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Severe Thrombocytopenia (severe + thrombocytopenia)
Selected AbstractsAtypical Plasmodium vivax Malaria in a Traveler: Bilateral Hydronephrosis, Severe Thrombocytopenia, and HypotensionJOURNAL OF TRAVEL MEDICINE, Issue 2 2008Pedro M. Rifakis MD We report a case of Plasmodium vivax infection manifested as severe thrombocytopenia, bilateral hydronephrosis, and hypotension in a returning traveler from a malaria,endemic area in Venezuela. While most of the efforts to prevent malaria in travelers focus on the life-threatening consequences of Plasmodium falciparum malaria, nonimmune travelers who encounter infection with P vivax may also develop serious complications. This case highlights the importance of preventing malaria cases among nonimmune or semi-immune individuals traveling to P vivax,endemic areas. [source] Thrombocytopenia due to hypotension unrelated to infection: shock marrowINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 7 2005T. A. Naqvi Summary Although peripheral blood cytopenias are observed in clinical practice following hypotensive episodes unrelated to infection, there has previously been no formal description of this in the medical literature. We retrospectively reviewed all medical intensive care unit records from two hospitals over a 5-year period to identify cases in which sustained hypotension had occurred that was unrelated to infection. After initial review, 10 records were identified that met our criteria (systolic blood pressure <90 mmHg for at least 6 h, with no evidence of sepsis or use of drugs commonly associated with suppression of haematopoiesis). All 10 of these patients were found to develop thrombocytopenia. The degree of thrombocytopenia correlated with the severity and duration of hypotension. Severe thrombocytopenia appeared to be associated with a poor outcome. Thrombocytopenia following shock unrelated to sepsis is common and is presumably related to hypoxic injury to haematopoietic progenitor cells. [source] Prognostic Factors for Mortality and Thromboembolism in Canine Immune-Mediated Hemolytic Anemia: A Retrospective Study of 72 DogsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2002Anthony P. Carr Medical records of 72 dogs diagnosed with immune-mediated hemolytic anemia (IMHA) were reviewed to find risk factors for the disease, for mortality, and for thromboembolism. Coagulation data of 32 patients were evaluated for mortality or thromboembolism risk factors. Cocker Spaniels were at increased risk for IMHA (P= .012). Timing of vaccination was not associated with development of IMHA. PCV ranged from 5 to 33%, with a mean of 16 ± 5%. Autoagglutination was present in 42% of the dogs. Platelet counts (n = 60) varied from 3,000 to 793,000/,L (mean, 160,117 ± 133,571; median, 144,000). Thrombocytopenia (platelet count, <200,000/,L) was present in 70% of the dogs, with severe thrombocytopenia (platelet count, <50,000/,L) being present in 22%. One-step prothrombin time (OSPT) was prolonged in 28% of the dogs tested, and activated partial thromboplastin time (APTT) was prolonged in 47% of the dogs tested. Fibrin(ogen) degradation products (FDPs) were detected in 16 of 28 dogs tested (57%). Disseminated intravascular coagulation (DIC) was diagnosed in 10 of 31 (32%) dogs and was suspected in 8 dogs. Thromboemboli were found in 20 of 25 dogs given postmortem examinations. Mortality rate was 58%. Thrombocytopenia (P= .008) and serum bilirubin concentration of >5 mg/dL (P= .015) were risk factors for mortality, and hypoalbuminemia approached significance (P= .053). Severe thrombocytopenia (P= .046), serum bilirubin concentration of >5 mg/dL (P= .038), and hypoalbuminemia (P= .016) were risk factors for thromboembolism. On evaluation of continuous data, decreased platelet count (P= .057), increased bilirubin (P= .062), and decreased albumin (P= .054) approached significance for decreased survival. A higher risk for thrombosis was found with increased alkaline phosphatase (ALKP) (P= .042), increased bilirubin (P= .047), and decreased albumin (P= .012). [source] Severe thrombocytopenia and fibrinolysis mimicking disseminated intravascular coagulation after rituximab infusion,AMERICAN JOURNAL OF HEMATOLOGY, Issue 2 2010Ioannis Kotsianidis No abstract is available for this