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PubMed1986

Amoxapine-associated agranulocytosis with thrombocytosis occurring early during recovery.

Agranulocytosis developed in a 35-year-old woman after she received 18 g of amoxapine, a tricyclic antidepressant, over 57 days. On the fifth day after cessation of amoxapine treatment, her platelet count rose from normal to a peak value of 999,000/mm3 on the 13th day. No cause for this thrombocytosis was apparent. Granulocytes appeared in the peripheral blood on the 15th day, and the thrombocytosis abated with the platelet count returning to a normal level by day 22. This confirms a previous report that amoxapine may be associated with agranulocytosis and suggests that thrombocytosis may occur as an early sign of recovery of the bone marrow in drug-associated toxic agranulocytosis.

Adult↗
PubMed1984

Some aspects of platelet glucose metabolism in thrombocytosis due to myeloproliferative disorders.

Some aspects of the glucose metabolism were investigated in platelets of 11 healthy donors and 11 patients suffering from thrombocytosis due to myeloproliferative disorders. Out of all the glycolytic compounds measured in resting platelets, dihydroxyacetonephosphate and fructose 1,6 bisphosphate were significantly higher in cells of subjects with thrombocytosis. No difference was observed in the basic net flux of glucose through the hexose monophosphate shunt. Addition of arachidonic acid to platelets of patients with thrombocytosis had a very poor effect in stimulation of the hexose monophosphate shunt, whereas high values of activation were obtained in control platelets. Lactate production determined by collagen was found significantly higher in all patients. These data observed in platelets of patients could be explained by a decreased pool of metabolic adenine nucleotides.

Adult↗
PubMed2005

[Thrombocytosis and essential thrombocythemia in childhood].

Thrombocytosis is frequently observed in pediatric patients. Among them the secondary thrombocytosis are the most frequent and result from several causes. The rarely primary thrombocytosis can be either constitutive (and often familial) or acquired (essential thrombocythemia). The purpose of this article is to give diagnostic orientation and to suggest which biological tests should be performed.

Bleeding Time↗
PubMed2006

Bortezomib is an effective agent for MDS/MPD syndrome with 5q- anomaly and thrombocytosis.

Thrombocytosis is not a frequent event in myelodysplasia (MDS) and is observed mainly in 5q- syndrome and MDS/myeloproliferative (MPD) overlap syndromes. The pathogenetic mechanism of thrombocytosis in 5q- has not been fully elucidated to-date. Bortezomib is a proteasome inhibitor which seems to be effective in MDS. We present here the first case in the literature with MDS/MPD syndrome, sole 5q- anomaly and thrombocytosis in which bortezomib administration normalized platelet count, produced a major erythroid response, and reduced levels of interleukin-6 (IL-6) and TNF-alpha while increased levels of IL-4 in the bone marrow plasma. The study of such cases will reveal the exact role of bortezomib in the management of MDS/MPD.

Antineoplastic Agents↗
PubMed1999

Peripheral retinal nonperfusion associated with essential thrombocytosis.

PURPOSE: To describe a patient with retinal complications of essential thrombocytosis. METHOD: Case report. A 24-year-old man with acute vitreous hemorrhage of the right eye underwent ocular and systemic examinations to elucidate the origin of this condition. RESULTS: Fluorescein angiography of the right eye showed an avascular peripheral retina with marked capillary nonperfusion, arteriovenous anastomosis, and sea fan neovascularization. Blood studies showed thrombocytosis without other associated systemic diseases. The peripheral retinal capillary nonperfusion and sea fan neovascularization were treated with dye-laser photocoagulation, and aspirin, 80 mg daily, was given for systemic treatment. CONCLUSIONS: In our patient, the avascular retina was associated with essential thrombocytosis, which may cause an avascular peripheral retina with neovascularization and vitreous hemorrhage in otherwise healthy persons.

Adult↗
PubMed1977

Rebound thrombocytosis after alcohol abuse: a possible factor in the pathogenesis of thromboembolic disease.

Five alcoholic patients had rebound thrombocytosis after withdrawal of alcohol. This rebound thrombocytosis was not always preceded by thrombocytopenia at admission. Two patients had a history of unexplained recurrent venous thrombosis and recurrent pulmonary embolism. It is suggested that recurrent rebound thrombocytosis after alcohol abuse can be a factor in the pathogenesis of thromboembolic disease in some patients.

