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PubMed2001

Prevalence of HTLV-I-associated T-cell lymphoma.

In order to assess the prevalence rate of HTLV-1-associated T-cell lymphomas and human retrovirus infection in general, approximately 21,000 individuals representing various patient populations, retroviral risk groups, and blood donors were examined for HTLV-I, HTLV-II, HIV-1, or HIV-2 infection using serologic and PCR assays. The prevalence rates among volunteer blood donors were 0.02% and 0% for HTLV and HIV, respectively. Significantly increased HTLV prevalence rates were observed among paid blood donors, African American health care clinic patients, Amerindians, recipients of HTLV-positive cellular blood products, intravenous drug users, sexual contacts and family members of HTLV-positive people, and patients with primary thrombocytosis and other-than-low-grade non-Hodgkin's lymphoma (NHL). Among some of these groups there were significant differences in the prevalence of HTLV-I versus HTLV-II. The eight HTLV-positive NHL patients all had mature, high-grade, CD4+ T-cell lymphomas with clonally integrated HTLV-I, for a prevalence of 4% among other-than-low-grade NHL patients. Seven of the eight died from their disease within 2 years despite treatment. Interestingly, two groups at risk for HTLV infection, namely needle stick victims and recipients of HTLV-infected and/or pooled plasma products, showed no evidence for infection. Significantly increased HIV-1 prevalence was observed among paid blood donors, African Americans, homosexuals, female prostitutes, hemophiliacs, and other-than-low-grade NHL patients. Only one patient was infected with HIV-2. Of the nine HIV-positive, other-than-low-grade NHL patients, seven HIV-1 positives had B-cell lymphomas, one HIV-1 positive had an HTLV-I-positive CD4+ T-cell lymphoma, and one infected with HIV-2 had a CD4+ T-cell lymphoma that was HTLV negative. The data indicate that HTLV-I lymphoma, while uncommon, is not necessarily rare among other-than-low-grade NHL cases in the United States and, given its poor prognosis, should probably be studied separately in clinical trials.

Black or African American↗

PubMed1976

Erythroleukemia-like syndrome due to busulfan toxicity in polycythemia vera.

Over a 19-year period, a patient with polycythemia vera who had undergone a splenectomy received six courses of busulfan for recurrent thrombocytosis. The total dose of busulfan given for the sixth course was greater than that used for the previous ones. Severe pancytopenia followed, which persisted for 4 months. During this period there was marked erythroid hyperplasia in the bone marrow with striking dyserythropoiesis; PAS-positive red cell precursors, as well as moderate numbers of circulating normoblasts and evidence of chronic and acute hemolysis, were present. All of these findings reverted to normal without therapy, and the polycythemic state eventually recurred. These events are interpreted as an unusual marrow reaction following busulfan overdosage rather than a transient erythroleukemia.

Adult↗

PubMed2003

Imatinib mesylate in idiopathic and postpolycythemic myelofibrosis.

Imatinib mesylate targets the adenosine triphosphate (ATP)-binding sites of the protein tyrosine kinase domains associated with Bcr-abl, the platelet-derived growth factor (PDGF) and c-kit. In idiopathic myelofibrosis (IMF) PDGF is considered to be one of the growth factors responsible for the development of bone marrow fibrosis. Recently, it has been shown that imatinib has antifibrogenic effect on bone marrow fibrosis in chronic myelogenous leukemia. Treatment with imatinib alone in IMF has been associated with significant side effects. In this study, the safety and efficacy of imatinib therapy in IMF, either administered as a single agent or in combination with hydroxyurea (HU) and/or alpha-interferon (IFN-alpha) are evaluated. Eleven patients (median age, 63 years; range, 33-82 years) with IMF (n = 8) or postpolycythemic myelofibrosis (PPMF) (n = 3) were studied All patients had been treated with HU (n = 9) and/or IFN (n = 7) before study entry. In all but one patient, treatment with these agents was discontinued when imatinib therapy was instituted. One patient continued IFN when treatment with imatinib was started. Imatinib was given at a dose of 400 mg/day. Nine patients were in an advanced disease phase. The patients have been followed for a median period of 2 months (range, 0.5-12 months). Treatment with imatinib has been stopped in six patients (55%), because of overt side effects (n = 4), recurrence of transitory dizziness and visual defects owing to a rising platelet count (n = 1), or the occurrence of an acute subdural hemorrhage that was evacuated without neurological deficits (n = 1). In nine patients imatinib treatment was followed by a rise in leukocyte and platelet counts that required combination with HU or IFN. The combined treatment modalities were followed by a rapid decrease in cell counts and were well tolerated apart from IFN side effects. A beneficial effect of imatinib was documented in three patients. It is concluded that leukocytosis and thrombocytosis are seen in most patients with myelofibrosis during treatment with imatinib. Combination therapy with HU or IFN seems safe and well tolerated and followed by a decrease in disease activity. A subgroup of patients in an early disease phase might benefit from imatinib therapy alone.

