In our study acute toxicities were mild
In our study, acute toxicities were mild, and there were no Grade 3 or above hematologic toxicities. Only one patient (3.2%) had Grade 3 esophagus toxicity and three patients (9.7%) had Grade 3 lung toxicity. Compared with studies that investigated regimens of oxaliplatin and 5-FU/leucovorin, the prevalence of Grade 3 or above hematologic toxicities ranged from 0% to 10%. Grade 3 or above gastrointestinal toxicity was noted in 25% to 43% of patients. Burmeister et al reported the best median overall survival (32.6 months), but Grade 3 or above gastrointestinal toxicity also increased to 43% compared with other studies. Thus, the study found that weekly oxaliplatin in combination with infusional 5-FU was not acceptable for routine use. Although oxaliplatin can be used as a radiosensitizing chemotherapy, it may increase the rate of esophagitis. After adjusting the dose and timing of oxaliplatin according to our design, gastrointestinal toxicity was lower than levels reported in the aforementioned studies. In this study, median overall survival rate, local control rate, and distant metastasis rate were not inferior to those of previous randomized trials. Comparing a meta-analysis and our study, 5-year overall survival rates were 38.8% and 37.8%, respectively. In addition, during chemoradiotherapy, there was also no need to adjust the dose of chemotherapy or withhold radiotherapy due to adverse effects.
Oxaliplatin and cisplatin were demonstrated to damage DNA via different pathways. One study showed that squamous cell carcinoma lxr agonists of the esophagus died via apoptosis due to cell-cycle arrest during the G2 phase after oxaliplatin treatment. Thus, oxaliplatin treatment still had noninferior efficacy in the treatment of locally advanced esophageal cancer in our study. Furthermore, cisplatin has a higher rate of hematologic toxicity, such as neutropenia and thrombocytopenia, and may damage renal function in the event of renal insufficiency or inadequate hydration. According to our investigation, oxaliplatin may provide an alternative choice for patients who are not suited to treatment with cisplatin.
A better regimen of chemotherapy when used concurrently with radiotherapy is needed to improve survival and decrease toxicity. Oxaliplatin with capecitabine, and oxaliplatin with S1 were evaluated for the treatment of esophageal cancer. Unfortunately, there were no significant improvements in survival rates compared with those achieved using a cisplatin-based regimen.
Introduction Myotonic dystrophy type 1 (DM1) is an autosomal-dominant disease caused by CTG repeat expansion within the DMPK gene. DM1 is a multisystemic disorder affecting muscles, eyes, endocrine system, central and peripheral nervous system and the heart. It is well known that one third of DM1 patients die suddenly, most of them due to the heart conduction abnormalities and arrhythmias. Thus, early identification and treatment of the cardiac impairments is the main key for prevention of sudden death in DM1 patients. DM1 patients are usually clinically asymptomatic regarding heart involvement, probably due to the limited level of activity and consequently reduced cardiac demand. However, significant impairments may be observed even on regular cardiologic examination. Standard and 24-h Holter electrocardiography (ECG) reveal atrioventricular and intraventricular conduction disturbances, prolonged QTc interval, non specific ST and T changes, and to a lesser degree supra-ventricular and ventricular arrhythmias. Relatively frequent findings on echocardiography are mitral valve (MV) prolapse and hypertrophy and dilation of the left ventricle (LV) with rare overt systolic and diastolic dysfunction. Severe conduction abnormalities and arrhythmias, as well as LV systolic dysfunction/heart failure (HF), are defined as significant predictors of mortality in DM1.
Methods The clinical charts were reviewed in order to obtain sociodemographic data and to assess severity of disease according to the Muscular Impairment Rating Scale (MIRS).