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PubMed1989

Low protein S in essential thrombocythemia with thrombosis.

Patients with essential thrombocythemia (ET) are at increased risk for large-vessel and microvascular thrombosis, presumably because of abnormal platelet number and function. To determine if another hemostatic abnormality might contribute to this thrombotic risk, we investigated protein C and protein S and the fibrinolytic system in four patients with ET. The patients segregated into two distinct groups. The first group consisted of two patients with moderate thrombocytosis who were without thrombotic symptoms and who had normal protein S and protein C and normal fibrinolysis. The second group consisted of two patients with mild to moderate thrombocytosis and thrombosis. Both these latter two patients had abnormalities in protein S. The first patient had only 31% free protein S and 67% total protein S, with normal protein C and normal fibrinolysis. Following treatment, vasoocclusive symptoms resolved and platelet count decreased, but protein S remained low (28% free protein S). The second patient in this group had only 35% total protein S at initial study. Other hemostatic abnormalities were also present. Following treatment, symptoms resolved and protein S returned to normal. Based on this limited series, it appears that, in some patients with ET, thrombotic phenomena may be due to the presence of a second hemostatic abnormality in addition to the high platelet count and abnormal platelet function. This abnormality may be acquired as part of the disease process. Some of these abnormalities may be corrected following treatment.

Adult↗
PubMed1990

The transferrin receptor system is not involved in the pathogenesis of hematological disorders with 3q inversion.

To clarify the idea that an alteration of the transferrin receptor (TF-R) gene, localized to 3q26, may be of pathogenetic significance in hematological disorders with 3q anomaly, we studied the TF-R systems of erythroblasts from both functional and genetic aspects. The patient described here had refractory anemia with an excess of blasts (RAEB), with paracentric inversion, inv(3)(q21q26). The patient had the characteristic findings of micromegakaryocytosis and thrombocytosis, with giant platelets. There was no functional abnormality of TF-R as far as number of binding sites, affinity, molecular weight, or recycling kinetics were concerned. Furthermore, we could not recognize any rearrangement of the TF-R gene with Southern blot analysis. These data suggest that TF-R is not involved in the pathogenesis of leukemogenesis and thrombocytosis of the disease.

Chromosome Inversion↗
PubMed2007

Hematological abnormalities during the first week of life among neonates with Down syndrome: data from a multihospital healthcare system.

Various hematological abnormalities have been reported among neonates with Down syndrome. Thrombocytosis, thrombocytopenia, polycythemia, neutrophilia, transient myeloproliferative disorder (TMD), and congenital leukemia have all been reported. The two largest case series previously reported involved 63 and 31 cases. To acquire hematological data from a larger case series, we obtained all CBCs done during the first week after birth on all neonates with Down syndrome cared for in an Intermountain Healthcare (IHC) hospital with a date of birth between January 1, 2001 and December 31, 2005. During this period, 145,522 live births were recorded at 18 hospitals. Down syndrome was recognized in 226 (1 in 644). One hundred fifty-eight (70%) of these had one or more CBCs obtained before the seventh day (144 hr). Neonates who did versus did not have a CBC in the first week had a similar gestational age, birth weight, percentage who were LGA and SGA, and length of stay. Neutrophilia was the most common hematological abnormality detected, with 80% of absolute neutrophil counts above the upper limit of normal for age. Six percent (9/158) had blasts identified on the blood film and three, where this was persistent, were referred to the pediatric hematology service for further evaluation. The next most commonly detected abnormality was thrombocytopenia, with 66% of platelet counts <150,000/microl, and with 6% of counts <50,000/microl. The mean platelet volume did not correlate with the platelet count, but tended to run slightly large (9.2 +/- 1.3 fl), with 24% of values above 10 fl. Only one had a platelet transfusion. Polycythemia was the next most common hematological abnormality detected, with 33% of hematocrit values above 65% or hemoglobin concentrations above 22 g/dl. Six had a reduction transfusion. One patient had significant anemia (hematocrit <15%) and received an erythrocyte transfusion. One had neutropenia associated with an infection after bowel surgery. Neutrophilia, thrombocytopenia, and polycythemia were the most common hematological abnormalities observed among neonates with Down syndrome. Anemia, thrombocytosis, and neutropenia were not more common than among neonates who do not have Down syndrome. Hematological abnormalities were so common in this group that it seems reasonable to recommend that one or more CBCs be obtained on all neonates with Down syndrome.

