1. European Federation of Internal MedicineAbstracts Book7 CongressthRome, Italy, Aurelia Convention Centre & ExpoMay, 7-10, 2008

2. European Federation of Internal MedicineScientific SecretariatG. LicataG. Gasbarrini, M.D. CappelliniG. Parrinello, A. Pinto, R. Scaglione, A. TuttolomondoSociet Italiana di Medicina Interna - SIMIViale dellUniversit 25 00185 Rome (Italy)Phone (+39) 06 44340373 Fax (+39) 06 44340474Presidents of the Congress Council of the Italian SocietyG. Licata Italyof Internal Medicine (SIMI)G. Gasbarrini ItalyG. Abbita Erice M.D. Cappellini MilanoHonorary PresidentsG.R. CorazzaPaviaU. CarcassiItaly G. Crippa PiacenzaF. DammaccoItaly A. DAvanzo AvellinoM. Sangiorgi Italy R. LauroRoma G. Licata PalermoSteering Committee G. MancusoLamezia TermeW. BauerSwitzerlandE. MannarinoPerugiaC. Davidson EnglandP.M. Mannucci MilanoJ.W.F. Elte The NetherlandsV. Marigliano RomaF. Ferreira Portugal M.A. MontiMilanoG. Gasbarrini ItalyR. Nuti SienaG. Licata ItalyM. Pagani MilanoS. Lindgren Sweden G. Palasciano BariP.M. Mannucci ItalyF. Rossi FanelliRomaD. Sereni France A. SaccoMatera M.B. Secchi MilanoEFIM Executive Committee G. TraisciPescaraW. BauerSwitzerlandF. VioliRomaC. Davidson EnglandJ.W.F. Elte The NetherlandsSIMI Executive SecretaryF. Ferreira Portugal F. PepeRomaS. Lindgren SwedenD. Sereni France SIMI Administrative Secretary S. PescetelliRoma EFIM Assistant Secretary I. Huis in t Veld The NetherlandsOrganizing SecretariatAristea GenovaSalita di Santa Caterina 4 16123 Genoa (Italy)Phone (+39) 010 583224 Fax (+39) 010 5531544E-mail efim2008@aristea.com www.aristea.com/efim2008 3. SUMMARYORAL COMMUNICATIONSWednesday, May 7, 2008RHEUMATOLOGY 1PUBLIC HEALTH4Thursday, May 8, 2008CARDIOVASCULAR DISEASE 7PNEUMOLOGY11GASTROENTEROLOGY15HAEMATOLOGY AND ONCOLOGY19CLINICAL CASES23PUBLIC HEALTH 27MISCELLANEOUS 31CLINICAL CASES35Fryday, May 9, 2008IMMUNOLOGY39STROKE42HEART FAILURE 45HYPERTENSION48INFECTIOUS DISEASE51GERIATRICS55GASTROENTEROLOGY59ENDOCRINOLOGY, DIABETES, NUTRITION63Saturday, May 10, 2008ENDOCRINOLOGY, DIABETES, NUTRITION66CLINICAL CASES69CARDIOVASCULAR DISEASE72EMERGENCY MEDICINE75CLINICAL CASES78NEPHROLOGY83POSTER PRESENTATIONSWednesday, May 7, 200886Thursday, May 8, 2008143Friday, May 9, 2008201Saturday, May 10, 2008 257Summary Oral Communications316Summary Poster Presentations 322 4. Oral CommunicationsWednesday, May 7, 2008 RHEUMATOLOGY 5. 1. ISCHEMIC HEART DISEASE AS THE PRESENTING FEATURE OF TAKAYASU 2. PROLIFERATIVE MYOSITIS ARISING IN THE STERNOCLEIDOMASTOIDARTERITISMUSCLELorenzo Dagna, Fulvio Salvo, Emanuel Della Torre, Mattia Baldini, Enrica Bozzolo,Joaquin Campos-Franco, Nieves Mallo-Gonzalez, Raimundo Lopez-Rodriguez,Elena Baldissera, MariaGrazia SabbadiniPaula Barros Alcalde, Ihab Abdulkader, Rosario Alende-Sixto, Arturo Gonzalez-QuintelaTakayasus arteritis (TA) is an inflammatory disease that affects the aorta and/or its major branches. INTRODUCTION Proliferative myositis is an uncommon benign condition affecting skeletal mu-Cardiac involvement from TA is often underestimated: the heart can be directly involved by TAscle and characterized by the presence of ganglion-like giant cells within a myofibroblastic back-or be affected as a consequence of its systemic vascular manifestations. Primary cardiac involve-ground. Usually involves muscles of the trunk and extremities but the localization of this conditionment causing ischemic heart disease (IHD) can be the presenting feature of TA. We studied 60 in head and neck is rare. We report a case of proliferative myositis involving the sternocleidoma-consecutive patients (56F, 4M) with TA followed at San Raffaele Scientific Institute in Milan. Seven stoid muscle. CASE REPORT A 70-year-old woman was admitted to the