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Immune thrombocytopenic purpura (ITP) is also known as idiopathic thrombocytopenic purpura. Increased platelet destruction and insufficient platelet production are both responsible for its etiopathogenesis. ITP can be diagnosed after excluding other possible causes of thrombocytopenia.One hundred forty-three cases of chronic ITP that were monitored in a hematology clinic were retrospectively evaluated. All cases received first line treatment of 1 mg/kg/day prednisolone. Corticosteroid nonresponsive (CN) cases and corticosteroid-dependent (CD) cases underwent splenectomies.The rate of CN/CD cases was found to be 53% (n=76). Sixty-six percent of these cases (n=50) underwent splenectomies. The ratio of non-responsive cases to relapse cases after splenectomy (SN/SR) was 30% (n=15). The total number of cases was 41, including those without splenectomy (n=26) and with SY/SR (n=15). Helicobacter pylori (Hp) eradication, immunosuppressive agents and danazol treatments were administered to patients (n=10, n=14 and n=4, respectively). Currently, 13 patients are being monitored without treatment. Fifteen patients who were non-responsive to Hp eradication treatment, immunosuppressive treatment or danazol treatment are still being monitored without any treatment.Optimal treatment is not available for splenectomy-resistant cases of ITP. The response rates for Hp eradication treatment, immunosuppressive treatments and anabolic agents are low. Therefore, larger studies with more patients are required using new agents, such as thrombopoietin (TPO) receptor agonists and anti-CD20 monoclonal antibodies.İmmün trombositopenik purpura (İTP), idiopatik trombositopenik purpura olarak da bilinir (3). Etiyopatogenezinden trombosit yıkımında artış yanında trombosit üretiminde yetersizlik de sorumludur (4). İTP tanısı trombositopeni yapan diğer sebeplerin dışlanması ile konulur (5). Çalışmamızda kronik İTP’li 143 olgunun klinik seyir ve tedavi cevabı açısından değerlendirmesi amaçlanmıştır.Hematoloji kliniğinde izlenen 143 kronik ITP olgusu retrospektif olarak değerlendirildi. Tedavi endikasyonu konan tüm olgulara başlangıç tedavisi olarak 1 mg/kg prednizolon verildi. Kortikosteroid yanıtsız (KY) ve kortikosteroid bağımlı (KB) olgulara splenektomi uygulandı.KY/KB olguların oranı %53 (n=76) bulundu. Bu olguların %66’sına (n=50) splenektomi yapıldı. Splenektomiye yanıtsız ve splenektomi sonrası relaps (SY/SR) olan olguların oranı %30 (n=15) olarak saptandı. Splenektomi yapılamayan n=26 ve SY/SR n=15 olmak üzere toplam 41 olgu vardı. Helicobacter pylori (Hp) eradikasyon, immunosupresif ilaç ve danazol tedavileri sırasıyla n=10, n=14, n=4 olguya verildi. 13 olgu halen tedavisiz izlenmektedir. Hp eradikasyon tedavisi, immunsupresif tedavi ve danazole yanıtsız onbeş olgu halen tedavisiz takip edilmektedir.ITP de splenektomiye dirençli olgularda optimal bir tedavi seçeneği mevcut değildir. Hp eradikasyon tedavisi ve immunsupresif tedaviler ve anabolizan ajanlarla cevap oranları düşüktür. Bu nedenle trombopoietin (TPO) reseptör agonistleri ve anti-CD20 monoklonal antikorları gibi yeni ajanların kullanıldığı çok sayıda olgu içeren geniş çalışmalara ihtiyaç vardır.

Factor VII (FVII) deficiency is a rare autosomal recessivecongenital coagulopathy associated withclinical bleeding and isolated prolongation of theprothrombin time (PT). Factor VII deficiency maypresent with hemorrhages of central nervous (CNS)and gastrointestinal (GIS) systems during infantileperiod or may be asymptomatic until adulthood.1However, acquired factor VII deficiency is extremelyrare.2,3,4,5 Although there are numerous reports regardingthe use of rFVIIa concentrate in patientswith hemorrhage owing to congenital FVII deficiency,little is known about secondary FVII deficiencyand its management. Here, we present the firstreport of an acquired FVII deficiency developed inan elderly woman during the course of communityacquiredpneumonia and discuss management approachesfor this very rare entity