article. [source] Biological and clinical features of low-molecular-weight heparin-induced thrombocytopeniaBRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2003Yves Gruel Summary. Heparin-induced thrombocytopenia (HIT) is a common adverse effect of unfractionated heparin (UFH) therapy. In contrast, only a few patients have been reported with HIT following low-molecular-weight heparin (LMWH) therapy (LMW-HIT). To define the clinical and biological characteristics of LMW-HIT, 180 patients treated for suspected HIT at 15 French centres were investigated. Clinical history was recorded and HIT was confirmed in 59 patients with positive serotonin release assay results: 57 of them had high levels of antibodies (Abs) to heparin,platelet factor 4 complexes (H/PF4) and two had Abs to interleukin 8. Eleven patients were treated exclusively with LMWH (LMW-HIT) and 48 with UFH either alone (UF-HIT, n = 34) or combined with LMWH (UF/LMW-HIT, n = 14). The LMW-HIT and UF-HIT groups were similar with respect to sex, age, platelet count before heparin therapy, frequency of bleeding and occurrence of disseminated intravascular coagulation. The interval to onset of HIT was longer in LMW-HIT patients compared with UF-HIT patients (P = 0·03). Severe thrombocytopenia (platelets <,15 × 109/l) was more frequent in the LMW-HIT group (P = 0·04). Thrombosis occurred in three of 11 LMW-HIT patients, i.e. as frequently as in UF-HIT patients. LMW-HIT is potentially severe and may be observed after longer heparin treatment compared with UF-HIT. It is highly recommended, therefore, that platelet counts be monitored carefully whenever LMWH is administered. [source] Aberrant increase in the immature platelet fraction in patients with myelodysplastic syndrome: a marker of karyotypic abnormalities associated with poor prognosisEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 1 2009Naomi Sugimori Abstract Objectives:, Some patients with myelodysplastic syndrome (MDS) show a marked increase in the percentage of immature platelet fraction (IPF%) despite the absence of severe thrombocytopenia. To determine the significance of such an unbalanced increase in the IPF%, we investigated the IPF% and other laboratory findings of 51 patients recently diagnosed with MDS. Method:, Subjects consisted of 80 healthy males, 90 healthy females, and 51 patients with MDS and 20 patients with idiopathic thrombocytopenic purpura (ITP). The IPF and IPF% were determined using a Sysmex XE-2100 system loaded with IPF Master software (XE IPF Master, Sysmex). Platelet counts were measured simultaneously. Results:, IPF% and platelet counts of these patients ranged from 1.1% to 25.1% (median, 5.3%) and from 6 to 260 × 109/L (median, 71 × 109/L), respectively. Twelve patients showed platelet counts more than 50 × 109/L with 10% or more IPF%. All of the 12 patients had chromosome abnormalities including monosomy 7 and complex abnormalities involving 7 or 5q. In the other 39 patients who did not show the aberrant IPF% increase, chromosomal abnormalities were seen only in seven patients and none of them had chromosome 7 abnormalities. The IPF% of two patients increased to more than 10% in association with the appearance of monosomy 7. Conclusions:, These findings suggest that a high IPF% in MDS patient may be a marker for karyotypic abnormalities with a poor prognosis, including chromosome 7 abnormalities. [source] Position of nonmuscle myosin heavy chain IIA (NMMHC-IIA) mutations predicts the natural history of MYH9 -related disease,HUMAN MUTATION, Issue 3 2008Alessandro Pecci Abstract MYH9 -related disease (MYH9 -RD) is a rare autosomal-dominant disorder caused by mutations in MYH9, the gene for the heavy chain of nonmuscle myosin IIA (NMMHC-IIA). All patients present from birth with macrothrombocytopenia, but in infancy or adult life, some of them develop sensorineural deafness, presenile cataracts, and/or progressive nephritis leading to end-stage renal failure. No consistent correlations have been identified between the 27 different MYH9 mutations identified so far and the variable clinical evolution of the disease. We have evaluated 108 consecutive MYH9 -RD patients belonging to 50 unrelated pedigrees. The risk of noncongenital manifestations associated with different genotypes was estimated over time by event-free survival analysis. We