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PubMed2000

Multicenter prospective study of children with sickle cell disease: radiographic and psychometric correlation.

After obtaining familial informed consent, between January 1996 and July 1997, 173 children (5 to 15 years old) with sickle cell disease were enrolled in a prospective multicenter study using blood screening, transcranial Doppler ultrasonography (n = 143), cerebral magnetic resonance imaging (n = 144), and neuropsychologic performance evaluation (n = 156) (Wechsler Intelligence tests WISC-III, WIPPSI-R), which were also performed in 76 sibling controls (5 to 15 years old). Among the 173 patients with sickle cell disease (155 homozygous for hemoglobin SS, 8 sickle cell beta0 thalassemia, 3 sickle cell beta+ thalassemia, 7 sickle cell hemoglobin C disease SC), 12 (6.9%) had a history of overt stroke, and the incidence of abnormal transcranial Doppler ultrasonography (defined as mean middle cerebral artery velocity > 200 cm/sec or absent) was 8.4% in the overall study population and 9.6% in patients with homozygous sickle cell anemia The silent stroke rate was 15%. Significantly impaired cognitive functioning was observed in sickle cell disease patients with a history of stroke (Performance IQ and Full Scale IQ), but also in patients with silent strokes (Similarities, Vocabulary, and Verbal Comprehension). However, infarcts on magnetic resonance imaging were not the only factors of cognitive deficit: Verbal IQ, Performance IQ, and Full Scale IQ were strongly impaired in patients with severe chronic anemia (hematocrit < or = 20%) and in those with thrombocytosis (platelets > 500 x 10(9)/L). Multivariate logistic regression analysis showed that abnormal magnetic resonance imaging (odds ratio [OR] = 2.76) (P = .047), hematocrit < or =20% (OR = 5.85) (P = .005), and platelets > 500 x 10(9)/L (OR = 3.99) (P = .004) were independent factors of cognitive deficiency (Full Scale IQ < 75) in sickle cell disease patients. The unfavorable effect of low hematocrit has already been suggested, but this is the first report concerning an effect of thrombocytosis and showing that silent stroke alone is not a factor of cognitive deficit when not associated with low hematocrit or thrombocytosis. The effect of hydroxyurea, which is known to increase hematocrit and decrease platelet count, on cognitive functioning of sickle cell patients should be evaluated prospectively.

Adolescent↗
PubMed2002

The diagnosis and management of polycythemia vera in the era since the Polycythemia Vera Study Group: a survey of American Society of Hematology members' practice patterns.

The Polycythemia Vera Study Group (PVSG) was organized in 1967 to identify the optimal approach to the diagnosis and treatment of polycythemia vera (PV). Nevertheless, a systematic assessment of US physicians' approach to PV has not been performed. To determine practice patterns in the management of PV, a random sample of the US American Society of Hematology (ASH) membership was surveyed. Thirty-three percent of 3000 surveys were returned. Significant variations in diagnostic and therapeutic approach were evident by region, practice type, specialty, and clinical experience. Red cell volume determinations (78% of respondents), serum erythropoietin levels (76%), and arterial blood gases (75%) were the most frequent tests used in the diagnosis of PV. Sixty-nine percent of physicians use phlebotomy as their first choice for erythrocytosis. Phlebotomy plus hydroxyurea (27.8%) and hydroxyurea alone (10%) were used less often. Despite PVSG recommendations, almost 16% of physicians used a target hematocrit of 0.55 (50%) or 0.55 (55%) for phlebotomy therapy. Eighty-two percent of physicians treated thrombocytosis only when platelet counts exceeded 1000 x 10(9)/L (1 000 000/microL) or in the event of symptoms. Hydroxyurea (62.8%) and anagrelide (35.4%) were the primary agents used to treat thrombocytosis. Thus, this national survey of US hematologists and oncologists has identified substantial variation in the approach to the diagnosis and treatment of PV. A significant minority of physicians undertreat erythrocytosis, and little consensus exists regarding the treatment of thrombocytosis.

