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In pandemic conditions, patients with febrile neutropenia are also at risk of COVID-19. Aim of this systematic review is to evaluate COVID-19 cases presented with febrile neutropenia and provide information regarding incidence, clinical course and prognosis.We systematically searched on COVID-19 and febrile neutropenia cases in PubMed, SCOPUS and Web of Science.A total of 19 febrile neutropenic patients were analyzed. A male predominance was noted. Eleven cases had hematological malignancies. Fourteen of the cases were previously received chemotherapy. Five patients had severe neutropenia: 3 had hematologic cancer and none died. 17 (89.5%) cases have pulmonary involvement and seven of them had severe disease with acute respiratory distress syndrome (ARDS). Three cases with ARDS were died. 12 of them received G-CSF for treatment. Five cases were developed respiratory failure after G-CSF use. Overall mortality was 15.8%, while death was not observed in patients without malignancy and solid organ tumors, the mortality rate was 27% in cases with hematological malignancies.In ongoing pandemic, febrile neutropenic patients should be precisely evaluated for COVID-19 disease. It should be remembered that there may not be typical signs and symptoms and laboratory findings of COVID-19 disease because of the immunosuppression.

Periferik kök hücre toplama rejimleri merkezden merkeze değişmekle birlikte, en sık tercih edilen kemoterapi ile birlikte büyüme faktörü (G-CSF, GM-CSF) veya yalnızca büyüme faktörü uygulanmasıdır. CD34+ kök hücreler standart toplama rejimleri ardından toplanabileceği gibi salvaj kemoterapileri takiben de toplanabilir. Çalışmamızda standart toplama ve salvaj kemoterapi protokollerinin mobilizasyon başarısı açısından karşılaştırılması amaçlanmıştır. Ağustos 2008- Ocak 2011 arasında otolog periferik kök hücre toplama programına dahil edilen 56 hastanın dosyaları retrospektif olarak tarandı. Yirmi sekiz hastaya (50.0%) filgrastim 10 µg/kg/gün (1. grupfilgrastim), 18 hastaya (32.1%) ifosfamid + etoposid + epirubisin + filgrastim 5 g/kg/gün veya siklofosfamid + etoposid + 5 µg/kg/gün’den oluşan bir standart toplama protokolü (2. grup-standart), 10 hastaya (17.9%) ise bir salvaj rejim + filgrastim 5 µg/kg/gün (3. grup-salvaj) uygulanmıştı. Mobilize edilen median CD34+ hücre ve yetersiz toplama sayıları her üç grupta da benzerdi. Mobilizasyon öncesi nakil öyküsünün olması, toplama işleminin başarısı üzerinde negatif bir etkiye sahip bulundu. Nakil öyküsü olanlarda, olmayanlara göre toplanan CD34+ hücre sayısı daha düşüktü. Bununla birlikte hastaların tanıları, nakil öncesi hastalık durumları, mobilizasyon öncesi radyoterapi öyküsü gibi parametrelerin toplama işleminin başarısı üzerine etkisi saptanmadı. Çalışmamızda CD34+ hücre mobilizasyonu açısından standart toplama ve salvaj kemoterapi protokolleri arasında fark saptanmamıştır. Standart toplama ve salvaj kemoterapi protokollerinin mobilizasyon başarısı açısından karşılaştırılması için çok sayıda olgu içeren prospektif ve randomize klinik çalışmalara ihtiyaç vardır. Although regimens of harvesting peripheric stem cell vary from one center to another, the most common ones are chemotherapy plus growth factor or growth factor alone. We aimed to determine which variables of harvesting peripheral stem cells are effective on the number of harvested CD34+ cells and successfull mobilisation defined as “the collection of >2.0 x 106 CD34+ cells/kg b.w. with a maximum of three leukaphereres”. From August 2008 to January 2011, the documents of 56 patients included in the autologous peripheral stem cell harvesting program were retrieved retrospectively. Regarding harvesting regimens, 28 patients (50.0%) were administered filgrastim 10 mg/kg/day (filgrastim group), 18 patients (32.1%) were administered a standard regime with ifosphamide + etoposide + epirubicin + filgrastim 5 mg/kg/day or cyclophosphamide + etoposide + filgrastim 5 mg/kg/day (standard group), and 10 patients (17.9%) were administered a salvage regime + filgrastim 5 mg/kg/day (salvage group). Rituximab was added if the disease was CD20 positive. The median number of CD34+ cells and the number of inadequate collection did not differ between these 3 groups. Transplantation before mobilization was found to have a negative effect on the harvesting success. The transplantated patients had a lower number of harvested CD34+ cells than the patients without transplantation history. But no clear relationship was seen between harvest success and the diagnosis of the patients, pretransplant response, radiotherapy history before mobilization, or mobilization with a standard regimen. Finally, the number of standard CT cycles before mobilization were found to have a borderline negative effect on the harvested CD34+ cells.

