Adjuvant chemotherapy versus surgery alone for esophageal squamous cell carcinoma: a meta‐analysis of randomized controlled trials and nonrandomized studies

The effect of adjuvant chemotherapy on survival of patients with thoracic esophageal squamous cell carcinomas is still controversial, and the subgroup of patients who will most likely benefit from the adjuvant chemotherapy on long‐term survival has not yet been identified clearly. Studies published from 1995 to May 2012 were searched in Medline, Embase, PubMed, Cancerlit, the Cochrane Library, CNKI and major scientific meetings. Randomized controlled trials and nonrandomized studies comparing surgery plus adjuvant chemotherapy with surgery alone in patients with resectable thoracic esophageal squamous cell carcinomas were included. Eleven studies with a total of 2047 patients were identified, consisting of the adjuvant chemotherapy arm (n = 887) and surgery‐alone arm (n = 1160). There was not statistically significant benefit on 3‐year overall survival for adjuvant chemotherapy (risk ratio [RR] = 0.89, 95% confidence interval [CI], 0.72 to 1.09; P = 0.25). Adjuvant chemotherapy could significantly prolong the 1‐year disease‐free survival (DFS) (RR = 0.68, 95%CI, 0.51 to 0.89; P = 0.006), but not 3‐year DFS (RR = 0.97, 95%CI, 0.73 to 1.29; P = 0.84). Further analysis showed that patients with stage III‐IV diseases could benefit from adjuvant chemotherapy on 3‐year overall survival (RR = 0.43, 95%CI, 0.31 to 0.61; P = 0.00001), but not in the case of patients with stageI‐IIdiseases (RR = 1.12, 95%CI, 0.65 to 1.93; P = 0.68). Additionally, patients with positive lymph node could benefit on 5‐year DFS from adjuvant chemotherapy (RR = 0.79, 95%CI, 0.64 to 0.99; P = 0.04). The modality treatment with adjuvant chemotherapy for patients with squamous cell carcinoma of thoracic esophagus might be determined according to pathological stage or the status of lymph node metastasis.     

Calcific left atrium:A rare consequence of endocarditis

Usually, cardiac calcifications are observed in aortic and mitral valves, atrio-ventricular plane, mitral annulus, coronary arteries, pericaridium(usually causing constrictive pericarditis) and cardiac masses. Calcifications of atrial walls are unusual findings that can be identified only using imaging with high spatial resolution, such as cardiac magnetic resonance and computed tomography. We report a case of a 43-year-old patient with no history of heart disease that underwent cardiac evaluation for mild dyspnoea. The echocardiogram showed a calcific aortic valve and a hyper-echogenic lesion located in atrio-ventricular plane. The patient was submitted to cardiac magnetic resonance and to computed tomography imaging to better characterize the localization of mass. The clinical features and location of calcified lesion suggest an infective aetiology causing an endocarditis involving the aortic valve, atrioventricular plane and left atrium. Although we haven't data to support a definite and clear diagnosis, the clinical features and location of the calcified lesion suggest an infective aetiology causing an endocarditis involving the aortic valve, atrio-ventricular plane and left atrium. The patient was followed for 12 mo both clinically and by electrocardiogram and echocardiography without worsening of clinical, electrocardiographic and echocardiographic data. Cardiac magnetic resonance imaging and computed tomography are ideal methods for identifying and following over time patients with calcific degeneration in the heart.     

Chlamydophila pneumoniae phospholipase D (CpPLD) drives Th17 inflammation in human atherosclerosis

Phospholipases are produced from bacterial pathogens causing very different diseases. One of the most intriguing aspects of phospholipases is their potential to interfere with cellular signaling cascades and to modulate the host-immune response. Here, we investigated the role of the innate and acquired immune responses elicited by Chlamydophila pneumoniae phospholipase D (CpPLD) in the pathogenesis of atherosclerosis. We evaluated the cytokine and chemokine production induced by CpPLD in healthy donors' monocytes and in vivo activated T cells specific for CpPLD that infiltrate atherosclerotic lesions of patients with C. pneumoniae antibodies. We also examined the helper function of CpPLD-specific T cells for monocyte matrix metalloproteinase (MMP)-9 and tissue factor (TF) production as well as the CpPLD-induced chemokine expression by human venular endothelial cells (HUVECs). We report here that CpPLD is a TLR4 agonist able to induce the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 in monocytes, as well as CXCL-9, CCL-20, CCL-4, CCL-2, ICAM-1, and VCAM-1 in HUVECs. Plaque-derived T cells produce IL-17 in response to CpPLD. Moreover, CpPLD-specific CD4(+) T lymphocytes display helper function for monocyte MMP-9 and TF production. CpPLD promotes Th17 cell migration through the induction of chemokine secretion and adhesion molecule expression on endothelial cells. These findings indicate that CpPLD is able to drive the expression of IL-23, IL-6, IL-1β, TGF-β, and CCL-20 by monocytes and to elicit a Th17 immune response that plays a key role in the genesis of atherosclerosis.     

