The efficacy of self-expanding metal stents for palliation of malignant esophageal strictures and fistulas.

OBJECTIVES: Esophageal strictures and esophagorespiratory fistulas are complications of malignant esophageal tumors, which are difficult to manage. The efficacy of self-expanding metal stents (SEMS) for palliation of malignant esophageal strictures and fistulas was investigated prospectively. METHODS: Forty-three SEMS were inserted in 41 patients with malignant esophageal stricture or fistula. Our series included 32 men and nine women, of whom median age was 61.4 years. Twenty nine stents were inserted for stricture, ten for esophago-tracheal fistula, and four esophago-pleural fistula. Stents were inserted endoscopically under fluoroscopic control. RESULTS: SEMS implantation was technically successful in 40 of 41 patients. A second stenting was needed in two patients. Median dysphagia score improved from 3.4 to 1.3. The covered SEMS was succesful in completely sealing 85.7% of the fistulas. Complication occurred in 11 (26.8%) patients. Especially in the case of tumor stenoses in the distal esophagus, complication rate was higher (44%). In total six patients (14.6%) died after stent placement during early postoperative period. Procedure-related mortality was 4.8% (2/41). CONCLUSIONS: We conclude that treatment of malignant esophageal obstructions, including esophagorespiratory fistulas, with SEMS is an alternative palliative procedure. Furthermore SEMS implantation seems more safe in the case of tumor stenoses locating in the middle esophagus.     

Effects of a low-molecular-weight CCR-3 antagonist on chronic experimental asthma

Eosinophils represent one of the main effector cell populations of allergic airway inflammation and allergic bronchial asthma. Their infiltration correlates with many characteristics of the disease, including airway hyperresponsiveness (AHR) and increased mucus production. CCR-3 is the principle chemokine receptor involved in eosinophil attraction into inflamed tissue. Therefore, antagonizing CCR-3 could be a novel promising approach toward asthma therapy. We investigated the effect of a low-molecular-weight CCR-3 antagonist on established airway inflammation in a chronic model of experimental bronchial asthma. For this purpose, BALB/c mice intraperitoneally sensitized with ovalbumin (OVA) were chronically challenged with OVA aerosol to induce chronic airway inflammation and airway remodeling. The effect of antagonizing CCR-3 on asthma pathology was examined in BAL and lung histology. Airway reactivity was assessed by head-out body plethysmography. Treatment with the CCR-3 antagonist resulted in a marked reduction of eosinophils in the bronchoalveolar lumen and in airway wall tissue, whereas infiltration of lymphocytes or macrophages remained unchanged. The reduction in eosinophil infiltration was accompanied by normalization of AHR and prevention of goblet cell hyperplasia, indicating reduced mucus production. Furthermore, antagonizing CCR-3 prevented airway remodeling as defined by subepithelial fibrosis and increased accumulation of myofibrocytes in the airway wall of chronically challenged mice. These data demonstrate that antagonism of CCR3 reduces eosinophil numbers, which is accompanied by diminution of asthma pathology in a mouse model of established chronic experimental asthma. Therefore, antagonizing CCR-3 represents a new approach toward a promising asthma therapy.     

MRI findings in thoracic outlet syndrome

We discuss MRI findings in patients with thoracic outlet syndrome (TOS). A total of 100 neurovascular bundles were evaluated in the interscalene triangle (IS), costoclavicular (CC), and retropectoralis minor (RPM) spaces. To exclude neurogenic abnormality, MRIs of the cervical spine and brachial plexus (BPL) were obtained in neutral. To exclude compression on neurovascular bundles, sagittal T1W images were obtained vertical to the longitudinal axis of BPL from spinal cord to the medial part of the humerus, in abduction and neutral. To exclude vascular TOS, MR angiography (MRA) and venography (MRV) of the subclavian artery (SA) and vein (SV) in abduction were obtained. If there is compression on the vessels, MRA and MRV of the subclavian vessels were repeated in neutral. Seventy-one neurovascular bundles were found to be abnormal: 16 arterial-venous-neurogenic, 20 neurogenic, 1 arterial, 15 venous, 8 arterial-venous, 3 arterial-neurogenic, and 8 venous-neurogenic TOS. Overall, neurogenic TOS was noted in 69%, venous TOS in 66%, and arterial TOS in 39%. The neurovascular bundle was most commonly compressed in the CC, mostly secondary to position, and very rarely compressed in the RPM. The cause of TOS was congenital bone variations in 36%, congenital fibromuscular anomalies in 11%, and position in 53%. In 5%, there was unilateral brachial plexitis in addition to compression of the neurovascular bundle. Severe cervical spondylosis was noted in 14%, contributing to TOS symptoms. For evaluation of patients with TOS, visualization of the brachial plexus and cervical spine and dynamic evaluation of neurovascular bundles in the cervicothoracobrachial region are mandatory.     

