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PubMed1979

Thrombocytosis and increased circulating platelet aggregates in newborn infants of polydrug users.

Thirty-three prospectively studied neonates born to mothers using methadone plus other drugs developed significant thrombocytosis by the second week of life compared to platelet counts performed during the first week. This increase persisted for over 16 weeks, with a further short-lived significant peak at 10 weeks of age. Platelet counts exceeding 1,000,000/mm3 were found in seven infants. Thrombocytosis was not related to withdrawal symptoms or treatment (phenobarbital or paregoric). No thrombocytosis was found in 36 normal control infants up to eight weeks of life. Twenty-eight of the study group infants were evaluated for circulating platelet aggregates. Thirteen patients had a normal aggregate index and a mean platelet count of 468,000/mm3; 15 patients had increased aggregates and mean platelet count of 754,000/mm3. The risk for increased circulating platelet aggregates correlated directly with an increase in platelet count. Thrombocytosis and increased circulating platelet aggregates may be factors in the pathogenesis of the focal infarcts, and subarachnoid and germinal plate hemorrhages, described at autopsy in infants of addicted mothers.

Amphetamine↗
PubMed2001

Clonality analysis using X-chromosome inactivation patterns by HUMARA-PCR assay in female controls and patients with idiopathic thrombocytosis in Taiwan.

OBJECTIVE: Analysis of X-chromosome inactivation patterns (XCIPs) is a useful tool in the diagnosis of clonal disorders. The human androgen receptor (HUMARA) locus is especially useful for clonality study. The present study was conducted 1) to determine the heterozygosity rate for HUMARA locus in Taiwanese women, 2) to determine the frequency of excessive skewing in different cell types, and 3) to determine the utility of XCIPs in the differential diagnosis of thrombocytosis. PATIENTS AND METHODS: XCIPs by HUMARA-PCR assay were performed on purified granulocytes and T cells from 73 female patients presenting with idiopathic persistent thrombocytosis (IT), 10 patients with reactive thrombocytosis (RT), and 46 bone marrow samples from female controls. XCIPs of buccal mucosa cells were also compared with those of T cells in 57 patients with IT. The percentage of clonal granulocytes was calculated after correcting for the degree of Lyonization in T cells. RESULTS: The heterozygosity rate for the HUMARA gene was 89.1% in Taiwanese females. The median age of informative IT patients and controls was 59 (18-92) and 58 (19-89), respectively. Excessive skewing (allele ratio <0.33) was more frequent in granulocytes than in T cells in both controls (12/43 vs 9/43, p = 0.080) and IT patients (56/64 vs 25/64, p < 0.001). XCIPs were the same for both buccal mucosa and T cells in 43 patients but were different in 14 patients. Of the 43 informative controls, 31 had a polyclonal pattern; an ambiguous pattern was found in nine; and the remaining three, aged 71, 73, and 80, respectively, had a clonal pattern. A clonal pattern was found in 42 IT patients, a polyclonal pattern in 12, and an ambiguous pattern in 10 of the 64 IT patients. The frequency of clonal, polyclonal, and ambiguous patterns in the 40 IT patients with age < or = 65 was 55.0%, 30.0%, and 15.0%, respectively. None of the IT patients aged >65 had a polyclonal disease. IT patients aged >65 had a significantly higher frequency of clonal pattern (p = 0.030) and a significantly lower frequency of polyclonal pattern (p = 0.002) than those with age <65. Of the eight heterozygous patients with RT, one aged 80 exhibited a clonal pattern, and the remaining seven had a polyclonal pattern. CONCLUSIONS: The present study on Taiwanese females showed a heterozygosity rate of 89.1% for the HUMARA gene. Our results confirmed that IT is a heterogeneous disorder in terms of clonality. Twenty-three percent of IT patients exhibited a greater than 20% difference in allele expression for buccal mucosa and T cells. Presence of a clonal XCIP in young patients with IT can serve as a positive marker for the diagnosis of clonal thrombocytosis, and elderly patients with polyclonal XCIPs are unlikely to have essential thrombocythemia.

Adolescent↗
PubMed1999

Preoperative lipid-control with simvastatin reduces the risk of postoperative thrombocytosis and thrombotic complications following CABG.

