Kasabach-Merritt-like syndrome in a dog secondary to isolated splenic haemangiomatosis

2020 ◽  
Vol 8 (2) ◽  
pp. e001090
Author(s):  
Paolo Pazzi ◽  
Sarah Clift ◽  
Marthinus Jacobus Hartman ◽  
Nicolize O'Dell
Keyword(s):  
Platelet Count ◽  
Immunosuppressive Therapy ◽  
Blood Count ◽  
Complete Blood Count ◽  
Abdominal Ultrasound ◽  
Severe Thrombocytopenia ◽  
Intact Male ◽  
Distended Abdomen ◽  
First Case ◽  
Ultrasound Findings

A 13-year-old intact male miniature schnauzer presented with lethargy, distended abdomen and pallor. Pancytopenia was identified on complete blood count with a severe thrombocytopenia. Cavitatory severe splenomegaly was identified on abdominal ultrasound. Two weeks of immunosuppressive therapy had no effect on the thrombocytopenia and a splenectomy was performed. The platelet count returned to normal within 24 hours of splenectomy. Isolated splenic haemangiomatosis was confirmed on histopathology and immunohistochemistry. The anaemia and severe thrombocytopenia in conjunction with the ultrasound findings and histopathology are characteristic of Kasabach-Merritt syndrome in people. This is the first case of Kasabach-Merritt-like syndrome described in the dog.

First Case of Platelet-Type Von Willebrand Disease (PT-VWD) Associated with Type 2B Von Willebrand Disease (2B VWD)

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 5313-5313
Author(s):  
Marie Dreyfus ◽  
Celine Desconclois ◽  
Corinne Guitton ◽  
Marie-Jeanne Baas ◽  
Helene Mandard ◽  
...  
Keyword(s):  
Platelet Count ◽  
Von Willebrand Disease ◽  
Biological Study ◽  
High Dose ◽  
Severe Thrombocytopenia ◽  
First Case ◽  
Platelet Receptor ◽  
Biological Phenotype ◽  
Neonatal Thrombocytopenia ◽  
Von Willebrand

Abstract Abstract 5313 Introduction VWD 2B and PT-VWD are rare diseases, due to mutations inducing a gain of function respectively of von Willebrand factor (VWF) and of its platelet receptor, Glycoprotein (GP)1bα Case history We report here the case of a young girl, born with an extensive purpura and a severe thrombocytopenia: platelet count: 16G/L. There was no associated biological nor clinical abnormality. A high dose of 1g/kg of immunoglobulin G infused on day 1 was unsuccessful, and a HPA-1a (−) platelet concentrate infusion led to a partial and transient increase of the platelet count up to 60G/L. Thrombocytopenia then resolved spontaneously. Biological study showed no sign of materno-fetal allo- or auto-immunity, parents were not consanguineous. The diagnosis of type 2B VWD was performed when she was 5 months old: VWF:RCo < 13 IU/dl, VWF:Ag 60 IU/dl, positive ristocetin induced platelet aggregation (RIPA) at a low ristocetin concentration (0.5 mg/ml). RIPA mixing studies were unconclusive. The same biological abnormalities were found in the father, whereas the mother had normal hemostasis tests. The biological phenotype also included a study of the multimeric VWF structure, showing a marked decrease in percentage of VWF high and intermediate molecular multimers. Genetic analysis performed on VWF gene showed the heterozygous p.Pro1266Leu missense mutation in the VWF A1 domain. This mutation ( o ) is only slightly deleterious, and induces usually a mild disease, without thrombocytopenia, even in stress situations, with normal VWF multimeric distribution; therefore, it could not explain the biological phenotype severity in this family. GPIBA was then analysed, and a candidate point mutation p.Met239Ile was evidenced. This mutation had not been described yet, but p.Met255Val had already been found in diagnosed cases of PT-VWD. Conclusion This case underlines the utmost importance to characterize precisely neonatal thrombocytopenia mechanism. Furthermore, it points out the difficulties to performing PT-VWD diagnosis, which incidence is most probably underestimated. In our case, it was the systematic and extensive biological workout performed in this case of isolated neonatal thrombocytopenia, without any obvious cause, which led to the diagnosis of a PT-VWD, inducing a severe biological phenotype, associated with type 2B VWD characterized by a mild expression. It is, to our knowledge, the first case described to date of such a morbid association. Disclosures: No relevant conflicts of interest to declare.