Ankaferd is a folkloric medicinal plant extract which has historically been used as an hemostatic agent in traditional Turkish medi- cine. Ankaferd Hemostat (ABS, Ankaferd BloodStopper®) includes the plants of Thymus vulgaris, Glycyrrhiza glabra, Vitis vinifera, Alpinia officinarum and Urtica dioica. The hemostatic effects of ABS have been established in the in vitro and in vivo studies in the Literature. The basic mechanism of action for ABS is the formation of an encapsulated protein network representing the focal points for the vital erythroid aggregation. The topical usage of ABS as a hemostatic agent in clinical hemorrhages and during dental inter- ventions provided the first clues about the safety and efficacy of ABS in humans. The aim of this study is to search topical safety of ABS in a phase I randomized, double-blinded, cross-over, placebo controlled clinical study in healthy volunteers. Twenty-four healthy volunteers (11 males and 13 females, aged 18-44 years) compatible with the study protocol were enrolled into the study. In this study, topical ABS application for 120 minutes is not different from the placebo, in terms of both the local skin findings and systemic laboratory tests. Based on those data, it is concluded that topical application of ABS is safe and tolerable in humans.

Multiple myeloma (MM) represents a malignant proliferation of plasma cells in bone marrow. The prognosis is highly variable and mar- kedly affected by a number of prognostic features. We aimed to determine the relationship between conventional cytogenetics and FISH (del13q, del17p, t(11;14), t(4;14)) findings and other prognostic factors in MM. In our study, we investigated the frequencies and the types of cytogenetic abnormalities in 50 MM patients. The most common chromosomal abnormality was hypodiploidy ob- served in 40.5% of 42 patients (17/42) screened with conventional cytogenetic analysis. Del 13q was detected in 37.5% of 48 pa- tients (18/48)) screened with fluorescence in situ hybridization (FISH). 29 patients were investigated for del 17p, t(11;14), and t(4;14). Del 17p was detected in 3 (10.3%), t(11;14) in 7 (24.1%), t(4;14) in one (3.4%) of them. "International Staging System" (ISS) stage was increased as the "Durie-Salmon" (DS) stage increased. We didn't find a relationship between the cytogenetic abnormalities that we studied and DS or ISS stages.

In this case report we overview the diagnostic and therapeutic approaches for pleural effusions encountered during the tre- atment and follow-up of patients with myeloma in the light of the current medical literature. A 73-year-old female patient with a stage IIIA multiple myeloma was being treated with melphalan and methyl prednisolone. In the third month of the treat- ment, she had complaints of coughing, dyspnea and right side pain. Computed tomographic examination of the thorax re- vealed pleural effusion. Pathological examinations of the pleural fluid and pleural biopsy specimen were compatible with ade- nocarcinoma. Repeated examinations did not reveal a progression in myeloma or a pleural involvement of myeloma. The pa- tient died of respiratory insufficiency due to the progression of the pleural adenocarcinoma.

Multiple myeloma has been associated with the development of thromboembolic events. Thrombin activatable fibrinolysis inhibitor (TAFI) is a carboxypeptidase B-like proenzyme, which potently inhibits fibrinolysis. The purpose of the present study was to assess the TAFI levels in patients with newly diagnosed multiple myeloma. Twenty-seven newly diagnosed multiple myeloma patients (16 women and 11 men) and 27 age-matched healthy individuals (14 women and 13 men) were included in the study. Serum TAFI levels were significantly increased in patients with multiple myeloma (46 ± 13. 3 vs. 36. 6 ± 9.7 μg/ml) compared with healthy individuals. Serum TAFI levels were negatively correlated with serum albumin (CC: -0.453, P < 0.05) and hemoglobin levels (CC: -0.392, P < 0.05) and positively correlated with the β-2 microglobulin levels (CC: 0.524, P < 0.05). In this study, we observed significantly elevated TAFI levels in patients with multiple myeloma and higher serum TAFI levels were suggested to be associated with higher disease stage. With these results, a possible role of elevated TAFI levels in thromboembolic manifestations in the course of multiple myeloma can be suggested.

