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PubMed1998

Portal vein thrombosis following splenectomy for hematologic disease: prospective study with Doppler color flow imaging.

We report the results of a prospective series of 60 consecutive splenectomies for hematologic disorders performed between February 1995 and May 1996. The portal venous flow of all the patients (34 men and 26 women with a mean age of 54.1 years) was systematically studied before and after intervention with Doppler color imaging (on the day before the intervention and on the 7th and 30th postoperative days). The objective of this study were to determine the real frequency of asymptomatic portal or splenic venous thrombosis (PSVT) after hematologic splenectomy. The intervention began with exteriorization of the spleen and the tail of the pancreas; ligation of the splenic vein was performed close to its junction with the inferior mesenteric vein. Twenty-three complications (38.3%) were noted with three deaths (5%). One symptomatic PSVT (1.6%) and three asymptomatic PSVTs (6.7%) were diagnosed and treated with no deaths. Three risk factors of PSVT, recognized by all the authors, were present in these four cases: large splenomegaly, thrombocytosis, or myeloproliferative disorder. The systematic ultrasonographic (US) examinations increased the frequency of diagnosis of PSVT sevenfold during the perioperative period. Patients with marked splenomegaly associated with lymphoma, chronic lymphocytic leukemia, or myeloid metaplasia probably require systematic US monitoring during follow-up, but this must be determined by further study.

Adult↗
PubMed2002

Cyclic thrombocytopenia and polycythemia vera.

A periodic fall of platelet number characterizes an acquired pathological condition named cyclic thrombocytopenia. We describe an unusual case of polycythemia vera in which the episodes of thrombocytopenia were followed regularly by thrombocytosis. The period of platelet count fluctuation was about 50 days, with the counts ranging from 34 to 820 x 10(9)/l. Bone marrow megakaryocytes were decreased in number during platelet nadir. Circulating thrombopoietin levels fluctuated out of phase with the platelet count. We suggest that at least some cases of polycythemia vera may have an unstable hematopoietic stem cell pool in nature, which could contribute to the development of unprovoked cyclic thrombocytopenia.

Aged↗
PubMed2004

Tricuspid regurgitation in patients with beta-thalassemia major.

Although cardiac complications remain the main causes of death in thalassemic patients, right heart dysfunction has been little studied and the mechanism is still unclear. Echocardiography was performed in 39 patients with beta-thalassemia major and 35 aged-matched controls. The gender, age, heart rate, blood pressure, left ventricular ejection fraction (LVEF), acceleration time (AcT) of right ventricular outflow and right ventricular ejection time (RVET), AcT/RVET, and the presence of tricuspid regurgitation (TR) were compared between the two groups. We also compared the gender, age, age at first blood transfusion, serum ferritin level, alanine aminotransferase (ALT), the presence of antibodies to hepatitis C virus, liver fibrosis, splenectomy, platelet counts, diabetes mellitus, arrhythmia, cardiomegaly, LVEF, AcT, RVET, AcT/RVET, and signal intensity ratio (SIR) of myocardial magnetic resonance imaging (MRI) between thalassemic patients with and without TR. The incidence of TR in thalassemic patients was significantly higher than that in the control group (30.8 vs 11.4%, p=0.03). The incidences of splenectomy (p=0.03), platelet counts (p=0.01), and SIR of myocardial MRI (p=0.03) in thalassemic patients with TR were significantly higher than in those without TR. The AcT was shorter and the AcT/RVET ratio was smaller, suggesting higher pulmonary pressure in the thalassemic patients with TR. Occurrence of TR in patients with beta-thalassemia major may be a consequence of cardiac iron deposit, thrombocytosis, splenectomy, or pulmonary hypertension.

Adolescent↗
PubMedDate not supplied

Hematopoietic turnover index in reactive and neoplastic bone marrow lesions: quantification by apoptosis and PCNA labeling.

