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PubMedDate not supplied

Severe withdrawal syndrome possibly associated with cessation of a midazolam and fentanyl infusion.

A 40-month-old child was sedated with a fentanyl and midazolam infusion for 7 days. After the drugs were discontinued he became unresponsive and globally aphasic, and had marked thrombocytosis. He was hospitalized for 4 weeks, during which time his motor and cognitive status slowly improved, and had almost returned to baseline at time of discharge. Severe neurologic abnormalities have been reported with midazolam and fentanyl, administered separately or together, and seem to be a consequence of a withdrawal syndrome. Of interest, this patient had a reactive thrombocytosis at the time of onset of the withdrawal syndrome, and his decreased platelet count coincided with the return to normal cognitive and motor status. Based on this experience and other reports, we believe midazolam-fentanyl combination should be administered with caution.

Aphasia↗
PubMed1982

Effects of cyclophosphamide on murine bone marrow and splenic megakaryocyte-CFC, granulocyte-macrophage-CFC, and peripheral blood cell levels.

The effect of cyclophosphamide (CY) on megakaryocytopoiesis in mice was examined with assays of megakaryocyte colony-forming cells (Meg-CFC) in bone marrow and spleen and simultaneous determinations of peripheral blood counts, after a single intraperitoneal dose (200 mg/kg) of CY. Significant rebound thrombocytosis (170% of normal) occurred at day 11 after injection with CY, although only modest preceding thrombocytopenia (70% of normal) was observed. After an initial 3-5 day period of suppression, total megakaryocyte colony-forming cells (Meg-CFC) in both bone marrow and spleen of CY-treated mice demonstrated rebound increases at 5 and 7 days, respectively, after administration of the drug. Granulocyte-macrophage colony-forming cells (GM-CFC) exhibited alterations which were similar to those of Meg-CFC, suggesting similar sensitivities of Meg-CFC and GM-CFC to CY. The increase in Meg-CFC in both bone marrow and spleen preceded development of thrombocytosis by 4-6 days. This suggests that increased platelet counts in CY-treated mice are attributable, at least in part, to alterations in feedback mechanisms which control megakaryocytopoiesis, with resultant stimulation of the megakaryocyte progenitor compartment.

Animals↗
PubMed1981

The possible value of platelet aggregation studies in patients with increased platelet number.

ADP, adrenalin and collagen platelet aggregation studies were performed in 54 patients with elevated platelet counts: 38 patients showed primary thrombocythemia and 16 secondary thrombocytosis. Patients with primary thrombocythemia (78.7%) showed a decrease aggregation pattern while in patients with secondary thrombocytosis platelet aggregation response was entirely normal. An increase in platelet aggregation was obtained in four patients with primary thrombocythemia. The platelet aggregation response did not appear to be related to circulating platelet number. A relationship between increased platelet aggregation and the occurrence of thrombosis was demonstrated. Similarly, a correction between impaired platelet aggregation and bleeding was also present. These results emphasize the diagnostic value of platelet aggregation studies in patients with elevated platelet number.

Adenosine Diphosphate↗
PubMed1988

[Clinical characterization of essential thrombocythemia in comparison with other myeloproliferative diseases and reactive thrombocytoses].

60 patients with essential thrombocythemia (ET) have been retrospectively and prospectively followed from 1974 through 1987. The presenting signs and symptoms and the course of the disease were analyzed and compared to 10 patients with persisting reactive thrombocytosis selected from 6,000 patients with reactive thrombocytosis and to 50 patients with other myeloproliferative diseases. 54 ET-patients presented with complications, 46 with thrombembolic, 3 with hemorrhagic problems and 5 with thrombembolic and hemorrhagic problems. In 6 patients ET was detected accidentally. Disturbances of the microcirculation, mainly of the fingers and the toes, were the most frequent symptom. The average maximal platelet count was 1,207,000/microliter. The average platelet count at diagnosis was 880,000/microliter. 16 patients had an elevation of the serum creatinine at diagnosis, which deteriorated during the course of the disease. Bone marrow examinations were performed in 56 patients, histology in 48 patients, cytology in 29 patients. In contrast to the clinical diagnosis the histological diagnosis was in 4 cases each polycythemia vera and myeloproliferative syndrome without further specification. 12 patients died thus far. The causes of death were thrombembolic complications in 9, acute leukemia in 2 patients, in 1 patient the cause of death is not known. 10 years after diagnosis 61% of the patients are still alive. It appears that ET is a more important risk factor for the disturbances of the micro- and macrocirculation than has been recognized until now. ET is, if thrombembolic complications are avoided, a disease with a relatively benign course.

