Canine Idiopathic Thrombocytopenic Purpura

Canine idiopathic thrombocytopenic purpura (ITP) is a disease in which antibodies bound to the surface of platelets mediate premature platelet destruction by macrophages. ITP in dogs and chronic ITP in humans are analogous diseases. This article draws on information from the literature on ITP in dogs and in humans, and reviews the pathogenesis, diagnosis, and treatment of ITP in dogs. J Vet Intern Med 1996;207–218. Copyright © 1996 by the American College of Veterinary Internal Medicine .     

Platelet activation in ponies with airway inflammation

REASON FOR PERFORMING STUDY: Platelet activation occurs in human obstructive airway diseases and in laboratory animal models. However, there is limited evidence that platelets may be involved in equine recurrent airway obstruction (RAO) and other inflammatory diseases. This study investigated whether platelet activation also occurred in RAO. HYPOTHESIS: Platelet function is altered in ponies with active RAO. This alteration can be detected ex vivo by measuring platelet adhesion. METHODS: An in vitro platelet adhesion assay measuring acid phosphatase (AcP) activity colorimetrically was adapted for use with equine platelets and responses to selected agonists were established. Platelet adhesion and aggregation was evaluated in vitro on platelets isolated from 6 ponies with RAO before, during and after a 7 h natural antigen challenge. Three ponies with no history of airway disease were also studied. RESULTS: Adhesion of equine platelets to serum coated plastic was detected at concentrations of 10-100 radicaló 10(9)/l. Adhesion increased in response to stimulation with platelet activating factor and thrombin, but not equine interleukin 8. Prior to the antigen challenge, adhesion of nonstimulated platelets was low and increased significantly (P<0.05) 24 h after initiation of the challenge in RAOs, but not in the normal animals. No changes in platelet aggregation were noted in either group. CONCLUSIONS: The described assay offers an alternative method to evaluate platelet function in healthy and diseased horses and can detect changes not observed using a classic aggregation assay. Circulating platelets are activated 24 h after antigen challenge of ponies with RAO and may play a role in pulmonary inflammation and/or the pathophysiology of RAO. POTENTIAL RELEVANCE: Investigating platelet function in RAO and airway inflammation may reveal new aspects of the pathogenesis of inflammatory lung disease in the horse.     

Flow cytometric detection of activated platelets in the dog

Background: Platelet activation appears to play a role in a variety of canine thrombotic disorders. At present, tests for the detection of activated platelets are not used routinely in veterinary clinical laboratories. Objective: The purpose of this study was to develop a clinically applicable method to detect activated canine platelets. Methods: A flow cytometric assay was developed to detect activated platelets, platelet aggregates, and platelet microparticles in the dog. Blood was collected from healthy dogs using EDTA or sodium citrate as the anticoagulant, and platelet‐rich plasma was prepared. Platelets were activated by adding phorbol myristate acetate. In some experiments, platelets were fixed by incubation with 0.5% paraformaldehyde. In other experiments, platelets were stored for 4 or 24 hours at 4°C before analysis. Activated platelets were detected by measuring surface expression of P‐selectin and by determining the percentages of platelet aggregates and microparticles using forward‐angle vs side‐angle light scatter plots. Results were analyzed by using 2‐way ANOVA and the SchefféF‐test. Results: Platelets collected in EDTA had minimal expression of P‐selectin, whereas platelets collected in sodium citrate had greater median fluorescence intensity. Fixation with 0.5% paraformaldehyde before labeling platelets with anti‐P‐selectin did not affect antibody binding or the percentages of platelet aggregates and microparticles. Storage of platelet‐rich plasma at 4°C for 4 hours did not affect antibody binding or the percentages of platelet aggregates or microparticles. Activation of platelets ex vivo by addition of 10 ng/mL phorbol myristate acetate resulted in a large increase in expression of P‐selectin but only slight increases in platelet aggregates and microparticles. Conclusion: Determination of platelet P‐selectin expression and percentages of platelet aggregates and platelet microparticles may provide a clinically applicable means for detection of activated platelets in dogs. The capacity to use EDTA‐anticoagulated blood samples and to fix platelets for evaluation at a later time makes the test attractive as a routine diagnostic tool.     