OBJECTIVE: It has earlier been suggested that postoperative thrombocytosis frequently occur after coronary artery bypass grafting (CABG) and may be linked to lipid disturbances. A prospective randomized study was undertaken to evaluate if preoperative lipid-control, using HMG-CoA-reductase inhibitor (Zocor), simvastatin, reduces the risk of postoperative thrombocytosis. METHODS: Seventy-seven patients with symptomatic coronary artery disease and hypercholesterolemia (total cholesterol > or =6.2 mmol/l), planned for CABG where randomly assigned to; undergo CABG without preoperation lipid control (group I, n = 37) or undergo simvastatin-treatment (20 mg daily) to control their lipids (4 weeks) prior to CABG (group II, n = 40). RESULTS: Patient characteristics and operation data did not differ between the groups. Serum-cholesterol, cholesterol/HDL-cholesterol, LDL-cholesterol, Apolipoprotein A1 and Plasminogen were all significantly higher in group I patients compared with group II just prior to surgery. Other laboratory parameters did not differ. RESULTS: In group II, total cholesterol and cholesterol/HDL-cholesterol quota were significantly lowered by simvaststin (-2 and -29%, respectively). Postoperative thrombocytosis (platelet counts > or =400000/microl) occurred significantly more frequently in group I 81% (30/37) compared with 3% (1/40) in group II, P<0.0001. Myocardial infarction after the 7th postoperative day was more often diagnosed in group I, 14 vs. 0% in group II. Postoperative transient renal failure occurred also more frequently in group I, 24% compared with 8% in group II. Other postoperative complications and laboratory data did not differ. CONCLUSIONS: This study once again underlines the importance of lipid control using HMG-CoA-reductase inhibitors (e.g. Zocor) in patients with established coronary artery disease. For the first time it is shown that lipid-control with simvastatin prior to CABG reduces the risk of postoperative thrombocytosis, thus lowers the risk for thrombotic complications.

Aged↗
PubMed2005

Patterns of thrombocytosis and thrombocytopenia in hospitalized neonates.

OBJECTIVE: We sought to identify changes in platelet (PLT) counts over time, and to evaluate the patterns of thrombocytopenia and thrombocytosis in hospitalized infants 23.8 weeks to term gestation. STUDY DESIGN: Neonates were divided into four gestational age groups and their PLT counts were retrospectively compared for prevalence of thrombocytopenia, thrombocytosis, and associated conditions. RESULTS: Postconceptional age, postnatal age, and sepsis (among other factors) affected PLT counts. When counts from noninfected appropriately grown infants were evaluated, the risk of thrombocytopenia and thrombocytosis were highest in the most preterm infants, and these risks changed with corrected gestational age. PLT counts increased weekly over the first 4 weeks of life for all but the most preterm infants. CONCLUSIONS: These data characterize the incidence of thrombocytopenia and thrombocytosis across a wide range of gestational ages and show that, even in noninfected neonates, these conditions are common, and risk decreases with increasing maturity. The age-related changes in PLT patterns may reflect maturation of platelet regulation.

Hospitalization↗
PubMed2001

Thrombocytosis and thrombocythemia.

Thrombocytosis is caused by three major pathophysiological mechanisms: (1) reactive or secondary thrombocytosis; (2) familial thrombocytosis; and (3) clonal thrombocytosis, including essential thrombocythemia and related myeloproliferative disorders. Recent work has begun to elucidate the abnormal megakaryocytopoiesis of essential thrombocythemia, which is associated with paradoxically elevated plasma levels of thrombopoietin. The clonal nature of all cases of essential thrombocythemia has been challenged. Thrombotic complications are the major causes of morbidity and mortality in this disease. Indications for platelet cytoreduction and antiplatelet therapy, as well as complications of treatment, are being clarified.

Clone Cells↗
PubMed1996

[Thrombocytosis in polymyalgia rheumatica].

BASIC PROBLEM AND OBJECTIVE OF STUDY: The diagnosis of polymyalgia rheumatica is made difficult by the absence of any pathognomonic findings. Erythrocyte sedimentation rate (ESR) and concentration of C-reactive protein are used as diagnostic criteria and to monitor the disease's course. It was the purpose of this study to evaluate prevalence of thrombocytosis and whether there is any correlation between thrombocytosis and ischaemic complications. PATIENTS AND METHODS: In a retrospective study the data of 23 patients (14 women, 9 men; mean age 67.3 [48-84] years) with polymyalgia rheumatica were analysed: platelet counts, ESR and C-reactive protein had been measured at the time of diagnosis and 7, 14 and 21 days after start of glucocorticoid treatment. At the time of diagnosis 17 of 23 patients (74%) had a thrombocytosis (> 400,000/microliter), at a mean value of 511,000 (418,000-638,000)/microliter. The platelet count decreased more slowly than the inflammatory parameters. On average the platelet count returned to normal on the 14th day. Ischaemic complications developed in three patients (visual disturbances, blindness, cardiac arrhythmias, neurological deficits): all had a high platelet count (462,000-524,000/microliter). CONCLUSIONS: Thrombocytosis can serve as an additional criterion in the diagnosis and follow-up of polymyalgia rheumatica. An association with ischaemic complications is especially likely in the elderly, in case of immobility and if there is evidence of giant-cell arteritis. Treatment with platelet aggregation inhibitors should be considered.

