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PubMed1984

Platelet aggregation induced in mice by whole-body hyperthermia.

Whole-body hyperthermia ( WBH ) induced by 2450-MHz irradiation resulted in a decrease in platelet number in the circulating blood 3.5 hr after irradiation. Afterward, the treated mice developed thrombocytosis which peaked 3 days after WBH . This phenomenon was suppressed by administration of antiinflammatory drugs (methylprednisolone acetate and indomethacin) or aggregating inhibitors (heparin, pentoxifylline and dibutyryl cyclic AMP). These facts suggest that thrombocytosis occurring in treated mice arises to offset a deficiency of platelets induced by aggregations and adhesions. Further investigation of platelets in vitro indicated that the addition of plasma extract from mice treated with WBH to heated platelets induced a significant aggregation of platelets.

Animals↗
PubMed1978

Role of the spleen and lymphocytes in regulation of the circulating platelet number in mice.

The role of the spleen in the regulation of the circulating platelet number was studied in mice. The increased 75Se-Met incorporation found after removal of the spleen indicates that postsplenectomy thrombocytosis is due to enhanced platelet production. The increased thrombopoietic activity observed in the plasma of splenectomized mice proves the presence of a humoral factor which mediates this process. Administration of spleen lymphocytes to control mice caused mild thrombocytopenia and prevented postsplenectomy thrombocytosis in splenectomized animals. Moreover, culture medium obtained from peripheral blood and spleen lymphocytes contained a substance which induces thrombocytopenia when injected into control mice. The mechanism by which the spleen and lymphocytes affect the amount of circulating platelets is discussed.

Animals↗
PubMed1995

The human thrombopoietin gene is located on chromosome 3q26.33-q27, but is not transcriptionally activated in leukemia cells with 3q21 and 3q26 abnormalities (3q21q26 syndrome).

We previously demonstrated that the EVI-1 gene was transcriptionally activated in the 3q21q26 syndrome and chromosomal breakpoints at 3q26 were clustered within 400 Kb of the EVI-1 gene. Since thrombocytosis is often observed in the 3q21q26 syndrome, we first mapped the thrombopoietin (TPO) gene and then we examined for transcriptional activation and chromosomal rearrangement of the TPO gene in four cases of the 3q21q26 syndrome. The TPO gene was assigned to chromosome 3q26.33-q27 by fluorescence in situ hybridization analysis. Although the TPO gene was mapped to the same locus as the EVI-1 gene, the distance between the TPO gene and the EVI-1 gene at 3q26 was more than 600 Kb and no gross chromosomal rearrangements of the TPO gene were detected by Southern blot analysis and pulsed field gel electrophoresis (PFGE) analysis. TPO transcripts were not detected in these leukemia cells by Northern blot analysis. These results indicate that activation of the TPO gene is not the main cause of thrombocytosis in the 3q21q26 syndrome.

Base Sequence↗
PubMedDate not supplied

Kawasaki disease presenting with disseminated intravascular coagulation: report of one case.

Thrombocytosis is always noted in patients with Kawasaki disease (KD). Here we present a case of KD with an unusual finding of thrombocytopenia. A 3 months old female baby was admitted to our hospital presenting with the classical symptoms and signs of KD. However, initially she also had thrombocytopenia and disseminated intravascular coagulation. She was treated successfully with a single high dose of intravenous immunoglobulin. (2 gm/kg). Thrombocytosis was found on the 10th day of illness, and treatment with low dose aspirin was administered for 3 months. No coronary aneurysm was found on cardiac echography. She was found to be well on a follow-up of 8 months.

Disseminated Intravascular Coagulation↗
PubMed1993

Gut inflammation in children with late onset pauciarticular juvenile chronic arthritis and evolution to adult spondyloarthropathy--a prospective study.

