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PubMed2004

[Essential thrombocythemia and retinal vein thrombosis].

CASE REPORT: Essential thrombocytosis is a disorder of the hematopoietic stem cell that causes proliferation of platelets. We report two cases: a 72-year-old woman with ischemic retina and tortuous and white veins in the superior retina and diffuse hemorrhages in the inferior retina with blot hemorrhages scattered throughout the equatorial region in the left eye; and a 62-year-old man with a central retinal vein occlusion in the left eye as signs of essential thrombocythemia. DISCUSSION: These cases are examples of potential complications of essential thrombocytosis. Vulnerable patients should be monitored for retinal vascular occlusions, especially when platelet counts do not exceed 106/mm3.

Aged↗
PubMedDate not supplied

Therapeutic plateletpheresis in thombocythemia.

Patients with myeloproliferative thrombocythemia have usually been managed with chemotherapy. Generally, removal of platelets from such patients has been performed intermittently to lower the platelet mass rapidly when neurologic or hemorrhagic complications were manifest or concurrently with the initiation of chemotherapy. A platelet count of 1,000,000/microliter or less was maintained by the use of repeated plateletpheresis over a period of three months in a patient with essential thrombocythemia, who had frequent syncopal episodes. A second patient with secondary thrombocytosis, who sustained two cerebrovascular accidents, underwent intermittent plateletpheresis over a 22-day period until her underlying disorder improved. It is concluded from the experience, combined with that of others, that plateletpheresis is not only a life-saving procedure in an acute episode but may also be used to maintain a lowered platelet count over a prolonged period in selected patients with primary thrombocythemia, in whom chemotherapy cannot be undertaken, and in symptomatic patients with secondary thrombocythemia.

Adult↗
PubMed2004

Pathophysiology and treatment of platelet-mediated microvascular disturbances, major thrombosis and bleeding complications in essential thrombocythaemia and polycythaemia vera.

Essential thrombocythaemia (ET) is associated with a broad spectrum of microvascular circulation disturbances including erythromelalgia and its ischaemic complications, episodic neurological symptoms of atypical and typical transient ischaemic attacks (TIAs), transient ocular ischaemic attacks, acute coronary syndromes, and superficial 'thrombophlebitis'. The microvascular circulation disturbances are caused by spontaneous activation and aggregation of hypersensitive thrombocythaemic platelets at high shear stress in the endarterial microcirculation involving the peripheral, cerebral and coronary circulation. As this microvascular syndrome is a pathognomonic feature of essential thrombocythaemia and of thrombocythaemia associated with polycythaemia vera (PV) in complete remission with normal haematocrit, we have labelled these two variants of thrombocythaemia as thrombocythaemia vera. The arterial thrombophilia of microvascular circulation disturbances in thrombocythaemia vera already occur at platelet counts in excess of 400 x 10(9)/l. Complete relief of microvascular circulation disturbances in thrombocythaemia vera is obtained with the platelet cyclooxygenase inhibitor aspirin 50-100 mg/day, but not with dipyridamole, ticlopidine, coumarin or heparin. Haemorrhagic thrombocythaemia (HT) is a clinical syndrome of recurrent spontaneous mucocutaneous and secondary haemorrhages associated with extremely high platelet counts far in excess of 1000 x 10(9)/l. The paradoxical occurrence of microvascular circulation disturbances and mucocutaneous bleeding is usually seen at platelet counts between 1000 and 2000 x 10(9)/l. At increasing platelet counts from below 1000 to in excess of 2000 x 10(9)/l, the arterial thrombophilia of thrombocythaemia vera changes into a spontaneous bleeding tendency of HT as a consequence of platelet-mediated increased proteolysis of the large von Willebrand factor multimers leading to a type 2 acquired von Willebrand syndrome. As PV is usually associated with thrombocythaemia, the vascular complications in PV patients are microvascular circulation disturbances typical of thrombocythaemia. On top of this, major arterial and venous thrombotic events and haemorrhages are related to increased haematocrit, red cell mass and its concomitant increased blood viscosity. Correction of increased blood viscosity and haematocrit to normal values (0.40-0.44) by bloodletting alone will significantly reduce the risk of major thrombotic complications, but does not prevent the microvascular circulation disturbances because thrombocythaemia persists. The microvascular syndrome associated with thrombocythaemia in PV patients in remission after bloodletting is best controlled by low-dose aspirin (50-100 mg/day) or by reduction of platelet count to normal (< 350 x 10(9)/l).