Adult↗
PubMed1989

Long-term interferon therapy for thrombocytosis in myeloproliferative diseases.

31 patients with thrombocytosis associated with myeloproliferative disorders were included in a prospective trial of long-term interferon therapy. 6 patients (19%) had side-effects which required withdrawal of interferon within one year. 22 patients (71%) achieved and maintained a complete response (platelet count less than 440 x 10(9)/l) for at least twelve months, with reduction or abolition of symptoms associated with thrombocytosis and a significant fall in bone-marrow megakaryocytes. At twelve months, 25 patients were randomly allocated to maintenance or withdrawal of interferon. Thrombocytosis recurred rapidly when treatment was stopped, but a second remission could be achieved by resumption of interferon therapy.

Aged↗
PubMed1988

Thrombocytosis elevates serum potassium.

Spurious elevation of the serum potassium can be seen if the platelet count exceeds 1,000 x 10(9)/L in patients with myeloproliferative disease. To see if serum potassium is increased at more modest elevations of the platelet count we studied these parameters in 283 controls and 161 patients with reactive thrombocytosis. The incidence of hyperkalemia was 34% in patients with over 500 x 10(9) platelets/L compared with 9% if the platelet count was below 250 x 10(9)/L. Over this range there was a significant correlation of potassium increasing with the platelet count. The higher potassium values could not be explained on the basis of leukocytosis, renal insufficiency, or acidosis, suggesting that the elevated serum levels were often spurious. In support of this conclusion, the serum potassium exceeded plasma potassium by a larger amount in patients with thrombocytosis. We conclude that serum potassium rises in direct proportion to the platelet count in normal patients and in those with thrombocytosis, and that this increment is an artifact.

Humans↗
PubMed2005

Anagrelide is effective in treating patients with hydroxyurea-resistant thrombocytosis in patients with chronic myeloid leukemia.

We report phase II trial results of the use of oral anagrelide hydrochloride for treating 38 patients with hydroxyurea (HU)-resistant thrombocytosis accompanying chronic myeloid leukemia (CML). Anagrelide's efficacy was well established during a phase II study of more than 400 patients with one of the four myeloproliferative disorders: essential thrombocythemia, polycythemia, idiopathic myelofibrosis, and CML. In the last subgroup, there were 114 CML patients with significant thrombocytosis treated with anagrelide. Out of these patients, 38 had symptoms of thrombosis or hemorrhage and had thrombocytosis resistant to HU. They were then treated with anagrelide at an initial dose of 2.0 mg/day, followed by modifications based upon response and toxicity. In all, 71% of these patients responded with platelet reductions of more than 50% in a median time of approximately 4 weeks. The response rate was not influenced by age, gender, or prior thrombosis or hemorrhage. Importantly, the response rate to anagrelide in patients refractory to prior HU was essentially the same as that of the other 76 CML patients. Treatment with anagrelide was well tolerated and without undue toxicity. Reduction of excessive platelet counts by anagrelide sometimes occurring in CML may lead to the prevention of thrombohemorrhagic complications occurring in this clinical setting and is relevant even in those patients in whom imatinib mesylate is primary therapy.

Adult↗
PubMed2002

Elevation of serum thrombopoietin precedes thrombocytosis in acute infections.

To clarify the mechanisms underlying thrombocytosis secondary to infections, we longitudinally studied serum levels of thrombopoietin (TPO) and interleukin (IL)-6 in 15 infants and young children with prominent thrombocytosis (platelets >700 x 10(9)/l) following acute infections and 116 age-matched controls using an enzyme-linked immunosorbent assay. The subjects included nine patients with bacterial infections, three with viral infections and three with non-determined pathogens. TPO values in the controls were 2.24 +/- 0.87 fmol/ml (mean +/- SD) with a 95% reference interval of 0.85-4.47 fmol/ml. In the first week of infection, platelet counts were normal, but TPO values increased (approximately 10.73 fmol/ml). TPO levels peaked on day 4 +/- 2 at 6.44 +/- 2.37 fmol/ml and then fell gradually. When platelet counts peaked in the second and third weeks, TPO levels were similar to the controls. IL-6 levels in the first week rose and dropped more rapidly than TPO. Serum TPO values were significantly correlated with C-reactive protein levels (r = 0.688, P < 0.001) and IL-6 levels (r = 0.481, P = 0.027). These results suggest that TPO contributes to thrombocytosis following infections in conjunction with IL-6, arguing for additional regulatory mechanisms of blood TPO levels.

