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PubMed1995

Atopic dermatitis and allergic diseases with thrombocytosis: a possible link.

BACKGROUND: Thrombocytosis can be present in patients with myeloproliferative disorders or can accompany various conditions, in particular chronic inflammatory diseases, namely chronic bowel diseases, rheumatoid arthritis, and nephritis. OBJECTIVE: We report our experience in 55 patients younger than 45 years of age with increased platelet counts (over 500 X 10(9)/L). Thirty-three were affected by essential thrombocytemia in agreement with polycytemia vera study group criteria and 22 by reactive thrombocytosis. Serotonin concentration has been determine in all the patients. RESULTS: Serotonin was decreased as expected in 23 out of the 33 patients with essential thrombocytemia. In the remaining ten subjects, serotonin was within normal limits as in reactive thrombocytosis. Eight of these subjects had positive histories for allergic rhinitis and two for atopic dermatitis. CONCLUSIONS: Chronic inflammation, present in patients with diseases of the immune system may cause an increased platelet number. One should consider with caution patients with thrombocytosis and positive histories for diseases of the immune system; probably a diagnosis of essential thrombocytemia is not justified.

Adult↗
PubMed1977

Prognostic significance of thrombocytosis in idiopathic sideroblastic anemia.

In order to determine the prognostic significance of thrombocytosis in idiopathic sideroblastic anemia, the clinical courses of 17 patients were reviewed. Six patients (36%) had thrombocytosis, and none developed acute leukemia. Nine patients (53%) had normal platelet counts, and one developed acute leukemia. Two patients (12%) were thrombocytopenic, and one died of acute leukemia. There was little correlation between survival and platelet count. Sixty-three additional case reports of idiopathic sideroblastic anemia were collected from the literature. Analysis of those patients and the patients in the present study documented transformation to acute leukemia in 5 of 9 (56%) thrombocytopenic patients, 4 of 54 (7.4%) patients with normal platelet counts, and 0 of 17 patients with thrombocytosis (p less than 0.05). Therefore patients with idiopathic sideroblastic anemia and thrombocytosis appear to have a decreased likelihood of leukemic transformation.

Aged↗
PubMed1997

[Thrombocytosis in patients with non-Hodgkin's lymphomas and Hodgkin's disease].

Secondary thrombocytosis appears in patients with various neoplastic and autoaggressive diseases and infections. Thrombocytosis occurrence among 358 patients with NHL and 46 with HD treated at the Department of Haematology of CMKP (Postgraduate Training Centre) and Warsaw Medical School in 1986-1993 is here presented. The 11 patients (3%) among the ones with NHL and the 11 (24%) with HD showed thrombocytosis. Much more frequently the increased thrombocyte count could have been found in patients with low grade T-cell lymphomas (14%) and in patients with Hodgkin's disease. The patients with chronic B-cell lymphocytic leukemia (1%) showed thrombocytosis in very few cases. Thrombocyte count in patients with NHL was not high (mean-596.0 x 10(9)/L median-558.0 x 10(9)/L) which was similar as in those with HD (mean-601.0 x 10(9)/L median-558.0 x 10(9)/L).

Adult↗
PubMed1998

A case of pseudohyperkalaemia and thrombocytosis.

An unusual cause of "hyperkalaemia" was observed in a neurosurgical patient admitted to our intensive care unit. The cause of the hyperkalaemia was not known initially and treatment with cation ion exchange resin was initiated to lower the elevated serum potassium level. The concurrent occurrence of thrombocytosis and hyperkalaemia raised the possibility of psuedohyperkalaemia associated with thrombocytosis. Simultaneous measurement of plasma and serum potassium with the Hitachi 917 Analyzer (indirect ion selective electrode, coefficient of variation = 1% to 2%) confirmed the diagnosis. Correlation between thrombocytosis and pseudohyperkalaemia was found to be highly significant (r = 0.54; P = 0.014). It is estimated that for for every 100 x 10(9)/L of platelets, an increase of 0.07 to 0.15 mmol/L of potassium is expected. In thrombocytosis, plasma rather than serum potassium should be measured.

