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Oral Communications / European Journal of Internal Medicine 19S (2008), S1S59

Discussion and Conclusions: Enterococci, most often E. faecalis, cause 5 to 20% of cases of infective endocarditis. According to a MEDLINE search, this is the the third report of endocarditis due to E gallinarum and the rst associated with colonic carcinoma. Several studies reported intestinal colonization by E. gallinarum in both hospitalized individuals and nonhospitalized healthy individuals. The low prevalence of motile enterococcal endocarditis may be due to the difculties in identifying these species. This case demonstrates the role of E gallinarum as a cause of native valve endocarditis and a very uncommon presentation for colorectal malignancy.

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HIP FRACTURE IN A YOUNG PATIENT WITH CHRONIC RENAL DISEASE Cristina Tanaseanu, Monica Popescu, Isabela Tiglea, Alina Dumitrascu, T. Irimia. UMF Carol Davila Bucharest Romania Background Bone disease develops relatively early in chronic renal failure. The high turnover variants secondary hyperparatiroidism (SHP) and a combined disorder are still the most frequent. Low turnover disorders include osteomalacia (OM) and adynamic bone disease. Case discussion: we present a case of a 28-years old woman with multiple pregnancies, without signicant medical history, who presents clinical symptoms compatible with a recent hip fractures. On physical examination patient presented kyphosis, hypostaturality, nger abnormalities. Of laboratory relevance there were: low grade anemia with feature of microangyopathic anemia, elevated alkaline phosphatase, moderately increased serum creatinine level (3,4 mg/dl), nephrotic syndrome, phosphorus 5,7 mg/dl, low calcium 4 mg/dl, increased PTH level, low 1,25(OH)2D3. Ultrasound examination revealed small hyperechoic kidneys with disorganized structure, compatible with chronic glomerulonephritis. Thyroid CT: thyroid and parathyroid structures in normal upper limits. Immunological tests for SLE were negative. Radiographs: demineralization with subperiosteal erosions and terminal resorbtion in the phalanges, pepper pot appearance on lateral radiographs of the skull and femoral neck fracture, kyphoscoliosis. Clinical, laboratory and radiological data are feature of long-standing hyperparathyroidism in a patients with silent glomerulonephritis and possible previous vitamin D deciency due to multiple pregnancies and a reduced alimentary intake. Conclusion: Renal osteodystrophy develops at the early stages of chronic renal failure covering a large spectrum of abnormalities. Increased PTH secretion is associated in most cases with diffuse hyperplasia of parathyroid tissue. Vitamin D deciency is one of major pathogenic factors for renal osteodystrophy via secondary hyperparatiroidism and osteomalacia via hypocalcaemia.