Caries preventive efficacy of silver diammine fluoride (SDF) and ART sealants in a school-based daily fluoride toothbrushing program in the Philippines

Background

Occlusal surfaces of erupting and newly erupted permanent molars are particularly susceptible to caries.The objective of the study was to assess and compare the effect of a single application of 38% SDF with ART sealants and no treatment in preventing dentinal (D3) caries lesions on occlusal surfaces of permanent first molars of school children who participated in a daily school-based toothbrushing program with fluoride toothpaste.

Methods

The prospective community clinical trial in the Philippines was conducted over a period of 18 months and included 704 six- to eight-year-old school children in eight public elementary schools with a daily school-based fluoride toothpaste brushing program. Children were randomly assigned for SDF application or ART sealant treatment. Children from two of the eight schools did not receive SDF or ART sealant treatment and served as controls. SDF or ART sealant treatment was applied on sound occlusal surfaces of permanent first molars. Surfaces that were originally defined as sound at baseline but which changed to dentinal (D3) caries lesions were defined as surfaces with new caries (caries increment). Non-compliance to the daily toothbrushing program in three schools offered the opportunity to analyze the caries preventive effect of SDF and sealants separately in fluoride toothpaste brushing and in non-toothbrushing children.

Results

In the brushing group, caries increment in the SDF treatment group was comparable with the non-treatment group but caries increment in the sealant group was lower than in the non-treatment group with a statistically significant lower hazard ratio of 0.12 (0.02-0.61). In the non-brushing group, caries increment in the SDF treatment group and the sealant group was lower than the non-treatment group but the hazard ratio was only statistically significant for the sealant group (HR 0.33; 0.20-0.54). Caries increment was lower in toothbrushing children than in non-toothbrushing children. Hazard ratios reached statistical significance for the non-treated children (HR 0.43; 0.21-0.87) and the sealant-treated children (HR 0.15; 0.03-0.072).

Conclusions

A one-time application of 38% SDF on the occlusal surfaces of permanent first molars of six- to eight-year-old children is not an effective method to prevent dentinal (D3) caries lesions. ART sealants significantly reduced the onset of caries over a period of 18 months.

Trial registration number

German Clinical Trial Register DRKS00003427

     

The chance finding at multislice computed tomography coronary angiography of myocardial bridging

Myocardial bridging is present when a segment of a major epicardial coronary artery, the ‘tunnelled artery’, runs intramurally through the myocardium. With each systole, the coronary artery is compressed. The pathophysiology of myocardial bridging is incompletely understood. With each systole, the coronary artery is compressed. Moreover, intravascular ultrasound analysis revealed a delayed relaxation after systolic compression, which may extend significantly into diastole. This explains both the impaired coronary flow reserve and ischemia. Evidence indicates that the intima beneath the bridge is protected from atherosclerosis, and the proximal segment is more susceptible to the development of atherosclerotic lesions because of haemodynamic disturbances. Myocardial bridging is sometimes associated with overt pathology, as well as it can just be an incidental finding without any significance. Myocardial bridging may cause angina pectoris, myocardial infarction, life threatening arrhythmias and even sudden cardiac death but most of them are harmless. Furthermore depressed left ventricular function, myocardial stunning, early death after cardiac transplantation has been also reported. Although the exact management is not well known, beta blockers seem to be the first choice. Stenting is controversial and one must think “twice” before stenting the bridged coronary artery. We report a case of chance finding at multislice computed tomography coronary angiography of two myocardial bridging. Also this case focuses attention on myocardial bridging and it confirms that multislice computed tomography coronary angiography technology represents a useful, noninvasive imaging method of its assessment.