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PubMed2001

Current opinion in essential thrombocythemia: pathogenesis, diagnosis, and management.

A working diagnosis of essential thrombocythemia (ET) is made in the presence of nonreactive thrombocytosis and after the exclusion of another chronic myeloid disorder that may mimic ET in its presentation. Clinically, ET is characterized by vasomotor symptoms, thrombohemorrhagic complications, recurrent fetal loss, and transformation of the disease into either myelofibrosis with myeloid metaplasia or acute myeloid leukemia. Median survival in the majority of patients is close to that of an age-adjusted normal population, and current therapy has not been shown to either retard or hasten leukemic transformation, which is reported to occur in 1% to 20% of patients. The use of hydroxyurea in high-risk patients with ET has reduced the incidence of thrombosis, and recent studies have suggested the value of keeping the platelet count below 400 x 10(9)/L in such cases. The incidence of thrombosis in low-risk patients may not be high enough to warrant the use of cytoreductive therapy. Although effective in controlling vasomotor symptoms, aspirin therapy has not been shown to influence the risk of either recurrent thrombosis or first-trimester miscarriage in ET. Recent laboratory studies have suggested that hematopoiesis in ET may not always be clonal. Similarly, there is substantial heterogeneity in both megakaryocyte/platelet surface expression of the thrombopoietin receptor (c-Mpl) and bone marrow microvessel density. Clinicopathologic correlates to these biologic parameters are currently being defined.

Cell Transformation, Neoplastic↗
PubMed1977

[Megakaryocytic myelosis: clinical and morphological features (author's transl)].

In general, megakaryocytic myelosis is nowadays considered to be a separate disease entity, one of the myeloproliferative syndromes. Morphologically there are localised or diffuse proliferations of usually large pleomorphic megakaryocytes and immature atypical megakaryocytes up to megakaryoblasts in the bone marrow, in the sense of a haemoblastosis. In the course of the disease megakaryocytic splenomegaly develops. A sarcomatous form (megakaryoblastoma, megakaryo-sarcoma) is rare. Megakaryocytic myelosis may arise from chronic meyloid leukaemia or polycythaemia vera, rarely as a transitional stage to an acute myeloblastic leukaemia or megakaryoblastic leukemia in the sense of a blast crisis. The mature form of the disease, which has an age peak at 59 years and is not sex-linked, often takes a course over years with increasing splenomegaly, anaemia, moderate leucocytosis and usually marked thrombocytosis (average value of 720 X 10(9)/1). Life threatening complications are haemorrhages, thromboembolism and increased frequency of infections due to antibody deficiency in the advanced stage.

Adult↗
PubMed1979

[Pseudo-hyperkalaemia in myeloproliferative diseases (author's transl)].

In two patients in the blast phase of chronic myeloid leukaemia there was a marked rise in serum potassium levels, while plasma potassium was at the lower range of normal and there were no signs of hyperkalaemia clinically. After reduction of the pathological cells under cytostatic treatment the serum potassium levels returned to normal. This in-vitro phenomenon seems to be more common in patients with marked thrombocytosis and leukaemia than has previously been thought. In such patients hypokalaemia may be undetected because serum potassium levels arenormal. Pseudo-hyperkalaemia exists when the potassium level is normal in plasma obtained by centrifugation immediately after the blood sample has been taken, without addition of plastic spheres and at once separated from the blood cells.

Adult↗
PubMed2001

Acute Budd-Chiari syndrome, portal and splenic vein thrombosis in a patient with ulcerative colitis associated with antiphospholipid antibodies and protein C deficiency.

We report the case of a female patient who had severe thrombotic complications in peripheral (V. jugularis, subclavia, brachialis, poplitea) and visceral (portal and splenic) veins 4 years after the first diagnosis of severe ulcerative pancolitis. A thrombolysis therapy for subclavian and jugular vein thrombosis was performed without complication, but she soon developed acute thrombosis of the hepatic veins (acute Budd-Chiari syndrome). She quickly recovered after liver transplantation and now - 6 years later - she lives a normal life with continuous anticoagulation and medical therapy of the colitis.3 possible causes for the severe coagulation defect in this patient can be supposed: Thrombocytosis, protein C deficiency and an antiphospholipid antibody syndrome.

