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A case of autoerythrocyte sensitization syndrome in a 59-year-old female is reported. She had several episodes of circular ecchymoses on her left thigh. Intradermal injection of autoerythrocytes reproduced a similar ecchymosis. Thrombocytosis was detected and treated with busulfan which induced a delayed improvement of the ecchymosis outbreaks over 2 years of follow-up.
We describe a 22-month-old boy with iron deficiency anemia and reactive thrombocytosis who developed vomiting, headache, mental status changes, and seizures. Computed tomography showed infarction of the basal ganglia and thalami. Magnetic resonance imaging revealed cerebral venous thrombosis, delineated the extent of the vascular and associated parenchymal involvement, showed the infarcts to be hemorrhagic (a finding not imaged by computed tomography due to our patient's depressed hemoglobin level), and obviated the need for invasive angiography.
The clinical and laboratory features of acute Henoch-Schönlein purpura in 18 patients are presented. Thrombocytosis was noted in 67 per cent of the patients and was significantly associated with the presence of abdominal pain and gastrointestinal bleeding. We found no correlation between increased serum IgA concentrations or elevated sedimentation rates and any of the clinical features of Henoch-Schönlein purpura.
In developing countries, a deficiency of cobalamine and folate contributes significantly to megaloblastic anaemia. Neurological observations in infants and young children with megaloblastic anaemia have included hypotonia, developmental regression, tremors and other abnormal movements. Following therapy with vitamin B12, coarse tremors occurred in six of 51 patients (12%) with megaloblastic anaemia. The tremors, which were noticed initially in the hands and feet, gradually became generalised and disappeared during sleep. They subsided within 5-11 days. Thirteen of 25 (52%) patients developed thrombocytosis between day 3 and week 5 of follow-up. In one child, the platelet count increased to >1300 x 10(9)/L. The importance of recognising these clinical findings during treatment of megaloblastic anaemia is emphasised.
P230 Bcr/Abl has been associated with indolent myeloproliferative disease (MPD). We generated transgenic mice expressing P230Bcr/Abl driven by the promoter of the long terminal repeat of the murine stem cell virus of the MSCV neo P230 BCR/ABL vector. Two founder mice exhibited mild granulocytosis and marked thrombocytosis and developed MPD. The disease of one founder mouse, no. 13, progressed to extramedullary myeloblastic crisis in the liver at 12 months old. The other founder mouse, no. 22, was found to have chronic-phase MPD with large populations of megakaryocytes and granulocytes in an enlarged spleen. The transgenic progeny of no. 22 clearly exhibited MPD at 15 months old. These results showed that P230Bcr/Abl had leukemogenic properties and induced MPD. The phenotype of the MPD caused by P230Bcr/Abl was characterized by mild granulocytosis, a high platelet count, infiltration of megakaryocytes in some organs, and a longer disease latency compared with the MPD caused by P210Bcr/Abl.
JAK2 V617F mutation recently was identified as a pathogenic factor in typical chronic myeloproliferative diseases (CMPD). Some forms of myelodysplastic syndromes (MDS) show a significant overlap with CMPD (classified as MDS/MPD), but the diagnostic assignment may be challenging. We studied blood or bone marrow from 270 patients with MDS, MDS/MPD, and CMPD for the presence of JAK2 V617F mutation using polymerase chain reaction, sequencing, and melting curve analysis. The detection rate of JAK2 V617F mutants for polycythemia vera, chronic idiopathic myelofibrosis, and essential thrombocythemia (n = 103) was similar to the previously reported results. In typical forms of MDS (n = 89) JAK2 V617F mutation was very rare (n = 2). However, a higher prevalence of this mutation was found in patients with MDS/MPD-U (9 of 35). Within this group, most of the patients harboring JAK2 V617F mutation showed features consistent with the provisional MDS/MPD-U entity refractory anemia with ringed sideroblasts and thrombocytosis (RARS-T). Among 9 RARS-T patients, 6 showed the presence of JAK2 V617F mutation, and in 1 patient without mutation, aberrant, positive phospho-STAT5 staining was seen that is typically present in association with JAK2 V617F mutation. In summary, we found that RARS-T reveals a high frequency of JAK2 V617F mutation and likely constitutes another JAK2 mutation-associated form of CMPD.