Effect of serum uric acid on the positive predictive value of dobutamine stress echocardiography

There is controversial data regarding the relationship between uric acid (UA) and coronary artery disease and cardiovascular events. Despite the deleterious effects of hyperuricemia on endothelial function, the effect of UA on myocardial ischemia has not been previously studied. We aimed to investigate the relationship between UA and myocardial ischemia that was identified using dobutamine stress echocardiography (DSE). In this retrospective study, the laboratory and DSE reports of 548 patients were reviewed. The patients were divided into two groups based on the presence of ischemia and further subdivided into three groups according to the extent of ischemia (none, ischemia in 1–3 segments, ischemia in >3 segments). Serum UA levels were compared. Determinants of ischemia were assessed using a regression model. UA was increased in patients with ischemia and was correlated with the number of ischemic segments (p < 0.001). A cutoff value of UA > 5 mg/dl had 63.9 % sensitivity, 62.0 % specificity, 42.5 % positive predictive value (PPV), and 79.6 % negative predictive value for ischemia. When the positive DSE exams were further sorted according to the UA cutoff, the PPV of DSE increased from 80.2 to 94.0 %. Uric acid (odds ratio 1.51; 95 % CI 1.14–1.99), diabetes mellitus, HDL and glomerular filtration rate were found to be independent determinants of myocardial ischemia in DSE. Increased UA is associated with both the presence and extent of DSE-identified myocardial ischemia. A UA cutoff may be a good method to improve the PPV of DSE.     

Vascular endothelial function and plasma homocysteine levels in Behcet's disease

The purpose of the present study was to test endothelial function and to determine if plasma homocysteine levels are associated with endothelial injury in patients with Behcet's disease (BD). Flow-mediated dilation in patients with BD was smaller than that of control subjects (p = 0.001), and mean plasma homocysteine levels in patients with BD were significantly higher (p = 0.0001). On regression analysis, only mean plasma homocysteine concentration was independently related to flow-mediated dilation (F = 5.7, p = 0.001).     

Subclinic arterial and left ventricular systolic impairment in autosomal dominant polycystic kidney disease with preserved renal functions

The International Journal of Cardiovascular Imaging - Subclinical atherosclerosis and cardiovascular events are common even in young normotensive patients with autosomal dominant polycystic kidney...     

Sudden Unilateral Vision Loss Arising from Calcified Amorphous Tumor of the Left Ventricle

Calcified amorphous tumor of the heart is a very rare non-neoplastic intracavitary mass. The clinical presentation is similar to that of other cardiac masses. The precise cause and best approach to treatment remain unclear. We describe a case of cardiac calcified amorphous tumor presenting with refractory unilateral vision loss that was successfully treated by surgical excision. To our knowledge, this is only the 2nd reported case of retinal arterial embolism due to cardiac calcified amorphous tumor in the English-language literature.Key words: Blindness/etiology, calcinosis/complications/radiography/surgery, diagnosis, differential, tumor, cardiac calcified amorphous, vision loss, suddenCalcified amorphous tumor (CAT) of the heart is a very rare non-neoplastic cardiac intracavitary mass. It was first described as a distinct pathologic entity by Reynolds and colleagues in 1997.¹ Since then, very few cases of cardiac CAT have been reported in the English-language medical literature^2–19 (12 TABLE I. Clinicopathologic Findings of Published Cases of Cardiac Calcified Amorphous Tumor Open in a separate window TABLE I, continued. Clinicopathologic Findings of Published Cases of Cardiac Calcified Amorphous Tumor Open in a separate window In the present report, we describe a case in which cardiac CAT presented with refractory unilateral vision loss, which was successfully treated by surgical excision.     

CEFEPIME VERSUS CETAZIDIME AMIKACIN AS EMPIRICAL THERAPY FOR FEBRILE NEUTROPENIA IN CHILDREN WITH CANCER: A Prospective Randomized Trial of the Treatment Efficacy and Cost

The efficacy, safety, and cost of cefepime and ceftazidime + amikacin as empirical therapy in children with febrile neutropenia is compared. A prospective randomized study in children with cancer was conducted. Patients were randomly assigned to receive either cefepime 150 mg/kg/day or ceftazidime 150 mg/kg/day combined with amikacin 15 mg/kg/day. Treatment modification was defined as all the changes in the empirical antimicrobials after the first 72 h. Overall treatment success was defined as cure of febrile episode with or without modification. Costs of hospitalization, antimicrobial drugs, and supportive therapy were calculated. Fifty febrile netropenic episodes were evaluated. Infectious agents were microbiologically identified in 28% of episodes. The incidence of gram-negative and gram-positive isolates was equal. Overall treatment success was 100% and success of initial empirical therapy without modification was 52 and 40% in the cefepime and cefepime + amikacin groups, respectively. The response rate after glycopeptides were added to the regimen was 64 and 52% in the cefepime and cefepime + amikacin arms, respectively. Glycopeptide and antifungal drugs were added more frequently in the ceftazidime + amikacin group. Duration of fever, hospitalization, and antimicrobial drug administration were longer in the ceftazidime + amikacin arm. The costs of the antimicrobial drugs, hospitalization, and total cost were lower in the cefepime arm. Cefepime monotherapy is as effective as ceftazidime + amikacin combination in febrile neutropenia of pediatric cancer patients and must be preferred due to shorter defervescence of fever, shorter hospitalization, and lower therapy cost.