Immune mediated destruction of platelets in dogs with heat stroke: A prospective study

2009 ◽  
Vol 37 (05) ◽  
pp. 314-318 ◽  
Author(s):  
L. Keller ◽  
K. Meichner ◽  
S. Unterer ◽  
K. Hartmann ◽  
I. Zenker

Summary Objective: Severe thrombocytopenia is a common sequelae to heat stroke in dogs. So far it has been hypothezised that it is due to disseminated intravascular coagulation. We hypothezised that it is due to immune mediated destruction via antiplatelet antibodies. Material and methods: Prospective evaluation of dogs with heat stroke from May 2005 to August 2008. Dogs that developed severe thrombocytopenia within 5 days of admission were included in the study. All dogs were treated with a standardized treatment protocol. In addition, they received either immunoglobulins or prednisolone. Results: Six dogs were presented with heat stroke during that time period. Four developed a severe thrombocytopenia. All four dogs tested positive for antiplatelet antibodies and did not have elevated D-Dimers at that time. Platelet count in three dogs recovered fully, one dog was euthanized due to liver and renal failure. Conclusion: In those cases thrombocytopenia was due to immune mediated destruction not due to DIC. Clinical rele-vance: Due to the severity of the thrombocytopenia and the high risk for bleeding in those patients, immunosuppressive therapy in addition to DIC prophylaxis should be discussed.

Pilomyxoid astrocytoma (PMA) is an atypical subtype of pilocytic astrocytoma (PA), which presents in children and young adults. The incidence of PMA is low, so there is no standardized treatment protocol for it. Here, we present a 62-year-old woman with recurrent PMA, which is important for the understanding and treatment of the disease.


2015 ◽  
Vol 8 (2) ◽  
pp. 256-263 ◽  
Author(s):  
Jiaxin Niu ◽  
Teresa Goldin ◽  
Maurie Markman ◽  
Madappa N. Kundranda

Background: Immune thrombocytopenic purpura (ITP) is a rare acquired bleeding disorder with an estimated incidence of 1 in 10,000 people in the general population. The association of ITP with breast cancer is an even rarer entity with very limited reports in the English literature. Case Presentation: We report a case of a 51-year-old female with no significant past medical history who presented with sudden onset of malaise, syncope, gingival bleed and epistaxis. She was found to have severe thrombocytopenia (platelet count 6,000/μl) and anemia (hemoglobin 7.2 g/dl). Her workup led to the diagnosis of metastatic ductal breast cancer with extensive bone metastasis. Bone marrow biopsy demonstrated myelophthisis which was initially thought to be consistent with her presentation of thrombocytopenia and anemia. Therefore, the patient was started on hormonal therapy for the treatment of her metastatic breast cancer. After 3 months of therapy, she did not improve and developed severe mucosal bleeding. Her clinical presentation was suspicious for ITP and immune-mediated anemia, and hence she was started on steroids and intravenous immunoglobulin. The patient had a dramatic response to therapy with normalization of her platelet count and hemoglobin within 2 weeks. Conclusion: To our knowledge, this is the first reported case of metastatic breast cancer presenting with symptomatic ITP and anemia, and both symptoms are postulated to be immune-mediated.


Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 225-232 ◽  
Author(s):  
Thomas L. Ortel

Abstract Heparin-induced thrombocytopenia (HIT) is an immune-mediated disorder caused by the development of antibodies to platelet factor 4 (PF4) and heparin. The thrombocytopenia is typically moderate, with a median platelet count nadir of ~50 to 60 × 109 platelets/L. Severe thrombocytopenia has been described in patients with HIT, and in these patients antibody levels are high and severe clinical outcomes have been reported (eg, disseminated intravascular coagulation with microvascular thrombosis). The timing of the thrombocytopenia in relation to the initiation of heparin therapy is critically important, with the platelet count beginning to drop within 5 to 10 days of starting heparin. A more rapid drop in the platelet count can occur in patients who have been recently exposed to heparin (within the preceding 3 months), due to preformed anti-heparin/PF4 antibodies. A delayed form of HIT has also been described that develops within days or weeks after the heparin has been discontinued. In contrast to other drug-induced thrombocytopenias, HIT is characterized by an increased risk for thromboembolic complications, primarily venous thromboembolism. Heparin and all heparin-containing products should be discontinued and an alternative, non-heparin anticoagulant initiated. Alternative agents that have been used effectively in patients with HIT include lepirudin, argatroban, bivalirudin, and danaparoid, although the last agent is not available in North America. Fondaparinux has been used in a small number of patients with HIT and generally appears to be safe. Warfarin therapy should not be initiated until the platelet count has recovered and the patient is systemically anticoagulated, and vitamin K should be administered to patients receiving warfarin at the time of diagnosis of HIT.


Hematology ◽  
2009 ◽  
Vol 2009 (1) ◽  
pp. 153-158 ◽  
Author(s):  
James N. George ◽  
Richard H. Aster

AbstractAlthough drugs are a common cause of acute immune-mediated thrombocytopenia in adults, the drug etiology is often initially unrecognized. Most cases of drug-induced thrombocytopenia (DITP) are caused by drug-dependent antibodies that are specific for the drug structure and bind tightly to platelets by their Fab regions but only in the presence of the drug. A comprehensive database of 1301 published reports describing 317 drugs, available at www.ouhsc.edu/platelets, provides information on the level of evidence for a causal relation to thrombocytopenia. Typically, DITP occurs 1 to 2 weeks after beginning a new drug or suddenly after a single dose when a drug has previously been taken intermittently. However, severe thrombocytopenia can occur immediately after the first administration of antithrombotic agents that block fibrinogen binding to platelet GP IIb-IIIa, such as abciximab, tirofiban, and eptifibatide. Recovery from DITP usually begins within 1 to 2 days of stopping the drug and is typically complete within a week. Drug-dependent antibodies can persist for many years; therefore, it is important that the drug etiology be confirmed and the drug be avoided thereafter.


