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The treatment of unprovoked venous thromboembolism (VTE) is anticoagulant therapy for at least 3 months [1]. As VTE recurs frequently and about 20 % of the patients with an unprovoked VTE develop recurrence within the first 2 years [2], extended vitamin K antagonist (VKA) treatment is often considered. The decision to prolong VKA therapy after the initial treatment period is a dilemma, since longer term therapy reduces the risk of recurrent thromboembolism, but increases the risk of bleeding. The last American College of Chest Physicians (ACCP) EvidenceBased Clinical guidelines suggest a strategy to balance the benefits and risks of different durations of anticoagulant therapy; in unprovoked VTE, ACCP guidelines suggest extended anticoagulant therapy if bleeding risk is low or moderate (Grade 2B) and recommend 3 months of therapy if bleeding risk is high. When extended anticoagulant therapy is contraindicated, aspirin might be appealing. In fact the annual risk of major bleeding is only 0.1 % in patients on long-term low-dose aspirin therapy, thus lower than VKA therapy [3]. A large meta-analysis by the Antiplatelet Trialists’ Collaboration shows that antiplatelet therapy significantly reduces the risk of fatal or non-fatal pulmonary embolism (PE) by 25 % [3]. Moreover, a large trial involving patients undergoing surgery for hip fracture shows a 36 % risk reduction in VTE in the aspirin therapy group, [4] suggesting that antiplatelet therapy may be an alternative to prolonged VKA therapy. Two randomized controlled studies were conducted to evaluate the use of ASA for the prevention of venous thromboembolism recurrence: the Aspirin for the Prevention of Recurrent Venous Thromboembolism (Warfarin and Aspirin [WARFASA]) [5] and the Aspirin to Prevent Recurrent Venous Thromboembolism (ASPIRE) study [6].

Dr. Montano: A 42-year-old man was admitted to our department because of migratory arthromyalgias predominantly involving large joints, with painful swelling for the prior 3 weeks. He had used large doses of non-steroid antiinflammatory drugs with limited pain control. The patient was eupneic and apyretic demonstrating pain and swelling of the left hand, and erythema and edema of the right leg and foot. Blood pressure and heart rate were, respectively, 120/80 mmHg and 80 beats/min. The remaining clinical history and physical examination were otherwise negative. The electrocardiogram and the chest X-ray were normal. Compressive ultrasound scan of the legs, looking for a deep venous thrombosis, was normal. Routine laboratory findings were within the normal ranges except for hypertransaminasemia (AST 287, ALT 740); for this reason an abdominal ultrasound scan was performed, but showed only a mild hepatosplenomegaly. Serologic profile revealed previous Epstein–Barr and cytomegalovirus infections, and detected hepatitis B virus (HBV) IgM antibodies, HBsAg and HBeAg, thus showing an acute HBV infection. Autoimmune screening (ANCA and ANA autoantibodies, rheumatoid factor, autoantibodies against gliadin and transglutaminase) were all normal as were the thyroid function tests. The migratory arthralgias were treated with tramadol, with a significant reduction in pain. Intravenous fluids were administered, and a specific diet for hepatic disease was prescribed; the patient was subsequently discharged with the diagnosis of ‘‘migratory arthralgias in an acute hepatitis B infection’’. A month after discharge, the patient was readmitted to our department for dysesthesias and hypoesthesia of both feet (predominantly the right) associated with motor deficits. On neurologic examination, flexion, extension and rotation movements of the right foot were not possible for the patient, and the Achilles tendon reflex was absent. The patient also showed a deficit in right thigh flexion with steppage gait, and a deficit in left foot extension. Laboratory findings showed a leukocytosis (12,000 WBC) and C-reactive protein (CRP) elevation (170 mg/l). A magnetic resonance (MR) examination of the spine was performed to test the hypothesis of spondylo-diskitis or multiple discopathies, but was normal. To evaluate the motor deficit, an electromyography (EMG) was performed. It revealed an acute axonal multineuropathy involving the right common peroneal nerve and the left femoral nerve, associated with chronic axonal damage in some of the studied districts. In particular, This case record was selected for the ‘‘Casi Clinici Gymnasium’’ session at the 2009 SIMI Annual Congress in Rome, and was reviewed by a Committee composed of Maria Domenica Cappellini and Luigi Pagliaro.

Ischemic stroke is a significant cause of mortality and of serious long-term morbidity. It is estimated that cryptogenic stroke (stroke whose underlying causes remain unknown despite a complete work-up,) accounts for about 20–40 % of all ischemic events, one quarter of which tend to be recurrent [1]. Paroxysmal and persistent atrial fibrillation (AF) is a well-recognized cause of ischemic stroke, and the risk may be reduced with anticoagulation. However, only 5 % of patients are diagnosed to have AF after an ischemic stroke. Indeed the use of traditional monitoring techniques may not detect episodes of asymptomatic paroxysmal AF, which might underlie some apparently ‘‘cryptogenic’’ strokes. Therefore, the most effective duration of ECG monitoring has not been determined by current guidelines [2]. Nowadays, external and implanted loop recorders may allow identification of silent AF, thus increasing AF detection rate. However, the effectiveness of prolonged heart rhythm monitoring in patients with cryptogenic stroke is still unproved [3, 4].

Case presentationDr Montano: A 60-year-old-man was admitted to ourEmergency Department (ED) for worsening dyspnea, andrecurrent episodes of oppressive chest pain that resolvedwithin a few minutes with rest. He had a history ofbenign prostatic hypertrophy (in therapy with Finasteride5 mg/day), mild chronic renal failure, a prior episode ofright lower limb thrombophlebitis (1992), pulmonary sar-coidosis diagnosed in 1991 and initially treated with6 months of steroid therapy without further follow-up in thepastfewyears.Hishistorywasnegativeforsmokingorothercardiovascular risk factors (Fig. 1).In ED, he appeared diaphoretic and dyspnoeic, wastachycardic and his blood pressure was 190/120 mmHg.The physical examination was otherwise substantiallynormal. An ECG showed sinus tachycardia (125 bpm), andisolated premature ventricular beats. The arterial blood gasshowed respiratory failure with a normal pCO