Pseudothrombocytopenia (PTCP) is a laboratory event of platelet clustering related to drugs used for anticoagulation. This condition is engendered by autoantibodies against platelets in usually EDTA-anticoagulated blood. Pseudothrombocytopenia has no clinical significance but when evaluated as true thrombocytopenia, this misconception may lead to unnecessary diagnostic procedures. Heparin-induced thrombocytopenia with thrombosis (HITT) is a complication of heparin treatment caused by heparin platelet factor 4 (HPF-4) antibodies, leading to platelet activation and hypercoagulability. In our study, 48 patients with PTCP and 36 healthy volunteers were included. Heparin platelet factor 4 antibody positivity was detected in 12 patients from PTCP group; nobody from control group had. Citrated serum samples and peripheral blood smears showed normal platelet count. Of the 4 patients using heparin derivative, 1 (2.1%) had antibody positivity but without any bleeding symptoms. In conclusion, HPF-4 antibody positivity might be a risk factor for PTCP. Clinicians should be aware of this kind of condition.

Inherited thrombophilia may cause important complications in pregnancies including maternal death, early and late pregnancy loss, preeclampsia, intrauterine growth restriction and placental abruption. This study was developed to investigate the fetal loss and successful birth rates in hereditary thrombophilic patients treated with low-dose acetylsalicylic acid and low molecular weight heparin to determine the necessity and effectiveness of this treatment. Ninety-three patients with the history of recurrent pregnancy loss or thromboembolism were included in this study. Eighty milligram acetylsalicylic acid treatment was started just after the diagnosis for the patients with hereditary thrombophilia, continued throughout pregnancy and ceased 3 days before the delivery. Low molecular weight heparin (LMWH) was started for the patients with the unsuccessful in-vitro fertilization (IVF) history, just after finishing the egg collection. For the other patients, LMWH was started after the positive result of the pregnancy test. Treatment was started for 67 (72%) of patients. Among the treated 67 patients, 38 had MTHFR C677T gene mutation, 25 had protein S deficiency, 19 had FV Leiden mutation, four had protein C deficiency, two had Prothrombin 20210A gene abnormality, two had antiphospholipid anticore syndrome and two had AT III deficiency. Fifty-seven (85.1%) of 67 patients under treatment had pregnancy. Forty-one (61.2%) of those 57 patients had a live birth, whereas 16 (23.9%) of them had abortus under treatment. In regression analysis, only protein C and S deficiencies were found to be independent risk factors. In conclusion, inherited thrombophilia should always be kept in mind as an etiological factor of recurrent abortus. With treatment, success rates are between 60 and 80%. Severe side effects due to treatment are rare. But randomized, double-blind, placebo-controlled studies are still necessary to evaluate the benefit of heparin and acetylsalicylic acid treatment in women with the history of inherited thrombophilia.

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.

OBJECTiVES: Oxidative stress plays a role in the pathogenesis of diabetic nephropathy. It has been reported in many studies that antioxidant therapy may decrease complications related to diabetes mellitus. We aimed to evaluate the protective effects of erdostein on diabetic renal injury in diabetic rats. maTERial and mETHOdS: Thirty rats were randomly divided into 5 experimental groups (Group 1: control, group 2: erdostein, group 3: alloxan, group 4: alloxan+erdostein, and group 5: alloxan+insulin, n=6 each). Rats were made diabetic using alloxan injection intraperiteonally. Erdostein (10 mg/kg/day) orally and insulin two times a day (3 g/kg) intraperitoneally were administered for four weeks. All rats were then sacrificed and kidney histopathological examinations were performed by light microscopy. RESulTS: The diabetic rats had diabetic nephropathic changes in the kidney on histological examination but the rats treated with erdostein showed significantly less histopathological changes, similar to the control group compared with the diabetic rats not treated with erdostein (p 0.05). COnCluSiOn: Based on the present data, we conclude that erdostein may show protective effects on renal injury due to diabetes mellitus. KEY WORdS: Diabetic nephropathy, Erdostein, Renal failure, Alloxan Yazisma Adresi: Faruk TuRGuT Fatih Universitesi Tip Fakultesi, Nefroloji Bilim Dali, Ankara, Turkiye Gsm : 0 505 642 17 12 E-posta : turgutfaruk@yahoo.com Gelis Tarihi : 07.06.2010 Kabul Tarihi : 25.08.2010 Faruk TuRGuT1 ayse CaRliOglu2 Rabia alKan3 derya aKdEnIz3 Hacer HalTas4 ozlem saHIn BalCiK5 Ebru uz1 omer Faruk KaRaTas6 1 Fatih Universitesi Tip Fakultesi, Nefroloji Bilim Dali, Ankara, Turkiye 2 Fatih Universitesi Tip Fakultesi, Endokrinoloji Bilim Dali, Ankara, Turkiye 3 Fatih Universitesi Tip Fakultesi, Ic Hastaliklari Anabilim Dali, Ankara, Turkiye 4 Fatih Universitesi Tip Fakultesi, Patoloji Anabilim Dali, Ankara, Turkiye 5 Fatih Universitesi Tip Fakultesi, Hematoloji Bilim Dali, Ankara, Turkiye 6 Fatih Universitesi Tip Fakultesi, Uroloji Anabilim Dali, Ankara, Turkiye Turgut F ve ark: Diyabetik Nefropatide Erdostein Etkisi Cilt/Vol: 19, No: 3, 2010, Sayfa/Page: 157-161 158 Turk nefroloji diyaliz ve Transplantasyon dergisi Turkish Nephrology, Dialysis and Transplantation Journal