Characterization of the equine platelet aggregation response.

Equine platelet aggregation responses to bovine collagen, adenosine diphosphate (ADP), serotonin, epinephrine, and arachidonate in a platelet aggregometer were recorded. Equine platelets exhibited irreversible aggregation when incubated with ADP at a final concentration of 10 microM and bovine collagen. A secondary aggregation wave was recorded from platelets from certain horses at final ADP concentrations of 1 to 5 microM. Serotonin and arachidonate induced a weak reversible aggregation response, but a response was not observed following epinephrine addition. Equine platelet aggregation was influenced by concentration of anticoagulant (sodium citrate). Platelet aggregation responses at 37 C were indistinguishable from those recorded at 39 C. Platelet aggregation responses also were altered if the aggregation tests were not performed within 4 hours of blood sample acquisition. An assessment of platelet aggregation from multiple blood samples from the same horse indicated that the procedures described provide a reliable method to assess equine platelet aggregation in vitro.     

Primary hemostasis

Objective: To review the current understanding of the mechanisms responsible for primary hemostasis and to give an overview of primary hemostatic syndromes in small animal patients. Current and future therapeutic options for dysfunction of primary hemostasis are discussed. Data sources: A thorough search of the human and veterinary literature using the keywords platelets, primary hemostasis, von Willebrand factor (vWF), von Willebrand disease, aspirin, thromboxane, and aggregation, were performed. Databases searched included OVID Medline, Pubmed, and CAB abstracts. Conclusions: Primary hemostasis occurs when platelets adhere to an injured or disrupted endothelial surface. Adherence is followed by activation, or the release of platelet granule contents. The agonists released from platelet granules recruit additional platelets and induce their activation and aggregation. Adhesion, activation, and aggregation are mediated by different receptors and ligands depending on the local blood flow conditions. vWF and adenosine diphosphate are the primary mediators of adhesion, activation, and aggregation under high shear conditions. During low shear conditions collagen, fibronectin, and laminin mediate adhesion, thromboxane A₂ promotes activation, while aggregation is mediated by glycoprotein Ib‐IX‐V (GP Ib–IX–V) and fibrinogen. Knowledge of the receptor interactions during different blood flow conditions is crucial to the understanding of the various inhibitors of primary hemostasis available to clinicians.     

Platelet Dysfunction Associated With Immune-Mediated Thrombocytopenia in Dogs

The effect of antiplatelet antibody on in vitro platelet function was investigated in 15 dogs with immune-mediated thrombocytopenia (ITP). Platelet aggregation was assessed after addition of serum from healthy dogs (n = 5) or dogs with ITP (n = 15) to platelet-rich plasma from a healthy donor dog. The aggregation responses to adenosine diphosphate, thrombin, and collagen/epinephrine were measured as the maximum aggregation observed after 2 minutes. In 13 of 15 dogs with ITP, maximal aggregation was significantly inhibited in response to ADP, thrombin, or collagen/epinephrine. The slope of the aggregation curve was decreased after addition of serum from 9 of 15 patients. A polyclonal rabbit anti—dog platelet antiserum induced inhibition of aggregation with all 3 agonists.
Serum from control dogs neither inhibited nor activated platelet aggregation. Aggregation experiments were repeated with all 3 agonists after addition of patient immunoglobulin (lg)G or IgG from a healthy dog to platelet-rich plasma. The IgG fraction from 9 of 10 dogs with ITP suppressed platelet aggregation. The IgG fraction from polyclonal rabbit anti—dog platelet antiserum inhibited platelet aggregation with all agonists. These results suggest that many canine ITP patients have circulating antibodies that, in addition to causing platelet destruction, may cause platelet dysfunction.     

