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Immune thrombocytopenia (ITP) is an autoimmune disease which is related to antiplatelet immunoglobulin production, characterized by thrombocytopenia and, mucocutaneous bleeding. A 34-year-old woman had spontaneous abortion three times. Having been detected deep venous thrombosis, thoracic computer tomography (CT) showed a massive pulmonary embolism (PE) involving bilateral pulmonary arteries and segmental branches. The patient with thrombocytopenia (13,000 mm³) was unable to be given low molecular weight heparin (LMWH). The patient's peripheral smear and bone marrow aspiration findings were compatible with ITP. Once MTHFR and Factor V mutation for thrombophilia were detected, anticoagulant treatment was planned life-long. As the platelet level decreased again, splenectomy was offered by a hematologist. While the patient was hospitalized in general surgery clinic for dyspnea, thoracic CT revealed acute embolism of the bilateral main pulmonary arteries. Our case is discussed due to difficulties in the treatment of recurrent pulmonary embolism and refractory ITP. [ABSTRACT FROM AUTHOR]

Faktör V Leiden (FVL) mutasyonunda tromboza eğilim olduğu gösterilmiştir. Lipoprotein A nın (Lpa) proaterojenik olduğu ve protrombotik olduğu düşünülmektedir. FVL mutasyonunun özellikle genç yaşlarda miyokard infarktüsünden sorumlu olabileceğine dair yayınlar vardır. 33 yaşında erkek hasta acile göğüs ağrısıyla başvurdu. Çekilen elektrokardiyografide akut anterior miyokard infarktüsü (AMİ) tanısı konularak koroner anjiyografisi yapıldı. Koroner anjiyografide sol ön inen arterin proksimalinde tam tıkanıklık saptandı. Diğer koroner arterler normal bulundu. Sol ön inen koroner arterdeki tam tıkanıklığa direk stent işlemi ile tam açıklık sağlandı. Polimeraz zincir reaksiyonu yöntemi ile FVL heterozigot mutasyonu saptandı. Aynı zamanda Lpa yüksekliği saptandı. Tekrarlayan anjinal ataklar nedeniyle 2 ay sonra yapılan kontrol anjiyografisinde stentin açık olduğu gözlendi.

Summary Factor V Leiden (FVL) mutation has been shown tendency to thrombosis. Lipoprotein a (Lpa) is thought to be proatherogenic and prothrombotic. There are several publications that were reported that FVL mutation might be responsible for myocardial infarction especially in a young age group. 33 year old male patient was admitted to the emergency room with chest pain. Acute anterior myocardial infarction was diagnosed with electrocardiography. Coronary Angiography was performed. Coronary Angiography showed that there was a total occlusion in the proximal part of the left anterior descending artery (LAD). Other coronary arteries were normal. Complete patency was achieved with direct stent procedures in the completely occluded part of the left anterior descending coronary artery. FVL heterozygous mutation was found with polymerase chain reaction method. Elevated Lpa was found in the same period. A control angiography was done 2 months after the stent application because of recurrent anginal attacks. In the control angiography, it was observed that stent was open. [Cukurova Med J 2013; 38(3.000): 525-527]

A 52 years old woman with a history of homozygous factor V leiden mutation and a mitral valve replacement operation 3 mounths ago was referred to the cardiology out-patient clinic with the complaint of dyspnea. The physical examination and transthoracic echocardiography of the warfarin treated patient revealed a pressure gradient over the replaced mitral valve, disfunctional leaflet movements and pulmonary hypertension. An urgent re-do mitral valve replacement operation due to the early stuck mitral valve was planned, as the movements of the replaced mitral valve leaflets were shown to be overtly restricted on cinefluoroscopy. During the operation, the thrombotic pannus causing severe movement disturbance was found to be spread over both of the leaflets on the replaced valve and was removed. A 27 mm St.Jude mechanical bileaflet prosthetic valve was replaced. The patient was discharged on the 10th day of the operation with an appropriate dose of oral anticoagulant therapy. As it is in the present case, we would like to emphasise that special care must be taken about the laboratory follow-up of the patients, who are known to have genetic predisposition to clotting disturbances, following the valve replacement operation regarding oral anticoagulant therapy. [ABSTRACT FROM AUTHOR]

A twenty one years old woman presented with sudden, painless visual loss in her left eye. In our ophthalmological examination, the best corrected visual acuity (BCVA) of right eye was 20/20 and counting fingers at 20 cm in the left eye. Anterior segment examination and intraocular pressure was normal in both eyes. Aferan pupillary defect was detected in the left eye. Right fundus was normal, but left fundus revealed retinal edema and attenuation of the retinal arterioles, the peripapillary retina was appeared swollen and opaque. Fundus fluorescein angiography showed a reduced arterial caliber and delayed arteriovenous transit time. Cilioretinal artery was normal. The central retinal arterial occlusion was diagnosed by these examinations and therapy was initiated. Systemic investigations showed that the patient had factor V Leiden Mutation. In our ophthalmological examination, the BCVA of left eye was 4/10 and retinal edema was regressed after two months. It should be remembered and investigated in young patients with arterial occlusion without any other predisposing factors. [ABSTRACT FROM AUTHOR]