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At least 1,387 records · Page 77Linked to original sources
PubMed1982

Determination of the density distribution of human platelets--methodological aspects and comparison with other tests for platelet activation.

Stimulation of human platelets to release results in decreased buoyant density. This decreased density provides a tool to detect circulating platelets which have participated in a thrombotic process. Platelet density gradient centrifugation using Stractan was standardized and the effects of anticoagulation, temperature, and osmolarity were investigated. In 7 out of 32 patients with thrombotic disease less dense platelets were found. Platelet activation in the patient group was also indicated by spontaneous aggregation (10/32), decreased circulating platelet aggregate ratios (5/24) and elevated plasma beta-thromboglobulin levels (2/ 11). Several of these tests were also abnormal in diabetes mellitus thrombocytosis, leukaemia and several systemic diseases with thrombotic complications. The platelet density test using Stractan is reproducible and independent of other tests for platelet activation and is therefore potentially a useful extension of platelet function testing in patients with thrombotic disease.

Adult↗
PubMed1981

The effect of partial splenectomy on platelet production in mice.

The effect of total and partial splenectomy on the number and production of circulating platelets was studied in mice. Five days after total and partial splenectomy the number of the peripheral blood platelets increased by 87% and 60%, respectively and the incorporation of 75selenium methionine (75Se-Met) into platelets was enhanced indicating that the thrombocytosis was due to increased platelet production. The results obtained by the two operative procedures were compared. Since previous work from our laboratory has shown that a factor produced by splenic lymphocytes affects the platelet number in mice, it is suggested that the differences in the number of circulating platelets observed in animals after total and partial splenectomy may reflect a difference in the number of spleen lymphocytes removed.

Animals↗
PubMed1981

Familial myeloproliferative disease. Hematological and cytogenetic studies.

A family is described in which a form of myeloproliferative disease involving the megakaryocytic cell line occurs in three generations, resulting in thrombocytosis in several members. An autosomal dominant transmission with variable penetrance is proposed, based on the distribution of involved members in the pedigree. Two family members appeared to have an abnormal chromosome 7, which is frequently observed in patients with hematological disorders. It is our opinion that the chromosomal aberration is primarily related to the mutagenicity of the cytostatic treatment, although a primary defect cannot be fully excluded.

Adolescent↗
PubMed1981

Pseudohyperkalaemia - a cause of diagnostic confusion.

Marked hyperkalaemia occurred on more than one occasion in 3 patients with thrombocytosis caused by the myeloproliferative syndrome. Initial failure to recognize that the elevation in the serum potassium level was an artefact resulted in unnecessary admissions to hospital and inappropriate investigations and treatment. Awareness of this entity and the use of suitable confirmatory tests should avoid such problems in management.

Aged↗
PubMed1980

Leg pain and platelet aggregates in thrombocythemic myeloproliferative disease.

In three patients with thrombocytosis secondary to myeloproliferative disorders, disabling intermittent lower extremity pain occurred in the absence of peripheral vascular insufficiency. In all patients, circulating platelet aggregates were detected. Antiplatelet therapy resulted in prompt relief of pain and the disappearance of platelet aggregates. These findings suggest that abnormal platelet function with the formation of platelet plugs in the microcirculation could be responsible for the observed symptoms and response to treatment. The value of the determination of circulating platelet aggregates in the management of this syndrome is highlighted.

Aged↗
PubMed1980

[Recurrent hemolytic uremic syndrome (author's transl)].

A hemolytic uremic syndrome (HUS) reoccurred 13 months after the first episode in an 8 years old girl. Both episodes were treated by peritoneal dialysis. They had all signs of HUS: renal failure, severe anemia with fragmented erythrocytes and thrombocytopenia. Interesting was the transient thrombocytosis following the primary thrombocytopenia. 2.5 years since the second episode the girl is healthy with intact renal functions.

Child↗
PubMed1980

Platelets in myeloproliferative disorders. I. A comparative evaluation with certain platelet function tests.