Adult↗

PubMed1981

Pure erythrocytosis: reappraisal of a study of 51 cases.

Fifty-one cases of pure, primary erythrocytosis were identified and followed at Hôpital Saint-Louis, Paris, and compared with 350 cases of polycythemia vera (PV) observed during the same period. At the initial evaluation, these cases did not differ from PV cases with respect to age, sex ratio, degree of red cell volume increase, and clinical symptoms. They did differ by the absence of splenomegaly, granulocytosis and thrombocytosis. At a late stage of evolution only a few cases developed classical criteria of PV. From this group of apparently homogeneous cases, two subgroups evolved. Sixty percent of the cases were highly responsive to myelosuppression with 32P. The median duration of the first remission was greater than five years, the mean yearly dose of 32P was very low, and there was a low incidence of complications. The other group (40% of cases) was relatively resistant to myelosuppressive agents. The development of better methods of investigate this disorder might help in discriminating these two groups from both an etiological and pathophysiological viewpoint. The thromboembolic risk of these diseases suggests that myelosuppressive therapy should be utilized in older patients with higher risk of vascular accidents, reserving phlebotomy for younger patients and those who are shown to be resistant to 32P therapy.

Adolescent↗

PubMed1987

Megakaryocytic colony formation (CFU-Meg) in essential thrombocythemia: quantitative and qualitative abnormalities of bone marrow CFU-Meg.

For the purpose of examining the mechanisms for the overproduction of megakaryocytes and platelets in essential thrombocythemia (ET), marrow megakaryocytic colony-forming units (CFU-Meg) were characterized using a methylcellulose culture system in nine patients with ET, and they were compared with those of 16 control subjects and four patients with secondary thrombocytosis (ST). The number of CFU-Meg per 10(5) cells in ET was significantly higher (p less than .001) than that in the controls (5.8 times of the controls) or that in ST. ET showed endogenous CFU-Meg (58 +/- 16% of the total CFU-Meg) that could form megakaryocytic colonies without phytohemagglutinin-stimulated leukocyte-conditioned medium (PHA-LCM) as a source of Meg-CSA. The controls and the patients with St revealed no endogenous CFU-Meg. The dose-response studies with PHA-LCM revealed that CFU-Meg from ET are highly sensitive to low concentrations of PHA-LCM compared to CFU-Meg from the control and ST. Erythropoietic burst-forming units (BFU-E) were monitored as a control progenitor, because the patients with ET studied did not have erythrocytosis. Although five out of nine patients with ET had endogenous BFU-E, the percentages of endogenous BFU-E were small (4-10%). The number of BFU-E in ET was not different from the control value. Thus, ET is associated with an enlarged CFU-Meg compartment that shows abnormal growth patterns when cultured in vitro, while the growth abnormality of BFU-E is small, which may underlie the hematological features of ET. The culture of CFU-Meg should be clinically useful for differentiating ET from ST.

Bone Marrow↗

PubMed1990

Effect of adherent cells on the regulation of BFU-E in patients with myeloproliferative disease.

The interaction between adherent cells and red cell progenitors from peripheral blood of patients with polycythemia vera (PV), essential thrombocytosis (ET), and healthy controls was studied. Various combinations of adherent and nonadherent cells were co-cultured in a semisolid system. Adherent cells from controls, when added at low concentrations, stimulated BFU-E proliferation, whereas high concentrations (40% of total cells in the culture) caused a significant decrease in the number of BFU-E colonies in 6/8 PV patients, 4/4 ET patients, and 8/12 controls. On the other hand, low and high concentrations of adherent cells from both patients with PV and ET caused a significant increase in BFU-E from either patients or controls. Moreover, adherent cells from these patients induced endogenous BFU-E proliferation (independent of erythropoietin) in nonadherent cells of 12/12 normal controls. The results show that BFU-E from patients with PV and ET are sensitive to suppression by normal adherent cells. On the other hand, adherent cells from these patients possess stimulatory activity on BFU-E from peripheral blood at all concentrations and are devoid of the inhibitory activity. This suggests a possible defect in the functioning of adherent cells in PV and ET patients which may contribute to the abnormal regulation of hematopoiesis in these disorders.