Ileocolonoscopy with biopsy of the colon and terminal ileum was performed prospectively on 12 patients under age 16 with late onset juvenile chronic arthritis (JCA). Inflammatory gut lesions were seen in 9 of these 12 patients; 4 were of the acute type, 5 of the chronic type. Chronic gut inflammation was related to axial inflammatory complaints, inflammatory serum variables, thrombocytosis and sacroiliac radiological abnormalities. A 2nd ileocolonoscopy was performed on 5 of the 12 patients, and a 3rd ileocolonoscopy on 2 of these with persistent synovitis. Gut inflammation and joint inflammation were related; moreover, all 5 patients had chronic inflammatory lesions by the time of the last investigation, one presented with Crohn's disease. The 12 patients were reviewed 3 to 9 years after the first ileocolonoscopy. Four patients were in remission, including the 3 patients with initial normal gut histology. Five patients had developed ankylosing spondylitis (AS), a 6th patient possible AS. Axial inflammatory complaints, a family history of spondyloarthropathies, HLA-B27 positivity, early sacroiliac and peripheral joints radiographic changes, persistence of inflammatory serum variables, thrombocytosis and chronic inflammatory lesions on gut biopsy, are predictive factors in juveniles for evolution to AS. Late onset pauciarticular JCA represents a form of spondyloarthropathy similar to adolescent forms. Persistent gut inflammation could play a role in the pathogenesis of the disease and persistent synovitis.

Adolescent↗
PubMed1993

[Sideroblastic anemia preceded by essential thrombocythemia with 20q- chromosome abnormality].

A 78-year-old man presented with marked thrombocytosis (126.4 x 10(4)/microliters), low neutrophil alkaline phosphatase (NAP) score and an abnormal karyotype of 46, XY, del(20) (q11q13) (18 of 20 cells), without obvious anemia or ringed sideroblasts in bone marrow. He received ranimustine (MCNU) with a diagnosis of essential thrombocythemia. After 2 years, he was admitted because of macrocytic anemia. The peripheral blood smear showed anisopoikilocytosis with a few nucleated red blood cells. Moderate thrombocytosis (71.7 x 10(4)/microliters) and a low NAP score were also observed. Bone marrow aspiration revealed erythroid hyperplasia with a significant increase in ringed sideroblasts (85% of erythroblasts). Cytogenetic studies showed the same abnormal karyotype 46, XY, del(20) (q11q13) in 100% of metaphase cells as those at initial diagnosis. A diagnosis of sideroblastic anemia preceded by essential thrombocythemia was made. No rearrangement or amplification of c-src was revealed. The observation of the same chromosome abnormality (20q-) in different phases of this patient's disease indicates that chronic myeloproliferative disorders and myelodysplastic syndrome may share some borderline or transitional cases with a similar pathogenesis.

Aged↗
PubMed1993

[Essential thrombocythemia. Apropos a case of cerebrovascular stroke].

The authors report the case of a 60-year-old white man with a previous history of pulmonary tuberculosis, smoking habits, hypertension, intermittent claudication and erythromelalgia, admitted to our ward with an ischemic cerebral event. Initial laboratory evaluation documented thrombocytosis (platelet-950000/mm3) and discrete anemia. Additional studies confirmed the diagnosis of essential thrombocythemia, meeting all the criteria proposed by the Polycythemia Vera Study Group in 1986, after exclusion of the possible causes of reactive thrombocytosis. Therapy was initiated with alpha-2b interferon (3 MU/m2 subcutaneously three times a week) and aspirin. Platelet count control was obtained and the patient remained asymptomatic. Nine months later cutaneous toxicity obliged the discontinuance of alpha-interferon. Due to a continuous increase of platelet count, hydroxyurea was introduced. The patient is asymptomatic, with platelet counts < 500000/mm3, without toxicity manifestations, two years after diagnosis. The contribution of cardiovascular risk factors versus thrombocythemia in the pathogenesis of the ischemic cerebral event and the benefit of platelet count control are discussed.

Aspirin↗
PubMed1993

Compensatory mechanisms in platelet production: lack of a paracrine response in W/Wv mice treated with 5-fluorouracil.

W/Wv mice maintain normal platelet levels despite having a reduced functional stem cell pool, indicating that platelet production in these mice is compensated by altered megakaryocytopoiesis. In this study the effect of 5-fluorouracil (5-FU) treatment on platelet production in W/Wv mice and their congenic normal littermates was assessed. Recovery of circulating platelet levels occurred 11 days after 5-FU administration in W/Wv mice and subsequently did not increase above control values. In contrast, normal littermates showed an increased platelet count by day 8 and significant thrombocytosis between days 11 and 14. Investigation of bone marrow megakaryocytopoiesis in W/Wv mice showed there was no recovery in the number of megakaryocyte progenitors (CFU-Meg) per femur between days 3 and 5, but control values were reached by day 10. In addition, by day 8 the number of mature megakaryocytes per unit volume of bone marrow in these mice had not returned to control values, although the megakaryocytes were of an increased size. In comparison, the number of CFU-Meg per femur in normal mice treated with 5-FU began to recover after day 3, returned to control values by day 8 and increased to supranormal levels by day 14. Bone marrow megakaryocyte concentration was increased 2-fold over the control by day 8 and an increase in mean megakaryocyte size was also observed. The data suggest that platelet production in mice is dependent on the rate of establishment of both the progenitor cell and megakaryocyte pools. The inability of W/Wv mice to enhance and accelerate progenitor cell levels led to a reduced bone marrow response and failure to produce a marked thrombocytosis.