Certain platelet functions were evaluated in 24 patients with secondary polycythaemia (SP) and in a large number of patients suffering from myeloproliferative disorders (MD'S): 89 patients with chronic myeloid leukaemia (CML) at different stages of development, 58 with polycythaemia vera (PV), 23 with essential thrombocythaemia (ET), and 25 with agnogenic myeloid metaplasia (AMM). Bleeding time, epinephrine-induced platelet aggregation and adhesiveness agreed with those generally reported in the literature; they are independent of thrombocytosis, the haemoglobin level and the leucocyte count. Macrothrombocytosis, evaluated by an electronic method, was only found in CML, mainly during acute blast crisis. An increased percentage of light platelets was a constant feature in all groups except in the SP and in 20% of the PV. The most severe abnormalities were observed in AMM and CML in the acute stage; in the chronic phase of CML there is no correlation between the severity of platelet abnormalities and the survival of the patients.

Blood Platelets↗
PubMed1995

Platelet unresponsiveness to collagen: involvement of glycoprotein Ia-IIa (alpha 2 beta 1 integrin) deficiency associated with a myeloproliferative disorder.

We studied a 66-year-old man with a myeloproliferative disorder who presented with a prolonged bleeding time and marked thrombocytosis (platelet count, 3,890 x 10(9)/l). There was no past history of a bleeding disorder. The patient had normal coagulation data. His platelets completely lacked collagen-induced platelet aggregation and adhesion, but showed normal responses to other agonists. All family members tested showed normal platelet aggregation with collagen. Analysis of 125I surface-labeled platelets by two-dimensional SDS gel electrophoresis disclosed absence of the spot corresponding to platelet membrane GPIa (alpha 2) but no other significant deficiencies of major platelet glycoproteins i.e., GPIb, IIb-IIIa, and IV. Immunoisolation studies of the patient's platelets indicated that neither anti-GPIa nor anti-GPIIa (beta 1) monoclonal antibody (mAb) isolated any surface membrane proteins corresponding to GPIa. GPVI, a putative collagen receptor, was immunoisolated from the platelets. Indirect immunofluorescence study using flow cytometry confirmed that the patient's platelets were totally deficient in surface expression of the GPIa-IIa complex (alpha 2 beta 1 integrin). In contrast, phytohemoagglutinin-activated T-lymphocytes from the patient expressed normal concentrations of this complex. The data suggest that our patient had an acquired deficiency of the platelet GPIa-IIa complex, due to a myeloproliferative disorder, which might account for the absence of responsiveness of his platelet to collagen.

Acute Disease↗
PubMed1978

[Relationship between digital necrosis of the upper limbs and malignant conditions (author's transl)].

The authors report six new cases of necrosis of the fingers occurring during the course of a malignant condition. None of the patient was suffering from any other disease which could explain the digital necrosis. They discuss the mechanism of the relationship between the two conditions : blood hyperviscosity, thrombocytosis, polycythaemia, cryoglobulin and the production of immune complexes. The particular role of bleomycin is mentioned. The possibility of a true paraneoplastic syndrome is suggested.

Adult↗
PubMed1995

Endogenous megakaryocyte and erythroid colony formation from blood in essential thrombocythaemia.

The in vitro cultures of haematopoietic progenitors have been reported to be useful in the diagnosis of myeloproliferative disorders since the so-called endogenous erythroid and megakaryocyte colony formation has, in most studies, been found in these diseases. In order to know their value as diagnostic criteria in essential thrombocythaemia (ET) we have studied megakaryocyte (with and without phytohaemagglutinin-stimulated leucocyte conditioned medium) and erythroid (with and without erythropoietin) colony formation in vitro by progenitors from blood in 60 patients with ET and in ten with reactive thrombocytosis (RT) using the methyl-cellulose assay. Out of 60 ET patients endogenous megakaryocyte colony growth was observed in 38 (63%) and endogenous erythroid growth in 42 (70%). None of the patients with RT or any of the controls showed either type of endogenous growth. Fifty-five (91%) of the patients with ET showed megakaryocyte and/or erythroid endogenous colony formation whereas five (9%) did not have any kind of endogenous colonies, although cultures were performed sequentially. In conclusion, a positive endogenous megakaryocyte and/or erythroid colony growth from blood is a frequent and characteristic finding in ET patients and should be used as a useful marker in this disease.