Cell Adhesion↗

PubMed1991

Platelet thrombospondin and glycoprotein IV abnormalities in patients with essential thrombocythemia: effect of alpha-interferon treatment.

Platelet aggregability and some biochemical parameters were evaluated in seven patients with essential thrombocythemia (ET) compared with seven patients with secondary thrombocytosis (ST). Defective platelet aggregation with one or more agonists was seen in five patients with ET whereas aggregation was increased in two other patients. In addition, three patients with ET demonstrated spontaneous platelet aggregation in citrated plasma. This was associated with increased level of thrombospondin (TSP) in the plasma membrane. Interestingly, the presence of a proteolyzed 160 kDa form of TSP was detected in all patients with ET, whereas it was never found in patients with ST. Furthermore, three patients with ET demonstrated increased levels of platelet surface glycoprotein IV (GP IV), the putative receptor for TSP in the plasma membrane. In two of these patients, this correlated with increased surface expression of TSP and spontaneous platelet aggregation. The results suggest a possible link between the increased number of plasma membrane GP IV molecules, the spontaneous expression of TSP on the platelet surface and platelet hyperaggregability in some ET patients. The levels of plasma membrane GP IV and platelet surface-associated TSP tended to be normalized during alpha-interferon treatment, whereas the presence of an altered form of TSP persisted. This last parameter might be of practical usefulness in the characterization of the disease, permitting a clear distinction from ST.

Aged↗

PubMed1994

Familial myeloproliferative syndrome.

Familial chronic myeloproliferative syndrome (CMS) was observed in five members from two different generations of the same kindred. Diagnosis included agnogenic myeloid metaplasia (case 1), polycythemia vera (case 2), and essential thrombocythemia (cases 3-5). Cases 1-3 were siblings, case 5 was the daughter of case 1, and case 4 was the cousin of cases 1, 3. Age at diagnosis ranged from 28 to 75 years, cases 1 and 3 were male, and the others were female. The diagnosis was made after an episode of cerebral thrombosis in one patient, during a study for headache and dizziness in another, and fortuitously in the three remainders. All patients had splenomegaly and varying degrees of thrombocytosis. The cytogenetic exam was normal in all four cases. A woman patient was treated with interferon during a pregnancy. Fetal growth was retarded, and the newborn showed bone and genital malformations. No environmental leukemogen factor was found. This familial case strengthens Dameshek's theory of a common pathogenesis of CMS and suggests a genetic and hereditary etiology.

Adult↗

PubMed1985

Evidence for intravascular coagulation in systemic onset, but not polyarticular, juvenile rheumatoid arthritis.

After observing a child with systemic onset juvenile rheumatoid arthritis (S-JRA) who developed purpura fulminans in association with disseminated intravascular coagulation, with subsequent gangrene and autoamputation, we undertook a prospective study of coagulation parameters in children with JRA. Ten consecutive children with S-JRA, 10 children with rheumatoid factor-negative, polyarticular juvenile rheumatoid arthritis (P-JRA), and 10 age- and sex-matched controls were studied. Routine coagulation screening tests were performed, as were tests for plasma fibrinopeptide A (a sensitive measure of intravascular thrombin generation), factor VIII-related antigen (an endothelial cell protein), and platelet factor 4 (a platelet-secreted protein). Our studies suggest that activation of intravascular coagulation is common in systemic onset JRA, but not in rheumatoid factor-negative, polyarticular disease. The coagulopathy may cause severe morbidity. In addition, marked elevations of plasma factor VIII-related antigen suggest perturbation of endothelial cells and vascular involvement in S-JRA, but not in P-JRA. Normal ranges of platelet factor 4 indicate that intravascular platelet consumption does not occur in either type of JRA, despite the thrombocytosis common in both.