Aged↗
PubMed1988

Anagrelide: a new drug for treating thrombocytosis.

Anagrelide is a member of the imidazo (2,1-b) quinazolin-2-one series of compounds, with a powerful antiaggregating effect on platelets. During studies in humans, anagrelide in small doses has produced thrombocytopenia. We therefore evaluated it in the treatment of thrombocytosis, and to date, platelet levels in 15 of 17 patients with primary thrombocythemia, 2 patients with polycythemia vera and thrombocytosis, and 1 patient with chronic granulocytic leukemia and thrombocytosis have been well controlled with the use of this agent. Induction doses of 1.0 to 1.5 mg given orally every six hours have produced a decrease in the platelet count, starting on day 5 and reaching a normal level by day 12. Side effects of anagrelide have been minimal. Maintenance therapy with 1.5 to 4.0 mg a day has continued to control the platelet count in patients for up to 28 months. This new agent appears promising in the treatment of thrombocytosis in patients with chronic myeloproliferative disease.

Adult↗
PubMed2006

Reticulated platelets are increased in chronic myeloproliferative disorders, pure erythrocytosis, reactive thrombocytosis and prior to hematopoietic reconstitution after intensive chemotherapy.

Reticulated platelets with a high RNA content represent the most recently released platelets and are regarded to reflect thrombopoiesis. In the present study we used flow cytometric analysis to determine the percentage of reticulated platelets in peripheral blood for patients with chronic myeloproliferative disorders (polycythemia vera, essential thrombocytosis) and acute myelogenous leukemia (AML) patients with severe chemotherapy-induced thrombocytopenia. Patients with essential thrombocytosis and polycythemia vera showed increased levels of reticulated platelets compared with healthy controls, and these levels persisted after normalization of the platelet count by hydroxyurea or interferon-alpha treatment. Patients with reactive thrombocytosis or thrombocytopenia with increased platelet turnover often had higher levels of circulating reticulated platelets than patients with myeloproliferative disorders. Furthermore, AML patients with severe chemotherapy-induced cytopenia showed low levels that started to increase 1-9 days prior to hematopoietic reconstitution. To summarize and conclude: (i) circulating reticulated platelets are increased in patients with chronic myeloproliferative disorders, reactive thrombocytosis and thrombocytopenia due to increased platelet turnover; (ii) patients with pure erythrocytosis often have additional abnormalities in the thrombopoiesis; and (iii) the levels of reticulated platelets seem to predict hematopoietic reconstitution for patients receiving intensive AML therapy.

Adult↗
PubMed2003

Bone marrow and peripheral blood C-kit ligand concentrations in patients with thrombocytosis and thrombocytopenia.

C-kit ligand (stem cell factor, SCF) is a hematopoietic growth factor with diverse effects. It has stimulatory effects on megakaryocytopoiesis acting in synergism with interleukin-3 (IL-3), thrombopoietin (TPO) and granulocyte-macrophage colony stimulating factor (GM-CSF). The relationship between SCF and megakaryocytopoiesis, especially the correlations between blood and bone marrow SCF levels have been not clearly established in the literature. We therefore, investigated peripheral and bone marrow SCF levels in patients with thrombocytosis and thrombocytopenia. Subjects were divided into three groups: those with (i) thrombocytopenia, (ii) thrombocytosis and (iii) healthy adults as controls. When the three groups were compared, the mean peripheral blood SCF level of the thrombocytosis group (2149±197) was significantly higher than the thrombocytopenia (1586±178) and normal control groups (1371±68; p<0.05) and the bone marrow SCF level was higher (2694±267) than the thrombocytopenia group (1700±182; p<0.05). In the correlation analysis, considering all the groups together the bone marrow and peripheral blood SCF concentrations were positively and significantly correlated (p<0.01; r=0.93). Correlations between platelet number and both bone marrow SCF concentration (p<0.01; r=0.51) and peripheral blood concentrations (p<0.01; r=0.40) were also shown. Our results indicate that SCF is operative in the pathological megakaryopoiesis of clonal origin and reactive thrombocytosis both in the local bone marrow microenvironment and the peripheral circulating blood. We feel that further studies on the platelet-SCF relationship and SCF levels in different disease states are required.

