988

Low incidence of familial occurrence of thrombocythaemia and/or thrombocytosis.

Several reports have been published about familial polycythaemia vera (PV) but no information is available about the incidence of thrombocytosis in the same family. In our population of thrombocytosic patients, both with primary thrombocytosis (133 cases) and secondary (37 cases), we found only two family related subjects. One of them had PV and the other essential thrombocytosis (ET). Our results seem to indicate that familial thrombocytosis is a rare phenomenon, much less frequent then familial thrombocytopenia.

Adolescent↗
PubMed1989

Thrombocytosis in childhood: a survey of 94 patients.

The introduction of the newer generation of electronic cell counters allows the routine reporting of platelet numbers when the peripheral blood count is requested. In a 12-month period, 100 episodes of marked thrombocytosis (platelet count more than 900 X 10(9)/L) were found among 94 children. These patients were young (median age 9 months). All but one episode of marked thrombocytosis occurred as a phenomenon secondary to a variety of disease states. Infections, especially those involving the central nervous systems were the commonest cause of an elevated platelet count in this series. Malignant diseases alone were rarely associated with thrombocytosis of this magnitude. The elevated platelet count began to decline at a mean of 3 days after diagnosis, and no thrombotic or hemorrhagic complications were encountered. Marked thrombocytosis is a benign, common phenomenon in young children, but specific treatment is not required.

Adolescent↗
PubMedDate not supplied

[Thrombocytosis in progressive generalized sclerosis (scleroderma) and in other rheumatic diseases].

A platelet count was made in 37 patients with Progressive Systemic Sclerosis (PSS), 6 with Sjögren's Syndrome, 11 with Rheumatic Polymyalgia with or without Horton's Arteritis (PMR-AH), 26 with Ankylosing Spondylitis (A.Sp.), 29 with Psoriatic Arthritis, 15 with Gout and in 65 healthy subjects. In this last group the mean platelet count was 215.692/mm3, S.E. 4.167. In the various groups of patients the following mean platelet counts were determined: PSS 242.108 +/- 11.766; Sjögren 245.000 +/- 22.620; PMR-AH 276.818 +/- 25.577; A.Sp. 272.846 +/- 14.124; Psoriatic Arthritis 245.833 +/- 9.374; Gout 265.333 +/- 24.628. Statistical analysis showed a significant difference (P less than 0.05), (P less than 0.01) or (P less than 0.001) between each group of patients and the controls. However, the platelet count in the majority of patients in each group was not higher than 300.000/mm3. Statistically significant correlations were found between platelet count and some biolgoical inflammation parameters. All patients with platelets higher than 300.000/mm3 showed a high disease activity. Yet some patients with marked inflammation did not present thrombocytosis. According to literature data thrombocytosis in Rheumatoid Arthritis is considered to be correlated to disease activity. The results of this study indicate that even in other rheumatic diseases thrombocytosis is often present, apparently correlated to the inflammation. Therefore thrombocytosis is an inflammation parameter; but it is less sensitive than other ones.

Adult↗
PubMed1977

The role of platelets in the pathogenesis of thrombosis and hemorrhage in patients with thrombocytosis.

Some patients with thrombocytosis due to myeloproliferative diseases or other etiologies experience thromboembolic complications and others may bleed excessively. It seems unlikely that elevations in platelet count per se are a direct cause either of thrombosis or of hemorrhage. In an effort to ascertain whether variations in platelet function might determine whether an individual patient experiences thrombotic or hemorrhagic complications we have evaluated platelet function in 22 patients with thrombocytosis due to a variety of etiologies. The results of platelet counts, bleeding time determinations, and studies of platelet aggregation were similar in patients with thrombosis, in patients with bleeding and in patients with neither complication. Therefore, detailed studies of platelet coagulant activities were carried out in 8 patients. The results of platelet coagulant activity assays were normal in all 3 patients with thrombocytosis and neither thrombotic nor bleeding complications and an additional 3 patients with myeloproliferative diseases, normal platelet counts and no thrombohemorrhagic complications. In 2 patients with thrombotic complications significant elevation of platelet coagulant activities concerned with the early phases of intrinsic coagulation were observed whereas in 2 patients with severe hemorrhagic complications deficiencies of either contact forming activity or collagen-induced coagulant activities were evident. This preliminary study suggests the possibility that variations in platelet coagulant activities concerned with the early stages of intrinsic coagulation may determine whether patients with thrombocytosis will experience bleeding or thrombotic complications.

Blood Platelets↗
PubMed1994

Vascular disease outcome and thrombocytosis in diabetic and nondiabetic end-stage renal disease patients on peritoneal dialysis.

STUDY OBJECTIVE: to evaluate vascular disease and its outcome in association with thrombocytosis in chronic peritoneal dialysis (PD) patients. DESIGN: the study was designed to investigate possible correlations between severity of vascular disease and thrombocytosis in PD patients. SETTING: tertiary-referral university hospital. PATIENTS AND METHODS: serial blood platelet levels were measured in 53 stable PD patients (32 male, 21 female; mean age 55 years; mean duration of PD 19 months) between January 1991 and July 1992. Twenty-four patients were diabetic and 29 were nondiabetic. Mean duration of PD was 23 and 36 months in diabetic and nondiabetic patients, respectively. Severity of coronary arterial disease (CAD), carotid arterial disease (CNS), and peripheral arterial disease (PAD) was assessed using the Craven et al. (1991) ESRD Severity Index, a measure of organ dysfunction. Functional status was assessed using the Karnofsky Performance Status Index (KPSI). RESULTS: eighteen out of 53 PD patients (34%) had platelet counts exceeding 300,000/mm3 for six months or longer. Thirteen of 24 diabetic PD patients (54%) had thrombocytosis. Blood platelets were significantly (p < 0.01) higher in diabetic (324,000 +/- 27,000/mm3) than in nondiabetic PD (236,000 +/- 11,000/mm3) patients. In the PD group as a whole, a positive correlation was observed between blood platelet and serum cholesterol (r = 0.5, p < 0.001), blood platelet and PAD (r = 0.5, p < 0.001), and blood platelet and CAD (r = 0.35, p < 0.05). No correlation was found with age or duration of PD. In diabetic PD patients, blood platelet counts correlated significantly with PAD (r = +0.5, p < 0.01) and CAD (r = +0.4, p < 0.05) indexes. No correlation was observed between blood platelet and CNS or KPS indexes. In nondiabetics, no correlation was observed between blood platelet and CAD, PAD, CNS, or KPS indexes. CAD, PAD, and KPS indexes were significantly higher in diabetics compared to nondiabetics. CONCLUSIONS: thrombocytosis, particularly in diabetic PD patients, appears to be associated with the severity of PAD and CAD.

Cholesterol↗