Data Collection↗
PubMed2001

Hepatic thrombopoietin mRNA is increased in acute inflammation.

The plasma concentration of thrombopoietin (TPO) in general is inversely related to the mass of platelets and megakaryocytes. However, reactive thrombocytosis of inflammatory disease is accompanied by elevated TPO levels. To investigate whether the rate of TPO mRNA expression is altered during acute inflammation, rats were injected with bacterial lipopolysaccharide (LPS). After 6 h, total RNA from liver and kidney was reverse transcribed and analyzed by competitive PCR for TPO and glyceraldehyde-3-phosphate dehydrogenase (GAPDH). LPS-treated rats showed a significant increase in hepatic TPO mRNA concentration. The ratio of TPO to GAPDH mRNA was 3.5 +/- 0.6% in the livers of control rats and 8.3 +/- 2.0% in the livers of LPS-treated rats (mean +/- SD). Thus, reactive thrombocytosis of inflammatory disease might result from an increase in hepatic TPO production. Since platelets are involved in the immune reaction, reactive thrombocytosis may be a mechanism of host defense.

Acute Disease↗
PubMedDate not supplied

Diagnostic significance of platelet count and other blood analyses in patients with lung cancer.

The objective of this study was to evaluate the clinical value of an elevated platelet count and other routine laboratory tests for predicting malignancy in patients with radiologically suspected lung cancer. Platelet count, haemoglobin, total leukocyte count, erythrocyte sedimentation rate (ESR) and serum lactate dehydrogenase (LDH) were analysed in 126 prospectively admitted patients with suspected lung cancer. The patients were divided by pathologic diagnosis into those with benign disorders (n=65) and with malignancies (n=61). Patients with lung cancer were staged (TNM) and the tumours were classified according to histological types (WHO). Thrombocytosis (platelet count >400x10(9)/l) was present in 8% (5/65) of patients with benign disease and in 57% (35/61) of patients with malignant disease (p<0.00001). The prevalence of thrombocytosis in patients with primary lung cancer was 53% (27/51). Elevated platelet count was more common in advanced disease (stage III and IV). No difference was observed between histological types. The sensitivity of thrombocytosis for predicting malignancy was 0.57 and the specificity 0.92. When elevated platelet counts, LDH and ESR were combined, a sensitivity of 0.71 and a specificity of 1.00 was achieved. The positive and negative predictive values were 1.00 and 0.89, respectively. Elevated platelet count is frequently observed in patients with lung cancer. When test results of platelet count and other routine blood analyses are combined, a high sensitivity and specificity for predicting malignancy can be achieved. These tests are clinically useful in the evaluation of patients with radiologically suspected lung cancer.

Blood Sedimentation↗
PubMed2004

[Clinical biological features of mixed myeloid diseases].

AIM: To characterize patients with mixed myeloid neoplasias with proliferation of neutrophils, platelets and eosinophils. MATERIAL AND METHODS: Examination and treatment results were analysed for patients with atypical myeloid leukemia (n = 4), myelodysplastic syndrome (MDS, n = 1) and thrombocytosis, MDS and eosinophilia (n = 1). The examination included morphological, histological, cytogenetic and molecular tests. RESULTS: One patient with atypical chronic myeloid leukemia was prior diagnosed to have primarily MDS with a typical aberration of chromosome 5. Two other patients had an initial morphological picture of resistant anemia with blast excess, signs of myeloproliferation and extramedullary hemopoiesis. One and two months after the first examination they received transfusions of erythrocytic mass. Just then they were found to have splenomegaly and leukocytosis due to proliferating and maturating forms of neutrophils. The course of the disease in patients with MDS, thrombocytosis and normal karyotype and in patients with MDS, eosinophilia and combined chromosomal breaks including translocation (3;12)(q21;p13) was characterized by resistance to standard programs of polychemotherapy and transformation into acute myeloblastic leukemia. CONCLUSION: In some cases atypical CML is a stage of a natural course of MDS. Some MDS variants with eosinophilia and thrombocytosis should be referred to the group of mixed myeloid neoplasias.

