ABSTRACT
Pulmonary thromboembolism (PTE) is rarely reported in Behçet's disease (BD) due to its distinctive thrombus-forming mechanism. In BD, the inflammation on vessel walls causes venous thrombosis. The thrombi are considered to be tethered to the inflamed walls making embolization less frequent. Thus, immunosuppressive agents are the mainstay of treatment. However, the necessity of anticoagulation therapy is controversial because of its uncertain efficacy of resolving thrombi and the possibility of fatal side effects of hemorrhage. A 25-year-old man with recurrent oral aphthae visited with abrupt onset of dyspnea and chest pain. Based on history, imaging studies and laboratory results, he was diagnosed with BD with vascular involvement and antiphospholipid syndrome (APS), causing PTE from deep vein thrombosis. The co-existing APS may have further promoted the thrombosis, shifting his blood profile toward the hypercoagulable state. Immunosuppressive therapy with glucocorticoid and azathioprine, and concomitant anticoagulation with warfarin were achieved successfully without any fatal complications. When atypical features of vascular involvement in BD develop, other coexisting diseases should be considered to design an optimal therapeutic plan.
Subject(s)
Antiphospholipid Syndrome/complications , Behcet Syndrome/complications , Pulmonary Embolism/etiology , Venous Thrombosis/etiology , Adult , Anticoagulants/therapeutic use , Antiphospholipid Syndrome/blood , Antiphospholipid Syndrome/diagnosis , Antiphospholipid Syndrome/drug therapy , Behcet Syndrome/blood , Behcet Syndrome/diagnosis , Behcet Syndrome/drug therapy , Computed Tomography Angiography , Humans , Immunosuppressive Agents/therapeutic use , Male , Phlebography/methods , Pulmonary Embolism/blood , Pulmonary Embolism/diagnostic imaging , Pulmonary Embolism/prevention & control , Risk Factors , Treatment Outcome , Venous Thrombosis/blood , Venous Thrombosis/diagnostic imaging , Venous Thrombosis/drug therapyABSTRACT
OBJECTIVE: Stress cardiomyopathy (SCM) sometimes develops in patients with non-cardiac medical illness. We hypothesized that soluble suppression of tumorigenicity 2 (sST2) can predict SCM. METHODS: In 76 patients admitted to non-cardiac medical intensive care unit (MICU), echocardiography and sST2 were assessed on admission day (D0) and on the third day (D2). Cardiac troponin I (cTnI) and B-type natriuretic peptide (BNP) were measured on D0. RESULTS: The SCM group (21%, 16/76) showed significantly higher cTnI, BNP, sST2 (D2), and sST2 changes than the non-SCM group. In receiver operator characteristics curve analysis, they equally predicted SCM. In 65 patients with normal cTnI, sST2 (D2) and sST2 changes predicted SCM better than cTnI or BNP. CONCLUSION: Follow-up sST2 and the change in sST2 have additional predictive value for SCM in patients with normal cTnI. A combination strategy of sST2 and cTnI would be useful to predict SCM in patients admitted to the MICU.