Adolescent↗
PubMed2002

[Wound botulism after drug injection].

CLINICAL PRESENTATION: A 32-year old male drug user presented with diplopia, ataxia and general weakness. The patient had abscesses on arms and legs at injection sites, bilateral ptosis, a bifacial weakness, nasal speech, severely reduced ability to raise his arms and a positive Trendelelenburg sign with normal motor neuron reflexes and normal sensation. CLINICAL AND LABORATORY TESTS: The haematological values indicated a hypochromic, microcytic anaemia (12,1 mg/dl), a slight leuko (10,8 G/L) - and thrombocytosis (582G/l) with elevated erythrocyte sedimentation rate (74 mm/h), and a reduced prothrombin time (67%). The HIV test was negative. The MRI scan of the brain and the bacterial, serological and cytological results of a lumbar puncture were normal. In the bloodculture no bacterial growth and no botulinum toxin was found. In a culture of the wound material grew coagulase-negative staphylococcus and Clostridium perfringens, diagnosed with PCR. The serum anti-acethylcholine antibodies were negative. The motor-nerve conduction test with repetitive stimulation of the ulnari nerve with a 3 Hz trigger showed no change in the amplitude, while a 20 Hz trigger showed an increment up to 160 %. DIAGNOSIS, TREATMENT AND RESPONSE TO THERAPY: Another possible diagnosis was excluded through MRI, CSF and serum examination. The typical presentation of a rapidly progressive descending paralysis without loss of sensation and the typical motor-nerve conduction disorder of a presynaptic block established the diagnosis of wound botulism. This was treated immediately by surgical removal of wound debris, antitoxin- and penicillin therapy. After 28 days the patient left the hospital with slight residual problems. He had been admitted to the intensive care unit for a short period only and intubation was not necessary at any time. CONCLUSION: After exclusion of any other possible diagnosis, it is possible to establish an early diagnosis of injection related wound botulism by its typical symptoms and signs. These are presented as wound abcesses at intramuscular drug injection sites together with rapidly progressive descending paralysis with preserved sensation. Treatment consists of surgical excision of wound debris combined with antitoxin and penicillin administration in order to prevent a possible build-up of residues. Early diagnosis and associated therapy overcome the necessity of intubation and prolonged intensive care.

Adult↗
PubMed2002

Platelets and cancer: implications for antiangiogenic therapy.

Thromboembolism is one of the most common causes of death in cancer patients. Among the most frequent thrombotic complications in patients with cancer are disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, and thrombocytosis. Clearly, these complications arise as tumor cells interact with almost all components of the hemostatic system including platelets. Platelets participate in tumor progression by contributing to the metastatic cascade, protecting tumor cells from immune surveillance, regulating tumor cell invasion, and angiogenesis. Platelets contain one of the largest stores of angiogenic and mitogenic factors and the tumor vasculature is leaky, which allows platelets to come in contact with the tumor and deposit multiple angiogenic factors including vascular endothelial growth factor (VEGF) and thrombin to tumor cells, which in turn contributes to tumor progression. This article reviews the recent literature on how platelets contribute to tumor growth, angiogenesis, and metastasis.

Angiogenesis Inhibitors↗
PubMed2003

Hyperviscosity in polycythemia vera and other red cell abnormalities.

Thrombosis is a major cause of mortality and morbidity in polycythemia vera (PV). The wide range of thrombotic events reflects the complex picture in PV. There are multiple factors involved in thrombogenesis in this disease, including increased hematocrit, thrombocytosis, impaired fibrinolytic activity, platelet activation, leukocyte activation, endothelial damage, interactions between platelets and endothelium, various modalities of therapy, and increased in whole-blood viscosity. Among them, the increase in blood viscosity, and hence the impairment of blood flow, is the major factor. In this article, the role of hyperviscosity in PV is reviewed. A high hematocrit occurs under PV and many other conditions with abnormal red blood cell aggregation. The impaired capillary blood flow results in neurological manifestations and increased bleeding risk in PV. Thrombotic complications can also occur in both arteries and veins and manifest as stroke, myocardial infarction, deep vein thrombosis, or pulmonary embolism. The hemodynamic principle is aptly applied in the management of PV. The most important objective is the reduction of the patient's hematocrit.