The plasminogen activator system consists of the serine protease urokinase plasminogen activator (uPA), two endogenous inhibitors of PAI-1 (plasminogen activator inhibitor-1) as well as the PAI-2 and uPA receptor (uPAR or CD87). The aim of this study was to determine the significance of flow cytometry and CD87, CD45 and CD56 expressions in the diagnosis, follow-up and prognosis of multiple myeloma (MM).Twenty-nine MM patients were included in the study. Bone marrow samples were used for flow cytometry. A panel of CD87, CD45, CD56, CD10, CD19, CD20, CD38, and CD138 was tested by flow cytometry.CD87 was negative in 8 (27.5%) cases, dim positive in 9 (31.1%) and bright positive in 12 (41.4%). CD87 expression was significantly higher in CD45 (-) cases.Flow cytometry has a significant role in the diagnosis and prognosis of MM. Further clinical studies including large numbers of patients are needed to determine the prognostic role of CD87 in MM.AMAÇ: Plazminojen aktivatör sistemi; serin proteaz ürokinaz plazminojen aktivatörü (uPA), iki endojen inhibitörü PAI-1 (plazminojen aktivatör inhibitör-1) ve PAI-2 ile uPA reseptöründen (uPAR veya CD87) oluşmaktadır. Bu çalışmada MM tanı, takip ve prognozunda akım sitometri metodunun ve CD87, CD45, CD56 ekspresyonunun önemini belirlemek amaçlanmıştır. YÖNTEMLER: Çalışmaya 29 MM hastası alındı. Akım sitometri için kemik iliği örneği kullanıldı. Hastalara akım sitometri yöntemi ile CD87, CD45, CD56, CD10, CD19, CD20, CD38, CD138’i içeren panel çalışıldı.Çalışmamızda CD87; 8 (% 27.5) olguda negatif, 9 (% 31.1) olguda zayıf pozitif, 12 (% 41.4) olguda ise kuvvetli pozitif bulundu. CD 45 (-) olgularda CD 87 ekspresyonu anlamlı olarak yüksek bulundu. SONUÇ: Akım sitometri MM tanısı ve prognozu belirlemede önemli role sahiptir. MM’da CD87 ekspresyonunun prognostik rolünü belirlemek için çok sayıda hasta içeren daha fazla klinik çalışmaya ihtiyaç vardır.

The increased risk for thrombosis is known as hypercoagulability or thrombophilia. Here, we investigated risk factors for thrombophilia which were screened in young adult patients presenting with thrombotic events or with recurrent abortions with unknown etiology. A total of 115 patients aged between 16 and 50 years who were found to harbor thrombophilia were retrospectively evaluated. The laboratory investigations performed for the assessment of thrombophilia included protein C, protein S, antithrombin III deficiencies, activated protein C resistance, factor V Leiden (FVL), prothrombin 20210A (PT 20210) and methylenetetrahydrofolate reductase (MTHFR) gene mutations, factor VIII elevation, lupus anticoagulant and antiphospholipid antibodies (APA). In 66% of the cases a single thrombophilic defect was identified while some of the patients had combined thrombophilic defects. The most common thrombophilic defect was mutation in the MTHFR gene, and was followed by FVL mutation, the presence of APA and PT 20210 gene mutation, respectively. The patients were divided into two different age groups, 16-35 and 36-50 years, and arterial thrombosis was more common in the older age group. Our results indicated that some important thrombophilic defects such as gene mutations may appear in young adult patients presenting with thrombotic events.

The colon and rectum are rare sites of malignant lymphoma, observed in frequency after adenocarcinoma and carcinoid tumors. In this article, a case with mantle cell lymphoma presenting with chronic diarrhea and with a simultaneous diagnosis of multiple myeloma is presented together with a review of the related cases in the literature., Kolon ve rektum malign lenfomaları nadir olup, adenokarsinom ve karsinoid tümörlerden sonra görülmektedir. Bu makalede kronik diyare nedeni ile başvuran ve mantle cell lenfoma ile eş zamanlı multiple myelom tanısı almış olan vakayı literatür bilgileri eşliğinde sunduk.