Reports about vanadium (V) inhalation toxicity on the hematopoietic system, specifically about coagulation are limited. Therefore, we decided to evaluate the effects of V with a complete blood count and morphologic analysis of platelets on blood smears. CD-1 male mice inhaled V2O5 0.02 M 1 h twice weekly over 12 weeks. Blood samples were obtained by direct heart puncture; Wright stained smears were used for platelet quantification. An increase in platelet count from the third week of exposure was observed, as well as the presence of megaplatelets. Our results demonstrate, for the first time, that V induces thrombocytosis and it might correlate with some thromboembolic diseases. Further analysis is needed to evaluate the functionality of these platelets as well as the cause of its increase.
The effects of interleukin-6 (IL-6) in vivo were assessed by inoculating Chinese hamster ovarian (CHO) cells which were transfected with the murine IL-6 gene in nude mice. Nude mice bearing CHO cells expressing IL-6 developed hypercalcemia. Tumor-bearing mice also showed increases in white cell count, platelet count, and decreases in body weight. In nude mice carrying CHO tumors which had not been transfected with the IL-6 gene, there were no changes in these parameters. These results suggest that increased circulating concentrations of IL-6 in patients with malignant disease may contribute to a number of paraneoplastic syndromes including hypercalcemia, cachexia, leukocytosis and thrombocytosis.
BACKGROUND: Thrombocytosis is one of several pre-analytical factors which contribute to spuriously high serum potassium concentrations, yet there is little published data to guide analysts in the selection of a specific platelet count threshold above which serum potassium results become unreliable. We have studied the sensitivity and specificity of blood platelet count as a predictor of false elevations in potassium. METHODS: Paired serum and plasma potassium measurements together with full blood count were performed for 300 patients. All samples were stored at room temperature and analysed within 4 h of collection. The difference between serum and plasma potassium was plotted against blood platelet count. RESULTS: When the difference (serum-plasma) in potassium concentration was plotted against platelet count, there was a direct linear relationship. Blood platelet counts of >500 x 10(9)/L will detect elevations in serum relative to plasma potassium of >0.5 mmol/L, with a sensitivity of 71% and a specificity of 89%. CONCLUSION: It is recommended that where blood platelet count is above 500 x 10(9)/L, potassium measurements should be repeated using lithium heparin plasma. When serum potassium results of >5.4 mmol/L are obtained, it is our policy to check the platelet count if a sample is available before reporting results. If available and above 500 x 10(9)/L, potassium results are withheld and plasma requested.
OBJECTIVE: To review the role of anagrelide in the management of essential thrombocythemia. DATA SOURCES: A MEDLINE search (January 1966-August 1998) was performed using the key terms anagrelide, thrombocytosis, and essential thrombocythemia. In addition, the package insert, product monograph, and patient information pamphlets were reviewed. DATA SYNTHESIS: Recently, there has been a trend toward the use of anagrelide in the management of thrombocythemia. Anagrelide lacks leukemogenic and mutagenic potential and possesses a more favorable adverse effect profile compared with other therapeutic agents. At recommended doses, anagrelide induces thrombocytopenia in thrombocythemic patients with a concomitant reduction in the incidence of disease-related symptoms. CONCLUSIONS: Although the treatment of choice for thrombocythemia is still an area of debate, anagrelide has distinct advantages over alternative therapies. Anagrelide represents an important therapeutic option in the treatment of patients with thrombocythemia.
A case of thromboembolic pulmonary hypertension associated with long-standing thrombocytosis is presented. In this patient we found a significant local pulmonary platelet activation and thrombin generation as indicated by the existence of a transpulmonary gradient for thromboxane A2, beta thromboglobulin and fibrinopeptide A. Prolonged heparin and acetylsalicylic acid treatment resulted in improvement of clinical and hemodynamic conditions. These findings support the usefulness of anticoagulating and antiaggregating therapy in selected cases of pulmonary hypertension.
We report the case of a 27-year-old male smoker with simultaneous myocardial infarction (MI) and acute peripheral ischaemia. At the time of his first hospitalization, the platelet count and the coronary angiogram were normal. Two years later, the patient presented again with a leg artery occlusion, followed, a few days later, by a recurrence of MI. At this time, the platelet count was high and the coronary angiogram revealed an occlusion of the right coronary artery. The diagnosis of primary thrombocytosis was made by bone marrow aspiration and biopsy. Different unusual mechanisms of MI in young people are discussed in this report.
