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Öğe Idiopathic thrombocytopenic purpura in children - A single centre experience(2006) Biner B.; Balci D.The objective of the study was to review retrospectively our institutional experience of childhood idiopathic thrombocytopenic purpura (ITP). Medical records of all children diagnosed with ITP and treated in our centre between ages of 2 months to 16 years from January 1999 to December 2004 were reviewed. There were 28 were girls and 26 boys with a F/M ratio of 1.07, and a mean age (SD) of 54 children was 6.2 (2.1) years The majority of our patients had only mild and moderate bleeding symptoms and no intracranial haemorrhage occurred. A preceding viral infection history was noted in 57.4%. Mean platelet count at presentation was 12.2×109/l, mean platelet count of cases with wet purpura was 6.8×109/l which was significantly lower (P<0.001). Only one patient required erythrocyte transfusion and none of the patients received platelet transfusion at the admission time. Initial management consisted of no drug treatment in 7.4%, IVIG in 76.2%, corticosteroids in 14.8% or both in 11.1% patients. Three children received anti-D immune globulin, 3 cases unresponsive to various treatments were treated with cyclosporine A. Four cases had a recurrence within 6 months and had a favourable outcome. A total of 74% had acute ITP, whereas 26% were classified as chronic ITP. Splenectomy was performed in 2 patients who had chronic ITP, 1 child had a good response the other one was unresponsive. In our chronic ITP cases, 64.3% were younger than 10 years of age, whereas 35.7% were older than 10 years at presentation. However, 22% of children < 10 years had a chronic form whereas 38.4% of children > 10 years developed chronic ITP. In conclusion, our results were in accordance with the literature. Copyright © Hellenic Society of Haematology.Öğe Nutritional vitamin B12 deficiency presenting as bicytopenia in an infant(2006) Biner B.In infancy, vitamin B12 deficiency is usually secondary to maternal deficiency, especially in their exclusively breastfed infants. Here, an 8-month-old male infant admitted for bicytopenia and developmental delay is presented. On admission the patient was pale, apathic, hypotonic and lethargic. He had severe anaemia (Hb 6.2 g/dl) and thrombocytopenia (65×10 9/l). Serum vitamin B12 levels of the infant and his mother were low and in bone marrow aspiration, megaloblastic changes were observed. A rapid response in haematological values was observed after commencement of vitamin B12 treatment. Vitamin B12 deficiency should be considered in the differential diagnosis of hypotonic infants with developmental delay accompanied by megaloblastic anaemia. Adequate nutrition of pregnant and nursing mothers must be emphasized. Copyright © Hellenic Society of Haematology.Öğe Systemic lupus erythematosus presenting with generalized lymphadenopathy: A case report(2001) Biner B.; Acunaş B.; Karasaliho?lu S.; Vatansever Ü.Systemic lupus erythematosus (SLE) is an immune complex disease with many different clinical presentations. Here we report a 13-year-old female patient presenting with generalized lymphadenopathy, who meanwhile developed butterflly rash and pericarditis. The diagnosis of SLE was based on the clinical features, positive antinuclear antibody, and positive antibodies to dsDNA. The patient had an active disease and developed renal involvement, despite steroid therapy. The patient's clinical presentation, course and response to therapy are detailed, and the literature on lupus lymphadenitis is reviewed.Öğe Von Willebrand factor and von Willebrand disease(2005) Biner B.Von Willebrand disease (vWD) is an autosomally inherited bleeding disorder caused by a deficiency or abnormality of von Willebrand factor (vWF). vWF is a large multimeric glycoprotein that mediates platelet adhesion at the site of vessel injury. Also, it protects factor VIII from proteolytic degradation in the circulation. vWD has a prevalence of about 1% in the general population but less than 10% of them have bleeding symptoms. Bleeding symptoms are usually mucocutaneous and postsurgical with varying severity. This disorder can result from either a quantitative (types 1 and 3) or qualitative (type 2) defect in vWF. Type 2 vWD has been further classified into four distinct subtypes; 2A, 2B, 2M and 2N. The diagnosis of vWD requires attention to personal and family history of excessive bleeding and confirmation by laboratory evaluation. If the patient has a chronic blood loss, there may be accompanying iron deficiency anaemia and a mild chronic thrombocytopenia is often seen with type 2B vWD. Patients with mild vWD often have both a normal bleeding time and normal aPTT. Specific tests for vWD diagnose involve vWF antigen level, vWF activity (ristocetin cofactor), and factor VIII activity. Once a diagnosis is established, additional tests that aid in classifying the type of vWD include ristocetin-induced platelet aggregation and vWF multimer analysis. There are two main options available for the treatment of bleeding episodes: desmopressin and replacement therapy with plasma-derived factor VIII/vWF concentrates. Antifibrinolytic agents and topical haemostatic preparations are also used as adjunctive therapies. Copyright © Hellenic Society of Haematology.