Refractory Severe Thrombocytopenia Associated with Intravenous Treprostinil Use: a Case Report

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4566-4566 ◽  
Author(s):  
Sherry Kuo ◽  
Rajive Tandon ◽  
Lisa Boggio
Keyword(s):  
Platelet Count ◽  
Case Report ◽  
Coagulation Factor ◽  
Similar Efficacy ◽  
Pulmonary Artery Hypertension ◽  
Caucasian Woman ◽  
Recurrent Bleeding ◽  
Severe Thrombocytopenia ◽  
Idiosyncratic Reaction ◽  
First Case

Abstract Background: Intravenous epoprostenol was the first drug approved by the U.S. Food and Drug Administration for the treatment of pulmonary arterial hypertension. Treprostinil, a tricyclic benzidene prostocycline analog of epoprostenol has been favored over epoprostenol due to its more advantageous mode of administration and similar efficacy. All prostocyclines are known to cause thrombocytopenia, but severe platelet reductions are rare below 100,000/μL. Aim: We report the first case of severe thrombocytopenia associated with intravenous treprostinil with subsequent recovery of a normal platelet count following transition to epoprostenol. Case Report: A 55 year-old Caucasian woman diagnosed with idiopathic pulmonary artery hypertension noted significant improvement in symptoms and exercise tolerance following initiation of intravenous treprostinil. However, she developed new onset severe thrombocytopenia with her platelet count falling to 51,000/μL (150,000–399,000/μL) and recurrent anterior epistaxis after receiving intravenous treprostinil for six months. She had no known hematologic disorders or history of recurrent bleeding and was not receiving any other new medications. There was no evidence of disseminated intravascular coagulation, hemolysis, coagulation factor deficiency, or splenic sequestration. Empiric treatment with corticosteroids was started for positive antiplatelet IgG direct antibody, but the platelet count further declined to 25,000/μL. The patient was subsequently transitioned from intravenous treprostinil to epoprostenol under the assumption that her severe thrombocytopenia was an idiosyncratic reaction rather than a class effect of prostocyclines. Her platelet count had returned to normal two weeks after the transition. Conclusion: In practice, patients developing thrombocytopenia from epoprostenol are frequently switched to treprostinil hoping to attenuate the degree of thrombocytopenia. This case is the first report of severe thrombocytopenia associated with intravenous treprostinil, as well as its successful resolution following transition to another prostocycline analog, epoprostenol. Although the exact mechanism of thrombocytopenia is unknown, it raises a question if the cyclohexane ring on treprostinil compared to the lactone ring on epoprostenol can potentially lead to more severe thrombocytopenia. Although at this point, it is uncertain if severe thrombocytopenia is an idiosyncratic reaction to treprostinil, this report will hopefully draw attention to this potential adverse effect and identify the mechanism of this reaction.

Severe Haemolytic Anaemia Secondary To Avian Allergy

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4654-4654 ◽  
Author(s):  
Taylor David ◽  
Russell Keenan
Keyword(s):  
Immunosuppressive Therapy ◽  
Haemolytic Anaemia ◽  
Blood Count ◽  
Full Blood Count ◽  
Costal Margin ◽  
Effective Measure ◽  
First Case ◽  
Short Period ◽  
Patient Consent