Blood Platelets↗
PubMed1987

Aspirin and risk of bleeding in patients with thrombocythemia.

Thirty-two patients with thrombocythemia associated with myeloproliferative syndromes were selected on the basis of normal bleeding time and absence of hemorrhagic or thrombotic history. Twenty-five control subjects were studied simultaneously. They were all given a single intravenous infusion of 500 mg of aspirin (lysine acetylsalicylate), and bleeding time was measured two hours later. Both in the control group and in the patient group, aspirin significantly prolonged the bleeding time, but the average prolongation was significantly more pronounced in the patients. In comparison with the control subjects, the patients had a statistically significant reduction of platelet serotonin content and no difference in the production of platelet lipoxygenase derivative 12-HETE or plasma von Willebrand factor properties. Fourteen patients had abnormal platelet aggregation in response to adenosine diphosphate, adrenaline (epinephrine), or collagen. In six of them, all with very low serotonin content, the bleeding time was prolonged above the upper limit of the post-aspirin values in the control group. Thus, cyclooxygenase inhibition by aspirin unmasked a bleeding tendency in patients with a severe reduction in platelet dense bodies content. These findings might be relevant in relation to the use of antiplatelet drugs.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1999

Acquired von Willebrand disease due to increasing platelet count can readily explain the paradox of thrombosis and bleeding in thrombocythemia.

The arterial microvascular thrombotic events in thrombocythemia including erythromelalgia, atypical and typical cerebral and ocular transient ischemic attacks, and acute coronary syndromes already occur at platelet counts > 400 x 10(9)/L and are sensitive to low-dose aspirin, which does not elicit bleedings at platelet counts < 1,000 x 10(9)/L. An increasing platelet count in thrombocythemia to above 1,000 x 10(9)/L is accompanied by the acquisition of a von Willebrand factor deficiency due to the loss of intermediate and large von Willebrand factor multimers. The arterial thrombotic condition in thrombocythemia changes into an overt spontaneous bleeding tendency at mean platelet counts of about 2,000 +/- 1,000 x 10(9)/L due to an acquired von Willebrand disease type II with normal values for von Willebrand factor antigen concentration but absence of intermediate and large von Willebrand factor multimers in plasma. At platelet counts between 1,000 and 2,000 x 10(9)/L, thrombosis and bleeding frequently occur in sequence or paradoxically, and low-dose aspirin does prevent thrombotic complications but aggravates or may elicit bleeding symptoms. Reduction of the platelet count < 1,000 x 10(9)/L significantly restores the von Willebrand factor deficiency with the reappearance of the intermediate and some of the large von Willebrand factor multimers and the disappearance of the bleeding tendency, but the thrombotic tendency persists as long as platelet counts are above the upper limit of normal. The acquisition of von Willebrand factor deficiency at increasing platelet counts can readily explain the paradox of thrombosis and bleeding in thrombocythemia and has important clinical implications.

Blood Platelets↗
PubMed1992

Remission may continue after termination of rIFN alpha-2b treatment for essential thrombocythemia.

Essential thrombocythemia, a myeloproliferative disorder of clonal origin, is often associated with various clinical manifestations resulting from thromboembolic or hemorrhagic complications. The long-established successful method of treatment with cytotoxic agents or radioactive phosphorus has recently been superseded by interferon alpha. We treated 14 symptomatic patients with 5 x 10(6) IU recombinant interferon alpha-2b s.c. daily. 12/14 pts responded within 14-75 days. When platelet counts decreased to below 450 g/l the frequency of administration was reduced stepwise. 7 patients remained in CR during this reduction phase and treatment was stopped in 5 pts after 12-32 months. Until now, 3 of them are still in continuous good PR without any drug therapy and free of symptoms for 3+, 19+ and 36+ months. Continuous response during maintenance was associated with age, initial platelet count and time required to reduce platelet counts to less than 450 g/l.

Adult↗
PubMed1983

[Primary thrombocythemia in childhood].