Animals↗
PubMed1993

Essential thrombocythemia: a relative benign long-term course.

The disease manifestations, response to therapy, and follow-up course of 35 patients with essential thrombocythemia seen in a single center were evaluated. The median age was 53 years (range 17-81). Twelve patients were asymptomatic on presentation and the diagnosis was incidental. Twenty-three patients presented with thrombocytosis-related symptoms, most commonly neurological, microcirculatory, or thromboembolic. In no patient did hemorrhage occur as a presenting symptom. The mean platelet count (+/- SD) at diagnosis was 858 +/- 223 x 10(9)/l and the mean maximal count during the follow-up period was 989 +/- 269 x 10(9)/l. The median follow-up of the entire group was 54 months (range 12-172). Ten of the 12 patients who were asymptomatic on presentation remained so during the observation period, while 10 patients who presented with thrombocytosis-related symptoms became asymptomatic following a single course of treatment with no recurrence of symptoms. Thirty of the 35 patients were treated with busulfan or hydroxyurea or both. Response to cytoreductive therapy was prompt and continuous in most patients. Essential thrombocythemia might be a disease of grave consequence but it seems that in general its course under treatment is more benign than previously thought.

Adolescent↗
PubMed1996

[Two cases of severe bacterial meningitis with paranasal sinusitis followed by cerebrovascular disease--pathophysiology and treatment of cerebrovascular disease].

We report two cases of pneumococcal meningitis with paranasal sinusitis followed by cerebrovascular disease. Both cases were occupational divers, and had past histories of head trauma and paranasal sinusitis. Despite the combined therapy with antibiotics and dexamethasone, they developed cerebrovascular complications. Case 1 developed cerebral infarction and hemorrhage on day 13, and in case 2 cerebral infarction occurred on day 15. In both cases, serum levels of TNF-alpha and IL-6 were elevated in the early stage of the illness (12 pg/ml and 21.3 pg/ml in case 1, and 50 pg/ml and 7,570 pg/ml in case 2, respectively). In case 2, TNF-alpha, IL-1 beta and IL-6 levels in the cerebrospinal fluid were also elevated on day 4 (25 pg/ml, 320 pg/ml and 6,870 pg/ml, respectively). Thrombocytosis was observed in both cases before the onset of the cerebrovascular complications. These cytokines may play significant roles in thrombocytosis leading to cerebrovascular complications in pneumococcal meningitis. Although the use of steroids as adjunctive therapy for bacterial meningitis has been found to be beneficial, the dosage of dexamethasone administered in our cases may not be enough to suppress the synthesis and release of the cytokines. Therefore, administration of large doses of glucocorticoid should be recommended before the treatment with antibiotics.

Adult↗
PubMed1997

Clonality analysis of hematopoiesis in essential thrombocythemia: advantages of studying T lymphocytes and platelets.

Essential thrombocythemia (ET) is a myeloproliferative disorder characterized by a sustained elevation of the platelet count in the absence of other causes of thrombocytosis. ET is difficult to diagnose, and the demonstration of clonal hematopoiesis may be of value. However, clonality analysis of hematopoietic cells based on the study of the X-chromosome inactivation pattern is complicated by the observation that some normal females present skewed lyonization. Moreover, DNA methylation of X-linked genes in hematopoietic cells may differ from that in other tissues. Appropriate controls for skewed lyonization are therefore critical for the study of clonality. We developed two techniques based on X-chromosome inactivation and polymerase chain reaction (PCR) analysis of polymorphisms, to study clonality in ET patients. Reverse transcriptase-PCR analysis of IDS, P55, and G6PD mRNAs was used to examine the different hematopoietic cell lineages including platelets in patients heterozygous for these polymorphisms and analysis of the HUMARA gene methylation pattern permitted us to study clonality in all nucleated cell fractions of the other patients. Using both types of assay and T lymphocytes as a control tissue for lyonization, clonal hematopoiesis was demonstrated in 28 patients. In 14 patients, the granulocytes were polyclonal; among these patients, platelets were monoclonal in 3 cases, polyclonal in 7 cases, and in the remaining 4 cases this fraction could not be studied because the patients were homozygotes for all RNA markers. No conclusion about clonality could be drawn in 6 cases. Polyclonal hematopoiesis was found in all the cases of reactive thrombocytosis. These findings confirm the high frequency of monoclonal hematopoiesis in ET, the utility of studying platelets, and the possibility of using T lymphocytes as a control tissues for X-chromosome inactivation patterns.