hospital complaining of(6F, 1M, mean age 35.8 y) out of the 60 TA patients (11.7%) showed symptoms of IHD on pre- a five days painful mass in the neck. On physical examination, the patient was afebrile, with ansentation. Among them, 6 presented with exertion angina and 1 with an acute myocardial infar-arterial blood pressure of 115/70 mmHg, and showed a firm and painful mass of approximatelyction. A coronary angiography was performed in 6 patients and showed severe stenosis of both 2.5x1.5 cm arising from the sternal head of the right sternocleidomastoid muscle, just upon thecoronary ostia in 2 patients, whereas distal coronary artery stenoses were present in 3 patients;manubrium sterni. The rest of the physical examination was normal. A cervical and chest CT-scancoronary angiography was negative in a patient who had a positive ECG-stress test and a posi-showed a poorly demarcated enlargement of the right sternocleidomastoid muscle and there wastive stress myocardial perfusion study. The last patient had positive ECG- and myocardial perfu- no collection or lymphadenopathy. Adjacent bone was normal. A fine-needle-aspiration-biopsy ofsion imaging-stress tests, but didnt undergo a coronary angiography. Interestingly, none of the the mass was performed and cytological smears obtained from lesion showed two populations ofpatients had known risk factors for IHD (only one was a mild smoker). Other signs and symptoms cells, fat cells and amorphous metachromatic material. The most prominent feature of the smearof TA were recognized on presentation in 4 out of 7 patients and a diagnosis of TA was consi-was a population of large polygonal cells resembling ganglion cells. The second population ofdered. In the 3 remaining patients, other signs of vascular involvement appeared later: the mean cells was composed of smaller oval to spindle-shaped cells with oval or bacillary-shaped nuclei. Thedelay in diagnosing TA was 38.7 months. Three patients were treated with CABG, 1 with a PTCA pathological diagnosis of the mass was proliferative myositis. No adjuvant therapy was admini-with stenting, 1 with a proximal aortoplasty. The other 2 patients were diagnosed with TA on pre-stered. After three weeks, the mass decreased and nearly disappeared. Actually, the patient issentation and received immunosuppressive therapy, with a marked improvement in IHD mani- asymptomatic. DISCUSSION PM is a benign tumor of the soft tissue that may mimic malignancy.festations. TA can present with signs and symptoms of IHD in many patients. Even though TA isOccur primarily in adults between 30 and 70 years and is extremely rare in children. The etio-rare, a vasculitic etiology of IHD should be considered in particular in young females with no logy is unknown, but trauma has been proposed as a possible precipitating factor suggesting anknown risk factors. An early diagnosis could allow prompt treatment and prevent possible com-inflammatory mechanism. Supporting this hypothesis, approximately one third of patients reportsplications.a history of recent trauma to the affected area. It usually appears as a solitary (exceptionally mul- tiple)rapidly growing mass that may be painful. The lesion is generally firm, non tender, fixed to muscle underneath, and without inflammatory signs. PM may present in shoulder, trunk, thigh, and head and neck. Presentation of PM as a sternocleidomastoid mass is rare and in a recent re- view considering only the English-language literature, eight cases have been described. Local ex- cision is curative and following biopsy, the lesion usually disappears as in our case. Some cases of PM were confounded with sarcoma, attributed to the unusual cellularity and alarming rate of growth, and radical surgery