Summary We present the first case of pigeon allergy causing severe haemolytic anaemia. Serology demonstrated very high titres of antibodies to avian proteins; in excess of those seen in the majority of cases of allergic lung disease1. Observation, immunosuppressive therapy and attempts at reducing antigen exposure were ineffective in controlling the disease. The only effective measure was culling the birds which resulted in a swift remission in the patient’s illness. Background Avian allergic diseases are well documented including extrinsic allergic alveolitis and asthma. However, from a review of the literature, haemolytic anaemia has not yet been described. Case Presentation An eight year old boy presented to accident and emergency with malaise, pallor and a sore throat. Haemoglobin was 53g/L. Further clinical examination revealed splenomegaly of 3.5cm below the costal margin. Investigations Full blood count demonstrated marked anaemia and a reticulocytosis (Hb 53g/L, WBC 2.2 x109/L, Neuts 1.3 x109/L, Lymphs 0.6 x109/L, Platelets 186 x109/L, Reticulocytes 375 x109/L). Blood film demonstrated increased polychromasia and microspherocytes. Direct coombes test was negative. Differential Diagnosis The patient’s haemoglobin stabilised following a short period of time in hospital. Red blood cell transfusion and immunosuppressive therapy were not required at this stage. Despite stable haemoglobin concentrations there continued to be evidence of haemolysis throughout the first year of follow-up. This was complicated by gallstone disease which required open cholecystectomy. School attendance was adversely affected. In view of the prolonged duration of the illness the patient was screened for congenital and acquired causes of haemolysis. No cause was found for the condition. Three years later the patient experienced decompensated haemolysis with a fall in his haemoglobin to 66g/L and symptoms of lethargy and malaise. His splenomegaly was more marked at 5.0cm. He was commenced on prednisolone (1mg/kg) which stabilised his blood count but was complicated by psychiatric disturbances. During a routine follow-up appointment the patient disclosed that he kept over 100 racing pigeons at his home. He was involved in their care on a daily basis and would regularly race the birds in competitions. Serological testing demonstrated high titres of antibodies to avian proteins (pigeon and budgie serum, feather and droppings >200x103 mg/L). These levels are in excess of those seen in the majority of cases of allergic lung disease1. Treatment Initial attempts to reduce exposure were ineffective. Following discussions with the family the birds were culled. There was an immediate and dramatic effect on reticulocytes and within a month it was possible to begin reducing the steroid dose. Over the following year there was a progressive rise in his haemoglobin associated with a continued fall in the reticulocytosis. Steroids were discontinued at four months. Three years following the removal of the causative agent the patient remains well and off treatment. Discussion Avian proteins are commonly cited as a cause for immune conditions, predominantly those affecting the respiratory system. This is the first case of avian allergic haemolytic anaemia. This case highlights the importance of consideration of unusual pathologies. Competing interests None Patient consent Not obtained. References 1) C I Baldwin, A Todd, J E Calvert. Pigeon fanciers' lung: effects of smoking on serum and salivary antibody responses to pigeon antigens. Clin Exp Immunol. 1998 Aug;113(2):166-72. Disclosures: No relevant conflicts of interest to declare.

Is anti-D immunoglobulin still a frontline treatment option for immune thrombocytopenia?

Hematology ◽  
2013 ◽  
Vol 2013 (1) ◽  
pp. 283-285 ◽  
Author(s):  
Jenny M. Despotovic ◽  
Cindy E. Neunert
Keyword(s):  
Platelet Count ◽  
Treatment Option ◽  
Drug Administration ◽  
Immune Thrombocytopenia ◽  
Blood Count ◽  
Complete Blood Count ◽  
Initial Therapy ◽  
Black Box ◽  
Frontline Treatment ◽  
Mucosal Bleeding

Abstract A 5-year-old boy presents with platelet count of 2 × 109/L and clinical and laboratory evidence of immune thrombocytopenia. He has epistaxis and oral mucosal bleeding. Complete blood count reveals isolated thrombocytopenia without any decline in hemoglobin and he is Rh+. You are asked if anti-D immunoglobulin is an appropriate initial therapy for this child given the 2010 Food and Drug Administration “black-box” warning.

scholarly journals Deranged hematological profile in patients presenting with malarial parasitaemia