Aged↗
PubMed1992

Anagrelide, a therapy for thrombocythemic states: experience in 577 patients. Anagrelide Study Group.

PURPOSE: To evaluate the safety and efficacy of anagrelide when used to reduce platelet counts in patients with thrombocytosis. PATIENTS AND METHODS: Five hundred seventy-seven patients were treated with anagrelide to control the thrombocytosis of chronic myeloproliferative diseases. Three hundred thirty-five patients had primary thrombocythemia, 114 chronic granulocytic leukemia, 68 polycythemia vera, and 60 undifferentiated myeloproliferative diseases. Of the 577 patients, 504 were known to have been previously treated unsuccessfully with other modalities. RESULTS: Of the 577 patients treated, 424 were evaluable for response. Anagrelide in doses of 0.5 mg to 1.0 mg four times a day reduced the platelet count by 50%, or to less than 600,000/mm3, for at least 28 days in 396 of the 424 (93%) evaluable patients. Acquired resistance to the drug was not observed. Major side effects were neurologic, gastrointestinal, and cardiac. In more than 5 years, 16% of patients discontinued treatment because of side effects. CONCLUSIONS: Our experience suggests that anagrelide should become a useful agent in controlling the thrombocythemia seen in chronic myeloproliferative diseases and can be effective in patients in whom treatment with currently available agents has failed.

Aged↗
PubMed1988

Prostacyclin degradation in patients with quantitative platelet disorders.

Plasma prostacyclin (PGI2) degradation rates were measured at 1, 5, 15 and 30 min in a group of patients with platelet quantitative disorders of various pathogeneses, including 13 with thrombocytosis, 16 with thrombocytopenia from impaired production in the bone marrow, 11 with thrombocytopenia from peripheral destruction, and 28 normal, healthy persons. Patients with thrombocytosis had a low PGI2 degradation rate, whereas patients with thrombocytopenia due to impaired production had a high PGI2 degradation rate. Of the patients with thrombocytopenia caused by peripheral destruction, six with idiopathic thrombocytopenia purpura (ITP) had a slow PGI2 degradation in contrast to five with systemic lupus erythematosus (SLE) - four concurrently had cryoglobulinemia - who had a rapid PGI2 degradation. The findings suggest that: (1) a platelet-derived substance in the human plasma may have a PGI2 stabilising activity; (2) presence of cryoglobulin or immune complex in plasma may interfere with PGI2 stability.

Epoprostenol↗
PubMed2006

Pseudohyperkalemia in serum: the phenomenon and its clinical magnitude.

We investigated in detail the difference between serum and plasma potassium levels in patients with several conditions associated with pseudohyperkalemia. In total, 435 patients with either thrombocytoses, erythrocytoses, leucocytoses, or a mixed-type disorder and 30 healthy controls were included. In each case, the index Dk [serum potassium minus plasma potassium] and the index Dk100 (Dk x 100,000/platelets), which indicates the Dk value that corresponds to platelets of 100,000/mm(3), were estimated. Median Dk was significantly higher in the groups with platelet, erythrocyte, or mixed-type disorders than in the controls (P=0.001). Among these groups, Dk values were significantly higher in patients with thrombocytosis or mixed-type disorders compared with those with erythrocytosis (P<0.001, for both). Furthermore, no significant difference was observed in Dk values between controls and patients with white blood cell disorders (P=0.74). Dk values did not exceed 2.61 mmol/L, whereas Dk100 values were inversely related to platelet counts (r=-0.351, P<0.01). In conclusion, pseudohyperkalemia is mainly present in patients with thrombocytosis or mixed-type disorders, probably as a result of the degranulation of platelets, which offers a potassium load to the surrounding plasma at the time of clot formation in vitro. However, the degree of pseudohyperkalemia does not increase proportionally with the increase of platelet counts, which may be associated with transfer of part of potassium load from the plasma back into red and white blood cells.

Adult↗
PubMed2003

Autosplenectomy and antiphospholipid antibodies in systemic lupus erythematosus: A pathogenetic relationship?