Detection of antiplatelet antibody: comparison of platelet immunofluorescence,agglutination, and immunoinjury tests using rabbit antiequine platelet serum

Immunofluorescence, tube agglutination, and platelet factor-3 immunoinjury tests for detecting antiplatelet antibody were compared using a heterologous system of equine platelets and rabbit antiequine platelet serum. Platelet immunofluorescence tests were performed using paratormaldehyde-fixed platelets in suspension as well as in air-dried smears on glass slides (solid phase). Bright homogeneous, membranous, specific fluorescence was seen in both assays with anti-immunoglobulin G (IgG) and protein G fluorescein isothiocynate conjugates (FITC-conjugates). Protein A conjugate gave nonspecific fluorescence irrespective of normal or antiserum treatment. Anti-IgG and protein G conjugates in suspension immunofluorescence tests with the same antiserum yielded antibody titers of 1:1024 and 1:128, respectively. Similarly, respective titers of 1:512 and 1:64 were obtained with solid phase immunoassay. Platelet suspension assay was slightly better than the solid phase assay. These observations indicated that anti-IgG was more sensitive than protein G in detecting antiplatelet antibody by fluorescence microscopy, while protein A was ineffective because of its nonspecificity. Chloroquine treatment of platelets failed to reduce the nonspecific fluorescence. Platelet agglutination and platelet factor-3 tests were relatively less sensitive to detect equine antiplatelet antibody.     

Resolution of severe thrombocytopenia in two standard Poodles with surgical correction of splenic torsion

Objective: To describe the diagnosis and treatment of 2 cases of severe thrombocytopenia associated with splenic torsion and to discuss the pathophysiologic mechanisms underlying the thrombocytopenia. Summary: We report 2 cases of severe thrombocytopenia associated with splenic torsion. Each dog presented with non‐specific clinical signs, radiographic evidence of an intra‐abdominal mass, and platelet counts of less than 25,000 platelets/μL. The diagnosis of splenic torsion was made with abdominal ultrasonography and was confirmed during exploratory laparotomy. Both dogs recovered rapidly following splenectomy. The cause of thrombocytopenia associated with splenic torsion is not fully elucidated, but may be because of either platelet sequestration within the torsed spleen, platelet consumption in disseminated intravascular coagulation, or a combination of both. New information provided: This report provides previously unreported evidence that the degree of thrombocytopenia associated with splenic torsion may be of a severity at which primary hemostasis is compromised, and resolution of thrombocytopenia occurs after splenectomy.     

Increased platelet aggregation response in Cavalier King Charles Spaniels with mitral valve prolapse

Mitral valve prolapse (MVP) is a fundamental feature of myxomatous mitral valve disease in the dog. In humans, primary MVP is associated with increased platelet reactivity. In Cavalier King Charles Spaniels (CKCS), a breed predisposed to myxomatous mitral valve disease, there is a high prevalence of hypomagnesemia and platelet anomalies, such as thrombocytopenia and macrothrombocytosis. The objective of this study was to evaluate platelet aggregation responses in CKCS and to determine the relationship between the platelet aggregation response and serum magnesium concentration, MVP, mitral regurgitation (MR), and platelet count. In 19 CKCS with MVP and 7 control dogs (not CKCS), the platelet aggregation response to 3 different agonists was compared. The CKCS with >100,000 platelets/microL (n = 10) had a significantly higher maximum aggregation response with regard to all tested agonists than the CKCS with <100,000 platelets/microL (n = 9) and control dogs (n = 7). The CKCS with <100,000 platelets/microL had a platelet aggregation response similar to the control dogs. There was no correlation between degree of MVP and platelet aggregation response. Platelet diameter increased (P = .006) and serum magnesium concentration decreased (P = .04) with lower platelet concentration. In conclusion, CKCS with MVP appeared to separate into 2 groups--1 group with <100,000 platelets/microL, normal platelet aggregation, low serum magnesium concentration, and enlarged platelets, and another group with >100,000 platelets/microL, increased platelet aggregation, and normal serum magnesium concentration and platelet size.     