Adolescent↗
PubMed1997

[A case report of aorto-coronary artery bypass surgery in patient with essential thrombocythemia].

Essential thrombocytosis was detected by chance in a 55-year-old patient with angina pectoris when cardiac catheterization was performed. The diagnosis of thrombocytosis (platelet count > 1,000000/mm3) was established by detailed investigations. This patient had stenosis of the coronary arteries and the right common iliac artery. About one month after cardiac catheterization, the patient underwent coronary bypass surgery following normalization of the platelet count with interferon therapy, which was also used to control the platelet count perioperatively. The operation was completed without major problems, and the postoperative course was uneventful. This case is reported in detail.

Angina Pectoris↗
PubMed1997

[Allopurinol induced pancytopenia in a patient with myeloproliferative disorder].

We reported a rare case of pancytopenia caused by allopurinol. A 61-year-old man was first admitted in May 1993, because of thrombocytosis. He had suffered from chronic glomerulonephritis. He was administered allopurinol for hyperuricemia from March 1993. On first admission the laboratory findings revealed leukocytosis (10,100/microliter) and thrombocytosis (971 x 10(3)/microliter) in the peripheral blood. Myelofibrosis was strongly suspected due to increased number of MgK and reticular fiber in the bone marrow. Two months later, he readmitted due to pancytopenia (WBC 1,300/microliter, Hb 6.2g/dl, Plt 10 x 10(3)/microliter). His bone marrow showed markedly hypocellular. Because we suspected that pancytopenia was induced by allopurinol, we discontinued allopurinol and administered oxymetholone, G-CSF, and EPO, WBC, RBC, and platelet count had been recovered about one and half months later. In vitro co-culture indicated that CFU-G, E, and Meg in the bone marrow cells after recovery from pancytopenia were markedly suppressed in the presence of patient's serum and oxipurinol. Pancytopenia due to allopurinol was reported to be rare, and some authors showed that it will sometimes be fatal. Because pancytopenia of this case had been recovered in a relatively short time with cytokine therapy, it was thought to be effective for pancytopenia due to drug like this case.

Allopurinol↗
PubMed1976

Unusual manifestations of Henoch-Schönlein syndrome.

Henoch-Schönlein syndrome represents a diagnostic challenge when the abdominal and/or joint manifestations precede the cutaneous lesions. Laparotomy is often performed unnecessarily. We describe a patient whose abdominal symptoms antedated the appearance of cutaneous lesions by three months. Gastrointestinal blood loss, thrombocytosis, hypoproteinemia, and the roentgenographic appearance of the small intestine suggested the correct diagnosis. His course was further complicated by hypertension associated with elevated plasma renin levels without evidence of nephritis. Joint manifestations were mild and transient as were testicular pain and swelling.

Child↗
PubMed2006

Prospective study of the incidence and risk factors of postsplenectomy thrombosis of the portal, mesenteric, and splenic veins.

HYPOTHESIS: Splenectomy is recognized as a cause of portal, mesenteric, and splenic vein thrombosis. The exact incidence of the complication and its predisposing factors are not known. DESIGN: Prospective observational cohort study. The median follow-up time of the patients was 22.6 months. SETTING: University surgical clinic in a teaching hospital. PATIENTS: A total of 147 consecutive patients who underwent splenectomy in a 4-year period were enrolled in the study. INTERVENTIONS: Preoperative and postoperative evaluation included ultrasonography with color Doppler flow imaging of the portal system, results of blood coagulation tests, fibrinogen levels, D-dimer levels, and complete blood counts. Operative sheets were recorded and reviewed. When portal system thrombosis (PST) was diagnosed, a complete control for acquired and congenital thrombophilia disorders was obtained. MAIN OUTCOME MEASURES: Primary end points of the study were the assessment of the incidence of postsplenectomy PST and the identification of risk factors for its occurrence. RESULTS: Portal system thrombosis occurred in 7 (4.79%) of 146 patients who underwent splenectomy. The age, sex, type or length of the operation, and use of preoperative and postoperative thromboprophylaxis with low molecular weight heparin did not prove to be significant factors in the occurrence of PST. Platelet count of more than 650 x 10(3)/microL and greater spleen weight (>650 g) was associated with the development of PST (P = .01, P = .03). Normal D-dimer levels on diagnosis of the complication showed a negative predictive value of 98%. Two of the affected patients were diagnosed with thrombophilia disorders. In a median follow-up period of 22.6 months, no other case of PST was recorded. CONCLUSIONS: Postsplenectomy PST occurs in approximately 5% of patients. Possible risk factors are thrombocytosis, splenomegaly, and congenital thrombophilia disorders.