2021 ◽  
Author(s):  
Amber Haroon ◽  
Huda Zameer ◽  
Aneeqa Naz ◽  
Sohaib Afzal ◽  
Tooba Ammar ◽  
...  
Keyword(s):  
Platelet Count ◽  
Plasmodium Vivax ◽  
Blood Count ◽  
Complete Blood Count ◽  
Hematological Parameters ◽  
Blood Film ◽  
Bleeding Disorders ◽  
Peripheral Blood Film ◽  
Duration Of Disease ◽  
Low Platelet Count

Background: Alterations in the hematological parameters are thought to have the capacity to act as an adjuvant tool in strengthening the suspicion of malaria, thereby prompting a more meticulous search for malaria parasites.Methods: 186 cases with malaria positive for immunochromatographic test (ICT) malaria presenting with fever ≥101 °F, confirmed on peripheral blood film, of 20-60 years were included. Patients with coagulopathy and bleeding disorders such as hemophilia, brain tumors, tuberculosis meningitis, viral or bacterial encephalitis and multiple sclerosis were excluded. Sample was taken to the laboratory, for routine investigations like ICT malaria and complete blood count (CBC) to diagnose anemia and low platelet count.Results: Patients of 20 to 60 years of age with mean 41.80±8.51. Out of 186 patients, 101 (54.30%) were male and 85 (45.70%) were female with 1:2:1 ratio. Mean duration of disease was 4.91±1.32 days. Frequency of derangement in hematological parameters was anemia in 27 (14.52%) patients and 142 (76.34%) with thrombocytopenia. 127 cases were of Plasmodium vivax and 59 cases were of Plasmodium falciparum. Patients were more anemic as disease period prolonged. Patients infected by Plasmodium vivax showed more tendencies towards anemia and reduction in platelet count as compare to Plasmodium falciparum.Conclusions: The frequency of derangement in hematological parameters i.e. anemia and low platelet count, among malarial patients is quite high and more cases were of Plasmodium vivax and it showed anemia and thrombocytopenia was more pronounced in Plasmodium vivax.

scholarly journals The First Case Report of Tazobactam Induced Thrombocytopenia

Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4897-4897 ◽  
Author(s):  
Minh-Tri H. Nguyen ◽  
Pavneet Kaur ◽  
Richard H. Aster ◽  
Vidya Krishnan
Keyword(s):  
Platelet Count ◽  
Lower Extremity ◽  
Immune Thrombocytopenia ◽  
Conflicts Of Interest ◽  
Complex Case ◽  
Chronic Obstructive ◽  
Severe Thrombocytopenia ◽  
Beta Lactam ◽  
Diffuse Abdominal Pain ◽  
First Case

Drug-induced immune thrombocytopenia (DITP) is a rare and often overlooked cause for thrombocytopenia. It is a particularly difficult diagnosis given its rarity and because at least 100 different medication have been implicated. Cases of piperacillin-tazobactam-induced DITP have sparked growing interest given how common this antibiotic is used. Few studies, however, have defined the specific moiety causing the suspected DITP by serologic testing. When this has been done, only piperacillin has been implicated. Here, we describe the first case of DITP in which tazobactam was implicated by serologic studies. Case A 62 year-old-male with a past medical history of Crohn's disease, alcohol use disorder and chronic obstructive pulmonary disease (COPD) presented to the hospital with bilateral lower extremity pain and redness, and diffuse abdominal pain for 1 week. His home medications included pravastatin, meloxicam, pantoprazole and adalimumab. Physical exam, lab testing and imaging studies provided evidence for lower extremity cellulitis, multifocal pneumonia and possible colitis. In the Intensive care unit the patient was started on broad-spectrum antibiotics (vancomycin and piperacillin-tazobactam). He developed new onset thrombocytopenia to <20 K/UL (>50% drop within 72 hours) by hospital day 3, and vancomycin was discontinued. A peripheral smear showed no evidence of schistocytes or platelet clumps. Subcutaneous heparin was discontinued and supportive care with vasopressors, antibiotics and RRT was continued. Patient's septic shock improved, and he was eventually weaned off the vasopressor support. However, his thrombocytopenia persisted which prompted further workup as shown in Table 2. After initial workup remained unrevealing, piperacillin-tazobactam was discontinued and he was started on cefepime on hospital day 11. On day 12, his thrombocytopenia started to improve and showed an upward trend over next 48 hours. At this point antibiotic associated thrombocytopenia was highly suspected so antibiotic specific antibodies to piperacillin-tazobactam were requested. Platelet count on the day of discharge (hospital day 18) was 72 K/UL (Figure 1). IgM antibodies that reacted with normal platelets only when tazobactam was present in the reaction mixture were identified in laboratory testing performed by the Platelet and Neutrophil Immunology Laboratory of Versiti-BloodCenter of Wisconsin. Discussion Serologic findings made in this very complex case indicate that severe thrombocytopenia was caused by an IgM antibody that recognized normal platelets only in the presence of tazobactam. Tazobactam is almost invariably given with piperacillin to inhibit bacteria-derived penicillinase and prolong the lifespan of piperacillin in vivo but, although numerous cases of piperacillin-induced thrombocytopenia have been described, this is the first report in which tazobactam has been documented as the trigger for immune thrombocytopenia. While tazobactam, like piperacillin, contains a beta-lactam structure, tazobactam-specific antibiotic testing may have implications on choosing future antibiotic therapies (particularly penicillins) for a patient. DITP occurring in the ICU can often be over-looked because patients tend to be critically ill and there may be many other reasons for a low platelet count. It is important to keep this diagnosis in mind whenever severe thrombocytopenia develops. Additionally, further work may seek to understand whether a patient's penicillin allergy may be specific to a moiety such as tazobactam, allowing continued use of other types penicillin-class drugs. Disclosures No relevant conflicts of interest to declare.