Cerebral Hemorrhage↗
PubMed2006

Multiple coronary thrombosis and stent implantation to the subtotally occluded right renal artery in a patient with essential thrombocytosis: a case report with review.

Essential thrombocytosis is a myeloproliferative disorder of unknown etiology manifested clinically by the overproduction of platelets in the absence of a definable cause. Platelet dysfunction in essential thrombocytosis results in both hemorrhage and thrombosis. It is one of the rare causes of ischemic cardiovascular events. Fewer than 20 cases of essential thrombocytosis with involvement of coronary arteries leading to acute coronary syndromes or myocardial infarction have been reported. We report a case of multiple coronary thrombosis involving the left anterior descending artery and circumflex artery and stent implantation to the subtotally stenotic right renal artery in a women with unstable angina pectoris, essential thrombocytosis and previous history of renal artery trombosis.

Angina, Unstable↗
PubMed1989

Recombinant interferon-alpha therapy of Philadelphia chromosome-negative myeloproliferative disorders with thrombocytosis.

PURPOSE: The clinical course of patients with myeloproliferative disorders and excessive thrombocytosis may be complicated by serious hemorrhagic or thrombotic events. We have previously reported that interferon-alpha can control severe refractory thrombocytosis in patients with advanced chronic myelogenous leukemia. Therefore, we treated a group of thrombocythemic patients with Ph-negative myeloproliferative disorders, including polycythemia vera and essential thrombocythemia, with recombinant interferon-alpha (rIFN-alpha 2a). PATIENTS AND METHODS: Eight patients with profound elevations in platelet counts received a median induction dose of 5.4 X 10(6) U/day (range, 5.0 to 10.0 X 10(6) U/day) of rIFN-alpha 2a administered intramuscularly or subcutaneously. RESULTS: We observed a significant decline in platelet counts from a median baseline value of 1,929 X 10(9)/L (range, 960 to 2,960 X 10(9)/L) to a median posttreatment value of 431 X 10(9)/L (range, 71 to 1,150 X 10(9)/L) (p less than 0.01). Concomitantly, white blood cell counts declined from a median baseline value of 20.8 X 10(9)/L (range, 10.5 to 40.8 X 10(9)/L) to a median posttreatment value of 6.1 X 10(9)/L (range, 2.9 to 29.0 X 10(9)/L) (p less than 0.02). Correction of thrombocytosis was rapid, with a median of only eight days from the start of therapy to the achievement of a platelet count less than 1,000 X 10(9)/L. Six of eight patients have shown an ongoing response with a median follow-up period of 11 months (range, one to 30 months). There have been no bleeding or thrombotic events during the study. Side effects of rIFN-alpha 2a therapy consisted of fever and flu-like symptoms, with tachyphylaxis developing after one to two weeks of therapy. CONCLUSION: Our observations suggest that alpha interferon may be a promising therapeutic agent for myeloproliferative disorders characterized by thrombocytosis.

Adult↗
PubMed1995

Hematologic effects of stem cell factor (SCF) and leukemia inhibitory factor (LIF) in vivo: LIF-induced thrombocytosis in SCF-primed mice.

Stem cell factor (SCF) administered as daily bolus injections in dose-response experiments in mice causes a progressive and dramatic dose-dependent panleukocytosis characterized by neutrophilia, eosinophilia, monocytosis, and lymphocytosis. SCF causes circulating platelet numbers to be dose-dependently increased after 2 weeks of daily injections. Leukemia inhibitory factor (LIF) administered as daily bolus injections in mice causes a peripheral leukopenia that is largely due to peripheral lymphopenia. LIF causes thrombocytosis peaking after approximately 1 w. Coinjection of SCF and LIF for 1 to 2 wk in mice does not cause a much greater thrombocytosis than the maximum thrombocytosis achievable with SCF or LIF alone. On the other hand, daily injection of SCF for 5 days followed by daily injection of LIF for 5 to 6 d in mice causes a very substantial increase in platelets that was lineage-specific in terms of not being accompanied by a generalized leukocytosis. In contrast, only a very modest thrombocytosis was noted in SCF-primed LIF-treated rats. LIF causes a large increase in the cytoplasmic volume of splenic megakaryocytes in mice, but not in rats. In conclusion, SCF-induced priming followed by LIF-induced maturation of megakaryocytes causes a substantial selective increase in the numbers of circulating platelets in mice.