OBJECTIVES: To describe a systemic lupus erythematosus (SLE) patient with functional asplenia and antiphospholipid syndrome (APS) and to review the literature to better define its pathogenesis and diagnosis, emphasizing a possible relationship with antiphospholipid antibodies (aPL). METHODS: Descriptive report of 1 case and review of the literature by means of a MEDLINE search from 1966 to 2002. RESULTS: A SLE patient presented with cutaneous vasculitis and an unexpected thrombocytosis which resulted from autosplenectomy. Subsequently, she developed full-blown APS. In the literature, autosplenectomy has been described only in 1 other case of APS secondary to SLE. However, clinical or laboratory features linked to aPL occurred in several other cases among the 17 cases reported with functional asplenia. CONCLUSIONS: Autosplenectomy in SLE may be pathogenetically related to aPL. Thrombocytosis, unusual in SLE, may be a diagnostic clue of this condition. Pneumococcal vaccination is warranted to prevent life-threatening infections that frequently complicate this asplenia.

Adult↗
PubMed1997

The omnipotent platelet. Part II: Further observations.

Observation of platelet responses during acute injury or pathology can provide important information. The initial response is thrombocytopenia followed by thrombocytosis. In the case of injury with negative X-ray and appropriate thrombocytosis, a bone scan is indicated. The platelet responds like a sedimentation rate, which indicates the course of the injury or pathology.

Aged↗
PubMed2001

Clinicopathology and histochemistry on bone marrow biopsies in chronic myeloproliferative disorders--a clue to diagnosis and classification.

A clinicopathological study was carried out to address the currently still controversial issues of: 1) thrombocythaemias in chronic myeloproliferative disorders (MPDs); 2) Initial, prefibrotic idiopathic myelofibrosis (IMF); 3) discrimination of spurious polycythaemic states or polyglobuly (PG) from polycythaemia vera (PV); 4) unclassifiable MPDs. Based on a synoptical approach which implicates a comparative evaluation of laboratory data and histopathology of the bone marrow, the discriminating efficiency of both diagnostic tools has been emphasized. An elaborate evaluation of histotopography and cytological appearance of megakaryopoiesis is an invaluable aid to distinguish the different subtypes of MPDs which may eventually present with a significant elevation of the platelet count. Prefibrotic IMF is not only associated with a certain set of clinical symptoms (minimal to slight anaemia, splenomegaly, thrombocytosis), but should also be characterized by specific alterations of bone marrow morphology. Moreover, follow-up studies are in keeping with the finding that these patients evolve into typical IMF regarding laboratory parameters and ensuing myelofibrosis. Smokers polycythaemia--PG may be separated from early PV by the significant raise in the red cell mass and also by a few, easily determinable clinical parameters (i.e. EPO level, thrombocytosis, LAP). Both conditions can be distinguished by regarding bone marrow features (megakaryopoiesis, interstitial changes) which exert a distinctive impact. According to our experience the majority of patients categorized as unclassifiable MPDs include cases in which clinical or morphological data are inadequate to permit a more precise diagnosis. Only in a small proportion not a failing methodology, but initial stages of the disease process requires sequential examinations to reach a correct diagnosis.

Aged↗
PubMed1998

Diagnosis and classification of erythrocytoses and thrombocytoses.

An erythrocytosis describes an increased peripheral blood packed cell volume (PCV) and is deemed to be absolute or apparent depending on whether or not the measured red cell mass (RCM) is above the reference range. This reference range must be related to the individual's height and weight to avoid erroneous interpretations using ml/kg total body weight expressions in obesity. Absolute erythrocytoses are divided into primary, where the erythropoietic compartment is intrinsically abnormal, secondary, where the erythropoietic compartment is normal but is responding to external pathological events leading to an increased erythropoietin drive, and idiopathic, where neither a primary nor a secondary erythrocytosis can be established. Both primary and secondary erythrocytoses have congenital and acquired forms. The only form of primary acquired erythrocytosis that has been defined is the clonal myeloproliferative disorder, polycythaemia vera (PV). Modified diagnostic markers for PV are proposed. Thrombocytoses can be classified into primary, where megakaryopoiesis is intrinsically abnormal, secondary, where megakaryopoiesis is normal but increased platelet production is a reaction to some other unrelated pathology, and finally idiopathic. This latter new group would be used for patients not satisfying the criteria for primary or secondary thrombocytoses, if these were more precise and rigidly used than currently is the case. While theoretically congenital and acquired forms of primary and secondary thrombocytoses might exist, only one cause of secondary congenital thrombocytosis has been established, and primary congenital thrombocytosis has not yet been precisely defined. Primary (essential) thrombocythaemia (PT) is one of the forms of primary acquired thrombocytoses. The diagnostic criteria of PT traditionally involve the exclusion of secondary thrombocytoses and other myeloproliferative disorders but marrow histology could hold a key positive diagnostic role if objective histological features of PT were agreed.