Blood Cell Count↗
PubMed1983

Comparison of auranofin, gold sodium thiomalate, and placebo in the treatment of rheumatoid arthritis. A controlled clinical trial.

A prospective controlled, double-blind multicenter trial compared placebo, auranofin (an orally administered gold complex), and parenteral gold sodium thiomalate (GST) in patients with active rheumatoid arthritis (RA). Of 193 patients who received any treatment, the only important improvement identified for either auranofin or GST was for pain/tenderness scores. When 161 patients who completed 20 weeks of treatment were examined, both auranofin and GST treatments were superior to placebo as measured by improvement in number of painful and/or tender joints, joint pain/tenderness scores, physician's assessment of disease activity, and decrease in erythrocyte sedimentation rate when elevated at entry. GST was superior to placebo in improvement of joint swelling scores, anemia, thrombocytosis, and rheumatoid factor. No drug-related remissions were observed. The only statistically significant advantages of GST over auranofin for efficacy were an increase in hemoglobin concentration and decrease of thrombocytosis with GST. Withdrawals for adverse effects were 5 times more frequent with GST treatment. Thrombocytopenia, proteinuria, elevated liver enzymes, "nitritoid" reactions, and "gold pneumonitis" were observed only in the GST treatment group. These results confirm that both parenteral and oral gold may be effective for the treatment of RA, that GST tends to show greater efficacy than auranofin, and that auranofin has fewer significant adverse effects than GST. However, long-term benefits, tolerability, and safety cannot be inferred from this study.

Adolescent↗
PubMed2003

Phase II study of alpha2 interferon in the treatment of the chronic myeloproliferative disorders (E5487): a trial of the Eastern Cooperative Oncology Group.

BACKGROUND: In vitro and clinical data suggest a therapeutic role for alpha2 interferon (IFN) in the treatment of the chronic myeloproliferative disorders. Accordingly, a multiinstitutional, Phase II trial of IFN in patients with agnogenic myeloid metaplasia (AMM), essential thrombocythemia (ET), and polycythemia rubra vera (PRV) in the spent phase was initiated. The objectives of this study were 1) to investigate the response rates that may be achieved with IFN in the treatment of patients with these disorders, 2) to estimate the durability of the responses, and 3) to assess the toxicities of IFN in these populations. METHODS: Enrollment was limited to patients with AMM, ET, or PRV who already had developed 1) anemia or transfusion dependency, 2) thrombocytosis uncontrolled by standard therapy, 3) hemostatic complications, or 4) symptomatic splenomegaly. Initially, patients were started on IFN at a dose of 5 MU/m(2) per day as a subcutaneous injection. After the first 16 patients had been treated, the starting dose of IFN was reduced to 2 MU/m(2) per day because of unexpected toxicities. RESULTS: IFN demonstrated different levels of efficacy and toxicity in each of the three diseases studied. The overall response rates achieved among the evaluable patients in each category were as follows: ET, 88.2% (n = 17 patients; 1 complete response and 14 partial responses); PRV, 41.7% (n = 12 patients; 1 complete response and 4 partial responses); and AMM, 3.2% (n = 31 patients; 0 complete responses and 1 partial response). Thrombocytosis and leukocytosis were controlled in nearly all patients, with reversal of splenomegaly and resorption of myelofibrosis achieved in fewer patients. The toxicities attributed to IFN differed notably among the three disease groups: patients who had AMM suffered systemic and neurologic toxicities more frequently than patients who had PRV or ET; whereas patients who had ET experienced a greater than expected incidence of hepatic abnormalities, most typically transient elevations of serum amino acid transaminase levels. CONCLUSIONS: The current study demonstrated the safety and efficacy of IFN in patients with ET, PRV, and AMM. Objective responses and/or disease stabilization were obtained in patients with all three disease entities, including the reversal of splenomegaly and resorption of myelofibrosis in some patients.