In order to determine the dynamics of hematopoietic cell turnover, proliferative activity and incidence of apoptosis (programmed cell death) were evaluated in bone marrow trephine biopsies. Selection of patients (20 in each group) included in addition to a control group, idiopathic thrombocytopenia (ITP), reactive thrombocytosis (TH), secondary polycythemia-smokers' polyglobuly (PG), primary (essential-hemorrhagic) thrombocythemia (PTH), polycythemia vera (PV), and finally acute myeloid leukemia (AML). Apoptosis was demonstrated by the in situ end-labeling technique (ISEL) and proliferative activity by applying the monoclonal antibody PC10 raised against proliferating cell nuclear antigen (PCNA). To assess dynamic features of hematopoiesis, an index was calculated consisting of the ratio between PCNA-positive nuclei and the apoptotic cell fraction. This factor was termed the hematopoietic turnover index (HTI). Morphometric analysis revealed that the HTI was significantly increased in AML and PV. According to cell culture studies both disorders are characterized by either a prevalent proliferation of the myeloid or erythroid cell mass. On the other hand, PG, PTH, and TH showed no relevant enhancement of this index in comparison to the control specimen. In vitro experiment results are in keeping with the finding that PG and PTH are not associated with a significant expansion of the erythroid lineage (CFU-E). Similar to ITP and TH, in PTH megakaryocyte proliferation (CFU-MEG) is the predominant feature of cell turnover. Differences between PTH and TH are in line with the reduced in vitro formation of CFU-MEG in the latter disorder. In conclusion, our in situ study on turnover rates of the bone marrow in various neoplastic and reactive lesions extends previous experimental data on hematopoietic cell kinetics.

Acute Disease↗
PubMedDate not supplied

Excessive prolongation of the bleeding time by aspirin in essential thrombocythemia is related to a decrease of large von Willebrand factor multimers in plasma.

Patients with essential thrombocythemia (ET), who frequently have bleeding complications, may manifest an excessive prolongation of the bleeding time (BT) after ingestion of aspirin (ASA). The reason for this excessive prolongation of the BT is unknown, but it is attributed to qualitative platelet defects. Since patients with ET may also have acquired abnormalities of plasma and platelet von Willebrand factor (vWF), we questioned whether the excessive prolongation of the BT by ASA was related to changes in either plasma or platelet vWF. To that end, we studied BT and plasma and platelet vWF in ten ET patients, ten patients with reactive thrombocytosis (RT), and ten normal individuals, both before and after administration of 500 mg ASA for 7 days. In a second study, the effect of DDAVP infusion on plasma vWF in relation to the BT was studied in ten normal individuals and ten ET patients after treatment with 100 mg ASA for 3 days. In the first study, treatment with ASA resulted in a significant prolongation of the BT in normal subjects, RT patients, and ET patients. However, in five ET patients an excessive (> 2 SD) prolongation of the BT by ASA was observed. Although ASA induced no direct changes in either plasma or platelet vWF levels in either normal subjects, RT patients, or ET patients, all five ET patients who showed an excessive prolongation of the BT by ASA had significantly decreased levels of large vWF multimers in plasma. In the second study, infusion with DDAVP resulted in a significant increase in plasma large vWF multimers, paralleled by a normalization of (excessively) prolonged BT. Our data suggest that in ET inhibition of platelet function by ASA in the presence of concurrently decreased levels of large vWF multimers in plasma may have provoked the excessive BT prolongation.

Adult↗
PubMed1999

Treatment of essential thrombocythemia with special emphasis on leukemogenic risk.

Acute leukemia and myelodysplastic syndromes are rare, but almost invariably fatal, evolutions of essential thrombocythemia (ET). Three major factors are associated with blastic transformation: cytogenetic abnormalities, myelofibrotic features, and the use of cytotoxic agents. Hematological malignancies have been reported in ET patients after treatment with alkylating agents, such as busulphan, as well as other cytoreductive drugs, such as hydroxyurea. Concerns about leukemogenicity have led some to suggest limiting the indications of these drugs to patients at higher risk of bleeding and thrombosis. Major risk factors for thrombosis are age above 60 years and a previous thrombotic event, whereas an increased bleeding tendency has been reported with platelet counts in excess of 1000-1500x10(9)/l. No myelosuppressive therapy is recommended for younger patients if they are asymptomatic or their platelet counts are below 1500x10(9)/l. The threshold of 1500x10(9)/l is controversial, however, and cytoreduction can be considered when platelets are above 1000x10(9)/l or in the presence of risk factors for cardiovascular disease. In the presence of thrombotic events or extreme thrombocytosis, young ET patients can be managed with cytoreductive agents theoretically devoid of leukemogenic risk, such as a-interferon or anagrelide. Nevertheless, the mutagenic risk of anagrelide has not been investigated in long-term follow-up studies, and the ultimate place of these 'new' drugs in the management of ET patients remains to be established in prospective and controlled clinical trials.

Antineoplastic Agents↗
PubMed2002

Pilot study of pegylated interferon-alpha 2b in patients with essential thrombocythemia.