Adult↗
PubMed2004

Platelet large cell ratio in the differential diagnosis of abnormal platelet counts.

Platelet volume indices, estimated by automated blood cell analyzers, are useful in the diagnosis of various conditions with abnormal platelet counts. Platelet count (PLT), Platelet large cell ratio (P-LCR), Platelet distribution width (PDW) and mean platelet volume (MPV) were studied in 779 patients with normal platelet counts, 74 patients with high platelet counts and 41 cases with low platelet counts. P-LCR was significantly decreased in patients with thrombocytosis than in normal while it was increased in thrombocytopenia. In patients with high counts, P-LCR was significantly decreased in reactive thrombocytosis than neoplastic thrombocytosis. P-LCR was increased in destructive thrombocytopenia than those with hypoproliferative thrombocytopenia though it was not statistically significant. P-LCR was inversely related to platelet count and directly related to PDW and MPV. Platelet large cell ratio if properly utilised can be a good aid in the differential diagnosis of conditions associated with abnormal platelet counts.

Blood Platelets↗
PubMed1978

Template bleeding time and clinical hemorrhage in myeloproliferative disease.

In 32 patients with myeloproliferative disorders (MPD), correlations were made among clinical observations of hemorrhagic tendency, template Ivy bleeding time, and platelet aggregation studies. Bleeding time was commonly prolonged, particularly in myelofibrosis. In two cases, this prolongation appeared to reflect a defect in platelet function, which resulted in clinical bleeding. Prolongation of bleeding time did not correlate with degree of thrombocytosis. Two patients with thrombocytosis had serious clinical bleeding at a time when bleeding time was normal. Of the patients, 35% had abnormal findings from aggregation studies, but there was no correlation between aggregation studies and prolongation of bleeding time or clinical hemorrhage. We conclude that bleeding in MPD arises either from a defect in platelet function, which is reflected in a prolonged bleeding time, or from thrombocytosis.

Blood Cell Count↗
PubMed1996

Hemostatic profile in nephrotic syndrome.

OBJECTIVE: To evaluate the coagulation profile and its relation to steroid therapy, and the frequency of thromboembolic complications and its correlation with coagulation parameters in nephrotic syndrome (NS). SETTING: Hospital based. SUBJECTS AND METHODS: Forty children with NS were subdivided into four groups, namely, fresh cases, steroid dependent, remission after therapy and steroid resistant. An equal number of age and sex matched children served as controls. In all the study and control subjects, detailed clinical examination, liver function tests, renal function tests and detailed coagulation profile were done. Evaluation of renal veins and inferior vena cava for the presence of thrombosis was also done by abdominal ultrasonography. RESULTS: Thrombocytosis was detected in 57.5% and the degree of thrombocytosis was directly related to the amount of proteinuria. The mean prothrombin and thrombin times were within normal range in the study children. The activated partial thromboplastine time (APTT) was prolonged in six cases (15%) and three out of these six children had thromboembolic complications. Antithrombin-III level was significantly lower (p < 0.001) whereas protein C and S were significantly elevated (p < 0.001) as compared to controls. The levels became normal with remission of the disease. Steroid therapy significantly increased the levels of proteins C, protein S. AT-III and fibrinogen as compared to controls. Thromboembolic complications were seen in 3 cases (7.6%) and were associated with very low levels of AT-III and protein C and all three had serum albumin below 2 g/dl. CONCLUSIONS: The importance of coagulation profile in nephrotic syndrome is highlighted and a high index of suspicion for thromboembolic complications is warranted in patients with thrombocytosis, hyper fibrinogenemia, prolonged APTT and in children with low levels of AT-III, protein C and protein S.

Antithrombin III↗
PubMed1998

Increased levels of the soluble adhesion molecule E-selectin in patients with chronic myeloproliferative disorders and thromboembolic complications.