Blood Viscosity↗
PubMed2003

Correction of hyperviscosity by apheresis.

Therapeutic apheresis is an extracorporeal blood purification technique designed for the removal of either plasma (plasmapheresis) or cellular blood components (cytapheresis). One of the main indications for the use of apheresis is in the treatment of the hyperviscosity syndromes that can result from either the presence of abnormal plasma components, such as antibodies, immune complexes, paraproteins, and cryoglobulins, or the excessive increase in blood cells as seen in polycythemia, leukemias, and myeloproliferative diseases. Apheresis involves withdrawal of anticoagulated blood via a vascular catheter, separation of different blood components by either centrifugation or membrane filtration, removal of the undesired component, and reinfusion of the remaining components with replacement fluid into the patient. The centrifugal method can be intermittent or continuous, the latter being faster and fully automated, and is principally used in North America. The membrane filtration technique, mainly used in Europe and Japan, involves the filtration of blood by filters of different pore sizes. These are used sequentially in a process called double or cascade filtration, enabling removal of specific plasma pathogens without need for replacement fluids. In paraproteinemias, hyperviscosity syndrome is most commonly seen with Waldenström's macroglobulinemia, followed by immunoglobulin (Ig) A and IgG (3) multiple myeloma. Single plasmapheresis with one plasma volume replacement (about 3 L) usually results in a dramatic improvement in patients with macrogobulinemia because of its predominant intravascular distribution, whereas repeated plasmapheresis is necessary with other types of paraproteins. Cryofiltration apheresis using a high-capacity cryofilter is specific for the removal of cryoglobulins. In leukemias with hyperleukocytosis, there are no evidence-based guidelines for use of leukapheresis, but it is commonly initiated when white blood cells (WBC) are > 100,000/microL or even with lower counts if leukostasis symptoms are present, especially in acute myeloid leukemia. Erythrocytapheresis and plateletpheresis are mostly used in the acute management of symptomatic patients with polycythemia vera (PV), essential thrombocytosis, and sickle cell disease.

Blood Component Removal↗
PubMed2003

[Fungemia after oral treatment with Saccharomyces boulardii in a patient with multiple comorbidities].

HISTORY AND CLINICAL FINDINGS: A 48-year-old diabetic with multiple co-morbidities presented with generalized micro- and macroangiopathy including peripheral artery disease stage IV with necroses in several digits of both feet. He was admitted to the department of surgery for the insertion of femoropopliteal bypasses. INVESTIGATIONS: Infectious parameters were elevated (CRP 66.1 mg/l, sedimentation rate 90/96), accompanied by anemia (Hb 7.1 mmol/l), leukocytosis (14.8 Gpt/l) and thrombocytosis (514 Gpt/l). Body temperature was normal (36.8 degrees C). With insulin treatment the patient became nearly normoglycemic (HbA1c 6.8 %). TREATMENT AND FOLLOW UP: After receiving different broad-spectrum antibiotics over seven weeks the patient developed Clostridium difficile toxin-positive diarrhea that resolved after administration of oral metronidazole and Saccharomyces boulardii (Perenterol ((R))). Three days after bypass insertion, both legs had to be amputated due to infection and beginning sepsis. The condition of the patient improved. However, eight days after bypass-insertion the patient developed a toxic megacolon and sepsis. Blood cultures yielded the growth of Saccharomyces cerevisae. Despite of intensive care treatment the patient died five days later from to multi-organ failure. CONCLUSION: S. boulardii (synonym: S. cerevisiae) is considered an non-pathogenic probiotic yeast, and live yeast cells are used for supportive therapy of diarrhea. The present case and a review of the literature demonstrate that fungemia and sepsis are rare complications of the administration of S. boulardii in immunocompromised patients. For this reason the therapeutic usage of probiotics should be carefully considered regarding its risk-benefit potential.

Administration, Oral↗
PubMed2004

[Prophylactic splenectomy for splenic vein thrombosis in patients undergoing resection for chronic pancreatitis].