demonstrated that all subjects with mutations in the motor domain of NMMHC-IIA present with severe thrombocytopenia and develop nephritis and deafness before the age of 40 years, while those with mutations in the tail domain have a much lower risk of noncongenital complications and significantly higher platelet counts. We also evaluated the clinical course of patients with mutations in the four most frequently affected residues of NMMHC-IIA (responsible for 70% of MYH9 -RD cases). We concluded that mutations at residue 1933 do not induce kidney damage or cataracts and cause deafness only in the elderly, those in position 702 result in severe thrombocytopenia and produce nephritis and deafness at a juvenile age, while alterations at residue 1424 or 1841 result in intermediate clinical pictures. These findings are relevant not only to patients' clinical management but also to the elucidation of the pathogenesis of the disease. Hum Mutat 29(3), 409,417, 2008. © 2007 Wiley-Liss, Inc. [source] Characteristics of puumala and Dobrava infections in Croatia,JOURNAL OF MEDICAL VIROLOGY, Issue 4 2002A. Markoti Abstract In this study, two different hantaviruses, Puumala virus (PUUV) and Dobrava virus (DOBV), were demonstrated for the first time to coexist and cause hemorrhagic fever with renal syndrome (HFRS) in Croatia. Phylogenetic analysis showed some differences among the nucleotide sequences of PUUV originating from Dinara mountain, which was more closely related to Austrian PUUV than other Croatian PUUV from Mala Kapela mountain. More consistency was found among the Croatian DOBV. HFRS was verified in 85 of 201 suspected cases recorded in 1995 during the largest HFRS outbreak in Croatia. Most of these cases were soldiers. With the exception of the coastal region and islands, all of Croatia was found to be an area endemic for HFRS. A statistically significantly higher proportion of DOBV-infected patients had acute renal failure, visual disturbance, severe thrombocytopenia, and elevated levels of nonsegmented leukocytes, creatine, and total bilirubin. The prevalence of gastrointestinal and electrocardiography disorders also was greater in DOBV-infected patients. Interestingly, significantly more PUUV-infected patients had elevated systolic blood pressure on admission to the hospital. Further prospective studies are necessary to shed more light on differences in HFRS severity associated with PUU and DOB viruses. J. Med. Virol. 66:542,551, 2002. © 2002 Wiley-Liss, Inc. [source] Evaluation of platelet activation in canine immune-mediated haemolytic anaemiaJOURNAL OF SMALL ANIMAL PRACTICE, Issue 6 2010A. E. Ridyard Objectives: To establish whether heightened platelet activation is a common feature of canine immune-mediated haemolytic anaemia, and to evaluate the hypothesis that platelet activation plays a role in the pathogenesis of thromboembolism. Methods: Using whole-blood flow-cytometric analysis, the proportion of activated platelets and platelet-leucocyte aggregates in blood samples from 14 dogs with immune-mediated haemolytic anaemia and 14 healthy dogs was calculated. General linear models with binomial errors were used to compare groups. Results from the immune-mediated haemolytic anaemia-affected dogs were then correlated with established risk factors for thromboembolism in canine immune-mediated haemolytic anaemia, D-dimer concentration and antithrombin activity. Results: There was a strong correlation between platelet activation and severe thrombocytopenia, with heightened platelet activation being observed predominantly in severely thrombocytopenic dogs. Clinical Significance: Dogs with immune-mediated haemolytic anaemia, particularly those with concurrent severe thrombocytopenia, are likely to have heightened platelet activation, which may play a role in the pathogenesis of thromboembolism. [source] von Willebrand factor activation, granzyme-B and thrombocytopenia in meningococcal diseaseJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 5 2010M. J. HOLLESTELLE Summary.,Background:,During invasive meningococcal disease, severe thrombocytopenia is strongly associated with a poor outcome. Objectives:,In order to elucidate the pathophysiological mechanism behind the development of thrombocytopenia, we studied the role of von Willebrand factor (VWF) in meningococcal