Adult↗
PubMed1993

Production of interleukin-1 beta and interleukin-6 in hepatoblastoma.

Thrombocytosis and fever are frequent symptoms in children with hepatoblastoma. Interleukin-6 (IL-6) has been shown to mediate thrombocytosis and an acute-phase reaction including fever. We therefore investigated samples from 14 untreated patients with hepatoblastoma for this cytokine and in addition for interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha), all of which are known to induce IL-6 production. High serum levels of IL-6 were only found in 3/14 patients; the other cytokines were not detectable. In contrast, 12/14 tumors produced substantial amounts of IL-6 in primary cell culture, while IL-1 beta was found in 3/14 supernatants; IL-1 alpha and TNF-alpha were always negative. Immunoenzymatic staining of fresh tumors revealed that IL-6 is not produced by the tumor cells, but rather by surrounding fibroblasts and endothelial cells. In tumor cells only IL-1 beta, but neither IL-1 alpha, TNF-alpha nor IL-6, could be detected. In co-culture experiments with fibroblasts and endothelial cells, addition of hepatoblastoma cells enhanced IL-6 production. Including an IL-1 receptor antagonist abolished this effect incompletely. Our results suggest that tumor cells in hepatoblastoma induce IL-6 production in surrounding fibroblasts and endothelial cells by virtue of their endogenous secretion of IL-1 beta and supposedly some other, as yet unidentified, mediator.

Carcinoma, Hepatocellular↗
PubMed1992

Effects of short-term administration of recombinant human erythropoietin on rat megakaryopoiesis.

Recombinant human erythropoietin (rHuEpo) was tested for its ability to stimulate rat megakaryopoiesis in vivo. Groups of Sprague-Dawley rats were injected with rHuEpo at a daily dose of 20, 80, or 200 U for 5 days. Significant thrombocytosis (a 30 to 40% increase over the control level) was found only in the rats that received 200 U/day, but some changes in the megakaryopoietic parameters were observed not only in the rats given 200 U/day, but also in those receiving 80 or 20 U/day. rHuEpo induced a dose-dependent elevation of megakaryocyte ploidy, with the maximum 45% increase in the mean ploidy over the control level seen in rats given 200 U/day. The size of the marrow megakaryocytes also increased dose-dependently. rHuEpo did not increase bone marrow megakaryocyte numbers, but it increased those in the spleen in a dose-dependent manner. A change of these parameters was seen as early as day 1 at 24 h after initiating the Epo injections at a time when significant thrombocytosis was already present. Moreover, a significant increase in the ratio of small acetylcholinesterase-positive bone marrow cells was also found, with the greatest response noted on day 1. Administration of a large dose of iron did not alter the thrombopoietic effect of rHuEpo. These results suggest that the in vivo administration of rHuEpo stimulates the maturation of mature as well as immature megakaryocytes already present in the bone marrow.

Animals↗
PubMed1998

Anagrelide for treatment of patients with chronic myelogenous leukemia and a high platelet count.