AIM: Chronic pancreatitis (CP) is the leading cause of splenic vein thrombosis (SVT). SVT occurs in about 15 % of patients with CP. The risk of variceal bleeding in SVT is approximately 10 %. Splenectomy is indicated in symptomatic SVT but its role in asymptomatic SVT is discussed controversially. Aim of our study was to evaluate the outcome of splenectomy performed during pancreatic resection in patients with CP and asymptomatic SVT. METHODS: 33 of 198 patients undergoing resection for CP underwent concomitant prophylactic splenectomy for asymptomatic SVT. Perioperative data were compared in the groups of patients with or without splenectomy. Follow-up was complete in 84 % (average 31 months). RESULTS: Median operative time, postoperative morbidity, reoperation rate and mortality were not different in patients with or without splenectomy. The median number of blood units transfused was higher in patients with prophylactic splenectomy (6 vs 4 units; p < 0.01). One complication of splenectomy (postoperative bleeding) occurred (3 %). During follow-up no variceal bleeding, no episode of postsplenectomy sepsis or thrombosis due to temporary thrombocytosis occurred. CONCLUSIONS: Complications of prophylactic splenectomy are rare and less frequent than reported episodes of variceal bleeding. In the presence of asymptomatic SVT splenectomy should be considered during pancreatic resection to facilitate surgery and to avoid further variceal bleeding.

Chronic Disease↗
PubMed2006

Influence of the assays of endogenous colony formation and serum erythropoietin on the diagnosis of polycythemia vera and essential thrombocythemia.

Formation of endogenous erythroid colonies (EECs) or endogenous megakaryocytic colonies (EMCs) is a hallmark of myeloproliferative disorders (MPDs). The diagnostic value of EEC for polycythemia vera (PV) using standardized media has been demonstrated, and has led clinicians to consider EEC as a major diagnostic criterion in the WHO classification. The interest of EEC currently needs to be considered taking into account recent data about V617F JAK2 mutation in MPD. In particular, EECs and EMCs should be helpful for the diagnostic and the vascular risk evaluation of essential thrombocythemia (ET) and for mutation negative patients. A low serum erythropoietin (EPO) level is a consistent finding in PV. Recent studies have shown that commercial serum EPO assays provided a reliable, accurate, and low-cost criterion for the diagnosis of a significant proportion of PV. It suggests that diagnostic algorithms integrating serum EPO level could be elaborated. The diagnostic value of EPO assay for thrombocytosis has not been proved, but some data suggest a predictive value of low EPO levels for thrombosis in ET.

Colony-Forming Units Assay↗
PubMed1991

[Cerebral ischemia in young adults].

An overview is given over etiology and prognosis of cerebral ischemias until the age of 40. In a time period of 19 years, 168 patients were diagnosed with cerebral ischemia until the age of 40 (91 females, 77 males). The most frequent etiology is premature atherosclerosis in patients with vascular risk factors (up to 50%). Cardiogenic embolism is responsible for 1 to 34% of the cases: cardiac valve diseases and endocarditis being the most frequent sources. In 2 to 19% a vasculitis is diagnosed. While infectious arteritis is especially frequent in countries of the third world, immunovasculitides are common in Europe and the USA. Noninflammatory vasculopathies include spontaneous or traumatic dissection, fibromuscular dysplasia and vascular malformations. A migrainous stroke is especially frequent in female smokers with intake of oral contraceptives. During pregnancy both sinus thrombosis and arterial ischemia occur. Hematologic causes for ischemia are polycythemia, thrombocytosis and genetic diseases (sickle cell anemia, AT3-deficiency). Cerebral ischemia may occur in connection with the ingestion of ergot-derivates. The prognosis of cerebral ischemia in young adults is better than in older stroke-patients.

Adolescent↗
PubMed1999

[Thoracic splenosis with symptoms of coronary heart disease].