Primary thrombocythemia is a myeloproliferative disease characterized by a sustained and marked increase in platelet count. The platelet number rises in excess of 1000 X 10(9)/l. Adult patients present with recurrent hemorrhages, thrombotic episodes and microvascular disturbances. It is a relatively benign disease and rarely reported in children. We describe two patients with a thrombocythaemia. The first, a 13 1/2 year old boy, had no complaints. A thrombocythemia (2167 X 10(9)/l) and splenomegaly were found by chance. He was treated with melfalan. Acetylsalicilic acid and dipyridamol were added as anti-coagulants. The second patient, a 12 year old girl, was submitted to a splenectomy at the age of 10, because of a traumatic rupture. Sixteen months later she was admitted to our hospital with symptoms of thrombotic as well as bleeding tendency. Periferal microvascular disturbances and symptoms on the basis of impaired cerebro-vascular bloodflow were found. The number of platelets was 5083 X 10(9)/l. She was treated in the same way as the first patient. Symptoms disappeared as soon as the number of platelets decreased. In both patients periferal blood and bonemarrow examination as well as platelet function, measured by aggregation studies, were abnormal. Consideration of the literature on children and our own case I indicate that this disease in the younger patient may exist without undue risk of complications. One might consider treatment with anti-aggregating agents only.

Adolescent↗
PubMed1999

Aspirin seems as effective as myelosuppressive agents in the prevention of rethrombosis in essential thrombocythemia.

The course of essential thrombocythemia (ET) is complicated by bleeding, major thrombosis, and microvascular complications. Because about one-half of ET patients remain asymptomatic long term, the decision to use aspirin acetylsalicylic acid, (ASA) or myelotoxic drugs has not yet been clearly established. While vasomotor symptoms are improved by small doses of ASA, higher doses (900 mg/day) induce an unacceptable rate of serious hemorrhagic complications in patients with polycythemia vera. This retrospective study evaluates the utility of therapy in preventing thrombosis in ET and the efficacy and a safety of 100 mg/day of ASA in these patients. One hundred ninety-five consecutive patients with ET diagnosed in agreement with the Polycythemia Vera Study Group (PVSG) criteria are evaluated. All vascular complication before, at, or after diagnosis were recorded and related to the treatment used: no therapy, ASA alone, myelosuppressive agents or both. All treated patients had a significant reduction of thrombotic complications without increased hemorrhagic complications, in spite of therapy adopted. In addition, a significant reduction of rethrombosis was obtained in 60 patients with a previous thrombosis. A low rate of thrombosis (5.1%) was observed during the follow-up of the 135 patients previously asymptomatic for major complications. No difference appears to exist between the use of ASA and cytotoxic drugs in preventing thrombosis and rethrombosis in ET patients. However, the possible increase of cancer and leukemia with myelosuppressive drugs is minimized in patients treated with ASA. A low dose of ASA would seem to be a safe and effective agent in ET.

Adolescent↗
PubMed2006

Condylar resorption following temporomandibular joint arthroscopy in a patient with essential thrombocythemia.

Condylar resorption of the temporomandibular joint (TMJ) is a poorly understood phenomenon that is the subject of much controversy. The following case report depicts a unique case of condylar resorption (CR) in a 49-year-old female patient with essential thrombocythemia who underwent arthrocentesis of the TMJ. The exact cause of the CR is unclear but it is speculated that it was likely due to hemorrhagic and thrombotic complications during surgery secondary to an elevated platelet count.

Arthroscopy↗
PubMed1998

Prognostic and diagnostic value of endogenous erythroid colony formation in essential thrombocythemia.

Endogenous erythroid colonies (EECs), a typical characteristic of polycythemia vera (PV), could be observed in essential thrombocythemia (ET). Erythroid progenitors culture carried out in 34 previously untreated patients with unequivocal ET showed EECs in 35% of the cases. During a mean follow up of 4 years after the culture, the 12 EECs(+) and the 22 EECs(-) patients did not show any difference for a thrombotic or haemorrhagic complication, and the only one patient who showed an involvement of erythropoiesis was in the EECs(-) group.

Adult↗
PubMed1990

Hemostatic complications in young patients with essential thrombocythemia.

PURPOSE: The purpose of this study was to determine the incidence of hemostastic complications in young patients with essential thrombocythemia (ET). PATIENTS AND METHODS: The clinical course of 44 patients under the age of 45 with the diagnosis of ET was reviewed in a retrospective manner. Patients were collected from three medical centers in the United States and Italy: the Brigham and Women's Hospital and the Harvard Community Health Plan, Boston, Massachusetts, and the Ospedali Riuniti di Bergamo, Bergamo, Italy. RESULTS: The overall incidence of hemorrhage or thrombosis, or both, in this group of patients was 39% (17 of 44), with serious complications occurring in 23% (10 of 44). Two patients died of thrombotic events. Neither the presence of symptoms at diagnosis nor any single laboratory parameter proved predictive of clinical sequelae. Treatment with antiplatelet drugs or platelet-lowering agents was not protective. CONCLUSION: We conclude that ET in young patients may result in serious and life-threatening hemostatic problems and consequently that young age is not a favorable prognostic factor in this disease.