Animals↗
PubMed2005

[A case report of idiopathic thrombocytosis in 27-year-old man treated for myocardial infarction].

We present the case of 27-year-old male, physical training teacher in whom the first clinical sign of idiopathic thrombocytosis was myocardial infarction. The infarct was complicated by heart arrest caused by ventricular fibrillation. Streptolysis (streptokinase) was used in treatment. Thrombocytosis 842 G/l was observed in blood tests at admission. To estimate its cause the bone marrow biopsy and trepanobiopsy of hip bone were performed. Tests were performed to exclude the secondary cause of thrombocytosis. The coronarography did not show relevant stenoses of coronary arteries. The results let diagnose myocardial infarction in a patient with essential thrombocytosis.

Adult↗
PubMed1986

Thrombocytosis in patients with malignant pleural mesothelioma.

Thrombocytosis above 40.0 X 10(4)/mm3 occurred in five of six (83%) patients with malignant mesothelioma. In contrast, the incidence of thrombocytosis was 7.5% in patients with lung adenocarcinoma, 12.5% in squamous cell carcinoma, 5.1% in small cell carcinoma, and 41.7% in large cell carcinoma, respectively. The platelet count in large cell carcinoma was significantly higher than that in other cell types of lung cancer; however, the platelet count in malignant mesothelioma was much higher than that in large cell carcinoma. These results show that the incidence of thrombocytosis seems to be high in malignant mesothelioma, although the mechanism is thus far unknown.

Adenocarcinoma↗
PubMed1992

Increased secretion of interleukin-6 in malignant mesothelioma cells from a patient with marked thrombocytosis.

BACKGROUND: A high prevalence of thrombocytosis in malignant mesothelioma has been reported, although its pathogenesis remains unknown. METHODS: The case of a patient with marked thrombocytosis in peritoneal malignant mesothelioma is reported. To investigate the cytokines responsible for thrombocytosis in this patient, enzyme-linked immunosorbent assay and immunohistochemical analysis were used. RESULTS: Tumor cells produced large amounts of interleukin-6 (IL-6) and small amounts of granulocyte macrophage colony stimulating factor (GM-CSF) and monocyte colony stimulating factor (M-CSF). Immunocytochemical staining of tumor cells showed strong positivity for IL-6. CONCLUSIONS: These results indicated that persistent secretion of IL-6 promoted thrombogenesis in this patient.

Humans↗
PubMed2004

A case of familial thrombocytosis: possible role of altered thrombopoietin production.

Familial thrombocytosis (FT) is an inherited disorder with clinical presentations similar to essential thrombocytosis (ET). In several pedigrees, overproduction of thrombopoietin (TPO) has been shown to be responsible for the disease. We report herein three cases of thrombocytosis in three successive generations. All cases had increased serum TPO levels. Sequence analysis of TPO gene and transmembrane domain of c-MPL, known as the TPO receptor, revealed no mutations. Platelet c-MPL expression was similar or slightly increased as compared to normal volunteers. These data suggest that altered regulation of the TPO gene might be involved in the pathogenesis of FT.

Adult↗
PubMed2004

Anagrelide for thrombocytosis in myeloproliferative disorders: a prospective study to assess efficacy and adverse event profile.