disease. Patients/methods:,Thirty-two children with severe meningococcal disease admitted to our university hospital were included in this study. VWF and related parameters were measured and results were correlated with the development of shock and thrombocytopenia. Results:,At admission, all patients had increased levels of (active) VWF and VWF propeptide. The highest VWF propeptide levels were observed in patients with shock, indicating acute endothelial activation. Although VWF propeptide levels in patients with shock, with or without thrombocytopenia, were similar, increased active VWF was significantly lower in patients with thrombocytopenia as compared with patients without thrombocytopenia. ADAMTS13 was moderately decreased. However, the VWF multimeric pattern was minimally increased. We assume that these findings are explained by VWF consumption and perhaps by granzyme B (GrB). In vitro experiments showed that GrB is able to cleave VWF multimers in plasma, whereas GrB was high in patients with shock, who developed thrombocytopenia. Conclusions:,Our results demonstrate that consumption of VWF, derived from endothelial cells, could be a key feature of meningococcal disease and primary to the development of thrombocytopenia during shock. [source] Atypical Plasmodium vivax Malaria in a Traveler: Bilateral Hydronephrosis, Severe Thrombocytopenia, and HypotensionJOURNAL OF TRAVEL MEDICINE, Issue 2 2008Pedro M. Rifakis MD We report a case of Plasmodium vivax infection manifested as severe thrombocytopenia, bilateral hydronephrosis, and hypotension in a returning traveler from a malaria,endemic area in Venezuela. While most of the efforts to prevent malaria in travelers focus on the life-threatening consequences of Plasmodium falciparum malaria, nonimmune travelers who encounter infection with P vivax may also develop serious complications. This case highlights the importance of preventing malaria cases among nonimmune or semi-immune individuals traveling to P vivax,endemic areas. [source] Immune-mediated hemolytic anemia and severe thrombocytopenia in dogs: 12 cases (2001,2008)JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 3 2010Elizabeth S. Orcutt DVM Abstract Objective , To identify and characterize the syndrome of immune-mediated hemolytic anemia (IMHA) with concurrent severe thrombocytopenia (,15.0 × 109 platelets/L; [15.0 × 103 platelets/,L]), and to evaluate prognostic factors, clinicopathologic findings, complications, treatment, outcome, and survival of dogs with this hematologic disorder. Design , Retrospective, observational study. Setting , Veterinary teaching hospital. Animals , Twelve client-owned dogs with IMHA and severe thrombocytopenia (,15.0 × 109 platelets/L; [15.0 × 103 platelets/,L]), without evidence of overt disseminated intravascular coagulation. Interventions , The following data were recorded and analyzed from the electronic medical record: signalment, history, concurrent diseases, clinical signs at presentation, clinicopathologic data, diagnostic testing, radiographic findings, treatment modalities, length of hospitalization, complications, and clinical outcome. All dogs were treated with immunosuppressive doses of corticosteroids. Measurements and Main Results , Twelve dogs were identified with the diagnosis of IMHA and severe thrombocytopenia; of these, 9 (75%) survived, 3 (25%) were euthanized, and none died. Dogs that survived were significantly younger than nonsurvivors (P=0.03). There were no specific clinical signs or therapies associated with survival. Conclusions , Dogs in this study had a mortality rate similar to reported rates for dogs with either disease alone. Overall, younger dogs were more likely to survive. No association between different treatment modalities and overall survival was identified. [source] Babesiosis Caused by a Large Babesia Species in 7 Immunocompromised DogsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2010L.E. Sikorski Background: A large unnamed Babesia species was detected in a dog with lymphoma. It was unknown if this was an underrecognized pathogen. Objective: Report the historical and clinicopathologic findings in 7 dogs with babesiosis caused by a large unnamed Babesia species characterize the 18S ribosomal ribonucleic acid (rRNA) genes. Animals: Seven immunocompromised dogs from which the Babesia was