Anthropometry↗
PubMed2001

Phase I trial of simultaneously administered GM-CSF and IL-6 in patients with renal-cell carcinoma: clinical and laboratory effects.

BACKGROUND: Metastatic renal-cell carcinoma is a neoplasm that is minimally responsive to cytotoxic chemotherapy. Tumor regression following therapy with cytokines such as interferon alpha and or interleukin-2 is seen in selected subsets of patients. Investigations with other immunomodulatory cytokines, such as GM-CSF and IL-6 are therefore of interest. PATIENTS AND METHODS: A phase I trial of concomitantly administered granulocyte macrophage-colony stimulating factor (3.0 mcg/kg/day s.c. d1-14) and escalating doses of interleukin-6 (1.0, 5.0 or 10.0 microg/kg/day d1-14) was conducted in patients with metastatic renal-cell carcinoma to explore the toxicity of the combination and its hematologic effects. RESULTS: The most common side effects seen were fever, fatigue and arthralgias. Dose limiting toxicity included thrombocytosis and hyperbilirubinemia in patients receiving 10 microg/kg/day of IL-6. The hematologic effects of IL-6 and GM-CSF included leukocytoses and thrombocytosis, with increases in peripheral blood progenitors (BFU-E, CFU-GM, and CFU-GEMM). Evidence of platelet activation demonstrated by increased platelet expression of CD62 was found. No clinical responses were observed. CONCLUSIONS: The combination of IL-6 and GM-CSF has pleotropic hematologic effects. Further studies with this combination for the treatment of renal-cell carcinoma are not recommended.

Adult↗
PubMed2000

Improvement of extrathymic T cell type of large granular lymphocyte (LGL) leukemia by cyclosporin A: the serum level of Fas ligand is a marker of LGL leukemia activity.

We report a case of gammadelta T-cell-type large granular lymphocyte (LGL) leukemia (CD3 +,CD8 +, CD57 +,TCR gammadelta+), which was accompanied by pure red cell aplasia, neutropenia and thrombocytosis. Southern blotting analysis of the T-cell receptor beta gene showed the germline configuration, but clonal TCR J gamma rearrangements were identified. These granular lymphocytes demonstrated non-major histocompatibility complex-restricted cytotoxicitity. The serum-soluble FasL (sFasL) concentration of this patient was very high, whereas the serum levels of tumor necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), interleukin-1 beta (IL-1beta), interleukin-2 (IL-2) and thrombopoietin were normal. After treatment with cyclosporin A, anemia and thrombocytosis were improved, and LGL and the elevated sFasL concentration decreased. These observations suggested that FasL may have played a role in the establishment of the clinical symptoms of this patient and could be useful as an indicator of disease activity.

CD3 Complex↗
PubMed1998

Serum thrombopoietin levels in Kawasaki disease.

Kawasaki disease (KD) is an acute febrile vasculitic syndrome with thrombocytosis occurring in childhood. Transient thrombocytosis of KD is sometimes the cause of complications such as coronary aneurysmal thrombosis and myocardial infarction. We have analysed blood TPO levels in KD and found that 26/31 acute-phase KD patients had detectable blood TPO levels (mean 173 pg/ml; range 89-294 pg/ml), which decreased immediately with the elevation of platelet counts in 5/12 patients studied. Elevated serum level of TPO may have an important role for this ill-defined disease.

Child↗
PubMed2004

Platelets and angiogenesis in malignancy.