Adolescent↗
PubMed1993

[Secondary and primary thrombocythemia].

Reactive thrombocytosis is an elevation of platelet count occurring in association with certain underlying diseases such as various infections, inflammatory, neoplastic and asplenic states. Essential thrombocythemia is a myeloproliferative syndrome affecting megakaryocytes, which leads to increased numbers of circulating platelets. This disorder is characterized by splenomegaly and a clinical course punctuated by hemorrhagic and/or thrombotic episodes.

Diagnosis, Differential↗
PubMed1996

Systemic hematologic effects of PEG-rHuMGDF-induced megakaryocyte hyperplasia in mice.

PEG-rHuMGDF injected daily in normal mice causes a rapid dose-dependent increase in megakaryocytes and platelets. At the same time that platelet numbers are increased, the mean platelet volume (MPV) and platelet distribution width (PDW) can be either decreased, normal, or increased depending on the dose and time after administration. Thus, PEG-rHuMGDF at a low dose causes decreases in MPV and PDW, MGDF at an intermediate dose causes an initial increase followed by a decrease in MPV and PDW, and PEG-rHuMGDF at higher doses causes an increase in MPV and PDW followed by a gradual normalization of these platelet indices. In addition to the expected thrombocytosis after 7 to 10 days of daily injection of high doses of PEG-rHuMGDF, a transient decrease in peripheral red blood cell numbers and hemoglobin is noted accompanied in the bone marrow by megakaryocytic hyperplasia, myeloid hyperplasia, erythroid and lymphoid hypoplasia, and deposition of a fine network of reticulin fibers. Splenomegaly, an increase in splenic megakaryocytes, and extramedullary hematopoiesis accompany the hematologic changes in the peripheral blood and marrow to complete a spectrum of pathologic features similar to those reported in patients with myelofibrosis and megakaryocyte hyperplasia. However, all the PEG-rHuMGDF-initiated hematopathology including the increase in marrow reticulin is completely and rapidly reversible upon the cessation of administration of PEG-rHuMGDF. Thus, transient hyperplastic proliferation of megakaryocytes does not cause irreversible tissue injury. Furthermore, PEG-rHuMGDF completely ameliorates carboplatin-induced thrombocytopenia at a low-dose that does not cause the hematopathology associated with myelofibrosis.

Anemia↗
PubMed1977

Traumatic splenic rupture.

71 patients with traumatic splenic rupture are reported. Most had severe associated injuries. In 44 patients the mechanism of trauma was blunt, in 10 penetrating, and in 17 iatrogenic, occurring most commonly (11/17) during operations for peptic ulcer. Splenectomy gave use to thrombocytosis which reached its peak about 2 weeks and returned to normal within one month after operation. Postoperative complications occurred in 24 of the 60 surviving patients (40%) of which most, 17 patients (30%) were infectious in origin. One patient developed deep venous thrombosis. Mortality was 16%. Associated injuries were the main cause of death in most patients (9/11), the ruptured spleen being responsible for only 2 deaths. None of the 17 patients with injury to the spleen alone died, whether associated with fractures of the left lower ribs or not. Primary unconsciousness, shock on admission, and multiple injuries, especially renal and hepatic, increased the mortality rate markedly. The necessity of drainage, the possibility of increased susceptibility of splenectomized patients to infection and thromboembolic complications and their prevention are briefly discussed.

Accidents↗
PubMed1996

[Radioactive phosphorus (32P); an old but not bad treatment for polycythemia vera].