2019 ◽  
Vol 55 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Alaina Moon ◽  
Julia Veir

ABSTRACT This study described the rate of vaccine reactions in a population of dogs receiving vaccines after diagnosis of primary immune-mediated hemolytic anemia (IMHA). A secondary objective was to describe the time elapsed between vaccination and initial diagnosis of IMHA. A medical record search identified cases meeting criteria for primary IMHA. Owners and referring veterinarians were surveyed regarding vaccination of the dog following diagnosis. Referring veterinarians were surveyed regarding vaccination prior to diagnosis of IMHA. A completed survey was returned in 44 cases. Twenty-two dogs received vaccinations after diagnosis, and 22 dogs did not. The median time elapsed between vaccination and initial diagnosis was 280 days. No dog was vaccinated within 30 days of diagnosis. Two of the following possible reactions were noted out of 22 dogs vaccinated: vomiting and urticarial eruption in a dog administered a rabies and canine distemper vaccine, and recurrent anemia in a dog administered a rabies vaccine. The rate of vaccine reactions was higher than previously reported, although the time period evaluated was longer than in previous studies. The relationship between initial vaccination and development of IMHA, and between vaccination and vaccine reaction, in this population is uncertain and may reflect coincidence or differences in susceptibility.


2010 ◽  
Vol 10 (2) ◽  
pp. 156-164
Author(s):  
Dženita Ljuca ◽  
Samir Husić

The goal of research was to determine the frequency, intensity, time of occurrence, duration and causes of breakthrough pain (BTP) in patients whose carcinoma pain was treated by transdermal fentanyl. (TDF). A prospective study was conducted in a hospice for recumbent patients of the Centre for Palliative Care (hospice) University Clinical Centre Tuzla from October 2009 to December 2010. 33 patients in terminal stage of carcinoma, who had been treated by transdermal fentanyl due to their excruciating pain (7-10 mark on numerica! scale) with initial dosage of 25 μg as a strong opiate analgesic, were monitored within the time period of 10 days. In the statistics we used the even T - test, the Wilcox test and Mann -Whitney test. The difference was seen to be significant at p < 0,05. Treatment by transdermal fentanyl significantly reduces the intensity of strong carcinoma pain (p < 0.0001), with a frequent requirement for dose increase with bone metastasis. The intensity of BTP is higher compared to the pain experienced upon reception. The frequency and intensity of BTP are significantly reduced already in the second day of treatment by transdermal fentanyl (p = 0,0024). The BTP is most intense in patients with neck and head tumours (9,26 ± 0,66), and most frequent with abdomen and pelvic tumour. The biggest number of BTP (68.3 %) occurs within first three days of treatment. BTP most frequently occurs in the evening or at night (between 18:00 and 06:00 h in 62,2 % of the cases), with the duration of usually less than 15 minutes (65,2% of the cases). In 61,6 % cases the occurrence of BTP is related to physical activities or psychosocial incidents, while the cause is undetermined in 38,4 % of examinees.BTP is most frequent within first three days of treatment by TDF. Using the optimal dosage a good control of carcinoma pain is enabled, regardless of the occurrence of bone metastasis, while it also helps reduce the frequency and intensity of BTP.


Blood ◽  
2004 ◽  
Vol 104 (7) ◽  
pp. 2102-2106 ◽  
Author(s):  
Andrei Musaji ◽  
Françoise Cormont ◽  
Gaëtan Thirion ◽  
César L. Cambiaso ◽  
Jean-Paul Coutelier

Abstract Antigenic mimicry has been proposed as a major mechanism by which viruses could trigger the development of immune thrombocytopenic purpura (ITP). However, because antigenic mimicry implies epitope similarities between viral and self antigens, it is difficult to understand how widely different viruses can be involved by this sole mechanism in the pathogenesis of ITP. Here, we report that in mice treated with antiplatelet antibodies at a dose insufficient to induce clinical disease by themselves, infection with lactate dehydrogenase-elevating virus (LDV) was followed by severe thrombocytopenia and by the appearance of petechiae similar to those observed in patients with ITP. A similar exacerbation of antiplatelet-mediated thrombocytopenia was induced by mouse hepatitis virus. This enhancement of antiplatelet antibody pathogenicity by LDV was not observed with F(ab′)2 fragments, suggesting that phagocytosis was involved in platelet destruction. Treatment of mice with clodronate-containing liposomes and with total immunoglobulin G (IgG) indicated that platelets were cleared by macrophages. The increase of thrombocytopenia triggered by LDV after administration of antiplatelet antibodies was largely suppressed in animals deficient for γ-interferon receptor. Together, these results suggest that viruses may exacerbate autoantibody-mediated ITP by activating macrophages through γ-interferon production, a mechanism that may account for the pathogenic similarities of multiple infectious agents. (Blood. 2004;104:2102-2106)


2021 ◽  
Author(s):  
Lotte van Ouwerkerk ◽  
Andrea E. van der Meulen ◽  
Maarten K. Ninaber ◽  
Onno YK Teng ◽  
Tom W.J. Huizinga ◽  
...  

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