Patients with chronic myeloproliferative disorders (CMD) show a high frequency of thrombosis. For this reason we evaluated endothelial cell markers, soluble adhesion molecule E-selectin (sELAM), and thrombomodulin (TM) in 25 patients with CMD. Among them nine presented thromboses in their past history. Data were compared with those obtained in a group of healthy subjects and a group of patients with secondary thrombocytosis. The mean plasma concentrations of sELAM were elevated in patients with CMD, as compared with healthy subjects (81.27 +/- 42.8 ng/ml vs. 41.75 +/- 13; P < 0.02). Similarly, the mean plasma concentrations of sTM were increased in CMD patients in comparison with the control group (102.0 +/- 73 ng/ml vs. 16.7 +/- 9.6; P < 0.01). More markedly elevated sELAM levels were observed in CMD patients with thrombosis than in patients without thrombosis (113.16 +/- 29.5 ng/ml vs. 55.11 +/- 19.1 ng/ml; P < 0.001), while no significant difference was found between CMD patients without thrombosis and secondary thrombocytosis (50.72 +/- 10.8 ng/ml). Plasma thrombomodulin values in CMD patients with thrombosis (131 +/- 93.8 ng/ml) were higher than those without thrombosis (65.77 +/- 43.9 ng/ml; P < 0.02). sTM values were also significantly increased in patients with secondary thrombocytosis (P < 0.01). It is speculated that the plasma, sELAM levels may reflect endothelium activation and that it is possibly useful in predicting the thrombotic risk in myeloproliferative disorders.

Adult↗
PubMed2000

5q- syndrome presenting chronic myeloproliferative disorders-like manifestation: a case report.

A 28-year-old Japanese woman with suspected essential thrombocythemia (ET) had marked thrombocytosis, mild leukocytosis with normal neutrophil alkaline phosphatase activity, and no anemia. She was monitored without being given any medication. Eleven years later, complete blood counts showed no remarkable changes but some non-lobulated mononuclear megakaryocytes were found in the bone marrow. Cytogenetic analysis revealed deletion of the long arm of chromosome 5 (5q-). Subsequently, hemoglobin and platelet counts decreased gradually, splenomegaly appeared and progressed, after which myelofibrosis developed. Acute leukemia developed 16 years after the first documentation of thrombocytosis. 5q- syndrome is known to be a myelodysplastic syndrome (MDS) with unique clinical features and cases with this syndrome presenting with thrombocytosis of more than 1,000 x 10(9)/L but without anemia are rare. Furthermore, it is noteworthy that in this patient transition to acute leukemia occurred following development of myelofibrosis and marked splenomegaly, which are generally observed in blastic crises resulting from chronic myeloproliferative disorders (CMPD). The patient showed features indicative of CMPD rather than of MDS in spite of presenting with 5q- chromosomal abnormality. This case supports the concept of "mixed myelodysplastic and myeloproliferative syndromes" and suggests the possibility of the appearance of CMPD-like manifestations in 5q- syndrome.

Adult↗
PubMed2007

Essential versus reactive thrombocythemia in children: retrospective analyses of 12 cases.

BACKGROUND: Essential thrombocythemia (ET) rarely occurs in the pediatric population and little is known about the clinical course and the molecular characteristics. PROCEDURE: In this retrospective multi-institutional study we examine the clinical, hematological, and molecular features of 12 children aged 5-16 years with thrombocytosis and a suspected diagnosis of ET. RESULTS: Median follow-up was 59 months (range 10-72). Seven patients presented with clinical symptoms potentially related to thrombocytosis. The remaining five patients were diagnosed incidentally. Median platelet count at diagnosis was 1,325 x 10(9)/L (range 600-3,050). In 11 out of 12 cases bone marrow morphology was consistent with ET, the remaining patient had chronic idiopathic myelofibrosis. Cytogenetic analyses were normal in all studied cases and only one out of nine analyzed cases harbored a JAK(V617F) allele. Within 6 months after initial presentation one patient who was initially asymptomatic developed thrombosis and another patient had mild bleeding. Eight patients were treated with acetylsalicylic acid, one patient received hydroxyurea, and two patients received anagrelide. At last follow-up, all patients were alive and none had developed leukemia. Five patients experienced hematological remission. Two children had not received any therapy. During the course of their disease, nine patients developed symptoms possibly attributable to an elevated platelet count. CONCLUSIONS: In JAK2 mutation negative cases, long-term follow-up is helpful to distinguish between primary and secondary thrombocytosis. Secondary cases are not associated with organomegaly but may present with unspecific symptoms. Indications for treatment in children remain unclear.