Objectives: The aim of this study was to determine the thrombophilic risk factors and their frequency among women with history of recurrent abortion and a detected thrombophilic defect. Materials and methods: In this study, 41 women with history of recurrent abortion, who have one or more detected thrombophilic defects including protein S, protein C, antithrombin deficiency, activated protein C resistance (APC-R), factor V Leiden (FVL), prothrombin G 20210A (PTG), methylenetetrahydrofolate reductase (MTHFR) C677 T gene mutation, antiphospholipid antibodies and elevated levels of factor VIII were retrospectively investigated. Results: The most common detected thrombophilia defect (53.7%) was MTHFR gene mutation. While 22 of 41 patients (53.7%) had more than one concomitant defect, 20 of them had two concomitant defects and the remaining had three defects. Conclusion: MTHFR gene mutation, alone and/or with, concurrent thrombophilic defects was the most frequent factor for hereditary thrombophilia among our patients with a history of recurrent abortion., Amaç: Bu çalışmada, tekrarlayan düşük nedeni ile hematoloji polikliniğine başvuran ve en az bir trombofilik defekt saptanan kadınlarda trombofilik risk faktörleri ve sıklığını değerlendirmek amaçlanmıştır. Gereç ve yöntem: Bir ya da daha fazla trombofilik defekt (protein S eksikliği, protein C eksikliği, antitrombin, aktive protein C direnci (APC-R), faktör V Leiden (FVL), protrombin G 20210A (PTG), metilentetrahidrofolat redüktaz (MTHFR C677 T) gen mutasyonları, antifosfolipid antikorları (antikardiyolipin antikoru IgM ve IgG, lupus antikoagülanı) varlığı ve Faktör VIII yüksekliği) ve tekrarlayan abortus öyküsü olan 41 olgu geriye dönük olarak araştırıldı. Bulgular: En sık saptanan trombofilik defekt %53.7 MTHFR 677T mutasyonu idi. Kırk bir hastanın 22'si (%53.7) (n:22; 20 ikili, 2 üçlü defekt) birden fazla defekti aynı anda birlikte taşımaktayken, 20'si aynı anda iki, geri kalanı üçlü defekte sahipti. Sonuç: Hasta grubumuzda MTHFR gen mutasyonu tek ve/veya diğer trombofilik faktörlerle kombine olarak, tekrarlayan abortuslu hastalarda en sık rastlanan herediter trombofili etkeni olarak saptandı.

Thrombophilia is defined as the general name for a group of genetic and acquired situations, arising from defects of hemostasis mechanism and generating tendency to thrombosis. Examples of the acquired risk factors that increase the tendency to thrombosis are venous catheters, sepsis, surgery, hyperlipidemia, congestive heart disease, increased lipoprotein a, old age, antiphospholipid syndrome, nephrotic syndrome, hyperviscosity, chronic myeloproliferative neoplasms, paroxysmal nocturnal hemoglobinuria, heparin induced thrombocytopenia, vasculitis, immobility, obesity, major surgery, trauma, burns, malignancy, pregnancy and oral contraceptive usage. Genetic tendency to venous thromboembolism in early ages, even without any known cause, is named as thrombophilia. Factor V Leiden, prothrombin G20210A, methylenetetrahydrofolate reductase gene mutations, factor VIII elevation, protein C, protein S and antithrombin deficiency parameters are suggested for evaluation, in patient groups suspected of inherited thrombophilia. Detection of inherited thrombophilic factors in selected patient groups is a guide in developing treatment strategies and in establishing prognosis. Due to the genetic heterogeneities, each society should determine their thrombophilic risk pool. Thus, with the determination of the risk factors, unnecessary assessments will be prevented and a cost-effective approach can be developed., Trombofili, hemostaz mekanizmalarındaki bozukluktan kaynaklanan ve tromboza eğilim oluşturan bir grup kalıtsal ve kazanılmış durumun genel adı olarak tanımlanmaktadır. Tromboza eğilimi artırdığı bilinen kazanılmış risk faktörleri olarak santral venöz kataterler, sepsis, cerrahi, hiperlipidemi, konjestif kalp hastalığı, artmış lipoprotein a, yaşlılık, antifosfolipid sendrom, nefrotik sendrom, hiperviskozite, kronik miyeloproliferatif neoplazmlar, paroksismal nokturnal hemoglobinüri, heparine bağlı trombositopeni, vaskülit, immobilite, obesite, büyük cerrahi girişim, travma, yanık, malignite, gebelik ve oral kontraseptif kullanımı sayılabilir. Genç yaşta bilinen bir neden olmaksızın venöz tromboemboliye genetik yatkınlık, kalıtsal trombofili olarak tanımlanmaktadır. Faktör V Leiden, protrombin G20210A, metilentetrahidrofolat redüktaz gen mutasyonları, faktör VIII yüksekliği, protein C, protein S and antitrombin eksikliği parametrelerinin kalıtsal trombofili düşünülen hasta gruplarında araştırılması önerilmektedir. Kalıtsal trombofilik etkenlerin seçilmiş hasta gruplarında saptanmaları tedavi stratejileri geliştirmede ve prognozda yol gösterici olmaktadır. Her toplum genetik heterojenite nedeni ile kendi trombofilik risk havuzunu belirlemelidir. Bu şekilde trombofilik risk faktörlerinin belirlenmesi gereksiz tetkik istenmesini engelleyecek ve maliyet-etkin bir yaklaşım geliştirilebilecektir..