BACKGROUND: Although the platelet count does not correlate with the rate of thrombosis, there is evidence that a strict control of the platelet count decreases the incidence of thromboembolic complications in essential thrombocythemia. In the current study, the authors evaluated the efficacy and tolerability of anagrelide in thrombocytosis associated with myeloproliferative disorders. METHODS: The study cohort comprised 97 patients (n = 69 females, n = 28 males) with a median age of 59 years (range, 21-80 years). Patients with essential thrombocythemia (n = 79) or with thrombocytosis due to polycythemia vera (n = 16) or to chronic idiopathic myelofibrosis (n = 2) were enrolled in the multicenter, prospective study. Patients received anagrelide at a starting dose of 0.5 mg twice per day, which was then adjusted for each patient. RESULTS: Treatment with anagrelide resulted in a rapid decrease in the platelet count, from a median baseline platelet count of 743 x 10(9)/L to a median platelet count of 441 x 10(9)/L after 6 months (P < 0.0001). The proportion of patients with a platelet count < 600 x 10(9)/L increased from 30% at baseline to 77% after the 6-month study period. The rate of major thrombotic complications significantly decreased from 5% to 2% (P = 0.2568). For patients with essential thrombocythemia, the reduction of major thromboembolic complications was significant (P = 0.0455). The rate of minor thromboembolic complications decreased from 25% before anagrelide treatment to 14% during anagrelide treatment (P = 0.0278). No severe side effects were observed during the study period. There was, however, evidence that concomitant administration of acetylsalicylic acid may increase bleeding tendency. CONCLUSIONS: Anagrelide was an effective and well tolerated treatment modality for reducing platelet counts in both newly diagnosed and pretreated patients with thrombocytosis due to myeloproliferative disorders.

Adult↗
PubMed2008

Extreme thrombocytosis associated with transient myeloproliferative disorder with Down Syndrome with t(11;17)(q13;q21).

A female patient with Down Syndrome (DS) had neonatal thrombocytosis with platelet counts exceeding 2,000 x 10(3)/microL and transient myeloproliferative disorder (TMD). Platelet counts remained elevated the first 2 months of life. A translocation located between chromosomes 17 and 11 was observed. We describe a patient with thrombocytosis and TMD showing an 11q13 translocation. The leukocytosis and thrombocytosis improved after an exchange transfusion.

Chromosomes, Human, Pair 11↗
PubMed1987

Interferon-alfa corrects thrombocytosis in patients with myeloproliferative disorders.

During previous therapeutic trials with interferon, decreased levels of peripheral platelet counts have been observed. Taking advantage of this effect, we investigated the efficacy of recombinant interferon (rec-IFN) in the treatment of thrombocytosis in myeloproliferative diseases. A total of 15 patients with polycythemia vera, essential thrombocytosis, or chronic myeloid leukemia received rec-IFN-alfa at initial doses of 25-70 x 10(6) units/week; maintenance therapy following week 8 of treatment consisted of 20-35 x 10(6) units/week rec-IFN. Observation periods ranged from 24 to 48 weeks. Significant reductions in the number of platelets were noted in all cases; 12/15 patients achieved platelet counts below 440 x 10(9)/l and maintained those normal values for at least 4 weeks. The number of bone marrow megakaryocytes, which had been increased prior to treatment, diminished during rec-IFN therapy, while the previously shortened platelet half-life further decreased with rec-IFN treatment. During rec-IFN-induced remission, the plasma levels of platelet factors, the activity of natural killer cells, and platelet aggregation showed changes between slight improvement and normal values. Severe side effects were only observed with the highest rec-IFN doses; dosage adjustments were effective in improving or eliminating all treatment-related symptoms. Rec-IFN may prove to be a valuable therapeutic alternative to cytostatic treatment of thrombocytosis in myeloproliferative disorders.

Aged↗
PubMed1989

Treatment of thrombocytosis in myeloproliferative disorders with interferon alpha-2a.