Adult↗
PubMed1981

The diagnostic value of the serum lactic dehydrogenase determination in the evaluation of unexplained thrombocytosis.

Thrombocytosis may reflect a primary myeloproliferative disorder or be a secondary reaction to other pathologic processes. Patients with persistent unexplained thrombocytosis meeting criteria of primary thrombocythemia had elevated levels of serum lactic dehydrogenase, whereas comparable patients with secondary thrombocytosis did not. The findings of an elevated serum lactic dehydrogenase supports the diagnosis of a myeloproliferative syndrome in patients who have unexplained thrombocytosis, and should be useful in the differential diagnosis of this hematologic abnormality.

Adult↗
PubMed2003

Levels of serum cytokines and acute phase proteins in patients with essential and cancer-related thrombocytosis.

Essential thrombocytosis (ET) is a myeloproliferative disorder resulting in an increased production of abnormal platelets. Reactive thrombocytosis (RT) is occasionally observed in clinical situations including chronic inflammation and malignancy. The aim of the present study was to evaluate the discriminatory efficiency of various laboratory tests in patients with ET and cancer-related RT. Forty-five patients with ET, 52 patients with RT, and 25 age-matched normal individuals comprised the study population. Plasma interleukin-1 alpha (IL-1a), IL-2, IL-6, tumor necrosis factor alpha (TNF-a), platelets, hematocrit, hemoglobin, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), lactate dehydrogenase (LDH) and ferritin were determined. We found increased levels of ferritin, LDH, CRP, ESR, IL-1a, and IL-6 in RT compared with ET (p < 0.01 to p < 0.0005). Hemoglobin, hematocrit, and platelets were significantly lower in RT than in ET (p < 0.0005). Furthermore, ferritin and ESR were negatively correlated with Hct, hemoglobin, and TNF-a, whereas ferritin was positively correlated with ESR, IL-1a, IL-6, and CRP, and IL-1a was positively correlated with IL-6. We consider that the aforementioned parameters should be included in the investigation of unexplained thrombocytosis for the differentiation of essential from cancer related thrombocytosis.

Acute-Phase Proteins↗
PubMed1998

Humorally mediated thrombocytosis in major lower extremity trauma.

Thrombocytosis in patients undergoing free tissue transfer for coverage of posttraumatic lower extremity defects may be associated with an increased incidence of microvascular thrombosis. Patients with isolated lower extremity trauma have an elevated platelet count that peaks approximately 2 weeks after injury. It is our theory that a humoral component of trauma sera is responsible for the induction of this thrombocytosis. Eight patients with isolated soft-tissue and bony trauma were included in the study. Serum was collected at baseline and throughout the study period. Platelet count, leukocyte count, hemoglobin concentration, and hematocrit were determined. Immunoassay for human interleukin-3 (IL-3), IL-6, and IL-11 as well as granulocyte macrophage colony stimulating factor (GM-CSF) were performed by solid-phase enzyme-linked immunosorbent assay. Balb-C mice were then injected intraperitoneally with the human trauma sera from all time points. Blood was collected at baseline and throughout the study period for determination of platelet count, hemoglobin, and hematocrit. Mean initial platelet count in the 8 human subjects was 152,000 per cubic millimeter with an average peak to 642,000 per cubic millimeter. IL-3, IL-11, and GM-CSF were not detectable in the serum of any patient. Elevated levels of IL-6 were detected in all patients in a nonspecific pattern. In the murine model, an early and late thrombocytosis was elicited. The early peak averaged 78.6% over baseline whereas the late peak average 81.0% over baseline. The induction by human trauma sera of an early and late thrombocytosis in this mouse bioassay supports the theory of humoral mediators. The humoral mediators are yet to be determined but may include IL-6.

Adult↗
PubMed2004

Thrombocytosis in an infant with high thrombopoietin concentrations.