An elevated platelet count is a common finding in both hospitalized and ambulatory patients. Thrombosis and bleeding complications are more frequently observed in patients with clonal thrombocytosis than secondary thrombocytosis. The aim of this study was to investigate the behaviors of thrombin-activatable fibrinolysis inhibitor (TAFI) activity, the inhibitor of fibrinolysis, and also prothrombin time (PT), active partial thromboplastin time, and D-dimer and fibrinogen levels in 21 patients affected with clonal thrombocytemia as compared with 21 patients with reactive thrombocytosis and 21 healthy controls. In the clonal thrombocytemia group, plasma levels of TAFI activity were significantly higher than in both the reactive thrombocytosis and the control group. Plasma levels of leukocyte and platelet counts were significantly higher in the clonal thrombocytemia group than in the other two groups and also higher in the reactive thrombocytosis group than in the control group, which was also significant. Fibrinogen and D-dimer levels were higher in patients than in the control group but showed no significant difference between the clonal and secondary thrombocytosis groups. Plasma levels of PT and aPTT were higher in secondary thrombocytosis group than the clonal thrombocytosis group. The results of this study showed for the first time that TAFI activity is increased in patients with clonal thrombocytosis. These increased levels in clonal thrombocytosis can be considered a factor to explain the thrombotic tendency in myeloproliferative disorders.

Inflammation, which is extremely useful process for humanbody is the response of living vascular tissues topathological phenomena that removes the pathogens andinitiates the healing procedure. Microorganisms, physicaltrauma, chemical, mechanical, irradiation, or thermal injury,ischemia and immune reactions are most commoncauses of this exceptionally important event for humanbody. Platelets are non-nucleated cells in blood that producedin bone marrow as derived from megakaryocytes.Apart from stop bleeding and achieving hemostasis thereare incredibly important roles of platelets in inflammation.Platelets contain important mediators for inflammationlike neutrophils or macrophages and can alter the courseof mechanism. In this article changing platelet function ininflammation and the effect of these functions to the processof inflammation will be discussed.Key words: Platelet, inflammation, cytokines

Erythropoietin, the major humoral regulator of red cell production, was reported to stimulate various levels of megakaryocytopoiesis. We investigated levels of thrombopoietin (TPO) and erythropoietin (EPO) in patients with reactive thrombocytosis (RT) and clonal thrombocytosis (CT). 17 patients with RT and 18 patients with CT and 15 healthy subjects were enrolled into the study. TPO levels were higher in both patient groups than the controls. EPO levels were significantly higher than these in reactive thrombocytosis and in controls (p < 0.05). We suggest that besides TPO, EPO may play an important role in the pathogenesis of RT.

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.

Nonalcoholic fatty liver disease (NAFLD) is an important cause of liver failure. Whatever its cause, the liver failure is accompanied by multiple changes in the hemostatic system. The objective of the current report was to study several homeostasis parameters such as protein C, protein S, factor 7, factor 8 levels, platelet counts, prothrombin time and activated partial thromboplastin time, and plasminogen activator inhibitor in patients with fatty liver. A total of 28 consecutive patients with ultrasound proven NAFLD and 33 healthy volunteers were included in the study. Plasma prothrombin time and activated partial thromboplastin time were within normal ranges in both NAFLD and control groups. Plasma factor 7, factor 8, protein S, and protein C levels were decreased in NAFLD patients but the difference was not statistically significant, whereas plasminogen activator inhibitor 1 levels were significantly increased in patients with NAFLD compared to controls. In conclusion, in all types of liver disease, some alterations in hemostatic parameters are awaited. As fatty liver disease is very common in clinical practice, clinicians should be aware of this kind of alterations.