isolated. Methods: Retrospective case review. Cases were identified by a diagnostic laboratory, the attending clinicians were contacted and the medical records were reviewed. The Babesia sp. 18S rRNA genes were amplified and sequenced. Results: Six of 7 dogs had been splenectomized; the remaining dog was receiving oncolytic drugs. Lethargy, anorexia, fever, and pigmenturia were reported in 6/7, 6/7, 4/7, and 3/7 dogs. Laboratory findings included mild anemia (7/7) and severe thrombocytopenia (6/7). Polymerase chain reaction (PCR) assays used to detect Babesia sensu stricto species were all positive, but specific PCR assays for Babesia canis and Babesia gibsoni were negative in all dogs. The 18S rRNA gene sequences were determined to be identical to a large unnamed Babesia sp. previously isolated. Cross-reactive antibodies against other Babesia spp. were not always detectable. Five dogs were treated with imidocarb dipropionate and 1 dog with atovaquone/azithromycin; some favorable responses were noted. The remaining dog was untreated and remained a clinically stable carrier. Conclusions and Clinical Importance: Dogs with pigmenturia, anemia, and thrombocytopenia should be tested for Babesia sp. by PCR. Serology is not sufficient for diagnosis of this Babesia sp. Asplenia, chemotherapy, or both might represent risk factors for persistent infection, illness, or both. [source] Ulcerative Dermatitis, Thrombocytopenia, and Neutropenia in Neonatal FoalsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2005G.A. Perkins This report describes transient ulcerative dermatitis, severe thrombocytopenia, and mild neutropenia in 6 foals from 4 mares from geographically diverse regions of the United States. The foals presented at <4 days of age with oral and lingual ulcers, and crusting and erythema around the eyes, muzzle, and perineal, inguinal, axillary, trunk, and neck regions. There was a severe thrombocytopenia (0,30,000 platelets/,L), leukopenia (1,900-3,200 white blood cells/,L), and mild neutropenia (500-1,800 neutrophils/,L). Four of the 6 foals had petechiae and ecchymotic hemorrhages and 3 had bleeding tendencies. Results of examination of a bone marrow biopsy from 1 foal were normal and results of a platelet surface immunoglobulin test in another were negative. Histopathology of the skin in all foals showed subepidermal clefting with subjacent vascular dilation, dermal hemorrhage, and superficial papillary necrosis. The foals were treated supportively with broad-spectrum antibiotics (5/6), corticosteroids (3/6), gastric ulcer prophylaxis (6/6), whole-blood transfusion (4/6), and platelet-rich plasma (1/6). The skin lesions and thrombocytopenia (>50,000 platelets/,L) improved in 2 weeks (4/6). Two foals had a decline in their platelet counts when the steroids were decreased and needed protracted treatment. All foals survived and were healthy as yearlings. Two mares that had 2 affected foals each, upon subsequent pregnancies to different stallions, had healthy foals when an alternate source of colostrum was given. The findings in the cases in this report suggest a possible relationship between colostral antibodies or some other factor in the colostrum and the thrombocytopenia and skin lesions, although further investigation is warranted to confirm or refute this hypothesis. [source] Prognostic Factors for Mortality and Thromboembolism in Canine Immune-Mediated Hemolytic Anemia: A Retrospective Study of 72 DogsJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2002Anthony P. Carr Medical records of 72 dogs diagnosed with immune-mediated hemolytic anemia (IMHA) were reviewed to find risk factors for the disease, for mortality, and for thromboembolism. Coagulation data of 32 patients were evaluated for mortality or thromboembolism risk factors. Cocker Spaniels were at increased risk for IMHA (P= .012). Timing of vaccination was not associated with development of IMHA. PCV ranged from 5 to 33%, with a mean of 16 ± 5%. Autoagglutination was present in 42% of the dogs. Platelet counts (n = 60) varied from 3,000 to 793,000/,L (mean, 160,117 ± 133,571; median, 144,000). Thrombocytopenia (platelet count, <200,000/,L) was present in 70% of the dogs, with severe thrombocytopenia (platelet count, <50,000/,L) being present in 22%. One-step prothrombin time (OSPT) was prolonged in 28% of