Dogs with heart diseases causing turbulent high-velocity blood flow have changes in platelet function and von Willebrand factor multimer distribution

The purpose of this prospective study was to investigate platelet function using in vitro tests based on both high and low shear rates and von Willebrand factor (vWf) multimeric composition in dogs with cardiac disease and turbulent high-velocity blood flow. Client-owned asymptomatic, untreated dogs were divided into 4 groups: 14 Cavalier King Charles Spaniels (Cavaliers) with mitral valve prolapse (MVP) and no or minimal mitral regurgitation (MR), 17 Cavaliers with MVP and moderate to severe MR, 14 control dogs, and 10 dogs with subaortic stenosis (SAS). Clinical examinations and echocardiography were performed in all dogs. PFA100 closure times (the ability of platelets to occlude a hole in a membrane at high shear rates), platelet activation markers (plasma thromboxane B2 concentration, platelet surface P-selectin expression), platelet aggregation (in whole blood and platelet-rich plasma with 3 different agonists), and vWf multimers were analyzed. Cavaliers with moderate to severe MR and dogs with SAS had longer closure times and a lower percentage of the largest vWf multimers than did controls. Maximal aggregation responses were unchanged in dogs with SAS but enhanced in Cavaliers with MVP (regardless of MR status) compared with control dogs. No significant difference in platelet activation markers was found among groups. The data suggest that a form of platelet dysfunction detected at high shear rates was present in dogs with MR and SAS, possibly associated with a qualitative vWf defect. Aggregation results suggest increased platelet reactivity in Cavaliers, but the platelets did not appear to circulate in a preactivated state in either disease.     

Canine platelet transfusions

Objective – To review potential platelet storage options, guidelines for administration of platelets, and adverse events associated with platelet transfusions. Data Sources – Data sources included original research publications and scientific reviews. Human Data Synthesis – Transfusion of platelet concentrates (PCs) plays a key role in the management of patients with severe thrombocytopenia. Currently PCs are stored at 22°C under continuous gentle agitation for up to 5 days. Chilling of platelets is associated with rapid clearance of transfused platelets, and galactosylation of platelets has proven unsuccessful in prolonging platelet survival. Although approved by the American Association of Blood Banks, cryopreservation of human platelets in 6% DMSO largely remains a research technique. Pre‐storage leukoreduction of PCs has reduced but not eliminated acute inflammatory transfusion reactions, with platelet inflammatory mediators contributing to such reactions. Veterinary Data Synthesis – Canine plateletpheresis allows collection of a concentrate with a high platelet yield, typically 3–4.5 × 10¹¹ versus <1 × 10¹¹ for whole blood‐derived platelets, improving the ability to provide sufficient platelets to meet the recipient's transfusion needs. Cryopreservation of canine platelets in 6% DMSO offers immediate availability of platelets, with an acceptable posttransfusion in vivo platelet recovery and half‐life of 50% and 2 days, respectively. While data on administration of rehydrated lyophilized platelets in bleeding animal models are encouraging, due to a short lifespan (min) posttransfusion, their use will be limited to control of active bleeding, without a sustained increase in platelet count. Conclusions – Fresh PC remains the product of choice for control of bleeding due to severe thrombocytopenia or thrombopathia. While cryopreservation and lyophilization of canine platelets offer the benefits of immediate availability and long‐term storage, the compromise is decreased in vivo recovery and survival of platelets and some degree of impaired function, though such products could still be life saving.     