Adolescent↗
PubMed1998

Thrombopoietin in patients with hepatoblastoma.

Marked thrombocytosis (over 50 x 10(4)/microl) is frequently seen in patients with hepatoblastoma. Thrombopoietin (TPO), c-mpl ligand, has recently been purified as the major physiological regulator of the thrombopoiesis and is mainly produced in the liver. Since it is possible that TPO participates in thrombocytosis and the tumor growth of this particular hepatic tumor, serum TPO levels in addition to interleukin 1beta (IL-1beta) and IL-6 levels were assessed in seven untreated patients by using a sandwich enzyme-linked immunosorbent assay. High serum TPO levels were observed in all of the examined patients. The level ranged from 3.15 to 11.02 (mean +/- standard deviation; 6.08+/-1.25) fmol/ml. IL-6 levels were also somewhat higher than normal. Platelet counts, however, appeared to correlate more with serum TPO levels (p = 0.1) than with IL-1beta (p = 0.5) and IL-6 (p = 0.2) levels. Furthermore, using the reverse transcriptase polymerase chain reaction method, the expression of c-mpl mRNA was found in five of eight hepatoblastoma tissues as well as TPO mRNA in all eight tissues. These observations suggest that thrombocytosis in hepatoblastoma patients results from the production of cytokine members, including TPO, within tumor tissues. Additionally, it is possible that TPO might act as a type of autocrine and/or paracrine system for cellular growth in this tumor.

Child, Preschool↗
PubMed2005

Anagrelide: analysis of long-term efficacy, safety and leukemogenic potential in myeloproliferative disorders.

Appropriate treatment for nonreactive thrombocytosis resulting from a myeloproliferative disorder (MPD) is surrounded by controversy. Although few doubt the association of thrombocytosis with increased risk for life-threatening events such as thrombosis or hemorrhage, or the association between clonal myeloproliferation and the progression to acute leukemia or myelofibrosis, controversy exists regarding the timing and nature of appropriate therapeutic intervention. Studies have shown that treatment with myelosuppressive agents such as chlorambucil, busulfan, radiophosphorus (32P), and hydroxyurea reduces the platelet count. However, investigators have also identified an increased risk of drug-related leukemic transformation. An ideal cytoreductive treatment for long-term use should minimize thrombosis and avoid long-term complications, especially acute leukemia (AL). Anagrelide, an imidazoquinolin, inhibits megakaryopoiesis and more selectively reduces platelet production in humans. A retrospective analysis of an open-label, multicenter, international trial reviewing 3660 anagrelide-treated patients was performed to assess efficacy and long-term safety, specifically potential for increased leukemogenicity. The study included MPD patients with thrombocytosis diagnosed according to Polycythemia Vera Study Group (PVSG) criteria. Of all patients enrolled, 81% had previously received other myelosuppressive agents; of these, 33% were transferred from the original agent to anagrelide due to toxicity and 31% were transferred because of poor platelet control. Over 45% of patients were symptomatic due to thrombocythemia, most commonly vascular sequelae (25%). Dosage was titrated to achieve a platelet count < 600 x 10(9) L(-1) and ideally between 130 and 450 x 10(9) L(-1). The safety cohort of 3660 patients, including 2251 with essential thrombocythemia (ET), 462 with polycythemia vera (PV), and 947 with chronic myeloid leukemia (CML) and other MPDs, was analyzed to establish the incidence of leukemic transformation in patients with ET and PV. From the Safety Population, 12.8% (467/3660) of patients were treated with anagrelide as the sole cytoreductive agent (naive patients). Acute leukemia/myelodysplasia developed in 2.1% of ET patients (47/2251) with a maximum follow-up of 7.1 years. Of the PV patients, 2.8% developed acute leukemia/myelodysplastic syndrome (13/462), with a maximum follow-up of 7.0 years. ET and PV patients who transformed to AL had all been previously exposed to other cytotoxics; there were no ET or PV patients in the study who transformed to AL exposed solely to anagrelide. With maximum follow-up over 7 years, anagrelide achieved platelet control in over 75% of MPD patients and did not increase the conversion to acute leukemia during the treatment duration analyzed. Longer follow-up is required to confirm these important observations regarding the long-term safety of anagrelide.

