The main clinical characteristics and hematologic data for the six patients (two boys and four girls, median age = 8.6 years) are shown in Table 1. IgG and IgM antibodies to platelets 11 were identified by flow cytometry (FACSort Becton Dickinson, Franklin Lakes, NJ). In one experiment, a preincubated (37☌ for 30 minutes) 1:1 mixture of normal PRP with PPP from patient 1 was tested with adrenaline and collagen. Abnormal results were verified with the same sample. Results were expressed as the percentage change in optical density and compared with previously established normal patterns. Studies were conducted on patients and a healthy control 30 minutes after preparing the PRP and were completed within two hours of blood collection. Louis, MO), 2 μg/mL of collagen (Hormon-Chemie, Munich, Germany), and 1.2 or 0.6 mg/mL of ristocetin (H. Platelets were adjusted to a concentration of 300 × 10 9/L with autologous PPP and stimulated with 11 μM adrenaline (Pulmobronk, Caracas, Venezuela), 2 μM adenosine diphosphate (Sigma, St. Platelet aggregation was read turbidimetrically 10 in PRP (Chrono-log PICA aggregometer Chrono-Log Co, Havertown, PA). 9 The Simplate device (Organon Teknika, Durham, NC) was used to determine bleeding times. Factor XIII was evaluated qualitatively by solubility in 5 M urea, factor VIII by the one-stage method, 7 von Willebrand factor antigen by immunoelectrophoresis, 8 and ristocetin cofactor activity by the MacFarlane method. Thrombin time, prothrombin time, and activated partial thromboplastin time in PPP 6 were determined using a coagulometer (Stago Diagnostica, Asniers, France). Platelet-poor plasma (PPP) was obtained by centrifugation at 2,500 × g for 20 minutes at 4☌, and platelet-rich plasma (PRP) was obtained by centrifugation at 200 × g for 10 minutes at 22☌. 5 Absolute eosinophils were calculated from the product of the number of leukocytes and the percentage of eosinophils in differential counts.Īll coagulation procedures were done on citrated venous blood (10% 0.129 M sodium citrate). Platelet morphology was examined on Wright-Giemsa–stained blood smears and leukocytes were counted manually. Venous blood was collected into tubes containing EDTA and blood cells were quantified in a Coulter Gen S System 2 analyzer (Coulter Electronics, Hialeah, FL). The study was reviewed and approved by the Universidad Central de Venezuela and the Research Unit of the José María Vargas School of Medicine. ![]() Parental permission was obtained for all procedures. Periodic follow-up studies were conducted between 15 days and 30 months post-parasite therapy. No underlying illnesses or exposure to recent drug intake were elicited. 3 who exhibited a three-year period of protracted recurrent symptoms and cyclical thrombocytopenia, the syndrome lasted a few weeks. They were referred over a period of 33 months from 1999 to 2001 without any association with the season of the year. These patients with intense eosinophilic responses (> 650 cells/μL) were referred to the parasitology department and had florid intestinal infections. This is the first report of this pathologic combination in Latin American children.Ī cohort of six eutrophic otherwise healthy children less than 12 years of age were referred to our hemostasis unit due to mild dermal and mucosal bleeding episodes, mainly represented by variable-size ecchymoses (1.5–8 cm) mostly confined to the upper and lower extremities. The possible pathogenic roles of eosinophilia and parasitism are reviewed. Thrombocytopathic features mimicked the intrinsic defect of storage pool disease. No relationship could be established between excess eosinophils, intensity of bleeding, or type and degree of platelet abnormalities. Anti-parasite therapy reversed the hemorrhagic manifestations and normalized eosinophil counts and platelet alterations. Antibodies to platelets were not detected. Main abnormalities included prolonged bleeding times (50%) and defective aggregation with collagen (100%) adrenaline (66%), or ADP (66%). ![]() All children showed intestinal parasites and marked eosinophilia (mean count = 2,615.2 cells/μL, 95% confidence interval = 1,259.6–5,429.8). Mild bleeding phenomena (ecchymoses, petechiae, epistaxis, and gingival) were transient. We conducted clinical evaluations, hematologic and platelet function tests, clotting studies (bleeding time, prothrombin time, partial thromboplastin time, thrombin time, factor XIII, factor VIII, and von Willebrand factor), assays for IgG and IgM antibodies to platelets, and a search for stool parasites. Platelet dysfunction was detected in six children with purpura and eosinophilia.
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