Adolescent↗
PubMedDate not supplied

[Cerebrovascular disease in the cancer patient].

OBJECTIVE: To make an up-to-date review of the literature on cerebrovascular disease of the patient with cancer. DEVELOPMENT: Approximately 15% of the patients with cancer have cerebrovascular disease. The frequency of cerebral infarcts is similar to that of cerebral hemorrhage. The commonest mechanisms of cerebral ischemia are atherosclerosis, non-bacterial thrombotic endocarditis, disseminated intravascular coagulation, infection, tumour embolism and thrombosis of the longitudinal venous sinuses. The most usual mechanisms of cerebral hemorrhage are intratumoural hemorrhage, hypertensive hemorrhage and the coagulopathies. In the Stroke Register of the Hospital del Sagrat Cor in Barcelona, of a total of 1,099 patients with their first cerebrovascular episode, in 14 patients the stroke (12 infarcts and two intracerebral hemorrhages) were the form of onset of a previously unrecognised hematological disorder. The hematological neoplasias were the commonest form of hematological disorders, mainly essential thrombocythemia, which was diagnosed in six patients. CONCLUSIONS: The clinical management and care of patients with stroke and cancer differ from that of patients with stroke alone, since the cause is different from that of non-neoplastic patients.

Brain Ischemia↗
PubMed1998

No treatment for low-risk thrombocythaemia: results from a prospective study.

Essential thrombocythaemia (ET) is a chronic myeloproliferative disorder characterized by the occurrence of thromboembolic episodes, particularly in patients aged > 60 years or with a previous history of thrombosis, and/or by haemorrhages in patients with an exceedingly high platelet count. In these subgroups of patients the use of cytoreductive therapy is beneficial in terms of risk/benefit ratio. Only limited anecdotal data are available on the thrombotic or haemorrhagic risk and survival in young asymptomatic ET patients with a platelet count < 1500 x 10(9)/l. Therefore the optimal management of these patients is unknown. To assess the incidence of thrombosis and haemorrhages in this group of patients we carried out a prospective observational study in a cohort of 65 patients with ET, aged < 60 years, with no history of thrombosis or haemorrhage and platelet count < 1500 x 10(9)/l, and in 65 age- and sex-matched controls. Patients were not treated with cytoreductive therapy until the occurrence of thrombosis or haemorrhage. Arterial or venous thrombotic events were objectively documented both in cases and in controls. The median follow-up was 4.1 years, with an incidence of thrombosis in patients and controls of 1.91 and 1.50 cases/100 patient-years, respectively. The age- and sex-adjusted risk rate ratio was 1.43 (95% CI 0.37-5.4). Only three minor haemorrhagic episodes occurred in patients, with an incidence of 1.12 cases/100 patient-years. Pregnancy and surgery were not associated with thrombosis in these patients. We conclude that the thrombotic risk in young ET patients, with no thrombotic history and a platelet count < 1500 x 10(9)/l, is not increased compared to the normal population and that a conservative therapeutic approach should therefore be considered in these patients.

Adolescent↗
PubMed2005

Thrombosis and haemorrhage in polycythaemia vera and essential thrombocythaemia.

Despite decades of clinical and laboratory research, relatively little has been accomplished concerning the pathogenesis as well as the identification of risk factors for thrombosis and bleeding in myeloproliferative disorders. In polycythaemia vera, the pro-thrombotic effect of an elevated haematocrit is well established. In contrast, thrombocytosis per se has not been similarly incriminated in essential thrombocythaemia. In both conditions, advanced age and the presence of a prior event identify thrombosis-prone patients. There is increasing evidence to suggest an additional role by leucocytes that might partly explain the antithrombotic effects of myelosuppressive therapy. A substantial minority of affected patients display reduced levels of high molecular weight von Willebrand protein in the plasma during extreme thrombocytosis and it is believed that this might explain the bleeding diathesis of such patients. Recent controlled studies support the therapeutic value of hydroxyurea and aspirin in essential thrombocythaemia and polycythaemia vera, respectively. The current communication will address the incidence, phenotype, pathogenesis, risk factors, prevention, and treatment of both thrombosis and haemorrhage in these disorders.

Aged↗