the dogs tested, and activated partial thromboplastin time (APTT) was prolonged in 47% of the dogs tested. Fibrin(ogen) degradation products (FDPs) were detected in 16 of 28 dogs tested (57%). Disseminated intravascular coagulation (DIC) was diagnosed in 10 of 31 (32%) dogs and was suspected in 8 dogs. Thromboemboli were found in 20 of 25 dogs given postmortem examinations. Mortality rate was 58%. Thrombocytopenia (P= .008) and serum bilirubin concentration of >5 mg/dL (P= .015) were risk factors for mortality, and hypoalbuminemia approached significance (P= .053). Severe thrombocytopenia (P= .046), serum bilirubin concentration of >5 mg/dL (P= .038), and hypoalbuminemia (P= .016) were risk factors for thromboembolism. On evaluation of continuous data, decreased platelet count (P= .057), increased bilirubin (P= .062), and decreased albumin (P= .054) approached significance for decreased survival. A higher risk for thrombosis was found with increased alkaline phosphatase (ALKP) (P= .042), increased bilirubin (P= .047), and decreased albumin (P= .012). [source] Transient TTP in childhoodPEDIATRIC BLOOD & CANCER, Issue 3 2009Naomi P. Moskowitz MD Abstract Thrombotic thrombocytopenic purpura (TTP) is a type of microangiopathic hemolytic anemia that is uncommon in childhood. Adults with TTP have a high mortality rate unless they are treated with plasma exchange. There are few reports of children with acquired idiopathic TTP, and most of those children received some form of treatment. We describe a child with acquired idiopathic TTP who had severe thrombocytopenia and anemia that resolved over several months without the use of any medications. This case suggests that some children with acquired idiopathic TTP might be safely observed without ill effects. Pediatr Blood Cancer 2009;52:424,426. © 2008 Wiley-Liss, Inc. [source] Intracranial hemorrhage following allogeneic hematopoietic stem cell transplantation,AMERICAN JOURNAL OF HEMATOLOGY, Issue 5 2009Yuho Najima Charts and radiographs of 622 allogeneic hematopoietic stem cell transplant (HSCT) recipients, over a 20-year period, were retrospectively reviewed for intracranial hemorrhage (ICH) following transplant. A total of 21 cases of ICH were identified (3.4%) including 15 cases of intraparenchymal hemorrhage (IPH), two cases of subarachnoid hemorrhage (SAH), and four cases of subdural hematoma (SDH). The median time from transplantation to the onset of ICH was 63 days (range, 6,3,488 days). The clinical features of post-transplant ICH patients were similar and included hypertension, diabetes mellitus, chronic graft-versus-host disease (GVHD), systemic infection, and veno occlusive disease (VOD), recently referred to as sinusoidal obstruction syndrome, in addition to severe thrombocytopenia. Mortality rate was especially high (89%) after IPH with a median survival of 2 days (range, 0,148 days). In contrast, all patients with SAH or SDH following HSCT survived. The cause of post-transplant ICH appears to be multifactorial, including thrombocytopenia, hypertension, acute GVHD, VOD, and radiation therapy. Most patients in our series displayed severe thrombocytopenia at the onset of ICH, even though adequate prophylactic platelet transfusions were given. By univariate analysis, cord blood transplantation, acute GVHD, systemic infection, and VOD were related to the incidence of ICH, whereas prior CNS episodes and radiation therapy did not reach statistical significance. A multivariate analysis with logistic regression identified acute GVHD as the only factor that significantly influenced ICH occurrence. Am. J. Hematol. 2009. © 2009 Wiley-Liss, Inc. [source] Very severe thrombocytopenia and fragmentation hemolysis mimicking thrombotic thrombocytopenic purpura associated with a giant intracardiac vegetation infected with Staphylococcus epidermidis: Role of monocyte procoagulant activity induced by bacterial supernatantAMERICAN JOURNAL OF HEMATOLOGY, Issue 8 2007Kathleen Selleng Abstract The pathogenesis of very severe thrombocytopenia in bacterial endocarditis is uncertain. We report a 50-year-old male with platelet counts < 10 × 109/l and fragmentation hemolysis complicating Staphyloccoccus epidermidis pacemaker endocarditis with a giant vegetation. Antibiotics, corticosteroids, high-dose intravenous gammaglobulin, and plasmapheresis (for