Chronic kidney disease presenting acutely is not uncommon, often avoidable and associated with adverse outcomes. In the early stages of chronic kidney disease, there may be no symptoms. However, when kidney function is less than one-tenth of normal, the symptoms may arise. The patients in end-stage renal disease may also present with nonspecific symptoms. A 46 year old man admitted to our hospital with knee pain. He had no other complaints. His blood urea and creatinin levels were 232 mg/dl and 19.5 mg/dl respectively. He was anemic and venous blood gas revealed pH: 7.10, HCO3-: 10 mEq/L. But his physical examination was normal. The glomerular filtration rate was greatly reduced, altough his blood pressure was within normal limits. Hemodialysis had been initiated immediately and within 24 hours blood urea nitrogen had decreased to 145 mg/dl. The clinicians must be aware of non-spesific symptoms such as arthralgia, which should masquerade the underlying chronic kidney disease. The identification, follow-up and appropriate referral of patients with raised serum creatinine is likely to reduce its incidence., Kronik böbrek hastalığının akut olarak ortaya çıkması nadir değildir. Bu durumdan sıklıkla kaçınılabilir, fakat gelişmesi halinde olumsuz sonuçlar doğurabilir. Kronik böbrek hastalığı erken dönemlerde asemptomatik seyredebilir. Böbrek fonksiyonları normal düzeyinin onda birinin altına düştüğünde semptomlar ortaya çıkabilir. Fakat, son dönem böbrek yetmezliği hastaları non-spesifik semptomlarla da başvurabilirler. Hastanemize başvuran 46 yaşındaki erkek hastanın diz ağrısı dışında şikayeti yoktu. Üre ve kreatinin değerleri sırasıyla 232 mg/dl ve 19.5 mg/dl idi. Anemisi mevcuttu. Venöz kan gazı değerlendirmesinde pH: 7.10, HCO3-: 10 mEq/L idi. Fakat hastanın fizik muayenesi normaldi. Hesaplanan glomerüler filtrasyon hızı oldukça düşük olarak bulunmasına karşın kan basıncı normal sınırlar içerisindeydi. Acil olarak hemodiyalize alınan hastanın kan üre nitrojeni 24 saat içerisinde 145 mg/dl\'ye geriledi. Klinisyenler kronik böbrek hastalığını maskeleyebilecek artralji gibi non-spesifik semptomlara karşı uyanık olmalılardır. Bu durumun insidansının azaltılabilmesi, yüksek serum kreatinini olan hastaların tanınması, takibi ve uygun olarak sevk edilmeleri ile sağlanabilir. Klin Deney Ar Derg 2010; 1(3): 216-8.

Dear Editor;Chronic lymphocytic leukemia (CLL) is a malign disease of the bone marrow, originating from the relatively mature cell stage of B or T lymphocytes, during which mature-appearing small lymphocytes infiltrate the hematolymphoid organs. When fludarabine (F) is used alone, or in combination with cyclophosphamide (C), against CLL, especially the latter becomes a quite efficient chemotherapy combination for the first diagnosis or for resistant, or refractory, cases who previously a different therapy administered1,2.The aim of this study was to evaluate the efficiency, as well as the hematologic and non-hematologic side-effect profile of the low-dose oral F and C combination regime (FC) in cases, who were resistant against the first-line therapy, or in post-treatment relapsing CLL cases.

Ankaferd Blood Stopper (ABS) is a novel topical hemostatic agent. ABS-induced formation of the protein network with vital erythro- id aggregation covers the entire physiological hemostatic process. ABS has pleiotropic cellular, proteomic, transcriptomic, and me- tabolomic effects. ABS also affects the expression of important hemostatic molecules namely PAR-1, EPCR and PAI-1. The aim of this study was to detect the macroscopic, biochemical, and cytopathological effects of ABS on myeloma monoclonal immunoglo- bulin (M-protein). Based on our results, the addition of ABS into the serum of both multiple myeloma (MM) and control groups resul- ted in significantly decrements in the level of total protein, albumin, IgG, IgA and IgM. Furthermore, the decrements in the MM pati- ents were more pronounced than in the healthy control subjects. ABS has a potential role in decreasing of serum proteins and mo- noclonal M- proteins. Moreover, the declining in the neoplastic monoclonal M-protein was more prominent. We hypothesized that ABS could be used as an "agglutination-controlling factor" for myeloma monoclonal proteins and the protein-aggregating effects of ABS may be helpful for expressing the regulatory molecules promoting or preventing the myeloma protein aggregation.

[No abstract available]