HISTORY AND REASON FOR ADMISSION: A 53-year-old man, who had undergone a splenectomy for a traumatic splenic tear 20 years previously, was admitted because an acute myocardial infarction was suspected. 20 years ago, a splenectomy had been performed because of traumatic rupture. INVESTIGATIONS: Laboratory values were normal except for a microcytic anaemia, thrombocytopenia (109,000/microliter) and a raised ferritin level (547 ng/ml). Coronary heart disease as well as other cardiac and upper gastrointestinal abnormalities were excluded. Computed tomography revealed a space-occupying mass in the left lower lobe of the lung near the heart. This filled with contrast medium on coelangiography at the same time as the liver and a subphrenic mass thought to be an accessory spleen. TREATMENT AND COURSE: At thoracotomy numerous splenic masses, maximally 7 cm in diameter, were removed from near the heart, the costal pleura and the lung margin. There were haematological changes similar to those after splenectomy: leucocytosis (32,400/microliter) and thrombocytosis (637,000/microliter) on the 11th postoperative day and Howell-Jolly bodies noted on the 16th day. CONCLUSION: In splenosis the disseminated pieces of splenic tissue can partly substitute for the normal spleen's functions. Splenosis tissue should, therefore, not be removed in every case, especially, if it does not cause symptoms.

Diagnosis, Differential↗
PubMed1999

Laboratory diagnosis of the thrombophilic state in cancer patients.

Perturbations of coagulation in cancer patients have been described for a long time. In up to 90% of cancer patients "routine" blood tests are abnormal leading to a hypercoagulable state in these patients. Among these tests are an increase in clotting factors, fibrinogen, fibrinogen/fibrin degradation products, and thrombocytosis. Markers of the activation of coagulation have been developed, and levels of FPA, F1+2, TAT, and D-Dimer have been found higher in cancer patients. More specific procoagulant activities in cancer (CP and TF) have also been described and can be measured but none of them have any predictive value for the occurrence of venous thromboembolism in these patients. Consistent with this hypercoagulable state in cancer is the finding that most cancer patients have reduced plasma levels of inhibitors of coagulation. These complex abnormalities are clinically expressed as thrombosis, low-grade or fulminant DIC which can be assessed by different laboratory tests, and as hemorrhage when the fibrinolysis system is impaired. However, no studies have shown to date a relationship between these abnormalities of the coagulation tests and the clinical expression in any single individual. Because these patients are at high risk for thrombosis in special conditions such as surgery or during chemotherapy, prophylaxis with various forms of heparin are recommended.

Blood Coagulation↗
PubMed1997

Anagrelide as a new platelet-lowering agent in essential thrombocythemia: mechanism of actin, efficacy, toxicity, current indications.

Anagrelide is an oral imidazoquinazoline agent with an anti-cyclic AMP phosphodiesterase activity and inhibits platelet aggregation in both humans and animals. In addition, it has in humans a species-specific platelet-lowering activity observed at dose levels lower than those required to inhibit platelet aggregation. Because of this, the drug has been tested in patients with clonal thrombocytosis and has been shown to have potent platelet-reducing activity in essential thrombocythemia (ET) and related disorders. The mechanism of action may involve the drug's interference with megakaryocyte maturation. More than 90% of patients with ET respond to anagrelide regardless of the presence or absence of previous therapy. The responses are durable with a median maintenance dose of approximately 2 to 2.5 mg/day. Side effects are related mostly to the drug's direct vasodilating and positive inotropic effects and include headache, fluid retention, tachycardia, and arryhthmias. The place of anagrelide therapy in the current management of patients with ET is discussed.

Animals↗
PubMed1997

Spontaneous erythroid colony formation as the clue to an underlying myeloproliferative disorder in patients with Budd-Chiari syndrome or portal vein thrombosis.