PURPOSE: Interferon-alpha (IFN-alpha) has been shown to control symptoms, reduce platelet counts, and reduce the bone marrow megakaryocyte mass in patients with essential thrombocythemia (ET). A semisynthetic protein-polymer conjugate of IFN-alpha 2b (PEG-IFN2b) increases the serum half-life of IFN-alpha 2b. We conducted a pilot study of Peg-IFN2b in patients with ET. PATIENTS AND METHODS: Patients with a history of persistent (greater than 2 months) platelet counts >600 x 10(9)/l, with hyperplasia of bone marrow megakaryocytes in the absence of an alternate identifiable cause of thrombocytosis were eligible. Patients were required to have either thrombohemorrhagic signs and/or symptoms if previously untreated; persistence of thrombohemorrhagic signs and/or symptoms if receiving anagrelide, IFN-alpha, or hydroxyurea; or intolerance to anagrelide, IFN-alpha, or hydroxyurea. The initial PEG-IFN2b dose was from 1.5 to 4.5 micro g/kg per week subcutaneously with subsequent dose adjustments as indicated by response and adverse events. RESULTS: Eleven patients (nine female, median age 54 years, range 26-69 years) were treated. PEG-IFN2b rapidly controlled platelet counts and resolved symptoms in all patients. The median duration of PEG-IFN2b therapy on-study was 9 months (range 4-17 months). No patient had signs or symptoms of thrombosis or hemorrhage while on study. After 2 months of therapy, 10 patients (91%) were in complete remission, and 11 (100%) after 4 months. One patient discontinued therapy at 4 months because of persistent grade 3 fatigue and a second at 5 months because of anxiety and depression. CONCLUSION: PEG-IFN2b has significant activity in patients with ET. Long-term follow-up of a larger cohort of patients is needed to define its role in this disease.

Adult↗
PubMed2005

Erythromelalgia as a presenting manifestation in a patient with essential thrombocythemia complicating renovascular hypertension due to unilateral renal artery stenosis.

Erythromelalgia is a kind of cutaneous manifestation, which appears as a thrombotic complication in patients with myeloproliferative disorders such as essential thrombocythemia and polycythemia vera. It is characterized by red, congested distal extremities and a painful burning sensation, and is usually confined to the feet and one or more toes or fingers. A 28-year-old woman visited our hospital due to severe pain in the left thumb, index fingers and right toes. Her right toes and left thumb were erythematous, congested, and warm. She had a high blood pressure level of 190/100 mmHg, and laboratory evaluation revealed marked thrombocytosis. Bone-marrow findings were compatible with essential thrombocythemia. Renal angiography showed obvious stenosis in unilateral right renal artery. Her erythromelalgia immediately disappeared following interventional therapy along with aspirin. A careful history and appropriate evaluation of underlying diseases are important, because erythromelalgia as a microscopic thrombotic complication may be accompanied by vascular stenosis and all the resulting manifestations.

Adult↗
PubMed1988

Morphological and kinetic abnormalities of platelets in hypercholesterolemic rabbits.

Hypercholesterolemia (HC = hypercholesterolemia or hypercholesterolemic) was produced in rabbits by feeding them diets supplemented with cholesterol and peanut oil. Platelet counts and volumes, white cell counts, reticulocyte counts, and hematocrits were determined at intervals for 8-12 weeks in blood from HC animals and controls on a normal rabbit diet. Microthrombocytosis was a consistent occurrence in the presence of HC, developing as early as 2 weeks into the diet. Microthrombocytosis was generally associated with normal platelet counts, but mild thrombocytosis occurred late in the diet at the time of the highest levels of serum cholesterol (greater than 1300 mg/dl). Platelets from HC rabbits were morphologically normal by transmission electron microscopy. Survivals of 51Cr-labeled platelets from HC and non-HC rabbits were measured in HC and non-HC recipients. The results identified an intrinsic defect in the ability of HC platelets to survive in the circulation. They also confirmed previous findings of an environmental defect in HC that causes shortened platelet survival.

Animals↗
PubMed1986

Plasma free and conjugated catecholamines in clinical disorders.