Patients with essential thrombocythemia (ET) usually have normal thrombopoietin (TPO) concentrations because of negative feedback from thrombocytosis. TPO mutations in familial ET cases result in increased translation efficiency with excessive TPO stimulation and thrombocytosis. The authors describe an infant with a high platelet count (1300 x 103/mm3) and an elevated TPO concentration who was successfully treated with anagrelide. Sequencing of TPO revealed no genetic cause. This case may represent a case of atypical ET in which thrombocytosis results from TPO stimulation rather than clonal proliferation. Measuring TPO concentrations may be warranted for children with unexplained extreme thrombocytosis.

Blood Platelets↗
PubMed1993

High IL-6 levels in ascitic fluid correlate with reactive thrombocytosis in patients with epithelial ovarian cancer.

Non-haematopoietic malignancies are commonly associated with thrombocytosis. The aetiology of tumour-associated thrombocytosis is still unclear but may be related to tumour-derived thrombopoietin-like factors. Epithelial ovarian tumour cells have been shown to release IL-6 in vitro and high IL-6 levels have been identified in ascites of patients with ovarian cancer. Since IL-6 is a potent stimulator of megakaryocytopoiesis we examined IL-6 production at the tumour site and its relationship to serum IL-6 levels and circulating platelet counts in patients with ovarian cancer. Forty patients undergoing exploratory laparotomy for epithelial ovarian cancer [stage I+II: 6 (15%); stage III: 25 (62.5%); stage IV: 9 (22.5%)] and 24 women with benign ovarian conditions were evaluated. Sera were available from 39 cases with ovarian cancer and from 19 cases with benign ovarian tumours. Ascites was obtained from 35 patients with ovarian cancer. IL-6 activity in serum and ascitic fluid was determined by the standard B9 proliferation assay (detection level: 1 pg/ml). IL-6 bioactivity was detectable in 22 (56%) sera from patients with ovarian cancer, but in only five (26%) of the serum samples obtained from benign cases (P < 0.001). Serum IL-6 levels in patients with ovarian cancer were significantly higher (median 3 pg/ml; range < 1 to 1221 pg/ml) than in patients with benign ovarian conditions (median 0 pg/ml; range < 1 to 4 pg/ml) (P < 0.001). However, much higher concentrations of IL-6 were measured in malignant ascites specimens (median 22,100 pg/ml; range < 1 to 182,600 pg/ml). IL-6 bioactivity in serum and ascites samples was completely inhibited by a neutralizing goat anti-human IL-6 antiserum. Thrombocytosis (platelet counts > 400 x 10(9)/l) occurred in 25 (62.5%) of the 40 patients with ovarian cancer, but in only two (8%) of the 24 cases with benign ovarian tumours. In eight (20%) cases with malignant disease platelet counts ranged between 600 x 10(9)/l and 1060 x 10(9)/l. IL-6 bioactivity in ascitic fluid correlated significantly with circulating platelet counts (r = 0.5916; P < 0.001). Maximum IL-6 bioactivity in ascites and highest platelet counts occurred in patients with undifferentiated ovarian adenocarcinoma or advanced disease. In conclusion, these observations strongly suggest a role for IL-6 in the development of tumour-associated thrombocytosis.

Adult↗
PubMed1996

Flow cytometric analysis of megakaryocyte ploidy in chronic myeloproliferative disorders and reactive thrombocytosis.

Megakaryocyte (MK) ploidy patterns were analysed by flow cytometry in 29 newly diagnosed and previously untreated patients with chronic myeloproliferative disorders (MPD) and concomitant thrombocytosis, in 9 patients with reactive thrombocytosis (RT) and in 12 healthy individuals. Unfractionated bone marrow from routine aspirates was used. MKs were identified with a fluorescein labelled monoclonal antibody specific for glycoprotein IIIa (GPIIIa) and DNA was stained with propidium iodide. For the 12 healthy volunteers the mean modal ploidy number was 16 N; the 9 patients with RT displayed an identical MK ploidy pattern. The frequency of MKs with a ploidy > or = 32 N was 45% among the patients with essential thrombocythaemia (ET) compared to 32% among the healthy volunteers (p < 0.001). MKs with ploidy number > or = 64 N, comprising approximately 13% of the total number of MKs, was a characteristic finding in the patients with ET. Similar findings were present in 8 patients with polycythaemia vera (PV). In patients with PV 34% and 6% of the MKs displayed ploidies > or = 32 N and > or = 64 N, respectively. In contrast, a distinct shift towards lower ploidy number, with 63% of MKs < or = 8 N, was found among the 4 patients with chronic myeloid leukaemia (CML). The present results indicate that by using flow cytometric analysis of MK ploidy distribution in patients with thrombocytosis, those with a reactive cause are likely to be discriminated from patients with myeloproliferative thrombocytosis, i.e. PV and ET on one hand and CML on the other hand. The distinction between ET and PV, however, has to be made on other grounds.