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.

A bone implant should integrate to the tissue through a bone-like mineralized interface, which requires increased osteoblast activity at the implant-tissue boundary. Modification of the implant surface with synthetic bioinstructive cues facilitates on-site differentiation of progenitor stem cells to functional mature osteoblasts and results in subsequent mineralization. Inspired by the bioactive domains of the bone extracellular matrix proteins and the mussel adhesive proteins, we synthesized peptide nanofibers to promote bone-like mineralization on the implant surface. Nanofibers functionalized with osteoinductive collagen I derived Asp-Gly-Glu-Ala (DGEA) peptide sequence provide an advantage in initial adhesion, spreading, and early commitment to osteogenic differentiation for mesenchymal stem cells (hMSCs). In this study, we demonstrated that this early osteogenic commitment, however, does not necessarily guarantee a priority for maturation into functional osteoblasts. Similar to natural biological cascades, early commitment should be further supported with additional signals to provide a long-term effect on differentiation. Here, we showed that peptide nanofibers functionalized with Glu-Glu-Glu (EEE) sequence enhanced mineralization abilities due to osteoinductive properties for late-stage differentiation of hMSCs. Mussel-inspired functionalization not only enables robust immobilization on metal surfaces, but also improves bone-like mineralization under physiologically simulated conditions. The multifunctional osteoinductive peptide nanofiber biointerfaces presented here facilitate osseointegration for long-term clinical stability. © 2014 American Chemical Society.

The widespread usage of blood count autoanalyzers has led to a major improvement in cellular hematology because of quick and accurate results found in most instances. However, spurious test results also can be observed like pseudothrombocytopenia (PTCP). In our study, we aimed to evaluate the clinical and laboratory factors associated with PTCP. Forty-six patients with PTCP and 69 healthy volunteers were enrolled in the study. Sex distribution was similar between the groups. Hospitalization, infection, the use of low-molecular-weight heparin and pregnancy increased the incidence of PTCP. Atherosclerosis and some drugs such as warfarin and calcium channel blockers were associated with PTCP, but the coincidence was not statistically significant. Antinuclear antibody positivity was higher in PTCP group (18.8% vs 7.2%; P=0.033) but anticardiolipin positivity rates were similar when compared to controls. Pseudothrombocytopenia was frequently misdiagnosed, which led to inappropiate treatments. Therefore, this situation should be kept in mind.

Introduction: Angiotensin converting enzyme (ACE) is a circulating enzyme that participates in the body's renin-angiotensin system (RAS) and is localized on the endothelial cell surface in the lung and other vascular beds. It catalyses the conversion of decapeptide angiotensin I to octapeptide angiotensin II. In the present study, we aimed to analyse the possible relationship between the levels of ACE in the context of RAS in multiple myeloma (MM) pathogenesis. Materials and methods: The study was conducted on 25 MM patients (13 males, 12 females; median age 66 years, range 47-88) and 20 healthy controls. The clinical features of MM patients including demographics and laboratory findings were summarized. Serum ACE levels were measured by using commercially available kits. Results: The serum ACE levels of MM patients and controls were 32.60 +/- 20.26 and 15.35 +/- 6.47 respectively. Serum ACE levels were significantly higher in MM patients compared with control groups (p

The aim of this study was to evaluate mean platelet volume (MPV), thrombopoietin (TPO), and platelet levels in patients with ischemic stroke and compare this with healthy controls.We prospectively studied 50 patients with ischemic stroke and compared them with 37 control participants who have evaluated in internal medicine polyclinic and had no history of cerebrovascular events. All patients were within 24 hours after stroke; MPV and TPO were measured on admission.Both TPO and MPV values were significantly higher in patients with stroke (P = .00; P = .001).Increased TPO levels may increase both platelet count and platelet size, resulting in more hemostatic tendency, which may contribute to the progression of ischemic stroke.

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.

