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AIM:To describe disease characteristics and treatment modalities in a group of rare patients with metastatic gastric carcinoid type 1(GCA1).METHODS:Information on clinical,biochemical,radiological,histopathological findings,the extent of the disease,as well as the use of different therapeutic modalities and the long-term outcome were recorded.Patients’data were assessed at presentation,and thereafter at 6 to 12 monthly intervals both clinically and biochemically,but also endoscopically and histopathologically.Patients were evaluated for the presence of specific symptoms;the presence of autoimmune disorders and the presence of other gastrointestinal malignancies in other family members were also recorded.The evaluation of response to treatment was defined using established WHO criteria.RESULTS:We studied twenty consecutive patients with a mean age of 55.1 years.The mean follow-up period was 83 mo.Twelve patients had regional lymph node metastases and 8 patients had liver metastases.The primary tumor mean diameter was 20.13±10.83mm(mean±SD).The mean Ki-67 index was 6.8%±11.2%.All but one patient underwent endoscopic or surgical excision of the tumor.The disease was stable in all but 3 patients who had progressive liver disease.All patients remained alive during the follow-up period.CONCLUSION:Metastatic GCA1 carries a good overall prognosis,being related to a tumor size of≥1 cm,an elevated Ki-67 index and high serum gastrin levels.  相似文献   

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Effective secondary prevention after acute coronary syndrome (ACS) is largely dependent on dual antiplatelet therapy (DAPT). Despite DAPT, however, patients remain at substantial risk of major adverse cardiovascular events (i.e., cardiovascular death, myocardial infarction, stroke), and, therefore, combination therapy of oral anticoagulant and antiplatelets has been previously proposed. Because of the increase in bleeding and the cumbersome management of vitamin K antagonists, such combination therapy has never gained much popularity. The recent development of new, non vitamin K antagonists, direct oral anticoagulants (NOACs), including dabigatran, apixaban, rivaroxaban, and darexaban, which have more favorable pharmacokinetics and pharmacodynamics, as well as higher safety, has renewed the interest on combination therapy. Whereas phase II trials with dabigatran, apixaban, rivaroxaban, and darexaban have consistently shown an increased bleeding risk with combination therapy, a potential increased efficacy has emerged for apixaban and rivaroxaban, thereby prompting phase III studies. Both APPRAISE-2 and ATLAS ACS 2-TIMI 51 trials confirm a dose-dependent increase in major bleeding events, including intracranial, with apixaban and rivaroxaban when combined with DAPT. Low-dose (2.5 mg twice daily) rivaroxaban on the other hand, is associated with a significantly higher efficacy on the occurrence of combined cardiovascular death, myocardial infarction, stroke, and of stent thrombosis. Owing to the persistent uncertainty regarding the net clinical benefit of combined therapy of NOAC, namely low-dose (2.5 mg twice daily) rivaroxaban and DAPT of aspirin and clopidogrel, further studies are warranted to identify the ACS patient who will benefit most from such treatment, also in comparison to the current therapeutic standard represented by DAPT of aspirin and ticagrelor (or prasugrel).  相似文献   

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Despite the benefits of first generation drug eluting stents (DES), concerns have been raised over their long term safety in particular the risk of stent thrombosis. As a result, the current generation and novel DES have been developed, the latter includes DES with biocompatible and biodegradable polymers, polymer free DES and completely bioresorbable stent platforms. Many of these stents are currently under evaluation in clinical trials, and early results are promising. This paper reviews the progress thus far in DES technology and aims to highlight the impact of recent DES innovations on clinical efficacy and safety.  相似文献   

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Frey N  Katus HA  Olson EN  Hill JA 《Circulation》2004,109(13):1580-1589
Recent studies call into question the necessity of hypertrophic growth of the heart as a "compensatory" response to hemodynamic stress. These findings, coupled with recent progress in dissecting the molecular bases of hypertrophy, raise the prospect of suppressing hypertrophy without provoking circulatory insufficiency. In this article, we focus on signaling pathways that hold promise as potential targets for therapeutic intervention. We also summarize observations from animal models and clinical trials that suggest benefit from an antihypertrophic strategy.  相似文献   

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