Equine recurrent uveitis: A clinical manifestation of leptospirosis

Leptospirosis is a zoonosis of worldwide distribution affecting domestic animals, wildlife and man. The bacterial disease is caused by pathogenic Leptospira spp., which are transmitted from reservoir hosts to accidental hosts. Horses are accidental hosts and can become susceptible to leptospiral infections. Widespread exposure to leptospires exists and is significantly more common than clinical disease. Leptospirosis can have different clinical manifestations including abortion, still birth, systemic disease with hepatic or renal dysfunction, and equine recurrent uveitis (ERU). ERU is the most frequently encountered clinical manifestation and this article will focus on the review of leptospira‐associated ERU. Equine recurrent uveitis is the most common cause of vision impairment and blindness in horses. The pathogenesis of leptospira‐associated ERU involves direct bacterial effects and immune‐mediated responses. Clinical signs vary between the acute and chronic phases of the disease and progress over time. The diagnosis of leptospira‐associated ERU can be difficult and usually requires a combination of diagnostic tests. Medical and surgical treatments have been described with varying outcomes. The prognosis for sight is usually poor, although core vitrectomy may improve the outcome. Avoidance of leptospiral exposure of horses is the only reliable prevention of leptospira‐associated disease.     

Equine platelet CD62P (P-selectin) expression: a phenotypic and morphologic study

Acute inflammatory diseases, such as colic, septicemia and endotoxemia are common in equines and have been shown to be correlated to vascular injury and thrombosis. In humans with similar thrombotic conditions, P-selectin and P-selectin glycoprotein ligand-1 (PSGL-1)-mediated platelet-leukocyte adhesion contributes to the pathogenesis of these disorders through the generation of inflammatory mediators and tissue factor. As such, we hypothesized that a P-selectin-PSGL-1 (platelet-leukocyte) interaction, similar to that in humans, may also exist in the horse. The objective of this study was to investigate phenotypic and morphological properties of equine platelet activation with a focus on CD62P (P-selectin) expression and CD62P mediated platelet-leukocyte interactions. To study high levels of platelet activation, we used 1 U/ml thrombin to induce secondary, irreversible aggregation in both human and equine platelets. Addition of glycyl-L-prolyl-L-arginyl-L-proline amide (GPRP) prior to thrombin activation blocked fibrin polymerization, allowing the use of flow cytometry to study alpha-granule expression as a measure of platelet activation. Thrombin activation resulted in high levels of activation, measured as P-selectin expression, in both humans and equines. Interestingly, our research illustrates that in healthy horses, P-selectin is also constitutively expressed on 20-25% of resting platelets. This finding is in direct contrast to humans, in which P-selectin expression is negligible (<5%) in the absence of agonist activation. The high baseline level of P-selectin expression among equine platelets may suggest that they are primed for leukocyte adhesion, possibly resulting in prothrombotic conditions. This phenomenon could be of significant clinical relevance, as it may be related to the rapid clinical decline often seen in equine patients with colic and endotoxemia, where vascular injury and thrombotic complications compromise patient survival. Based on these findings, further investigation into the mechanisms of platelet P-selectin-mediated inflammation and platelet-leukocyte mediated vascular injury in the horse appears warranted.     

Effects of WEB 2086, an antagonist to the receptor for platelet-activating factor (PAF), on PAF-induced responses in the horse.