Chronic lymphocytic leukemia (CLL) is a clonal lymphoproliferative disease characterized by clonal expansion of B lymphocytes. Richter Transformation (RT) must be considered if CLL patient had fever, weight loss, cytopenia and resistance to standard therapy. Despite CLL usually transforms to diffuse large cell lymphoma, some rare lymphomas may occur as RT such as Hodgkin variants, lymphoblastic lymphoma nad mantle cell lymphoma. Here, we report a case of Mantle cell lymphoma has become secondary to chronic lymphocytic leukemia due to its being a rare entity. J Clin Exp Invest 2011; 2 (4): 443-445

Primary effusion lymphoma (PEL) is a rare type of non-Hodgkin lymphoma that presents with serosal effusion in body cavities, without obvious tumor masses. Although PEL occurs in immunocompromised patients that are human immunodeficiency virus (HIV) positive, it also occurs in immunocompetent human herpes virus-8 (HHV-8)-positive patients. Herein we present an immunocompetent, HIV-negative, CD-20-negative, HHV-8-positive patient with pleural effusion that was diagnosed as PEL. The CHOP protocol and talc pleurodesis were administered. HHV-8 plays a causative role in PEL and is important for differentiating PEL from other types of lymphoma. As such, in addition to pleurodesis antiviral treatment should be considered for optimal treatment outcome.None declared.Primer efüzyon lenfoması (PEL) vücut boşluklarındaki seröz zarlarda tümör kitlesi olmaksızın, sadece serozal effüzyonla karakterize, nadir görülen bir hodgkin dışı lenfomadır. PEL immünsupresif ve özellikle HIV pozitif olgularda görülmekle birlikte Human herpes virus-8 (HHV-8) pozitif immün sistemi sağlam olgularda da tespit edilmektedir. Bu olguda immünkompetan, HIV negatif, plevral effüzyonu olan HHV-8 pozitif, primer effüzyon lenfomalı erkek hasta sunulacaktır. HHV-8 pozitif CD-20 negatif PEL olgumuzda tedavide CHOP protokolü ve talk plörodezis uygulandı. HHV-8 pozitifliği PEL tanı ve ayırıcı tanısında önemli role sahiptir. Bu yüzden, PEL tedavisinde plörodezise ek olarak antiviral tedavinin uygulanmasıyla başarılı sonuçlar elde edilebileceği düşünülmektedir.

[No abstract available]

Dear Editor,The myeloproliferative disorders (MPDs) constitute a subcategory of chronic myeloid disorders and include chronic myeloid leukemia (CML), essential thrombocytemia (ET), polycythemia vera (PV) and myelofibrosis (MF). In 1960, the discovery of the Philadelphia chromosome (Ph) became a cornerstone in CML treatment and led to the development of moleculary targeted therapy. Recently, an acquired mutation in the Janus kinase 2 (JAK2) gene has been discovered in nearly all patents with PV and approximately half of the patients with primary MF and ET. Subsequently, the mutation has been demonstrated in atypical MPDs (chronic neutrophilic leukemia, unclassified), de novo myelodysplastic syndrome or acute myeloid leukemia.1 It has been hoped that targeted inhibition of JAK2V617F should achieve similar disease control as thyrosine kinases has produced in CML.

Chronic myeloproliferative disorders such as polycythemia vera (PV), essential thrombocytosis (ET), and idiopathic myelofibrosis arise from clonal proliferation of neoplastic stem cells in the bone marrow. Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that have potential to degrade all types of extracellular matrix (ECM) and also play a role in remodeling of the ECM. It is known that MMPs play a role in bone marrow remodeling. The primary goal of our study is to explore the relationship between chronic myeloproliferative diseases and some of MMP gene polymorphisms. The demonstration of a relationship will help to understand whether these polymorphisms may be a potential early diagnosis marker of the diseases. Patients were selected from outpatient clinics of Turgut Ozal University Hospital, Ankara, Turkey, between December 2010 and May 2011. Twenty-eight patients that previously diagnosed and followed-up with PV, 17 with secondary polycythemia (SP), and 12 with ET were enrolled in the study, along with a control group of 22 healthy people. DNA was isolated from peripheral blood. Using polymerase chain reaction–restriction fragment length polymorphism method, MMP2 and MMP9 gene polymorphisms were analyzed with agarose gel electrophoresis. There was a statistically significant difference between the study groups and the control group in terms of Gln279Arg polymorphisms rates of MMP9. The highest MMP9 Gln279Arg polymorphism rate was observed in the ET group. But nobody from the control group had polymorphic MMP9. There was no statistically significant difference between the groups in terms of MMP2-735 C > T polymorphism rates. In conclusion, MMP9 gene Gln279Arg polymorphism was associated with ET, SP, and PV diseases. Hence, we believe that these gene polymorphisms may play a role in the mechanism of bone marrow fibrosis and may be a factor that increases the risk of thrombosis. Illumination of the molecular basis of the relationship between MMP-thrombosis and MMP-fibrosis provides a better understanding of the pathophysiology of PV and ET diseases and will allow new approaches to diagnosis and treatment.