Chronic myelogenous leukemia (CML) is usually treated with hydroxyurea or interferon-alpha. In some patients high platelet counts develop although leukocyte counts are well controlled with these drugs. If in such a situation cytoreductive therapy has to be intensified by a increase of the dosage, anemia and leukocytopenia as well as adverse effects of the drugs are likely to occur. In twelve CML patients we have therefore combined the basic CML treatment with anagrelide. This drug which selectively reduces platelet counts has been shown to be efficacious in the control of thrombocytosis in essential thrombocythemia. The diagnosis had been confirmed in all CML patients by cytogenetic and/or molecular biological analysis. The median age of our group was 58 years. Five were women and seven men. All patients were on treatment with hydroxyurea, some of them had previously received treatment with interferon-alpha (alone or in combination with hydroxyurea), busulfan or melphalan. Prior to the initiation of anagrelide treatment the platelet count was between 970,000 and 3,600, 000/microl (median about 2,000,000/microl). Seven patients had thrombohemorrhagic complications. All twelve patients, experienced hematologic responses, since their platelet counts decreased to less than 600,000/microl. The median platelet count after reduction was 343,000/microl. The median dosage required to achieve these responses and to maintain them for a period of at least four weeks was 1.9 mg/day. Thrombohemorrhagic complications disappeared or did not recur in all symptomatic patients. Adverse effects were seen in 3/12 patients: headache (1), tachycardia (1), palpitation (1) and fluid retention (1). Whereas these symptoms were mild and transitory they caused one patient to request discontinuation of treatment. Currently five patients are still on treatment with anagrelide (median duration of treatment 11 months) while therapy had to be discontinued in the seven others because of bone marrow transplantation, development of osteomyelofibrosis, blast crisis or on patient request. In our experience anagrelide is a useful therapeutic adjunct when thrombocytosis in patients with CML cannot properly controlled alone with traditional drugs.

Aged↗
PubMed1994

Liver transplantation for Budd-Chiari syndrome--palliation or cure?

This report documents two cases of Budd-Chiari syndrome (BCS) with essential thrombocytosis and antithrombin (AT) III deficiency as underlying etiological factors. Orthotopic liver transplantation was successfully performed in both patients but with different therapeutic intention. In the patient with essential thrombocytosis, hepatic transplantation only relieved the symptoms of the predisposing thrombogenic condition; it did not cure the underlying disorder. Prophylactic long-term anticoagulation, as well as adjuvant therapy for the causative disease, remained necessary. On the other hand, in the patient with AT III deficiency, liver transplantation was curative, resulting in complete reconstitution of serum AT III activity with resolution of the hypercoagulable state postoperatively. Thus, depending on the underlying etiology, liver transplantation for BCS can be considered as palliative, necessitating long-term adjuvant therapy, or as curative, with correction of a metabolic defect.

Adult↗
PubMed1989

Prothrombotic abnormalities in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is known to be associated with a thrombotic tendency, which is often attributed to thrombocytosis, elevated fibrinogen, or decreased antithrombin III. We prospectively studied eight patients with IBD, seven of whom had little or no disease activity, to determine if they had any laboratory abnormality known to be associated with an increased risk of thrombosis. Abnormalities in fibrinolysis were noted in five patients: four with high plasminogen activator inhibitor levels and one with poor release of tissue plasminogen activator following venous occlusion. Circulating immune complexes were present in the sera of five patients. Fibrinogen was mildly elevated in one patient, and two patients had mild thrombocytosis. Decreased levels of antithrombin III, protein C, or protein S were not observed. There appears to be a high incidence of abnormalities in fibrinolysis in inactive IBD, which may contribute to the high frequency of thrombosis seen in IBD. The presence of circulating immune complexes may contribute to vascular injury and thrombosis.

Adult↗
PubMed2004

Philadelphia (Ph) chromosome-positive thrombocythemia without features of chronic myeloid leukemia in peripheral blood: natural history and diagnostic differentiation from Ph-negative essential thrombocythemia.