OBJECTIVE: To determine if there is a place for radiophosphorus (32P) in the treatment of polycythaemia vera (PV) and essential thrombocytosis (ET). DESIGN: Retrospective. SETTING: Leyenburg Hospital, The Hague, the Netherlands. METHOD: Data on 144 patients with the diagnoses 'PV' or 'ET' from 1965 to 1994 were collected. Available data were insufficient in 19 of these. Regarding 125 patients, 80 with PV and 45 with ET, the survival and the frequency of acute leukaemia with various forms of treatment (32P, busulfan or combination of several treatment modalities) were studied. Moreover, in the PV group the duration of survival was compared with the expected duration of survival in a comparable group of the population. RESULTS: Of the 80 PV patients, five developed acute leukaemia: two in the 32P group (5%), two in the busulfan group (12%) and one in the group given combination therapy (4%). Of the 26 patients of the ET group treated with busulfan, one developed acute leukaemia (4%). The survival in the PV group was 4 years shorter than the expected duration of survival in a comparable group of the population. CONCLUSION: Since 32P is efficacious and causes little inconvenience, it should be the drug of first choice in the treatment of PV in the elderly.

Adult↗
PubMed1997

[Traumatic splenic rupture--fatal increase in thrombocytes after splenectomy].

A patient with CMGM developed after traumatic splenectomy a severe thrombocytosis up to 4 millions. 25 days after the accident he died of acute right heart failure caused by vascular occlusion of lung vessels due to thrombocyte aggregations. According to the regulations of professional cooperatives in Germany the death is caused by the occupational accident. A bereaved pension will be payed. For the private life insurance the blood disease is with 33% partial responsible for the fatal development and reduces the payment. According to german penal law the death of the victim will tighten the punishment, if someone else is guilty for the accident. A professional error on the part of a doctor is not provable.

Accidents, Occupational↗
PubMed1997

Markedly reduced expression of platelet c-mpl receptor in essential thrombocythemia.

Thrombopoietin (TPO) is implicated as a primary regulator of megakaryopoiesis and thrombopoiesis through binding to the cytokine receptor c-Mpl (the product of the c-mpl proto-oncogene). In an effort to determine the pathophysiological role of TPO-c-Mpl system in essential thrombocythemia (ET), we have examined the levels of serum TPO and the expression and function of platelet c-Mpl in 17 patients with ET. In spite of extreme thrombocytosis, serum TPO levels were slightly elevated or within normal range in most, if not all, patients with ET (mean +/- SD, 1.31 +/- 1.64 fmol/mL), as compared with normal subjects (0.76 +/- 0.21 fmol/mL). Flow cytometric and Western blot analyses revealed that the expression of platelet c-Mpl was strikingly reduced in all patients with ET. Furthermore, the expression of platelet c-mpl mRNA was found to be significantly decreased in the ET patients tested. In contrast, almost identical levels of GPIIb/IIIa protein and mRNA were expressed in platelets from ET patients and normal controls. In addition to expression level, activation state of platelet c-Mpl was investigated in ET patients. Immunoblotting with anti-phosphotyrosine antibody showed that no aberrant protein-tyrosine phosphorylation was observed in platelets of ET patients before treatment with TPO, and the levels of TPO-induced protein-tyrosine phosphorylation, including c-Mpl-tyrosyl phosphorylation, roughly paralleled those of c-Mpl expression, suggesting that c-Mpl-mediated signaling pathway was not constitutively activated in platelets of ET patients. These results suggested that the TPO-c-Mpl system may not be directly linked to pathogenesis of ET, and that gene(s) mutated in ET may be important in regulating the levels of c-mpl gene expression in addition to the growth and differentiation of multipotential hematopoietic stem cells.

Adolescent↗
PubMed1997

Inflammatory bowel disease and immune thrombocytopenic purpura: is there a correlation?

Different hematologic abnormalities are often encountered in patients with inflammatory bowel disease. Among them anemia, leukocytosis, and thrombocytosis are commonly seen. Leukopenia and thrombocytopenia are observed mostly as a side effect of therapy, particularly with use of immunosuppressive drugs. Immune thrombocytopenic purpura is rarely reported in association with inflammatory bowel disease. We present two cases with combination of these entities along with a literature review and treatment options. Immune thrombocytopenic purpura in these patients presented as an extraintestinal manifestation of inflammatory bowel disease mediated by a disturbance of the immune system.

Adolescent↗