Adult↗
PubMed1976

Thrombocytosis in rheumatoid arthritis.

Of 75 patients with rheumatoid arthritis, 39 had a thrombocytosis and 36 normal platelet count. A highly significant relationship existed between the platelet count and disease severity and an inverse correlation with level of haemoglobin. An association appeared to exist between thrombocytosis and extra-articular manifestations of rheumatoid disease. By 75Selenomethionine labelling platelet and fibrinogen survival and turnover were determined. In 3 rheumatoid patients with thrombocytosis platelet survival was decreased and turnover increased. In these and a further rheumatoid patient with a normal platelet count there was reduced fibrinogen survival and increased fibrinogen turnover, and in addition excess fibrin degradation products were detected. The results suggest that thrombocytosis accompanies the more severe cases of rheumatoid disease and is due to a compensatory increase in platelet production associated with active intravascular coagulation.

Arthritis, Rheumatoid↗
PubMed2005

Potential role of interleukin 6 in reactive thrombocytosis and acute phase response in pulmonary tuberculosis.

OBJECTIVE: Reactive thrombocytosis is found in a number of clinical situations including infectious diseases such as pulmonary tuberculosis (PTB). To examine the possible role of interleukin (IL6) in reactive thrombocytosis and acute phase response in PTB this study measured serum IL6, C reactive protein (CRP), erythrocyte sedimentation rate (ESR), albumin concentrations in 62 PTB patients and 20 healthy volunteers. METHOD: PTB patients were divided into two groups based on thrombocyte counts. Twenty seven PTB patients with normal thrombocyte counts constituted group 1, 35 PTB patients with thrombocytosis constituted group 2, and 20 healthy volunteers constituted group 3. RESULTS: The median IL6 concentration of group 1 was 12.8 pg/ml (95% CI: 12.1 to 56.9 pg/ml) and group 2 was 40.6 pg/ml (95% CI: 67.1 to 168.7 pg/ml). The comparison of IL6 concentrations in the three groups was significant (p = 0.0001). Patients in group 1 had a higher concentration of CRP (p = 0.0001) and lower concentration of albumin (p = 0.002) than group 3 whereas group 2 had higher concentration of CRP (p = 0.003) and lower concentration of albumin (p = 0.002) than group 1. Serum IL6 concentrations were significantly correlated with thrombocyte counts (p = 0.004, r = 0.36), CRP (p = 0.007, r = 0.34), and albumin concentrations (p = 0.005, r = -0.34). IL6 concentrations were significantly correlated with the number of involved zones (p = 0.005, r = 0.35) and acid fast bacilli positivity (p = 0.03, r = 0.27). Patients in group 2 had weight loss (p = 0.004), fever (p = 0.038), and night sweats (p = 0.007) more frequently than group 1. Also, group 2 had more extensive radiological findings (involved zones p = 0.001, bilateral disease p = 0.0001, presence of cavity p = 0.02) than group 1. CONCLUSIONS: IL6 might play a contributory part in reactive thrombocytosis and acute phase response in PTB.

Acute-Phase Reaction↗
PubMed2000

Thrombopoietic cytokines in patients with iron deficiency anemia with or without thrombocytosis.

Iron deficiency anemia is a cause of reactive thrombocytosis. A moderate increase in platelet numbers is common but sometimes counts may exceed 1,000 x 10(9)/l. The mechanisms causing reactive thrombocytosis are unclear. In this study, we evaluated 15 women with iron deficiency anemia and thrombocytosis (platelets >450 x 10(9)/l) and 16 women with iron deficiency anemia with normal platelet counts. Serum samples were taken before oral iron replacement therapy, after 1 and 3 months and at the end of replacement therapy. Thrombopoietin, erythropoietin (EPO), leukemia inhibitory factor, interleukin-6 and interleukin-11 levels were assayed. There was no change in the levels of thrombopoietic cytokines except for EPO. The correlation between high EPO levels and high platelet counts may suggest that EPO increases platelet counts, but the same EPO level changes can also be demonstrated in women with iron deficiency anemia but normal initial platelet counts. The fact that the levels of other cytokines remained unchanged during treatment suggests that either these cytokines have no effect on reactive thrombocytosis or the change in platelet counts in our patients is in a narrow range and is thus not affected by the cytokine levels.

Adolescent↗