We have evaluated the clinical symptoms, hematological features, and natural history of 3 cases and 20 reported cases described as Philadelphia chromosome-positive (Ph+) essential thrombocythemia (ET). The presence of increased small mononuclear megakaryocytes in bone marrow smears and biopsy material in patients with pronounced thrombocytosis and no evidence of chronic myeloid leukemia (CML) in peripheral blood appeared to be a diagnostic clue to the diagnosis of Ph+ (essential) thrombocythemia. As compared to cases of reactive thrombocytosis, the megakaryocytes in Ph+ thrombocythemia are smaller than normal ones and typically have hypolobulated round nuclei. This contrasts with the finding of clustered mature and enlarged megakaryocytes in Ph-negative true ET. Patients diagnosed as Ph+ ET may progress to CML and show a high tendency to myelofibrosis and blastic transformation. These observations indicate that both Ph+ ET and Ph+ thrombocythemia associated with CML can be regarded as early manifestations of the chronic stable phase of CML.

Aged↗
PubMed1998

Essential thrombocythemia at diagnosis: causes of diagnostic evaluation and presence of positive diagnostic findings.

The reasons for diagnostic evaluation and the clinical and laboratory data at diagnosis of 170 patients with essential thrombocythemia (ET) were studied retrospectively. The age distribution was 19-88 years (median 52 years), and 52 patients were under the age of 45 years. In 111 patients (65%) thrombocytosis was a chance finding, but the past history of 37 of these patients revealed symptoms known to be related to ET. The diagnosis was based on a chance finding in a significantly higher proportion of female (74%) than male (53%) patients. The diagnosis of ET is based mostly on negative findings, i.e., on the exclusion of other causes of thrombocytosis, and positive diagnostic tests would be useful. We evaluated the presence of positive diagnostic findings of myeloproliferative disorders in ET. Splenomegaly was seen in 26% and an abnormal karyotype in 5% of the patients. Abnormal megakaryocyte morphology was seen in 80%, abnormal in vitro growth of hematopoietic progenitors in 74%, and abnormal platelet function in 83% of the patients. Both in vitro cultures of hematopoietic progenitors and platelet functions were studied in 36 patients, and in only two of these were both tests normal. We conclude that in most patients with ET the diagnosis can be strongly supported by positive findings, especially by in vitro cultures of hematopoietic progenitors and studies of platelet function.

Adult↗
PubMed1975

Advances in management of splenic injuries.

Because there is no such thing as "minor splenic injury", the diagnosis of splenic rupture is a major problem after abdominal trauma. Since it is our policy to explore all penetrating abdominal injuries, the problem of early recognition arises in patients with blunt trauma. When abdominal evaluation is difficult because of associated injuries, we increasingly use peritoneal dialysis. This has been particularly helpful in patients with head injury or drug intoxication and has also contributed to earlier operation in patients with signs of hypovolemia but minimal abdominal findings. Angiography has been useful in doubtful cases. Review of our experience in the last five years with splenectomy (298 cases) has revealed complications, particularly thromboembolic, that have changed our management of these patients. The incidence of clinical pulmonary embolism was 4 per cent in patients having splenectomy for trauma as contrasted with 0.5 per cent in patients having laparotomy for trauma without splenectomy. Postoperative platelet evaluations in patients after splenectomy for trauma revealed thrombocytosis. Detailed follow-up platelet studies showed a peak thrombocytosis at about two weeks, averaging 976,000/mm3. In contrast, similar studies in other patients having laparotomy for trauma showed counts of about 200,000/mm3. Because of the high incidence of thromboembolic complications, a low-dose heparin regimen was initiated. There was a 30 per cent incidence of infection postoperatively.

Abdominal Injuries↗
PubMed2006

Autoimmune manifestations in acquired idiopathic splenic atrophy: A puzzling association.

Splenic atrophy is an uncommon diagnosis associated with celiac sprue or other well-characterized connective tissue diseases, drepanocytosis, or amyloidosis. We report two patients with splenic atrophy revealed by thrombocytosis. Both patients had anti-nuclear antibodies. Patient 1 also had a grade III Chisholm lymphocytic sialadenitis with a rheumatoid factor, anti-extractable nuclear antibodies, and a polyclonal hypergammaglobulinemia consistent with the diagnosis of Sjögren's syndrome. Patient 2 displayed a previous history of idiopathic pericarditis. An anti-pneumococcal vaccination was given to both patients and neither experienced infectious complications. Splenic atrophy should be suspected in patients with thrombocytosis of unexplained origin and a blood smear consistent with asplenia. Such patients must be checked for clinical and biological symptoms of autoimmune disorders.