initially-suspected thrombotic thrombocytopenic purpura) failed to produce significant platelet count increase. However, therapeutic-dose heparin anticoagulation was associated with a platelet count increase from <10 to ,40 × 109/l, with parallel reduction in thrombin-antithrombin complexes (from 8.9 to 3.5 ,g/l), facilitating surgical intervention. The thrombocytopenia promptly resolved following surgical removal of the vegetation. Culture supernatant from S. epidermidis isolated from the patient's blood induced monocytes to express procoagulant activity (assessed by factor Xa generation) equivalent to lipopolysaccharide (1 ,g/ml), with half-maximal activation seen with culture supernatant diluted to 1:12,800. These data are consistent with previous animal models of endocarditis demonstrating staphylococci-induced procoagulant changes in monocytes. This case demonstrates that heparin anticoagulation can be therapeutic in infective endocarditis-associated severe thrombocytopenia in a non-bleeding patient, and that such therapy may ameliorate the platelet count enough to permit surgical intervention. Am. J. Hematol 2007. © 2006 Wiley-Liss, Inc. [source] Superior effect of intravenous anti-D compared with IV gammaglobulin in the treatment of HIV-thrombocytopenia: Results of a small, randomized prospective comparisonAMERICAN JOURNAL OF HEMATOLOGY, Issue 5 2007Andromachi Scaradavou Abstract This small, prospective, randomized study compared increases in platelet counts and duration of response after intravenous gammaglobulin (IVIG) and IV anti-D in patients with HIV-related thrombocytopenia (HIV-TP). Nine Rh+, nonsplenectomized HIV-positive patients with thrombocytopenia were treated sequentially, in random order, with IVIG and IV anti-D in a cross over design, receiving each therapy for 3 months. Peak platelet counts and duration of effect after each treatment were compared. In addition, viral load measurements and CD4 counts were followed serially, as well as thrombopoietin levels. IV anti-D resulted in a mean peak platelet count of 77 x 109/L compared to only 29 x 109/L after IVIG (P = 0.07). The mean duration of response was significantly longer in patients treated with anti-D (41 days) compared to IVIG (19 days, P = 0.01). No consistent changes were seen in the CD4 counts or viral load measurements as a result of either therapy. Thrombopoietin levels were normal in all patients despite often severe thrombocytopenia. Anti-D was more efficacious than IVIG for the treatment of HIV-TP, confirming and extending previous results. Anti-D should be the first line therapy in HIV-positive, Rh+ patients, when antiretroviral agents are not indicated, not effective, or there is an urgent need to increase the platelet count. Am. J. Hematol. 82: 2007. © 2006 Wiley-Liss, Inc. [source] Refractory thrombotic thrombocytopenic purpura following influenza vaccinationANAESTHESIA, Issue 4 2009P. J. Dias Summary Thrombotic thrombocytopenic purpura (TTP) is characterised by the systemic microvascular aggregation of platelets causing ischaemia of the brain and other organs. We describe the case of a 54 year-old man who presented with neurological signs, fever, severe thrombocytopenia, microangiopathic haemolytic anaemia and renal failure 5 days after receiving an influenza vaccination. He was diagnosed with acute refractory TTP caused by autoantibody-mediated ADAMTS-13 deficiency. He required stabilisation on the critical care unit before being successfully treated with 3 l plasma exchanges for 21 days and rituximab (MabThera®) at a dose of 375 mg.m,2, given weekly for a total of 4 weeks. Vaccination is an important part of preventative medicine and reduces morbidity and mortality. Only in a few rare cases has vaccination been associated with autoimmune pathology. We could find only one similar case report of thrombotic thrombocytopenic purpura following influenza vaccination. In addition to plasma exchange, rituximab appears to be effective and well tolerated in the treatment of refractory thrombotic thrombocytopenic purpura. [source] Anti,c-Mpl (thrombopoietin receptor) autoantibody,induced amegakaryocytic thrombocytopenia in a patient with systemic sclerosisARTHRITIS & RHEUMATISM, Issue 6 2003Yasuhiro Katsumata Amegakaryocytic thrombocytopenia (AMT) associated with systemic sclerosis (SSc) has