Background and aims. There is an increasing number of patients with cardiovascular diseases who require anticoagulant treatment to address the underlying disease. Types of anticoagulants include vitamin K antagonists, such as warfarin and coumarin derivatives, and also newer oral anticoagulants, including rivaroxaban, apixaban, edoxaban, and dabigatran. The use of these anticoagulants may impact the condition of patients undergoing oral surgery. If the treatment is discontinued, the patient may be at risk of thrombosis. On the other hand, if the treatment is continued, the patient may experience a postoperative bleeding episode, placing them at risk of both thrombosis and bleeding. Method. The present article systematically reviews two different therapeutic regimens and their influence on hemorrhagic and thromboembolic events. The review included research from three databases and four specialized journals. The regimens examined were continuous versus discontinuous anticoagulant treatment and continuous versus interruption and switch to bridging therapy. Results. The most common surgical procedure examined in the review was tooth extraction, with a few studies also including soft tissue procedures. A total of seven eligible articles were identified, with five using the first treatment regimen of continuous versus discontinuous anticoagulant. These studies reported several cases of bleeding under continuous anticoagulant treatment during surgery. Two articles used the second treatment regimen of continuous versus interruption and switch to bridging therapy. Conclusions. The results of both treatment categories (continuous versus discontinuous anticoagulant and continuous versus interruption and switch to bridging therapy) showed no significant differences in terms of bleeding events. However, the use of scores that assess the risk of thrombosis and bleeding can assist surgeons in anticipating the degree of ostoperative complications and making informed treatment decisions.
Periodontal medicine is a broad term commonly used to define the relationship between periodontitis and systemic health. Periodontitis is a highly prevalent, chronic multifactorial infectious disease, induced by the dysbiotic biofilm that triggers a persistent systemic inflammation and recurrent bacteremia. There is a growing body of scientific evidence that suggests the potential implication of periodontitis in the causation and progression of various systemic disease and conditions, such as diabetes, cardiovascular disease, pulmonary disease, adverse pregnancy outcomes and cancer. Some studies consider periodontitis as an independent risk factor for preterm birth, growth restriction, low birth-weight and pre-eclampsia. However not all studies support the association. Despite sparse scientific data, some studies indicate that individuals with periodontitis are at increased risk for cancer development, due to the increased inflammatory burden sustained by the presence of periodontal pathogens. This chapter emphasis the relationship between periodontitis and adverse pregnancy outcomes and the underlying mechanisms that link peridontitis to oral carcinogenesis.
Pancreatic cancer is associated with high rates of mortality especially due to advanced stages of diagnosis. Adjuvant chemotherapy role is thus essential in the attempt to downstage the tumoral grade. In cases of locally advanced tumors, this step could be followed by curative surgical resection. Characterization of predictor biomarkers for adjuvant chemotherapy has drawn increasing interest in molecular biology research of pancreatic cancer. Personalized treatment is one of the solutions proposed for advancing towards a better outcome. In this paper we discuss available predictor biomarkers with focus upon gemcitabine and FOLFIRINOX (5-fluoro uracil (5-FU), irinotecan and oxaliplatin) chemotherapy regimens, present approaches in advanced pancreatic cancer. Many data are current available in relation with gemcitabine chemotherapy regimen, where biomarkers like ribonucleotide reductase large subunit (RRM1), human equilibrative nucleoside transporter-1 (hENT1), deoxycytidine kinase (dCK), human antigen R (HuR), and secreted protein acidic rich in cysteine (SPARC) were proposed. Regarding the response to FOLFIRINOX components, other markers such as thymidylate synthethase (TS), topoisomerase I, and excision repair cross-complementation 1 (ERCC1) or KRAS mutation status were also investigated.
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