scholarly journals An Interesting Presentation of Severe Bicytopenia in A Case of SLE

2021 ◽  
Vol 8 (1) ◽  
pp. C17-19
Author(s):  
M Aswin Manikandan ◽  
A Josephine ◽  
Vindu Srivastava ◽  
S Mary Lilly
Keyword(s):  
Platelet Count ◽  
Haemolytic Anaemia ◽  
Blood Count ◽  
Complete Blood Count ◽  
Reticulocyte Count ◽  
Coombs Test ◽  
Peripheral Smear ◽  
History Of ◽  
Wbc Count ◽  
Transfusion Reactions

We present a case of 25-year-old female who was brought to the hospital for complaints of generalised weakness, fever, and history of melena and haematuria. Following admission complete blood count and peripheral smear was asked; Complete blood count (CBC) findings were haemoglobin 4.2 gm/dl, total WBC count was 14,990, platelet count 7000, reticulocyte count 4%, NRBCs were 15/100 WBCs. Peripheral Smear showed fragmented RBCs, polychromatophils microspherocytes and multiple foci of autoagglutination suggestive of autoimmune haemolytic anaemia. Pertaining to these findings immune workup was done for this patient; coombs test was negative for this patient, but ANA was positive. This identification proved valuable to the patient as; administration of corticosteroids helped to prevent haemolytic transfusion reactions and improved the patient’s haemoglobin and platelet count.

Rapid onset vancomycin-induced thrombocytopenia confirmed by vancomycin antibody test

2021 ◽  
Vol 14 (7) ◽  
pp. e243027
Author(s):  
Thakul Rattanasuwan ◽  
Yael Marks ◽  
Jess Delaune ◽  
Adonice P Khoury
Keyword(s):  
Platelet Count ◽  
Blood Count ◽  
Complete Blood Count ◽  
Clinical Symptoms ◽  
Antibody Test ◽  
Rapid Onset ◽  
Antibody Testing ◽  
Drug Dependent ◽  
Related Reaction ◽  
Vancomycin Level

We report a case of vancomycin-induced thrombocytopenia (VIT) with rapid onset after re-exposure to vancomycin. A 58-year-old man with cellulitis was initiated on vancomycin. Approximately 1 hour into the vancomycin infusion, the patient developed an infusion-related reaction. Vancomycin infusion was stopped. A complete blood count obtained 4 hours after discontinuation of the vancomycin infusion revealed a platelet count of 31 ×10­9/L. Investigations ruled out likely causes of thrombocytopenia. VIT was diagnosed based on clinical symptoms and confirmed with drug-dependent platelet antibody testing. Without complications, platelet counts recovered within 7 days after discontinuation of vancomycin. No correlation between vancomycin level and VIT was observed.