Adolescent↗
PubMed2002

Marked improvement of thrombocytopenia in a murine model of idiopathic thrombocytopenic purpura by pegylated recombinant human megakaryocyte growth and development factor.

OBJECTIVE: We examined the stimulatory effect of pegylated recombinant human megakaryocyte growth and development factor (PEG-rHuMGDF) on platelet production in male (NZW x BXSB) F(l) (W/B F(1)) mice, a murine model of idiopathic thrombocytopenic purpura. MATERIALS AND METHODS: A cohort of 19- to 25-week-old, severely thrombocytopenic male W/B F(1) mice were given PEG-rHuMGDF at different dosing schedules. Before and at various times after therapy, platelet counts, reticulated platelets, platelet lifespan, and levels of platelet-associated immunoglobulin G were measured. Analysis of megakaryocytic cells was performed. RESULTS: Treatment of male W/B F(1) mice with PEG-rHuMGDF (30 microg/kg/day) three times per week for several weeks resulted in sustained thrombocytosis, accompanied by increased megakaryocytopoiesis in both the bone marrow and spleen. The degree of the platelet response to PEG-rHuMGDF varied between individual mice, likely reflecting the heterogeneity of the disease. Production of new platelets in response to PEG-rHuMGDF was manifested by an increase in reticulated platelets. Levels of platelet-associated immunoglobulin G decreased inversely during periods of thrombocytosis. PEG-rHuMGDF therapy also improved thrombocytopenia in male W/B F(1) mice refractory to splenectomy. Platelet lifespan was not affected by PEG-rHuMGDF. Male W/B F(1) mice treated with pegylated murine MGDF, a homologue of PEG-rHuMGDF, had persistent thrombocytosis for at least 7 months, suggesting that antiplatelet antibody production was not enhanced. CONCLUSIONS: PEG-rHuMGDF therapy potently stimulated platelet production, effectively ameliorating thrombocytopenia in a murine model of idiopathic thrombocytopenic purpura.

Animals↗
PubMed1997

Uteroferrin and recombinant bovine GM-CSF modulate the myelosuppressive effects of 5-fluorouracil in young female pigs (Sus scrofa).