We describe a case of cyclic thrombocytopenia and thrombocytosis, whose cytokine levels, granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin-6 (IL-6) in plasma, fluctuated in synchrony with platelet count. The levels of the two cytokines correlated significantly with the platelet count for 11 observations over an 8-month period (r = 0.79, p < 0.01 for GM-CSF and r = 0.87, p < 0.001 for IL-6). No inverse relationship between platelet-associated immunoglobulin G (PAIgG) and platelet count was observed (r = 0.39, p > 0.20). These findings suggest that the fluctuation of platelet count in this case may result from an aberration of the cytokine network regulating megakaryopoiesis and platelet formation.
Splenic venous thrombosis is a rare disease in which an underlying hypercoagulable state can often be found. A 27-years old female patient with recurrent mesenteric venous and splenic thrombosis as a severe complication of an association of resistance to activated protein C and essential thrombocythemia is presented in this report. Establishing the diagnosis of essential thrombocytosis was particularly difficult because this was the case of the so called "silent" myeloproliferative disorder. The number of thrombocytes was almost normal before the splenectomy performed because of the splenic venous thrombosis. Thus, spontaneous growth of erythroid and megakaryocyte colonies in vitro and the clinical course of the disease were the clues for establishing the diagnosis, because the number of thrombocytes reached the values over 1500 x 10(9)/l after only 1.5 years of the follow-up. The case of this patient was interesting particularly from the surgical point of view because of the management strategy.
Two groups of suckling rabbits were studied from the 15th to the 40th day after birth, one group receiving mothers milk only, the other having the choice of iron-containing food pellets from the 20th day. In the milk-only group, the plasma iron concentration (P-Fe), blood hemoglobin concentration (B-Hb), red blood cell count (B-RBC), and mean corpuscular volume (MCV) declined continuously, whereas the hemoglobin mass of the blood (Hb-mass) remained unchanged, and the blood platelet count (B-PLTS), plasma platelet count (P-PLTS), and the estimated platelet release to the blood (PLT-release) showed a continuous rise. The milk-pellet group showed the same pattern until the 25th-30th day; thereafter, P-Fe, B-Hb, and Hb-mass rose markedly, whereas B-PLTS and PLT-release declined. At the time of weaning, both groups showed bimodal erythrocyte volume distribution curves. Thereafter, the milk-only group developed a pure microcytemia, whereas the milk-pellet group got normovolemic erythrocytes only. In conclusion, the erythropoiesis in suckling rabbits is characterized by a balanced recycling of an essentially constant amount of available iron, preventing rise of Hb-mass. The anemia thus reflects a failure of the Hb-mass to keep up with the growth-related rise in plasma volume. A close relationship exists between postnatal iron deficient microcytic anemia and thrombocytosis.
A 17-year-old girl known to suffer from essential thrombocytosis (ET) was admitted with severe abdominal pain that was due to sonographically verified portal and hepatic vein thrombosis. ET is a well-documented disease and portal vein thrombosis has often been reported in adults but not in children and adolescents suffering from ET. Coincidence of ET, urinary tract infection, oral contraception, and cessation of acetylsalicylic acid therapy might be responsible for the early manifestation of portal and hepatic vein thrombosis in our patient.
The breakpoints on chromosome 22 in CML occur within a 5.8 kb region called the Major breakpoint cluster region (M-bcr). DNA mapping within the M-bcr region was performed in 41 long term followed Ph1-positive CML patients using the Southern blot technique. The purpose of this study was to determine whether localization of M-bcr breakpoint correlates with the length of chronic phase of the disease, blastic crisis lineage and thrombocytosis at the time of initial diagnosis. Our results fail to indicate any correlation between breakpoint localization and duration of chronic phase, blastic crisis lineage and platelet count at diagnosis.
For most patients, elevated platelet counts are benign and require no treatment, but for some, severe complications or death may ensue. This article discusses how to classify thrombocytosis and identify which patients require treatment, describes the characteristic complications that may arise, and provides an algorithm for management.