Journal Article↗
PubMed2004

All-trans retinoic acid directly up-regulates thrombopoietin transcription in human bone marrow stromal cells.

OBJECTIVE: All-trans retinoic acid (ATRA) has been used as the first-line therapy for patients with acute promyelocytic leukemia (APL). We previously reported that ATRA increased serum thrombopoietin (TPO) levels accompanied by thrombocytosis during ATRA therapy for APL. In this study, we investigated the mechanism of transcriptional regulation of TPO gene by ATRA using human bone marrow stromal cells. PATIENTS AND METHODS: Real time reverse transcriptase polymerase chain reaction and Western blotting were performed to quantify TPO mRNA and protein levels in cells from the human bone marrow stromal cell line KM101. Luciferase-based reporter assay, electrophoretic mobility shift assay (EMSA), and chromatin immunoprecipitation (ChIP) assay were performed to identify a retinoic acid responsive element in the promoter region of TPO gene (TPO-RARE). RESULTS: TPO mRNA expression was up-regulated by approximately 2.9 times 8 hours after stimulation with 10(-6) M ATRA in KM101 cells. In contrast, ATRA did not alter TPO mRNA expression in cells from the human hepatoma cell line HepG2. Protein level of KM101 cells also was increased with 10(-6) M ATRA for 48 hours in KM101 cells. We found the synthesized RARalpha protein bound to [gamma-32P]-labeled TPO-RARE probe and its binding was competed by adding 200x amount of cold TPO-RARE probe by EMSA. In addition, [gamma-32P]-labeled TPO-RARE probe bound to KM101 nuclear protein extract was supershifted by anti-RARalpha antibody and modified by treatment with ATRA. The relative luciferase activity of TPO gene was increased by 2.2x and the histone H4 was acetylated through TPO-RARE after ATRA stimulation in KM101 cells by ChIP assay. CONCLUSION: These data support the direct up-regulation of TPO transcription by ATRA stimulation in human bone marrow stromal cells and propose one of the mechanisms of thrombocytosis during ATRA therapy for APL.

5' Flanking Region↗
PubMed2004

Interleukin-1beta up-regulates the expression of thrombopoietin and transcription factors c-Jun, c-Fos, GATA-1, and NF-E2 in megakaryocytic cells.

The multifunctional cytokine interleukin-1beta (IL-1beta) plays a central role in the body's immune and inflammatory responses. The mechanism of IL-1beta on thrombocytosis and megakaryocytopoiesis has remained controversial. In previous reports, we have demonstrated the expression of IL-1 receptors (IL-1RI and IL-1RII) and enhancing effects of IL-1beta on primary human megakaryocytic (MK) cells. In this study, we investigated the possible direct effects of IL-1beta on the expression of thrombopoietin (TPO) and transcription factors c-Jun, c-Fos, GATA-1, and p45 nuclear factor-E2 (NF-E2) in MK cell lines CHRF and Meg-01. Our results demonstrated that IL-1beta up-regulated messenger RNA (mRNA) and protein expressions of these transcription factors in a dose- and time-dependent manner. In CHRF cells, mRNA: c-Jun [3.4-fold, peaked at 15 minutes], c-Fos [4.2-fold, 15 minutes], GATA-1 [4.0-fold, 60 minutes], NF-E2 [3.2-fold, 120 minutes] and protein expression: c-Jun [3.0-fold, 30 minutes], c-Fos [1.7-fold, 30 minutes], GATA-1 [11.5-fold, 60 minutes], NF-E2 [12.5-fold, 120 minutes] were evidently enhanced after treatment with IL-1beta. The response to IL-1beta was consistent in the total cell and nuclear extracts and was significantly reduced by pretreatment with actinomycin D or cycloheximide. An IL-1-receptor antagonist (IL-1RA) inhibited the stimulatory effects of IL-1beta on these transcription factors by as much as 78%. TPO expression was increased by more than 9.9-fold on stimulation with IL-1beta. A TPO-neutralizing antibody did not significantly reduce the effects of IL-1beta. We conclude that IL-1beta up-regulates the expression of TPO, c-Jun, c-Fos, GATA-1, and NF-E2 in MK cells. The mechanism might be mediated by IL-1beta receptors and require transcription or protein synthesis. The direct involvement of IL-1beta in the MK lineage may provide an explanation for the phenomenon of thrombocytosis during inflammatory responses.