The present study investigated the ability of uteroferrin and recombinant bovine granulocyte monocyte/macrophage-colony stimulating factor (rbGM-CSF) to modulate the myelosuppressive effects of 5-fluorouracil (5-FU) in young female pigs (Sus scrofa). Pigs (N = 3/treatment) were infused with 5-FU (32.5 mg/kg) on days 0 and 1 of the experimental period. Uteroferrin (100 micrograms/kg in 0.9% NaCl), rbGM-CSF (10 micrograms/kg in 0.9% NaCl), uteroferrin + rbGM-CSF (as above) or control (0.9% NaCl) were administered as intramuscular injections twice daily (0800 and 2000 hr). Peripheral blood cell number, composition, and progenitor cells were determined over 28 days. Treatment of pigs with 5-FU resulted in a rapid leukocytopenia and thrombocytopenia (nadirs on days 5 and 7, respectively) and a modest decrease (P < 0.05) in red blood cell (RBC) number (nadir on day 14). Although nor affecting RBC and thrombocytes, treatment of pigs with uteroferrin had an initial protective effect (P < 0.05) on the 5-FU-induced leukocytopenia (63 and 64 vs 48 and 39 +/- 6% of baseline on days 3 and 5, respectively). In contrast, rbGM-CSF enhanced (P < 0.05) the rate of the leukocytopenia and had only minor effects on thrombocyte numbers relative to controls. These effects appeared to be additive, as pigs treated with uteroferrin + rbGM-CSF had a reduced rate of leukocytopenia compared to pigs treated with rbGM-CSF alone. Uteroferrin + rbGM-CSF also attenuated (P < 0.05) the suppression and enhanced (P < 0.05) recovery of RBC and thrombocyte numbers following 5-FU treatment. In control pigs, a modest rebound leukocytosis (122 +/- 6% of baseline) and thrombocytosis (141 +/- 9% of baseline) was evident. Uteroferrin enhanced (P < 0.05) the rebound leukocytosis (135 +/- 6% of baseline), but attenuated (P < 0.05) the thrombocytosis. In contrast, rbGM-CSF enhanced (P < 0.05) the duration of the leukocytosis during the recovery phase, an effect augmented by the combination of uteroferrin + rbGM-CSF. In addition, treatment with uteroferrin + rbGM-CSF resulted in a sustained thrombocytosis (days 12 to 21). As indicated by changes in CFU-GM, BFU-E, and CFU-GEMM progenitor cells in peripheral blood, the effects of uteroferrin and rbGM-CSF appeared to reflect their ability to enhance the proliferation and/or differentiation of both similar and distinct hematopoietic progenitor cells.

Acid Phosphatase↗
PubMed1995

Platelet count and the outcome of operation for ruptured abdominal aortic aneurysm.

PURPOSE: The purpose of this study was to determine the relationship between admission and postoperative platelet count (PC) and mortality and morbidity rates after emergency surgery for ruptured abdominal aortic aneurysm (AAA). METHODS: We performed a case record review of 65 consecutive patients admitted with ruptured AAA. RESULTS: Five patients did not undergo operation because of poor clinical condition, 12 patients died at operation, 13 patients died after operation, and 35 patients survived (operative mortality rate of 58%). Fifteen patients had an admission PC of less than 150 x 10(9)/L, of whom 14 (93%) died; 27 patients had an admission PC of 150 to 250 x 10(9)/L, of whom 8 (30%) died; and 18 patients had an admission PC of greater than 250 x 10(9)/L of whom 3 (17%) died. At the end of operation 29 patients had a PC of less than 100 x 10(9)/L, of whom 13 (45%) died, 20 (69%) had development of multiorgan failure (MOF), and 6 (21%) required relaparotomy for bleeding complications. By contrast, all 19 patients having a PC of 100 x 10(9)/L or greater at the end of the operation survived, three (16%) had development of MOF, and none required further surgery for bleeding. There was a significant inverse correlation between PC at the end of the operation and the number of postoperative days spent on a ventilator, in the intensive therapy unit, and in hospital. After operation, 15 patients had development of thrombocytosis (PC > 400 x 10(9)/L), of whom 10 had development of deep venous thrombosis and 8 had development of pulmonary embolism. There were no deep venous thromboses or pulmonary embolisms in patients who did not have development of a postoperative thrombocytosis. CONCLUSIONS: There is a direct correlation between PC on admission to the hospital and death after emergency repair of ruptured AAA. Thrombocytopenia at the end of the operation is associated with a high risk of morbidity from continuing hemorrhage or MOF. The development of postoperative thrombocytosis is associated with a high risk of thromboembolic complications. PC provides a simple marker of outcome in patients diagnosed with and undergoing operation for ruptured AAA.