Adolescent↗
PubMed1980

Changing indications for splenectomy. 30 years' experience.

During the last three decades, 2,4117 splenectomies have been performed at The Ohio State University Hospital. Indications for splenectomy include hypersplenism, incidental to other abdominal procedures, trauma, Hodgkin's staging, and other splenic disease. Hodgkin's staging has become the most frequent indication for splenectomy during the past five years, whereas splenectomy for hypersplenism has decreased. Thrombocytosis (platelet counts greater than 400,000/cu mm) was observed in 47% of all patients. Ninety-three percent of all thromboembolic complications occurred in this group. The overall morbidity of 39% has been decreased to 15% during the last five years. In-hospital mortality has decreased from 9.5% to 6%. Incidental splenectomy, even for benign disease, continues to be associated with complications and death.

Hodgkin Disease↗
PubMed1999

Portal, mesenteric, and splenic vein thromboses after splenectomy in a patient with chronic myeloid leukemia variant with thrombocythemic onset.

Portal, mesenteric, or splenic vein thrombosis is a very uncommon complication with significant mortality in the patients undergoing splenectomy for hematologic disorders. We report a 49-year-old woman who developed portal, superior mesenteric, and splenic vein thromboses after splenectomy. Four years before the event, she presented with a marked thrombocytosis and was diagnosed to have chronic myeloid leukemia variant with thrombocythemic onset as evidence by Philadelphia (Ph1) chromosome and a b3a2 BCR/ABL transcript. Six weeks after splenectomy, she developed severe epigastric pain. The diagnosis of thromboses of portal, mesenteric, and splenic veins was made by computed tomography scan and Doppler sonogram. She was successfully treated with antegrade intraarterial urokinase therapy via superior mesenteric artery and long-term anticoagulant therapies. To our knowledge, our patient is the first case of portal, mesenteric, and splenic vein thromboses after splenectomy in a patient with CML variant with thrombocythemic onset successfully treated with antegrade intraarterial thrombolytic therapy followed by anticoagulant therapies.

Female↗
PubMed2000

Derivation of a new hematopoietic cell line with endothelial features from a patient with transformed myeloproliferative syndrome: a case report.

BACKGROUND: During embryonal development primitive hematopoiesis can be observed first in the yolk sac, in which both hematopoietic and endothelial cells are derived from a common precursor, the hemangioblast. Whether cells with this dual differentiation potential persist during postnatal life is unknown. METHODS: A cell line was derived from a patient with secondary acute leukemia. Because of its ability to grow in soft agar and in SCID mice, this cell line was analyzed for expression of differentiation antigens by fluorescence-activated cell sorter analysis, immunocytochemistry, fluorescent in situ hybridization (FISH) analysis with simultaneous cell surface staining, and polymerase chain reaction (PCR). RESULTS: A new cell line was established from a patient with essential thrombocytosis that transformed into acute leukemia. The patient's initial clinical presentation included skin and lymph node infiltrations that were taken for an angiosarcoma due to positivity for CD34, CD31, and von Willebrand factor on immunohistology. In addition to hematopoietic markers, leukemic cells expressed endothelial antigens such as CD62E, CD105, and bound Ulex europäeus lectin-1. Immunocytochemistry revealed positive staining for vascular endothelial growth factor receptor type 2 (KDR), Tie-2/Tek, the angiopoietin receptor, and vascular endothelial cadherin. These results were confirmed by PCR analysis. Simultaneous staining for CD62E and FISH analysis showed that cells with endothelial characteristics belonged to the leukemia. FISH analysis of histologic sections of the lymph node infiltration confirmed this manifestation as part of the leukemic process. The derived cell line, UKE-1, forms colonies in soft agar and is tumorigenic in SCID mice. CONCLUSIONS: This new cell line, UKE-1, appears to combine hematopoietic and endothelial features, indicating the close ontogenic relation of both lineages.

Adult↗