Plasma free and sulfoconjugated norepinephrine (NE), epinephrine (E) and dopamine (DA) concentrations measured in patients with thrombocytopenia or thrombocytosis, in newborns and pregnant women were not statistically different from values determined in 41 healthy volunteers. The percentage free to total NE, E and DA was 30 +/- 10%, 35 +/- 11% and 1.5 +/- 1.1% (mean +/- SE) in the controls, resp; not different from the previously described patients or from patients with liver failure who showed significantly higher free and conjugated NE and E levels when compared with controls (p less than 0.01, resp.). Conjugated catecholamine (CA) levels from the femoral artery and from multiple sites in the venous system sampled in patients undergoing intracardiac measurements were identical. The data suggest that sulfation of CA may not be simply ascribed to platelets, to the liver, to vascular beds, or to organs along the vena cava including the adrenal glands. The parallel increase of free and conjugated NE with age in healthy controls, as well as the unchanged degree of conjugation in patients with increased spillover of NE and E caused by a pheochromocytoma or by a heart attack, suggest that there is a balance between free and sulfated CA. A normal ratio of free to conjugated NE and E observed in patients receiving high dosage DA infusion further indicates that there is an adequate sulfate supply and no apparent substrate inhibition of the conjugation process. Because the percentage free of total NE, E and DA were significantly lower in patients in the hypothyroid state when compared with controls (p less than 0.01, resp.), hypothyroidism may affect the balance of free to conjugated CA in a yet unknown way.

Adolescent↗
PubMed1991

Idiopathic thrombocythemia and pregnancy; a case report.

A 28-year-old women with idiopathic thrombocytosis was treated with melphalan before pregnancy, which resulted in a normal platelet count. During pregnancy 80 mg acetylsalicyclic acid was given daily to prevent microcirculatory thrombotic complications. Fetal outcome was normal.

Adult↗
PubMed1984

Hematological and bone marrow effects of ribavirin in rhesus monkeys.

Ribavirin (Virazole, 1-beta-D-ribofuranosyl-1,2,4-triazole-3-carboxamide), a broad-spectrum antiviral compound, was evaluated for effects on blood and bone marrow of rhesus monkeys when administered by intramuscular injection for 10 days in doses of 30 or 100 mg/kg/day (four monkeys/group). Both groups developed a normochromic, normocytic anemia that was mild in the low-dose group and severe in the high-dose group. A dose-related erythroid hypoplasia occurred during the treatment period. Myeloid precursors were not affected. Differential counts of erythroid precursors showed a significant decrease in late erythroid forms while early erythroid forms were either unchanged or increased. Megakaryocyte numbers were increased in both groups. Qualitative changes in marrow cells included vacuolization of erythroid precursors and of occasional white cell precursors and megakaryocytes, and the appearance of bone marrow histiocytes containing red cells in various stages of disintegration. Thrombocytosis occurred in both treatment groups, with platelet counts returning to control values after drug withdrawal. Platelet function was not affected by treatment. No drug-related changes were seen during the treatment period for total and differential leukocyte counts, mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration. Reticulocyte counts and mean corpuscular volume increased after treatment then returned to control values. Osmotic fragility of erythrocytes was not changed. These data show that in monkey, ribavirin causes a dose-related decrease in circulating red blood cell mass that is due in part to suppression of late erythroid precursors in bone marrow. These effects are reversible when treatment is discontinued and are not predictive of potentially serious or lasting untoward effects of ribavirin.

Animals↗
PubMed1986

MPLV: a retrovirus complex inducing an acute myeloproliferative leukemic disorder in adult mice.

A novel murine retrovirus complex was derived from the in vivo passage of a molecularly cloned Friend ecotropic helper virus. The virus isolate, myeloproliferative leukemia virus (MPLV), causes an acute (2-3 weeks) and generalized myeloproliferative disorder in adult mice. All strains of mice examined, including the C57BL/6J strain, developed the acute syndrome. This syndrome is characterized by a rapid hepatosplenomegaly, no thymus or lymph node involvement, granulocytosis, thrombocytosis, and erythroblastosis leading to polycythemia. The most prominent feature at the terminal phase of the disease is a granulocytic hyperplasia. The MPLV isolate replicates in vitro on NIH 3T3 fibroblasts but does not induce foci of transformed cells. Thus, MPLV exhibits unique biological properties that distinguish it either from the Friend virus complexes or from acutely transforming sarcomatogenic murine retrovirus which also induced a rapid splenomegaly.

Animals↗
PubMed1992

Measurement of the zeta potential of human platelets by the use of laser-light scattering.

An instrument was developed to detect the shift in scattering of laser light that occurs when particles in suspension move in a chamber with an electrical load. The instrument measures the zeta potential of particles. We applied the instrument to study human blood cells. Platelet-rich plasma was used because of the stability of the suspension, without the sedimentation or autoaggregation that is often seen with red or white blood cells. The reproducibility of the measurements was satisfactory when there were enough platelets in the suspension. Platelets from healthy controls (n = 136) had a potential of -14.20 +/- 1.64 mV at the detection angle of 17.1 degrees. Platelets from patients with essential thrombocytosis (n = 16) or polycythemia vera (n = 8) had higher potentials than the healthy controls.