were performed (occasionally in conjunction with lymphadenectomy, chemotherapy and radiation therapy), even with fatal consequences. Recurrence is extremely rare. The diagnosis can be made on needle aspiration cytology alone, as many authors proposed. Re- cognition of this condition is important in order to avoid a misdiagnosis of a malignant tumor, par- ticularly high-grade sarcoma. Consultation with an experienced pathologist, conservative management and a careful clinical evaluation (watch and wait policy) can spare unnecessary sur- gery in these patients. The case described here is unusual because of its location in the sterno- cleidomastoid muscle.3. DIAGNOSTIC UTILITY OF ANTI-CYCLIC CITRULLINATED PEPTIDE AND 4. THE INFLUENCE OF ADIPOKINES ON BONE MINERAL DENSITY INANTI-MODIFIED CITRULLINATED VIMENTIN ANTIBODIES IN RHEUMATOIDELDERLY MENARTHRITISStefano Gonnelli, Carla Caffarelli, Katie Del Santo, Alice Cadirni, Carmine Guerriero,Goksal Keskin, Ali Inal, Lek Keskin, Aysel Pekel, Ozan Baysal, Ufuk DizerLoredana Tanzilli, Stella Campagna, Ranuccio NutiPURPOSE: Several autoantibodies found in RA are directed to epitopes in citrullinated proteins.Body weight is commonly considered a significant predictor of bone mineral density (BMD). Adi-One of them is anti modified citrullinated vimentin (Anti-MCV). We tested the value a newly de-ponectin, an adipocyte-derived hormone, could modulate BMD. Moreover recent studies repor-veloped ELISA for the detection of antibodies againts a genetically modified citrullinated vimen-ted that ghrelin, an orexigenic peptide secreted by the stomach, is able to stimulate bonetin (anti-MCV) in comparison with an anti-CCP based ELISA system for the diagnosis of RA.formation. This study aimed to investigate whether there is any association between ghrelin levels,MATERIALS AND METHODS: Thirty-five patients with RA (mean age; 42.6 10.87 years, meanadiponectine levels, body composition and BMD in elderly men. We studied 117 men aged 55disease duration; 9.37 3.98 years) were enrolled in this study. Twenty five ankylosing spondylitisyears and older (mean age: 67.4 5.4 yrs) who were participating in an epidemiological(mean age; 35.88 6.64 years, mean disease duration; 10.25 4.61 years), and 19 healthy sub- study. In all subjects we evaluated ghrelin, adiponectin, parathyroid hormone (PTH), 25-hydro-jects (mean age; 40.26 5.11 years) served as controls. Anti-CCP antibodies and Anti-MCV an-xyvitamin D (25OHD), bone alkaline phosphatase (B-ALP) and the carboxy-terminal telopeptidetibodies were measured using ELISA. RESULTS: In all RA patients, mean anti- CCP level wasof type I collagen (CTX). BMD was assessed at lumbar spine (BMD-LS), at femoral neck (BMD-69.07 90.43 U/ml and anti-MCV level was 665.77 1040.19 U/ml. In patients with AS, theFN) and at total femur (BMD-TF). Body composition (fat mass and lean mass) was assessed bymean anti-CCP level was 10.7 5.22 U/ml and anti-MCV level was 40.54 20.15 U/ml. In he- using a DXA device (Prodigy, Lunar GE). A Food Frequency Questionnaire was used for calcula-althy controls, the mean anti-CCP level was 11.11 7.65 U/ml, anti-MCV level was 23.12 12.04tion of dietary calcium intake. The values of ghrelin were lower in osteoporotic men than in osteo-U/ml. In patients with active RA, the mean serum anti-CCP level was 100.54 98.07 U/ml andpenic and normal men but the difference did not reach the statistical significanceanti-MCV level was 998.74 1154.93 U/ml. In patients with inactive RA, the mean serum anti- (737.582.4; 825.3112.5 and 853.6136.8 pg/ml, respectively). A si-CCP level was 8.77 1.55 U/ml and anti-MCV level was 27.59 23.10 U/ml. According to these gnificant correlation was found between ghrelin and lean mass (r=0.20; p