Acute Disease↗
PubMed1998

Leg ulceration with associated thrombocytosis: healing of ulceration associated with treatment of the raised platelet count.

Thrombocytosis is the cause of various complications in myeloproliferative disorders. We present the case of a 54-year-old woman with chronic myelogenous leukaemia who developed large ulcers on both lower legs that were refractory to standard treatment. As concomitant thrombocytosis persisted despite treatment with hydroxyurea, the new megakaryocyte inhibitor anagrelide (Agrelin) was administered and led to normalization of the platelet count within 11 days. The leg ulcers started to heal after 2 weeks and disappeared over a period of 5 months. Our findings argue for a pathogenic role of platelets in the development of leg ulcers in patients with thrombocytosis due to a myeloproliferative disorder.

Female↗
PubMed1996

Thrombocytosis in patients with acute promyelocytic leukaemia during all-trans retinoic acid treatment.

In 26 acute promyelocytic leukaemia (APL) patients treated with all-trans retinoic acid (ATRA), 23% had platelet counts between 459 and 800 x 10(9)/I during treatment. These values, observed between days 28 and 45 of ATRA treatment, were transient and asymptomatic. We report two APL cases with platelet counts > 1000 x 10(9)/I during ATRA therapy who were treated with recombinant interferon alpha. In both cases ATRA doses were not modified, no complications secondary to thrombocytosis were seen, and they subsequently achieved complete remission. It is suggested that IL-6 may play an important role in the pathogenesis of the thrombocytosis induced by ATRA. To our knowledge, this is the first report of thrombocytosis occurring during ATRA treatment.

Adolescent↗
PubMed1997

Thrombopoietin measurement in thrombocytosis: dysregulation and lack of feedback inhibition in essential thrombocythaemia.

Essential thrombocythaemia (ET), a myeloproliferative disorder (MPD) manifested by excessive platelet production, lacks a specific diagnostic test to facilitate differentiation from other thrombocytoses. We studied thrombopoietin (TPO) levels in 41 patients with thrombocytosis: 25 ET patients, eight with other MPD, and eight with reactive thrombocytosis. Mean age and platelet counts for these groups were comparable. TPO levels for 96 healthy individuals provided a reference range for normal. The majority of ET patients (19/25 or 76%) had normal TPO levels. No patient with ET had a TPO level below 75 pg/ml, compared with 57% of healthy donors and 8/16 (50%) patients with other thrombocytoses (P<0.05). TPO levels in ET are not appropriately down-regulated, as occurs with cytokines relevant to other MPD. In thrombocytosis, a TPO level <75 pg/ml indicates that ET is unlikely.

Adolescent↗
PubMed2002

The role of blood component removal in essential and reactive thrombocytosis.

An elevated platelet count is now a common finding in both hospitalized and ambulatory patients with the advent of automated complete blood cell counters. Clinicians may be called upon to make a distinction between a reactive process and a primary hematologic disorder as the cause of a thrombocytosis and to determine whether treatment is indicated. Essential thrombocythemia and other myeloproliferative disorders may present with marked increases in the platelet counts and may be associated with thrombohemorrhagic complications. Reactive thrombocytosis can be caused by iron deficiency and a variety of inflammatory conditions, infections, malignancy, bleeding or hemolysis, splenectomy, and drugs. Acute therapy for all of these disorders has included blood component removal, specifically plateletpheresis. The role of plateletpheresis in current management of thrombocytosis is considered, based on current knowledge of pathophysiology and a review of the literature.

Female↗
PubMed2002

Serum proinflammatory cytokines and its relationship to clinical parameters in lung cancer patients with reactive thrombocytosis.