DISCOSPONDYLITIS IN A 7-MONTH-OLD FRENCH BULLDOG: A CASE REPORT

2019 ◽  
Vol 45 (03) ◽  
pp. 91-96
Author(s):  
Chung-Chao Chen ◽  
Shu-Fang Yang ◽  
Shei-Wen Lee ◽  
Heng-Leng Yang ◽  
Feng-Yi Hsieh ◽  
...  
Keyword(s):  
Case Report ◽  
Pain Perception ◽  
Complete Blood Count ◽  
Old French ◽  
Intact Male ◽  
Normal Limits ◽  
First Case ◽  
Staphylococcus Epidermis ◽  
Bacteria Culture ◽  
French Bulldog

A 7-month-old, intact, male French bulldog presented for paraplegia for two days, and persistent fever and diarrhea for seven days. Complete blood count and biochemical profiles were within normal limits. Radiography and computed tomography (CT) revealed destructive endplate lesions between T11 and T12. Surgery of intervertebral disc (IVD) curettage was performed because the dog was beginning to lose deep pain perception. Staphylococcus epidermis was isolated from blood culture and specimens of the IVD. After surgery, intravenous and oral antibiotics were continued for three weeks. The dog regained ambulatory status one month after surgery. Diagnosis of discospondylitis of T11 and T12 was confirmed according to CT and positive bacteria culture. To our knowledge, this case is the youngest dog confirmed with discospondylitis managed successfully, and the first case report of discospondylitis in a French bulldog. Aggressive surgical treatment is highly recommended in young dogs with rapidly progressive neurologic deficits from discospondylitis.

scholarly journals Postpartum hemorrhage risk is driven by changes in blood composition through pregnancy

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Matthew R. Robinson ◽  
Marion Patxot ◽  
Miloš Stojanov ◽  
Sabine Blum ◽  
David Baud
Keyword(s):  
Platelet Count ◽  
Blood Cell ◽  
Postpartum Hemorrhage ◽  
Mean Platelet Volume ◽  
Blood Count ◽  
Complete Blood Count ◽  
Platelet Volume ◽  
Distribution Width ◽  
Cell Counts ◽  
Blood Cell Counts

AbstractThe extent to which women differ in the course of blood cell counts throughout pregnancy, and the importance of these changes to pregnancy outcomes has not been well defined. Here, we develop a series of statistical analyses of repeated measures data to reveal the degree to which women differ in the course of pregnancy, predict the changes that occur, and determine the importance of these changes for post-partum hemorrhage (PPH) which is one of the leading causes of maternal mortality. We present a prospective cohort of 4082 births recorded at the University Hospital, Lausanne, Switzerland between 2009 and 2014 where full labour records could be obtained, along with complete blood count data taken at hospital admission. We find significant differences, at a $$p<0.001$$ p < 0.001 level, among women in how blood count values change through pregnancy for mean corpuscular hemoglobin, mean corpuscular volume, mean platelet volume, platelet count and red cell distribution width. We find evidence that almost all complete blood count values show trimester-specific associations with PPH. For example, high platelet count (OR 1.20, 95% CI 1.01–1.53), high mean platelet volume (OR 1.58, 95% CI 1.04–2.08), and high erythrocyte levels (OR 1.36, 95% CI 1.01–1.57) in trimester 1 increased PPH, but high values in trimester 3 decreased PPH risk (OR 0.85, 0.79, 0.67 respectively). We show that differences among women in the course of blood cell counts throughout pregnancy have an important role in shaping pregnancy outcome and tracking blood count value changes through pregnancy improves identification of women at increased risk of postpartum hemorrhage. This study provides greater understanding of the complex changes in blood count values that occur through pregnancy and provides indicators to guide the stratification of patients into risk groups.

Sign in / Sign up

Export Citation Format

Share Document