Base Sequence↗
PubMed2004

Differences of soluble CD40L in sera and plasma: implications on CD40L assay as a marker of thrombotic risk.

INTRODUCTION: Soluble CD40L (sCD40L) ELISA has emerged as a promising predictor of poor outcomes in acute coronary syndrome. Yet many blood processing techniques have been used with little consideration of their effect on the results. METHODS: We measured sCD40L by ELISA in 10 patients with thrombocytopenia and 12 with normal or high platelet counts and 8 healthy controls using three sampling techniques: serum clotted on ice (serum-I) or at room temperature (serum-RT) and platelet poor plasma (PPP). RESULTS: Serum-RT samples, compared to serum-I, gave significantly higher CD40L values (p=0.003), demonstrating that ex vivo sCD40L release by activated platelets is inhibited by cold temperature. Although serum-I and PPP were comparable in patients with normal platelet counts, serum-I gave significantly higher values than PPP in the thrombocytosis group (p=0.01), suggesting that cold inhibition is insufficient in the latter group. To estimate the fraction of sCD40L that was microparticle-bound CD40L (mp-CD40L), 16 samples underwent 0.1-microm filtration. 50.6% of sCD40L was mp-CD40L in serum-RT, whereas 21.3% and 29.9% were observed in serum-I and PPP, respectively. Lastly, plasma sCD40L was assayed in 46 patients with and 35 without thrombosis. Plasma sCD40L did not correlate with platelet count in non-thrombotic, non-inflammatory patients but did (p<0.01) in those with thrombosis. CONCLUSIONS: Sample processing and temperature profoundly affect sCD40L assay. Serum-I and PPP minimize the release of sCD40L ex vivo and better represent sCD40L in vivo. However, PPP may be preferable particularly in patients with thrombocytosis. The existence of mp-CD40L highlights the importance of centrifuge conditions.

Adult↗
PubMed1994

Issues in the diagnosis and management of essential thrombocythemia.

OBJECTIVE: To summarize the current trends in the diagnosis and management of essential thrombocythemia (ET) and to discuss the treatment of young and pregnant patients with ET. DESIGN: We review our experiences in the diagnosis and management of ET. MATERIAL AND METHODS: A definitive diagnosis of ET at initial examination is seldom possible because of the low incidences of associated clonal cytogenetic abnormalities and palpable splenomegaly. The criteria of the Polycythemia Vera Study Group for the diagnosis of ET are provided, as are the clinical and laboratory features that help to distinguish ET from reactive thrombocytosis. RESULTS: Patients with ET have an almost normal life expectancy if thrombohemorrhagic complications are controlled. Although a previous history of thrombosis is an established risk factor for further episodes, the adverse effects of extreme thrombocytosis and age are less well defined. Determining which patients require therapy is controversial. The management of young or pregnant patients necessitates special considerations. CONCLUSION: Until additional data become available, no strong recommendations can be given in support of or against specific therapy for asymptomatic young patients. We favor treatment in asymptomatic patients with cardiovascular risk factors but not in asymptomatic women who are pregnant or are of childbearing age.

Female↗