Platelet-activating factor (PAF) causes oedema and neutrophil accumulation when injected into the skin of normal horses. PAF is also known to induce aggregation of horse platelets in vitro. The selective PAF receptor antagonist WEB 2086 has now been used to determine whether these effects are mediated by PAF receptor activation. Addition of WEB 2086 to equine platelets in vitro inhibited PAF-induced aggregation in a competitive reversible manner (pA2 = 7.14). Inhibition of in vivo inflammatory responses to PAF occurred after local administration of WEB 2086: wheal formation induced by 0.1 micrograms PAF/site was reduced by 1-10 micrograms WEB 2086/site. PAF (1 micrograms/site)-induced neutrophil accumulation was also inhibited by co-administration of 10 micrograms WEB 2086/site. Systemic administration of WEB 2086 (3 mg/kg iv) to 4 normal ponies inhibited PAF-induced wheal formation and ex vivo platelet aggregation. At 30 min after drug administration the concentration of PAF required to produce a half maximal aggregation response was increased 496 +/- 137 fold. At 6 h the degree of inhibition was markedly reduced and responses had returned to pre-treatment values by 24 h. PAF-induced increases in cutaneous vascular permeability were also reduced by 80% as early as 30 min after iv administration of WEB 2086 in these animals, the inhibition persisting for at least 6 h. These results suggest that in vitro and in vivo responses to PAF in the horse are mediated via activation to PAF receptors. WEB 2086 will therefore be a useful agent for studying the role of PAF in the pathogenesis of equine inflammatory conditions.     

Platelet size,platelet surface-associated IgG,and reticulated platelets in dogs with immune-mediated thrombocytopenia

Abstract: Immune-mediated thrombocytopenia (IMT) is a disorder in which bound IgG on the surface of platelets results in platelet removal and alterations in mean platelet volume. Using flow cytometry, alterations in platelet size, platelet surface-associated IgG (PSAIgG), and numbers of reticulated platelets were determined in 13 dogs with primary IMT and 4 dogs with secondary IMT induced by experimental infection with Babesia gibsoni . Effects of sample age on platelet parameters also were determined, using samples from 20 dogs with normal platelet counts analyzed within 4 hours and after 24, 48, and 72 hours of storage in EDTA. No significant changes in platelet count, platelet size, or reticulated platelet percentage were observed in samples assayed within 4 and 24 hours of blood collection; whereas PSAIgG values increased 3 to 7 fold in samples stored for 24–72 hours. Using reference values for freshly collected or 24-hour-old samples, 10 of 13 (77%) dogs with primary IMT and all B gibsoni-inf ected dogs had increased PSAIgG levels. In 12 (75%) of the 16 dogs with thrombocytopenia the percentage of reticulated platelets was increased; however, absolute numbers of reticulated platelets were within reference values. Moreover, PSAIgG level and the percentage of reticulated platelets were not always increased concurrently in dogs with primary and secondary IMT. Platelet microparticles were detected in all B gibsoni-infected dogs, 8 of 13 (62%) dogs with primary IMT, and transiently in a dog that responded to immunosuppressive treatment. The results of this study indicate that sample age and time of sampling during disease affect interpretation of platelet parameters in dogs with IMT.     

Phenylbutazone inhibition of equine platelet function.

Nonsteroidal anti-inflammatory drugs impair platelet aggregation and secretion in man, pigs, and rabbits and inhibit platelet thromboxane/prostaglandin synthesis. The present investigation studied the effects of phenylbutazone on platelet aggregation and bleeding times in the horse. Aggregation responses to adenosine diphosphate and collagen were markedly impaired 15 minutes and 2 hours after treatment, but 4 hours after treatment, platelet responses approximated those prior to treatment. The in vivo effect of phenylbutazone correlated with its plasma concentrations. Phenylbutazone, like aspirin, appeared to exert its effect by inhibiting thromboxane/prostaglandin synthesis, because thrombin-induced malondialdehyde formation was inhibited. However, unlike aspirin, free arachidonate-induced malondialdehyde synthesis was reduced but not eliminated, which suggested that phenylbutazone may have more than one site of action. Although collagen-induced platelet aggregation was impaired, a response was still present, and bleeding times were not altered by phenylbutazone treatment. To account for these findings, it is proposed that equine platelets can respond to collagen by thromboxane/prostaglandin independent pathways. The physiologic and pathophysiologic importance of these findings is discussed.     