Aged↗
PubMed1997

Changes in platelet count, coagulation and fibrinogen associated with elective repair of asymptomatic abdominal aortic aneurysm and aortic reconstruction for occlusive disease.

BACKGROUND: Mortality and morbidity following aortic surgery, particularly repair of ruptured abdominal aortic aneurysm (AAA), is frequently associated with the development of coagulopathy. OBJECTIVES: To examine changes in platelet count (PC), fibrinogen, and coagulation in patients undergoing elective repair of asymptomatic abdominal aortic aneurysm (AAA) and aortic surgery for occlusive disease. DESIGN: Prospective clinical study in a University Department of Vascular Surgery. PATIENTS: Thirty-three patients undergoing elective repair of asymptomatic AAA and 19 patients undergoing aortic surgery for occlusive disease. METHODS: Full blood count (FBC), clotting screen, and fibrinogen measured pre-operatively; 6, 12, 24, 48 h postoperatively; and thereafter as clinically indicated in 23 consecutive patient's undergoing AAA repair (Group 1). Pre- and postoperative PC measured weekly for 4 weeks following operation in a further 10 consecutive patients undergoing AAA repair (Group 2) and perioperative PC measured in 19 consecutive patients undergoing aortic surgery for occlusive disease (Group 3). RESULTS: Group 1: Preoperative haematological parameters were normal. There was no mortality. Postoperatively, 21 (91%) patients developed thrombocytopenia (PC < 150 x 10(9)/l). The postoperative fall in PC (median 90, range 12-160 x 10(9)/l) was significantly related to the duration of aortic cross-clamp (median 46, range 20-127 min, r2 = 0.33, p < 0.01). At 10 days all patients had developed thrombocytosis (PC > 350 x 10(9)/l) Postoperatively, by 48 h, 17 (74%) patients had developed hyperfibrinogenaemia. One patient suffered a myocardial infarction associated with a PC of 105 x 10(9)/l and a fibrinogen of 7.2 g/l. GROUP 2: In a further 10 patients undergoing AAA repair postoperative thrombocytosis was found to persist for several weeks in five of nine survivors. GROUP 3: Patients undergoing aortic surgery for occlusive disease had significantly higher preoperative PC than AAA patients (median 292, range 179-251 x 10(9)/l vs. median 204, range 140-293 x 10(9)/l, p < 0.01). CONCLUSIONS: Patients undergoing elective repair of AAA demonstrate similar, albeit less dramatic, changes in platelet count to those we have previously reported in patients undergoing repair of ruptured AAA. Aortic clamping leads to platelet sequestration and thrombocytopenia in the early postoperative period. Later, patients develop hyperfibrinogenaemia and thrombocytosis which may persist for several weeks. Similar changes are seen in patients undergoing aortic surgery for occlusive disease. These changes may represent a hypercoagulable state that predisposes these patients to thrombotic complications.

Aged↗
PubMed2005

Acroparesthesia and acral arterial occlusions as first manifestations of essential thrombocythemia.

Thrombocytosis is either caused by a reactive process (secondary thrombocytosis) or by a clonal bone marrow disorder The latter category includes essential thrombocythemia with bleedings and thrombotic complications as major causes of illness and death in this patients. We describe a 43-year-old man with a 6 months history of acroparesthesia in his toes. Half a year after onset of these symptoms, he noticed a bluish discoloration of digit V of his left foot. On first presentation physical examination revealed a bluish discoloration of all toes and a cold and blue digit V of the left foot. Peripheral pulses were all palpable, normal ankle systolic pressure measurements and normal pulse volume recordings except for digit V of the left foot were found. Laboratory tests revealed thrombocytosis of 800000/microliter. On treatment with acetylsalicylacid, prostanoids intravenously and low molecular weight heparin, the patient became asymptomatic and pulse volume recording of digit V was normalized. After exclusion of cardial or vascular sources of embolism by utrasonography bone marrow aspirate and biopsy supported the diagnosis of essential thrombocythemia.

Adult↗