been described in several case reports, but the underlying mechanisms have not been identified. Here we describe a rare case of SSc accompanied by thrombocytopenia and megakaryocytic hypoplasia, in which autoantibody against thrombopoietin receptor (c-Mpl) was detected. A 61-year-old woman with limited SSc was admitted to our hospital because of severe thrombocytopenia (platelet count 0.2 × 104/mm3) with gingival bleeding. Her bone marrow was hypocellular with absent megakaryocytes, consistent with AMT. Treatment with corticosteroids and intravenous immunoglobulin infusions resulted in an increased platelet count, and she sustained a remission over a 1-year period, with a platelet count averaging 10.0 × 104/mm3. Her serum was strongly positive for anti,c-Mpl antibody, and IgG fraction purified from her serum inhibited thrombopoietin-dependent cell proliferation in vitro. Our case report suggests that AMT in patients with SSc could be mediated by the anti,c-Mpl antibody, which functionally blocks an interaction between thrombopoietin and c-Mpl. [source] Progressive neurological signs associated with systemic mastocytosis in a dogAUSTRALIAN VETERINARY JOURNAL, Issue 2 2001D TYRRELL A 9-year-old dog was presented with nonregenerative anaemia and severe thrombocytopenia, diarrhoea, spinal hyperalgesia and progressive hindlimb paresis. A moderately well differentiated cutaneous mast cell tumour (MCT) was removed from the skin of the right elbow along with the enlarged right prescapular lymph node. Due to deterioration of the dog's neurological condition, euthanasia was performed. On necropsy examination, haemorrhage and accumulations of poorly differentiated mast cells were found in the lumbosacral region and cauda equina. This article describes an unusual presentation of systemic mastocytosis and the previously unreported finding of metastasis of mast cells to the spinal cord. [source] Thrombocytopenia in hydropic fetuses with parvovirus B19 infection: incidence, treatment and correlation with fetal B19 viral loadBJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 1 2008TR De Haan Objective, To examine (1) the incidence of fetal thrombocytopenia in hydropic fetuses with congenital B19 virus infection, (2) the effect of intrauterine platelet transfusions and (3) the correlation between fetal B19 viral load and severity of thrombocytopenia. Design, Retrospective analysis of data from prospectively collected fetal blood samples. Setting, Leiden University Medical Centre, the national centre for management of intrauterine fetal disease in the Netherlands. Population, Thirty hydropic fetuses treated with intrauterine red blood cell and platelet transfusions for human B19 virus-induced severe fetal anaemia and thrombocytopenia over a 10-year period. Methods, Fetal blood samples (n= 30) taken before and after intrauterine transfusion were investigated. No cases were excluded, and there was no loss to follow up. Main outcome measures, Parameters recorded were gestational age, experienced fetal movements, gravidity and parity, severity of fetal hydrops, severity of fetal anaemia and thrombocytopenia and megakaryocyte and reticulocyte counts. Survival and procedure-associated complications were documented. Quantitative B19 viral load measurements were performed on all fetal samples. Results, Forty-six percent of all hydropic fetuses showed severe thrombocytopenia. No antenatal intracerebral haemorrhage or procedure-associated bleeding occurred. Overall, survival was 77%. Platelet counts increased following platelet transfusion and decreased significantly following red blood cell transfusion alone. No correlation was found between fetal viral loads and platelet counts. Conclusion, Thrombocytopenia was frequently encountered in fetal B19V infection, but fetal bleeding complications were not noted. Absence of a direct relationship between fetal B19 viral load and platelet counts suggests a temporal dissociation between these findings. Dilutional thrombocytopenia is frequently seen in the fetus following red blood cell transfusion alone. The clinical significance of this phenomenon is unclear. The risk of fluid overload by fetal platelet transfusion in a severely hydropic fetus should be weighed against the low incidence of fetal bleeding complications. [source] | ||||||||||||||||||||||||||||