There is increasing evidence that platelets play an important role in the process of tumor angiogenesis. Thrombocytosis is a frequent finding in cancer patients (10-57%). Although the mechanisms underlying thrombocytosis are not yet fully elucidated, tumor-derived factors with thrombopoietin-like activity and growth factors, platelet-derived microparticles, and factors secreted from bone marrow endothelial cells, as well as growth factors released by megakaryocytes (acting via an autocrine loop), are postulated to influence this process. The progression of cancer is associated with hypercoagulability, which results from direct influences of tumor cells and diverse indirect mechanisms. Activated platelets serve as procoagulant surfaces amplifying the coagulation reactions. It is well known that hemostatic proteins are involved in different steps of the angiogenic process. Furthermore, platelets adhering to endothelium facilitate adhesion of mononuclear cells (which exert various proangiogenic activities) to endothelial cells and their transmigration to the extravascular space. It was also documented that platelets induce angiogenesis in vivo. Platelets are a rich source of proangiogenic factors. They also store and release angiogenesis inhibitors. In addition, platelets express surface growth factor receptors, which may regulate the process of angiogenesis. Platelets also contribute directly to the process of basement membrane and extracellular matrix proteolysis by releasing proteinases, or indirectly via inducing endothelial cells and tumor cells to release proteolytic enzymes, as well as through the proteolytic activities of platelet-derived growth factors. The multidirectional activities of platelets in the process of new blood vessel formation during tumor development and metastasis formation may create the possibility of introducing antiplatelet agents for antiangiogenic therapy in cancer patients. Thus far experimental studies employing inhibitors of glycoprotein IIb-IIIa have yielded promising results.

Blood Platelets↗
PubMed1997

Interferon-alpha therapy in polycythemia vera and essential thrombocythemia.

Essential thrombocythemia (ET) and polycythemia vera (PV) are chronic clonal myeloid disorders that originate from the multipotential hematopoietic stem cell. They are characterized, respectively, by excessive thrombocytosis and erythrocytosis, a high incidence of thrombohemorrhagic events, vasomotor symptoms, and an inherent tendency to undergo leukemic transformation. Current standard therapies to control the excess accumulation of myeloid cells and to provide symptomatic relief carry either a persistent risk of thrombosis, as in the case of phlebotomy, or, in the case of hydroxyurea, the potential for inducing leukemia. None alter the natural history of these diseases. Interferon-alpha has been shown to have potent antiproliferative effects on the hematopoietic stem cells and bone marrow fibroblasts and, as a result, has received much attention as a therapeutic agent for chronic myeloproliferative disorders. The ability of interferon-alpha to induce hematologic and cytogenetic remission in chronic phase chronic granulocytic leukemia has further increased interest in this agent. Interferon-alpha has shown therapeutic activity in PV and ET, as demonstrated in multiple small studies and single-arm trials reviewed in this article. Reported beneficial effects include the ability to control excessive erythrocytosis and thrombocytosis and such disease-related features as vasomotor symptoms, pruritus, and splenomegaly. Recent reports of cytogenetic remission and reversal of bone marrow fibrosis after interferon therapy are of interest. Advantages over current therapeutic standards include lack of known leukemogenic and teratogenic effects and the potential to alter the underlying course of disease. Nevertheless, none of the information available allows definite therapeutic recommendations for the use of interferon-alpha in PV or ET. The available data support the need for randomized controlled trials comparing interferon-alpha with standard therapy.

Cell Division↗
PubMed1989

Maternal death from carotid artery thrombosis associated with the syndrome of hemolysis, elevated liver function, and low platelets.

A case is presented of cerebral infarction secondary to carotid artery thrombosis in a patient with hemolysis, elevated liver function, and low platelets (HELLP) syndrome. The patient's rebound thrombocytosis may have contributed to a hypercoagulable state. Severe preeclamptic patients with HELLP syndrome who experience a reactive thrombocytosis may represent a subset of women who have postpartum thrombosis.

Adult↗
PubMed2005

Variant translocation with a deletion of derivative (9q) in a case of Philadelphia chromosome positive (Ph +) essential thrombocythemia (ET), a variant of chronic myelogenous leukemia (CML) with a poor prognosis.

Patients presenting with thrombocytosis require thorough clinical and laboratory evaluation to determine whether they suffer from essential thrombocythemia or another myeloproliferative disorder. This distinction becomes increasingly relevant as targeted agents become available to treat specific myeloproliferative diseases. Cytogenetic testing plays a major role in this analysis. This study presents a patient with Philadelphia chromosome positive (Ph + ) thrombocytosis and a cryptic der(9q)t(5;9)t(9;22) not found by conventional cytogenetics, whose disease progressed within 2 years to typical myeloblastic crisis of CML. It discusses the entity of Ph + ET, the utility of molecular cytogenetic testing in the diagnosis of this unusual disease entity and the importance of cytogenetic testing in the prognosis of ET.

Aged↗