In an open prospective pilot trial, we tested the effect of recombinant interferon alpha-2 a (rIFN alpha-2 a) on thrombocytosis in myeloproliferative disorders (MPD). Since October 1986, 13 patients with MPD (4 with chronic granulocytic leukemia, 4 with polycythemia vera, 3 with essential thrombocythemia and 2 with myeloid metaplasia) were treated with rIFN alpha-2 a. Platelet counts decreased in all treated patients within 2 to 10 weeks from a median value of 1,050 x 10(9)/l (range 610-1,940 x 10(9)/l) to 340 x 10(9)/l (range 230-495 x 10(9)/l). The response was dose-dependent. In 11 patients we observed a simultaneous reduction of the white blood cell count. Six patients still continue the IFN alpha-2 a therapy. In 7 treatment was discontinued, because of chronic side effects in 3, and because of noncompliance in one. In these patients, thrombocytosis recurred after discontinuation of the therapy. These results show that rIFN alpha-2 a is effective in controlling thrombocytosis in MPD. However, the long-term benefit of interferon in these disorders remains to be established.

Adult↗
PubMedDate not supplied

Thrombocytosis associated with acute osteomyelitis.

Thrombocytosis is rarely observed during infection. We are describing a patient with acute osteomyelitis and bacteremia who developed thrombocytosis. In the patient described the platelet count paralleled the activity of the infection and the response to therapy. The causes of thrombocytosis and its implications are briefly reviewed.

Female↗
PubMed1988

Thrombocytosis in active rheumatoid arthritis. Relation to other parameters of inflammatory activity and confounding effect of automated cell counting.

The magnitude of thrombocytosis and the possible confounding effect of platelet clumping, an in vitro artifact resulting in spuriously low platelet counts, in active rheumatoid arthritis (RA) was evaluated by a prospective survey of 57 consecutive patients, 60% of whom had thrombocytosis. Five cases (9%) of platelet clumping, assessed by H6000 pictures, were found. A low-grade platelet loss in many of the samples anticoagulated by EDTA was suggested by comparison with platelet counts obtained in parallel blood samples anticoagulated by citrate. Thus, the possibility of spuriously low platelet counts due to laboratory artifacts must always be taken into consideration in RA patients. The relation between thrombocytosis and other estimates of disease activity was also studied. The platelet count in citrated blood in active RA was significantly correlated with ESR, acute phase plasma proteins, and neutrophil, basophil and monocyte counts. In a multivariate regression model, however, only the correlation with haptoglobin (p = 0.06) approached significance.

Arthritis, Rheumatoid↗
PubMed2005

Thrombocytosis in preterm infants: a possible involvement of thrombopoietin receptor gene expression.

Transient thrombocytosis is commonly observed in preterm infants after birth, but its physiological mechanism is still unknown. To understand the mechanism of the transient thrombocytosis in preterm infants we firstly evaluated a correlation between platelet counts and thrombopoietin (TPO) levels in preterm infants and next c-mpl mRNA levels on platelets in healthy preterm infants longitudinally during a half-year of life. The mean platelet counts in 45 very low birth weight infants (mean gestational age 27.4+/-1.8 weeks, mean birth weight 1047+/-249 g) was 230+/-71x10(9)/l just after birth and thereafter gradually increased to 579+/-178x10(9)/l by 5 weeks of age. The platelet counts continued this level for about next 8 weeks. Serum TPO levels soon after birth and at 1 month of age were significantly higher than those at the age of 2-6 months. There was a significant negative correlation between platelet counts and serum TPO values. The c-mpl expression levels on platelets at birth and at 1 month of age tended to be lower than those on platelets from adults, and the c-mpl levels gradually increased through 6 months of age, although they were still lower than those of adults. Our results suggest that low expression of TPO receptor on platelets until 1 month after birth cause a decreased TPO clearance and keep a high level of free TPO in blood, thereby promoting platelet production from megakaryocytes or their progenitors in bone marrow, resulting in the subsequent thrombocytosis in preterm infants.

Adult↗