Budd-Chiari syndrome is a severe disease characterized by occlusion of large hepatic veins leading to death if untreated. Using the classical criteria for the diagnosis of polycythemia vera (PV), essential thrombocythemia (ET), and idiopathic myelofibrosis (IMF), overt PV was the underlying cause in about 10% of the cases and ET or IMF in only a very few. Using spontaneous endogenous erythroid colony (EEC) formation in vitro and/or bone marrow biopsies, a primary myeloproliferative disorder (PMD) was present in 78% of the patients with apparently idiopathic Budd-Chiari syndrome and in about half of the patients with portal, splenic, and/or mesenteric vein thrombosis. The diagnoses in 40 reported cases with hepatic vein thrombosis and spontaneous EEC were overt PV in 25 and latent unclassified PMD in 15 patients. The diagnoses of 40 reported cases with splanchnic vein thrombosis and spontaneous EEC were overt PV in 12, ET in 2, IMF in 2, and latent unclassified PMD with the presence of EEC in 24 patients. Thrombocytosis as a manifestation of myeloproliferative disease was recorded in 34 of 80 (42.5%) patients with spontaneous EEC and Budd-Chiari syndrome or portal vein thrombosis. Thrombocythemia was present in 15 of 41 patients with a proven and in 19 of 39 patients with a latent myeloproliferative disorder. Patients with hepatic vein or splanchnic vein thrombosis associated with a PMD are predominantly females younger than 45. It is concluded that both spontaneous EEC and histopathology from bone marrow biopsy provide specific information as sensitive clues to the diagnosis of all variants of overt and latent myeloproliferative disorders. The association of hepatic and splanchnic vein thrombosis and PMD is not fully understood. Therapeutic options of Budd-Chiari syndrome include anticoagulation with heparin, fibrinolysis followed by oral anticoagulation, and appropriate treatment of the underlying PMD. In case of failure, invasive options include local procedures such as angioplasty or stenting, venous decompression by portal-systemic shunts, or liver transplantation.

Biomarkers↗
PubMed1997

[TIPSS in the Budd-Chiari syndrome with portal vein thrombosis].

HISTORY AND CLINICAL FINDINGS: A 41-year-old woman, known for 10 month to have polycythaemia vera, developed severe right upper abdominal pain. The abdomen was tense from marked ascites and the liver enlarged by 18 cm in the mid-clavicular line. INVESTIGATIONS: Serum bilirubin was slightly elevated to 2.2mg/dl, liver synthesis being much reduced (recalcifying time minimally 23%, albumin minimally 2.8 g/dl). Doppler sonography detected no flow in the right and middle hepatic veins, indicating Budd-Chiari syndrome. Portal vein flow was diminished. TREATMENT AND COURSE: Heparin treatment had to be stopped because of heparin-associated type II thrombocytopenia and hirudin was substituted. Attempted lysis with a total of 100 mg r-tPA failed. As the patient's condition deteriorated a TIPSS was implanted to provide portal decompression. Incomplete portal vein thrombosis was demonstrated and worsened during the procedure until nearly complete occlusion. Local lysis treatment for 2 days with urokinase, 50,000-60,000 U/h, and two shunt revisions finally succeeded in completely dissolving the thrombus. Portocaval pressure fell from 32 to 21 mm Hg, and the size and function of the liver became almost normal and the ascites disappeared. Anticoagulation with a coumarin derivative was started and hydrocarbamide again given for recurrent thrombocytosis. The patient remained largely symptom-free one year after TIPSS. CONCLUSION: This case demonstrates the effectiveness of TIPSS in Budd-Chiari syndrome, even in complicated portal vein thrombosis.

Adult↗
PubMed1980

[Treatment of central retinal venous and arterial occlusion by isovolemic hemodilution (author's transl)].

(1) Ten patients (mean age 71) with fully developed central retinal venous occlusion were treated by isovolemic hemodilution over a period of four to six weeks. Hematocrit was lowered in steps to about 30% to improve retinal microcirculation. For two to four days, 500 ml whole blood were exchanged daily for about 250 ml hydroxyethyl starch and 250 ml plasma. The procedure was repeated every five to ten days whenever the hematocrit exceeded 35%. Visual acuity was considered to be improved when the patient could read at least two more lines on the test card. Four to six weeks after starting hemodilution therapy visual acuity had improved in seven patients, deteriorated in one, and was unchanged in two. In the follow-up study six months after treatment visual acuity, as compared to data before treatment, had improved in four patients, deteriorated in two and was unchanged in four. Three patients developed a neovascular glaucoma and had to undergo photocagulation treatment. (2) As expected, hemodilution failed to improve visual acuity in five patients who had had a complete central retinal arterial occlusion for more than four hours. (3) This is the first time that a beneficial effect of isovolemic hemodilution on visual acuity, probably mediated by an improvement in retinal blood flow, has been demonstrated in man. However, only in retinal tissue with at least minimal blood flow (venous but not arterial occlusion) can this method be effective. Except for severe anemia or thrombocytosis there are no absolute contraindications. No adverse side-effects were observed. To prevent neovascularization it is planned to use a combination of hemodilution and photocoagulation.

Aged↗