Splenectomy in the management of primary immune‐mediated hemolytic anemia and primary immune‐mediated thrombocytopenia in dogs

BackgroundCurrent reports about the use of splenectomy for the management of immune‐mediated hemolytic anemia (IMHA) or immune‐mediated thrombocytopenia (ITP) or both in dogs are limited.ObjectivesTo retrospectively describe the use of splenectomy as part of the management for IMHA, ITP, and concurrent IMHA and severe thrombocytopenia (CIST) in dogs. It was hypothesized that splenectomy would be beneficial in allowing for reduction of dose of immunosuppressive drugs or discontinuation in 1 or more of these groups.AnimalsSeventeen client‐owned dogs (7 with IMHA, 7 with ITP, and 3 with CIST) were identified across 7 UK‐based referral hospitals from a study period of 2005 to 2016.MethodsData were collected retrospectively via questionnaires and included information about diagnosis, management and treatment response before and after splenectomy. Based on clinical outcome, treatment with splenectomy as part of the management protocol was classified as either successful or unsuccessful.ResultsSix of 7 dogs with ITP were managed successfully with splenectomy as part of their management protocol (3 complete and 3 partial responses), although 1 subsequently developed suspected IMHA. Of the 7 dogs with IMHA, splenectomy was part of a successful management protocol in 4 dogs (2 complete and 2 partial responses). In the CIST group, 1 case (1/3) responded completely to management with splenectomy as part of the management protocol.Conclusions and Clinical ImportanceSplenectomy was considered successful and well tolerated in most cases of isolated ITP. Whether there is a benefit of splenectomy in cases of IMHA and CIST could not be determined in the current study.     

Canine idiopathic thrombocytopenia: clinical observations and long-term follow-up in 54 cases

Idiopathic thrombocytopenia purpura (ITP) was diagnosed in 54 dogs. Bleeding was associated with platelet counts less than or equal to 30,000/mm3, and occurred most frequently at mucosal surfaces and in the skin. Other hematologic changes were variable, the most common being regenerative anemia with leukocytosis. Bone marrow examination revealed variable megakaryocyte numbers, but hyperplasia was most commonly observed. Results of the platelet factor 3 test were positive in only 7 of 25 dogs so tested. Treatment included various combinations of corticosteroid, vincristine, cyclophosphamide, and splenectomy. The dogs could be classified into 4 groups on the basis of the course of disease: (1) 14 dogs that died or were euthanatized during the first episode of thrombocytopenia, (2) 17 dogs that recovered after a single episode of thrombocytopenia (acute ITP), (3) 8 dogs in which thrombocytopenia recurred over a period of up to 8 months before recovering (acute, recurrent ITP), and (4) 15 dogs that experienced repeated episodes of ITP for periods of up to 8 years (chronic ITP).     

26例犬免疫介导性血小板减少症回顾性分析

旨在调查犬免疫介导性血小板减少症(immune thrombocytopenia，ITP)的发病和治疗情况，并探讨预后相关因素。本研究自2018―2019年于中国农业大学动物医院接诊的病例中筛选出26例符合要求的ITP病例，记录患犬的基本信息、临床表现、实验室检查结果以及治疗和预后情况，并进行统计学分析。结果显示，贵宾犬为主要的发病品种(58%)；伊文氏综合征(Evans syndrome)与诊断后短期内(14 d)死亡显著相关(P=0.02)；初诊时，所有患犬皆具有出血的临床表现，根据一种新型犬ITP出血评估工具(DOGiBAT)所得出的评分范围为3~10分，其中,评分>5的患犬与诊断后短期内死亡显著相关(P=0.03)，提示出血评分对判断疾病转归有一定的指导意义。此外，出血评分>5的犬C反应蛋白(C-reactive protein, CRP)检测结果显著高于出血评分≤5的犬(P=0.01)，初步提示CRP具有辅助判断ITP严重程度的意义。本研究建议在评估ITP预后时引入出血评分工具，相比单一的临床表现更能量化疾病的严重程度，并提供可靠的预后判断。