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A 73-year-old woman with an 11-year history of type 2 diabetes mellitus and hypertension was admitted to hospital because of acute confusion. Laboratory analysis showed severe hyponatremia with a serum sodium concentration of 109 mEq/L. No edema was found in her extremities. Neurologic examination revealed no abnormalities. She had been taking pioglitazone for 4 months. Sodium level was normal before the start of pioglitazone. Her blood pressure was 150/90 mm Hg. Serum and urine osmolalities were 245 and 613 mOsm/kg, respectively. Thyroid function tests, plasma corticotropin, and serum cortisol concentrations were normal. Clinical history and laboratory findings suggested that the cause of the severe hyponatremia was the syndrome of inappropriate antidiuretic hormone secretion caused by pioglitazone therapy. After withdrawal of pioglitazone, she was treated with infusion of hypertonic saline (3% sodium chloride, 300 mL/24 h) for 3 days. The patient's sodium concentration increased gradually and the clinical situation improved rapidly. Her serum sodium returned to nearly normal ranges within 1 week and she was discharged.

Background One of the option for reconstruction of segmental mandibular defect is the vascularized free fibular flap. However, difference in height between mandible and fibula causes aesthetic and functional problems. But lack of a flap wide enough to completely fill the mandibular defect is an important disadvantage for us(1). The double barrel fibula flap has been useed to eliminate this disadvantage, but this flap is too large(2-4). A piece of non-vascularized residual fibula have used as graft in addition to vascularized fibula flap(5). We designed one and a half barrel vascularized free fibular flap to overcome the disadvantages of both techniques. Methods Eight centimeter length mandibular body segment was excised because of giant cell reparative granuloma diagnosis. Vascularized fibular flap was harvested and shaped as follows. A small piece of bone (segment B) was removed at the middle of the flap to fold the flap (Figure 1). The distal half of the flap had been splitted longitidunally, and the bone segment away from the perforator vessels (segment D) were removed. And then two remaining fibula segments were folded, and placed in parallel to each other in the defect (Figure 2). Results The flap has survived. Radiography revealed bone healing between the fibula and mandible. Conclusions One and a half barrel technique may be a good solution for incompatibility of the sizes of the segmental mandibular defect and the vascularized fibula flap. This technique eliminates volume insufficiency of the classical technique, and volume excess of the double-barrel technique. One and a half vascularized fbula flap perfect fit for mandibular defect. Figure 1. Schematic drawing of the flap (arrow is showing the direction of the folding) Figure 2. The final view of the flap in the defect. References 1. Chang YM, Tsai CY, Wei FC. One-stage, double-barrel fibula osteoseptocutaneous flap and immediate dental implants for functional and aesthetic reconstruction of segmental mandibular defects. Plast Reconstr Surg. 2008;122(1):143-5. 2. Jones NF, Swartz WM, Mears DC, Jupiter JB, Grossman A. The "double barrel" free vascularized fibular bone graft. Plast Reconstr Surg. 1988;81(3):378-85. 3. Horiuchi K, Hattori A, Inada I, et al. Mandibular reconstruction using the double barrel fibular graft. Microsurgery. 1995;16(7):450-4. 4. Bahr W, Stoll P, Wachter R. Use of the "double barrel" free vascularized fibula in mandibular reconstruction. J Oral Maxillofac Surg. 1998;56(1):38-44. 5. Lee JH, Kim MJ, Choi WS, et al. Concomitant reconstruction of mandibular basal and alveolar bone with a free fibular flap. Int J Oral Maxillofac Surg. 2004;33(2):150-6. Disclosure/Financial Support None of the authors has a financial interest in any of the products.

e22227 Background: Thromboembolism is frequent in patients with cancer. Although it is known that several acquired factors take place in this process, the role of the genetic factors is controversial. In this study we analysed the most common genetic polymorphisms which have a role in the development of thrombosis. Methods: Study population consists of 292 (158 with thrombosis and 134 without thrombosis) patients treated between 2004 and 2008. Thrombosis was diagnosed by clinically and radiological measures in any time during the course of disease. Factor V Leiden G1691A, Prothrombin G20210A, Methlene Tetra Hydrofolate Reductase (MTHFR) C677T and Plazminogen Activator Inhibitor (PAI-1) 4G/5G were analysed with PCR-RFLP (Polymerase Chain Reaction- Restriction Fragment Length Polymorphism). Results: In the study group 48 and 1 patient had heterozygot and homozygot polymorphism for Factor V Leiden G1691A respectively. In the control group 32 heterozygot and 1 homozygot polymorphism and there was no statistically significant differents between study and control group (p=0,462).For Protrombin G20210A 11 and 4 heterozygot polymorphism were observed in control and study group respectively. While there was 1 homozygot polymorphism in study group there was no in control group and the difference between two groups was not statistically significant (p=0,198). For MTHFR C677T, 48 and 24 heterozygot polymorphism, 15 and 12 homozygot polymorphism were observed in study and control group respectively. The difference between two groups were statistically significant (p=0,04). There was no statistically significant difference between two groups for PAI-1 4G/5G polymorphisms (p=0,362). In subgroup analyses, statistically significant difference was found only in MTHFR C677T polymorphism in patients with GI cancer and with and without thrombosis (p=0,028). Conclusions: The studies investigating the relationship between genetic factors and thrombosis revealed controversial results. However, we found no genetic factor relevant to thrombosis other than MTHFR C677T polymorphism. Further studies investigating genetic and acquired factors in the development of the thrombosis in detail are warranted for documenting clearly the role of genetic polymorphisms. No significant financial relationships to disclose.

Pituitary consequences of chronic head trauma in boxing have not been investigated in detail.To investigate the pituitary function in retired or active amateur boxers.Cross-sectional, observational study.Turkey.61 actively competing (n = 44) or retired (n = 17) male boxers of the Turkish National Boxing Team.Body composition variables, pituitary volume (in 38 of 61 boxers), and pituitary function.9 of 61 boxers (15%) had growth hormone (GH) deficiency and 5 of 61 boxers (8%) had adrenocorticotropic hormone deficiency. All boxers with GH deficiency except 1 were retired from boxing. Of 17 retired boxers, 8 (47%) had GH deficiency. Retired boxers with GH deficiency had significantly lower pituitary volume than retired boxers with normal GH.Pituitary volume was measured in only 38 of 61 boxers, and the study had no comparison group.This study suggests that retired boxers have a high rate of pituitary dysfunction. Therefore, investigation of pituitary function in boxers, particularly retired ones, is recommended.

Monitoring of multiple myeloma patients during and after treatment for the presence of remaining myeloma cells (minimal residual disease, MRD) has been shown to give major insight into the effectiveness of treatment. However, so far applicabile genetic markers amenable to sensitive detection by PCR for MRD in myeloma patients. Previouse studies showed that Wilms tumor gene (WT1) expression level, measured by quantitative reverse transcriptase polymerase chain reaction (RT-PCR), was useful as an indicator of minimal residual disease in leukemia and myelodysplastic syndrome. In this study was to measure, by real-time polymerase chain reaction, levels of WT1 expression, in order to find a possible association between this gene and the minimall residual disease. We investigated peripheral blood WT1 expression level in 41 newly diagnosed multiple myeloma cases using quantitative reverse transcriptase polymerase chain reaction. All patients carried normal WT1-mRNA levels. WT1 expression analyse may be not useful genetic marker for monitoring MRD in routine clinical use of multiple myeloma patients.