Blood Platelets↗
PubMed1992

Cytogenetic and molecular studies of the Philadelphia translocation in myelodysplastic syndromes. Report of two cases and review of the literature.

We report two patients with a myelodysplastic syndrome and the Philadelphia (Ph) chromosome. The first patient was a 73-year-old man who was diagnosed as having a chronic myelomonocytic leukemia in combination with features suggestive of a myeloproliferative syndrome. Chromosomal analysis showed a normal karyotype in the majority of cells, mixed with metaphases containing a standard Ph translocation, t(9;22)(q34;q11), as well as a translocation between chromosome 4 and 6: t(4;6)(p15;p12). Southern blot analysis showed breakpoint cluster region rearrangement as observed in classic chronic myeloid leukemia. The second patient was a 63-year-old man with a myelodysplastic syndrome, type refractory anemia. Cytogenetic study of bone marrow cells at the time of diagnosis revealed a normal karyotype: 46,XY. The initial myelodysplastic syndrome evolved to a myeloproliferative phase with progressive leukocytosis and thrombocytosis. During the terminal phase the Ph chromosome was discovered in 100% of the examined cells. We discuss the correlation between MDS and myeloproliferative diseases, the de novo acquisition of the Ph chromosome during the course of a myelodysplastic syndrome, and review the literature.

Aged↗
PubMed2005

c-Myb and p300 regulate hematopoietic stem cell proliferation and differentiation.

Precise control of hematopoietic stem cell (HSC) proliferation and differentiation is needed to maintain a lifetime supply of blood cells. Using genome-wide ENU mutagenesis and phenotypic screening, we have identified a mouse line that harbors a point mutation in the transactivation (TA) domain of the transcription factor c-Myb (M303V), which reduces c-Myb-dependent TA by disrupting its interaction with the transcriptional coactivator p300. The biological consequences of the c-Myb(M303V/M303V) mutation include thrombocytosis, megakaryocytosis, anemia, lymphopenia, and the absence of eosinophils. Detailed analysis of hematopoiesis in c-Myb(M303V/M303V) mice reveals distinct blocks in T cell, B cell, and red blood cell development, as well as a remarkable 10-fold increase in the number of HSCs. Cell cycle analyses show that twice as many HSCs from c-Myb(M303V/M303V) animals are actively cycling. Thus c-Myb, through interaction with p300, controls the proliferation and differentiation of hematopoietic stem and progenitor cells.

Animals↗
PubMed2005

Focal nodular hyperplasia after busulfan treatment.

The case of a 48-year-old woman in whom focal nodular hyperplasia of the liver developed after busulfan therapy was administered for essential thrombocytosis is described. Focal nodular hyperplasia is a reactive disorder related to a circulation disorder. The close temporal relation between the haematological disease, busulfan treatment and the appearance of hyperplastic diseases of the liver in our patient supports the possibility that the association of the events might not be casual.

Busulfan↗
PubMedDate not supplied

Fever of unknown origin caused by late-onset rheumatoid arthritis.

Fever of unknown origin (FUO) is always a diagnostic challenge. The causes of FUO are legion and may be due to malignancy, infection, collagen vascular disease, and a variety of other unusual disorders. Currently, malignancies-followed by infectious etiologies-are the most common cause of FUO. We present an elderly female patient with an FUO who was thought to have subacute bacterial endocarditis because of an antecedent history of recent dental work. Subacute bacterial endocarditis was ruled out on the basis of negative cultures and negative transesophageal echocardiography. No evidence for an infectious disease or neoplastic etiology could be demonstrated in this patient. The diagnosis of FUO is most difficult when there is a paucity of clues from the history and physical examination, as was the case in this patient. Nonspecific laboratory tests included highly increased erythrocyte sedimentation rate (>or=100 mm/h), highly increased C-reactive protein, relative lymphocytopenia, and chronic thrombocytosis. These findings are compatible with a variety of infectious and inflammatory disorders. No evidence could be found for vasculitis. The only laboratory diagnostic findings present in her case were a highly increased rheumatoid factor titer and perinuclear antineutrophilic cytoplasmic antibody level. Polymyalgia rheumatica/temporal arteritis, systemic lupus erythematosus, and adult Still's disease were ruled out. The patient's FUO was best explained by the finding of late-onset rheumatoid arthritis (LORA), which is characterized by acute onset in elderly patients without the usual musculoskeletal manifestations of rheumatoid arthritis. Both the highly increased rheumatoid factor titer and perinuclear antineutrophilic cytoplasmic antibody level in the absence of an alternate explanation indicate that the FUO in this patient was caused by LORA.

Aged↗