Adolescent↗

PubMed2006

Palliative goals, patient selection, and perioperative platelet management: outcomes and lessons from 3 decades of splenectomy for myelofibrosis with myeloid metaplasia at the Mayo Clinic.

BACKGROUND: Although splenectomy may palliate massive splenomegaly in patients with myelofibrosis with myeloid metaplasia, this procedure carries significant risks. The authors retrospectively analyzed their experience with splenectomy over the course of 30 years to analyze the impact of improved techniques, antimicrobials, and aggressive postoperative control of platelet counts on outcome. METHODS: A total of 314 patients underwent splenectomy between 1976 and 2004 for mechanical symptoms (= 156 patients [49%]), anemia (= 78 patients [25%]), portal hypertension (= 47 patients [15%]), or thrombocytopenia (= 33 patients [11%]). Of a total of 91 patients studied during the last decade, 69 patients (76%) experienced a palliative benefit for their primary surgical indication for a median of 12 months (range, 1-91 months). RESULTS: Perioperative complications occurred in 87 patients (27.7%) including infection (= 31 patients [9.9%]), thrombosis (= 31 patients [9.9%]), or bleeding (= 44 patients [14%]), 21 of which (6.7% of all patients) were fatal. Perioperative thrombohemorrhagic complications decreased in the last decade through the use of platelet apheresis and the prompt use of cytoreductive agents to counteract postsplenectomy thrombocytosis. Survival after splenectomy was found to be decreased in patients with preoperative thrombocytopenia (<100 x 10(9)/L [P = 0.006]) but not by indication, myelofibrosis with myeloid metaplasia (MMM) prognostic score, or the decade in which splenectomy was performed. CONCLUSIONS: The lack of improvement in overall postsplenectomy survival over time may be a reflection on the failure of medical therapy to improve survival in patients with MMM.

Adolescent↗

PubMed2007

Long-lasting partial remission by Interferon-alpha treatment in a child with essential thrombocythemia.

Essential thrombocythemia (ET) is a clonal myeloproliferative disorder characterized by sustained thrombocytosis, isolated hyperplasia of megakaryocytic lineage, and association with thrombotic or bleeding episodes. It is extremely rare in childhood and frequently presents without evident clinical signs. We describe a 3-year-old girl with severe headache and dizziness suffering from ET, who was treated with Interferon-alpha-2a (IFN) based on the potent effect of this agent to inhibit myeloid colonies induced by phytohemagglutinin A stimulated leukocyte conditioned medium (PHA-LCM). Bone-marrow-derived mononuclear cells of this patient did not exhibit spontaneous colony formation but responded to recombinant human (rh) erythropoietin (EPO), rh granulocyte-colony stimulating factor (G-CSF), granulocyte-macrophage (GM)-CSF, and stem-cell factor in addition to PHA-LCM. After 65 months of in vivo IFN treatment, the patient experienced a sustained partial remission with platelet counts varying between 400 and 600 x 10(3)/microl.

Bone Marrow Examination↗

PubMed1995

Primary thrombocythemia: a current perspective.

The relationships among thrombocytosis, abnormal platelet aggregation and altered hemostasis in primary thrombocythemia remain poorly understood. Consequently, the appropriate management of asymptomatic patients is controversial and needs to be individualized. For symptomatic patients, conventional therapy, usually hydroxyurea, is directed primarily at lowering the platelet count by suppression of megakaryocyte activity. Recombinant interferon alpha can selectively lower platelet counts and may offer a reasonable alternative. Recent experience with anagrelide is also most promising in both symptomatic and asymptomatic patients. Current thoughts on the pathogenesis and management guidelines are presented here.

Aspirin↗

PubMed1993

Myocardial infarction in young patients with Hodgkin's disease--potential pathogenic role of radiotherapy, chemotherapy, and splenectomy.

