Objective: To compare effects of the fluoropyrimidines S-1 and capecitabine on prothrombin time international normalized ratios (PT-INR) of warfarin following coadministration and after discontinuation of each fluoropyrimidine treatment.
Methods: Medical records of patients receiving warfarin with either S-1 (6 patients) or capecitabine (7 patients) were obtained from four hospitals.
Results: Increased PT-INR was observed until peak levels of warfarin were achieved in all patients in S-1 and capecitabine treatment groups.　Moreover, PT-INR significantly changed after coadministration within each group (p＜0.05).　Specifically, ratios of peak PT-INR after coadministration of each fluoropyrimidine and those following administration of warfarin alone (PT-INR elevation ratio) were 3.31 and 3.29 in S-1 and capecitabine coadministration groups, respectively.　Moreover, numbers of days to peak PT-INR were 38.3 and 31.3 days, respectively, and did not significantly differ between the treatment groups.　Furthermore, PT-INR returned to pretreatment levels by 17.5 and 15.1 days after discontinuation of S-1 and capecitabine, respectively, and did not significantly differ between the treatment groups.
Conclusion: Coadministration of S-1 and capecitabine similarly prolongs PT-INR by approximately 3-fold compared with administration of warfarin alone; therefore, these drug-drug interactions were clinically suggested to be of high risk for episodes of bleeding and remarkable alterations in coagulation parameters.　Therefore, blood coagulation ability should be more carefully monitored with regard to PT-INRs in patients receiving warfarin with S-1 or capecitabine not only during coadministration but also after discontinuation of fluoropyrimidine treatments.

Cerebral air embolism caused by lung cancer is extremely rare, especially if not associated with invasive procedures such as needle biopsy. We describe the case of an 86-year-old man with squamous cell lung carcinoma of the left lung. He developed a bad cough and subsequently suffered left hemiplegia. Brain computed tomography (CT) on admission showed no abnormal findings. Diffusion-weighted magnetic resonance (MR) imaging revealed high intensity lesions in the right frontal lobe and right parietal lobes. Repeated brain CT revealed air densities around the high intensity lesions on previous MR imaging, compatible with air embolism causing cerebral infarction. Chest CT confirmed a left pulmonary hilar mass invading the left pulmonary vein, left atrium, and main bronchus. Air densities were found in the left heart ventricle. These radiological findings were attributed to cerebral air embolism associated with advanced lung cancer. Shortly afterwards he died of progressive respiratory failure. Our case reveals two important aspects. First, cerebral air embolism can be caused by lung cancer invading the pulmonary vein, left atrium, and main bronchus without iatrogenic causes. Therefore, we should pay special attention to the etiology when the patients with lung cancer in the advanced stage developed cerebral infarction. Second, repeated CT is recommended if cerebral air embolism is suspected because initial head CT does not always reveal air bubbles.

A 76-year-old man with a history of total esophagectomy and retrosternal gastric tube reconstruction for esophageal cancer was transferred to our hospital because of consciousness disorder. It became an emergency operation on diagnosis of Stanford type A acute aortic dissection on enhanced CT. Because CT showed the retrosternal gastric tube ran along the right side of the body of the sternum through the back side of the manubrium, we opted for skin and the suprasternal incision on the left side from center. We could perform total aortic arch replacement without the damage of the gastric tube except that the right side of the operative view was slightly poor. We did not recognize digestive organ symptoms such as postoperative passage disorders nor mediastinitis. The patient was discharged from our hospital on postoperative day 24.

Objective: Poor R wave progression in right precordial leads is a relatively common electrocardiogram (ECG) finding that indicates possible prior anterior myocardial infarction (MI); however, it is observed frequently in apparently normal individuals. In contrast, reversed R wave progression (RRWP) may be more specific to cardiac disorders; however, the significance of RRWP in daily clinical practice is unknown. The purpose of this study was to clarify the significance of RRWP in clinical practice.Materials and Methods: We analyzed consecutive ECGs obtained from 12,139 patients aged ≥20 years at Mito Kyodo General Hospital in Ibaraki between November 2009 and August 2012. Our setting is a secondary emergency hospital in the community, and the study participants were inpatients or patients who visited the general or emergency outpatient departments. RRWP was defined as RV2 < RV1, RV3 < RV2, or RV4 < RV3. Regarding ECGs considered to show RRWP, we confirmed the presence or absence of an abnormal Q wave and whether ultrasound cardiography, contrast-enhanced computed tomography, coronary angiography, and/or left ventriculography were performed to obtain detailed information.Results: RRWP was identified in 34 patients (0.3%). Among these patients, 29 (85%) had undergone cardiac evaluation. The final diagnosis was previous anterior MI in 12 patients (41%) and ischemic heart disease (IHD) without MI in 5 patients (17%). All 17 patients with IHD had left anterior descending (LAD) artery stenosis. The other patients were diagnosed with dilated (two patients, 7%) and hypertrophic (one patient, 3%) cardiomyopathy, left ventricular hypertrophy (one patient, 3%), or pulmonary embolism (one patient, 3%). Only seven patients (24%) were normal.Conclusions: RRWP is rare in daily clinical practice; however, it is a highly indicative marker for cardiac disease, particularly IHD with LAD artery stenosis.