Proinflammatory cytokines Interleukin-1 beta (IL-1 beta) and Interleukin-6 (IL-6) play a significant role in the pathogenetic processes related to various malignant and inflammatory conditions. Leukocytosis, thrombocytosis and increased acute phase protein levels are part of a systemic inflammatory response. In this study, we measured the concentrations of IL-1 beta, IL-6 and ferritin as well as hemoglobin, lactate dehydrogenase (LDH), C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) in 23 patients (male 15, female 8, median age 68 years) with lung cancer and reactive thrombocytosis (LCRT), in 27 (male 18, female 9, median age 64 years) with benign inflammatory lung disorder (BILD) and 18 (male 10, female 8, median age 62 years) lung cancer patients with a normal platelet count (LCNP). IL-1 beta levels were significantly higher in the three patient groups in comparison with control subjects (P < 0.001) but without significant difference among the three patient groups. IL-6 was higher in all three patients groups but only in the BILD group it was significantly higher than the control group (P < 0.05). However, no significant difference in IL-6 serum levels was found between the two lung cancer groups. CRP and LDH were significantly higher in the LCRT group in comparison with the other two patient groups (P < 0.01 and 0.001, respectively), while ferritin was higher in both lung cancer groups in comparison with the BILD group (P < 0.001). Our data suggest that in lung cancer patients, reactive thrombocytosis is part of the systemic inflammatory reaction for which IL-1 beta and IL-6 may be intermediate but not independent mediators.

Adult↗
PubMed1995

Thrombocytosis in childhood.

Until recently, thrombocytoses in childhood were considered to be rare. The literature on this subject is scarce and contradictory. When thrombocytosis is defined as a platelet count of more than 500 x 10(9)/L (500 000/mm3 or 500 000/microL), the occurrence in routine examinations at pediatric hospitals can be estimated as 3 to 13%. These are almost exclusively secondary thrombocytoses, which are the result of infections (most frequently), trauma and surgery, hypoxemia, immunologic disturbances, premature birth, gastrointestinal disorders, medications, stress situations, or previous loss of platelets. The secondary thrombocytosis usually has less then 800 x 10(9)/L platelets, is temporary, and occurs predominantly in infants and young children. If only thrombocytosis is present, thrombotic complications are practically nonexistent. Antithrombotic prophylaxis is not necessary unless other risk factors for thrombosis are present, such as vessel damage, permanent iron deficiency, hyperviscosity, immobilization. Primary thrombocytoses due to a defect of stem cells are extremely infrequent in childhood.

Child↗
PubMed2002

Development of thrombocytosis in HIV+ drug users: impact of antiretroviral therapy.

With the exception of hemolytic anemia, the potential hematological toxicity of antiretrovirals (ARV) and combination treatments in HIV treated individuals has not been well established. We report, for the first time, hematological toxicity defined as thrombocytosis in 9% of the HIV+ patients receiving highly active antiretroviral treatment (HAART) being followed in a nutritional clinical trial. Participants were evaluated every 6 months during a 2-year period (1998-2000) and blood drawn for biochemical, hematological and immunological parameters. NK cells were negatively correlated with platelet counts in the total cohort (P = 0.018) and persistently elevated with ARVT. Chronic thrombocytosis was associated with significantly lower NK percentages (P = 0.005). Twenty-five percent of the patients with thrombocytosis developed a cardiovascular disease. Together, these results support the proposal that HAART may increase the risk of hematological dysfunction and impact the risk of cardiovascular disease.

Acquired Immunodeficiency Syndrome↗
PubMed2003

Thrombocytosis under ciprofloxacin and tazobactam/piperacillin.

Whether the simultaneous administration of ciprofloxacin or tazobactam/piperacillin increases the risk of thrombocytosis is unknown. Broncho-pulmonary infection in a 50-year-old male with acute, hypertensive, intracerebral bleeding, necessitated therapy with cefpirome (2 g/day, 6 days), ciprofloxacin (800 mg/d, 11 days) and tazobactam/piperacillin (9 g/day, 11 days). Starting with the 8th hospital day, the thrombocyte count steadily increased from 410000/microl to a maximum of 1132000/microl on hospital day 16. Afterwards the thrombocyte count continuously decreased to normal values. Primary thrombocytosis and secondary causes were excluded. Since the thrombocyte count started to increase immediately after initiation and dropped immediately after discontinuation of ciprofloxacin and tazobactam/piperacillin and all other drugs were discontinued already before or were started after the nadir of the thrombocyte count, these two antibiotics were regarded causative. It is concluded that simultaneous administration of ciprofloxacin and tazobactam/piperacillin may cause marked thrombocytosis. Discontinuation of these two antibiotics results in an immediate decline of the thrombocyte count to normal values within three weeks.

Anti-Bacterial Agents↗