Among a total of 2147 patients admitted to our hospital for acute myocardial infarction between 1978 and 1987, three young patients aged 24, 29, and 39 years had previously been treated for Hodgkin's disease. Staging laparotomy, including splenectomy, had been performed in all three patients. Two patients had both mediastinal irradiation (21 and 27 months before infarction) and chemotherapy. In the first patient, postmortem histologic examination of the coronary arteries revealed fibrotic changes, which were probably induced by radiotherapy. In our second patient, myocardial infarction developed 5 days after vinblastine treatment; early angiography showed thrombotic occlusion of the proximal right coronary artery, which was recanalized using the diagnostic Sones catheter. Subsequent angiography revealed normal coronary arteries. This is, to our knowledge, the first case of documented coronary artery thrombosis after treatment with vinca-alkaloids. In our third patient, neither mediastinal irradiation nor chemotherapy had been performed prior to myocardial infarction. However, a marked increase in platelet counts following splenectomy was observed in this patient. The role of radiotherapy, chemotherapy, and splenectomy with consecutive thrombocytosis as a third possible pathogenic factor for subsequent development of myocardial infarction is discussed.

Adult↗

PubMed1978

Hemostatic alterations in inflammatory bowel disease: response to therapy.

Twelve patients with acute, untreated inflammatory bowel disease (IBD) were followed prospectively for coagulation and platelet function. With no symptomatic coagulopathy, abnormalities were found in all patients. With acute diseases, elevations of fibrinogen (9/12), factor V (8/12), and factor VIII (6/12) were common. Depressions of antithrombin III levels were also observed acutely (8/12). Abnormalities of platelets were both quantitative and qualitative. Thrombocytosis was present (11/12), and abnormalities in the rate and percent platelet aggregation were seen (9/10). During therapy, factors V and VIII, antithrombin III levels, and the quantitative and qualitative platelet abnormalities returned towards normal in direct correlation with sedimentation rate and clinical disease activity.

Adolescent↗

PubMed1996

Microembolization from a carotid mural thrombus detected by transcranial Doppler.

Over the last few years, many authors have described the possibility of using transcranial Doppler to demonstrate the passage of microemboli in the cerebral arteries. We report the case of a 44-year-old woman with thrombotic diathesis and thrombocytosis who was admitted twice within a short period of time (one and a half months) to a neurological department because of multiple cerebral infarctions. On the occasion of the second admission, a colour-Doppler examination of the epiaortic vessels, which had previously been negative, showed a carotid lesion due to a mural thrombus and, on the same side as the carotid lesion, transcranial Doppler detected short-duration, high-intensity signals in the middle and anterior cerebral arteries, an expression of the passage of microemboli. As already described by other authors in similar clinical situations, our case confirms that transcranial Doppler can identify the passage of microemboli in the circle of Willis.

Adult↗

PubMed1986

Cerebral infarction complicating Fontan surgery for cyanotic congenital heart disease.

We report on four children who had cerebral vascular events in the first three months after the Fontan procedure for complex cyanotic congenital heart disease. Potential risk factors in these children included congestive heart failure, postoperative thrombocytosis, and cardiac arrhythmias. These cases suggest that children who undergo Fontan surgery may be at increased risk for cerebral infarction.

Adolescent↗

PubMed2006

Leg ulcers in elderly on hydroxyurea: a single center experience in Ph- myeloproliferative disorders and review of literature.

Hydroxyurea (HU) is effective in controlling thrombocytosis while reducing the risk of thrombosis in essential thrombocythemia (ET), polycythemia vera (PV) and myelofibrosis (MF). However, HU may carry more or less severe side-effects. Rare cases of patients with painful leg ulcers have been published. We report our experience on such a side-effect in a large cohort of patients with ET and PV treated with HU and review the literature on the topic. Five (4%) out of our 124 patients (69 ET, 51 PV, 4 MF; 49 males, 75 females; mean age at diagnosis 59.1+/-11.8 years) treated with HU developed painful leg ulcers. Sixty-one other patients affected with Phmyeloproliferative disorders (Ph- MPD) developing HU-related painful leg ulcers are described in the English literature. All our five patients were women and developed leg ulcers over the age of 75. Sixty-five percent of all described cases are women; 59% were over 65 years of age and 45% over 70. Most cases received over 1 gr HU per day for at least 1 year. The pathogenesis of HU-induced skin ulcers remains elusive. Treatment is difficult and requires prompt cessation of HU therapy.

Age Factors↗

PubMed1997

Magnetic resonance imaging features of chloroma of the shoulder.

A patient with a history of essential thrombocytosis presented with diffuse skeletal pain and restricted motion of the left shoulder. Magnetic resonance imaging (MRI) of the left glenohumeral joint showed a soft tissue mass that displaced the rotator cuff. Biopsy of the mass revealed chloroma. MRI is the method that best characterizes this lesion.

Aged↗