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DECOMPRESSION SICKNESS IN A SEA-HEDGEHOG DIVER Giovita A. Piccillo, Aurelio Pant, L Manfr, Enrico G.M. Mondati, Riccardo Polosa, Luca Miele, Giovanni Gasbarrini. Department of Emergency Medicine, Cannizzaro Hospital, Catania, Italy Introduction: Decompression sickness, physiological disorder caused by rapid decrease in atmospheric pressure, resulting in presence of nitrogen bubbles into the body tissues. It is also known as caisson disease and represents the hazard of persons who work under greatly increased atmospheric pressure below the surface of the earth when their return to normal atmospheric pressure is made too quickly. At high atmospheric pressure the respiratory gases are compressed and larger amounts are dissolved in the tissues. During ascent from depths greater than 30 ft (9.1m), these gases escape as the external pressure decreases. The decrease in air pressure releases gas bubbles that block the small veins and arteries and collect in the tissues, cutting off the oxigen and causing nausea, vomiting, dizziness, pain in the joints and abdomen, paralysis, and other neurological symptoms. There may be shock, total collapse, and, if treatment is not prompt, death. Decompression illness from breath-hold diving is quite rare but can occur. It is usually seen in divers who are making many deep dives in a short period of time with little surface interval. Taravana (to fall crazily) syndrome, rst described by Cross in 1958, is a diving condition seen in working Tuamotu Island natives diving in the Takatopo Lagoon (French Polynesia). It represents a decompression illness in divers. The symptomatology is characterized by vertigo, nausea and lethargy, paralysis and death. The treatment consists on recompression. Case Report: A male 38-year-old subject was admitted to our Department because of nausea, vertigo, paresthesias of left emibody and lethargy. He was been diving during the morning as apneist, making almost 30 immersions at 30 meters of deepth with very short interval of surface in search of sea-hedgehogs. At history, mother and father affected with hypertension, appendicectomy at the age of ten years The patient appeared pale and suffering, polypnoic, extremely anxious, with nausea, vomiting, dizzness and paresthesias of left arm and leg. Normal BP (130/80 mmHg), EKG, HR (90 b/m), T 37C, SaO2 97%. Respiratory clinical evaluation revealed normal vesicular breathing. Neurological evaluation no showed left body impairment, but conrmed the presence of paresthesias. Laboratory data no pointed out alterations except for moderate anaemia (RBC 3.780.000/mmc, Hgb 12.4 g/dl, Hct 30.6%, MCV 80.9 ), slight increase of LDH (786 U/L).There was no evidence of C and S proteins deciency and negative resulted antiphospholipid antibodies, lupic anticoagulant Chest-X-ray, immediately executed, no pointed out abnormalities as well as chest-CT, apart for slight emphysema signs. Brain magnetic resonance detected few right little hyperintense lesions On the grounds of these ndings, we suspected a case of Taravana syndrome and submitted our patient to prompt recompression. The patient at last of hyperbaric session (180 min) appeared ameliorated with resolution of his symptomatology. Discussion: Taravana syndrome is a rare and very often misdiagnosed diving disturb with good prognosis in most cases. It seems be due to nitrogen load of the blood. Of particular relevance to the sport dive is what happens to the snorkelling breath-hold diver who repeatedly dives during the surface interval between sub dives. Very little nitrogen is transferred from the alveoli to the blood during one breath-hold dive. But repeated dives alter the off-gassing process as well as taking on more gas and would completely change the dive proles. Free diving on-loads N2, to a small degree, more or less depending upon the depth and time at depth of the dives and this time should be taken into consideration when calculating residual nitrogen. Snorkelers between scuba dives should stay on the surface. The gold standard of therapy is recompression and it should be started as soon as possible to beseech the rare but possible death of these patients.

Saturday, 10 May 2008, 9.4511.15

Room C

Cardiovascular Diseases
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GENETIC POLYMORPHISMS THAT INFLUENCE LONG TERM RISK OF MAJOR ADVERSE CARDIAC EVENTS AFTER PERCUTANEOUS CORONARY INTERVENTION M.I. Mendona, A.I. Freitas, A. Pereira, A.C. Sousa, P. Faria, S. Gomes, N. Santos, B. Silva, M. Serro, S. Freitas, I. Ornelas, A. Brehm, A. Cardoso. Hospital Central do Funchal Introduction: In spite of drug eluted stents, double anti-platelet aggregation and statin therapy, the occurrence of precocious restenosis and late major adverse coronary events (MACE) remains signicant. Artery morphology, medical therapy or the presence of risk factors, cannot totally explain those complications. Genetic background namely through the expression of several polymorphic genes that codify for endothelium proliferation and/or platelet aggregation, can contribute to explain MACE (death, non fatal acute myocardial infarction, unstable angina, and late revascularisation), after percutaneous coronary intervention (PCI). Aims: To study which rennin angiotensin axis polymorphisms, inuence the emergence of MACE, after PCI. Methods and Population: Prospective observational study of 10 years) with symptomatic coronary artery?189 consecutive patients (54.9 disease who underwent successful coronary stent implantation from November 2001 and December 2003, with a medium follow up 3.81.5 years. Long term clinical outcome was prospectively evaluated and the rates of MACE (death, non fatal acute myocardial infarction, unstable angina, and late revascularisation) were obtained. The environmental, clinical and biochemical variables, were studied as well as ACE (I/D), ACE 8 A2350G, Angiotensinogen AGT T174M and M235T, ATIR A1166C, Paraoxonase 1 (PON1) L55M; Q192R, and IIIa Glycoprotein (PLA1/PLA2) polymorphism. The frequency of MACE was analysed and the groups with and without MACE, were compared by Chi square test and Student T test. Through a logistic regression (Coxs multivariate analysis), we studied which variables were, in a signicant and