Partial thrombosis of the inferior vena cava in a patient with non-Hodgkin lymphoma and history of lumbar spine surgery

Complete or partial thrombosis of the inferior vena cava is usually due to pre-existing malformation of the vessel, malignant tumors, ascending thrombosis, or thrombophilic disorders. We report the case of an 81-year-old woman, in whom a partial thrombosis of the vena cava was observed in the CT scan when re-staging was performed after six cycles of R-CHOP because of high-grade malignant non-Hodgkin lymphoma. Before chemotherapy was started, the patient had undergone an operation of the lumbar spine using cement augmentation. Retrospective analysis showed that cement had penetrated a segmental vein and spilled into the vena cava leading to formation of an adhering blood thrombus. The patient was free of symptoms and anticoagulation was started. Spillage of cement frequently occurs in the process of vertebroplasty and kyphoplasty and may result in serious sequelae. As these procedures are increasingly being used, physicians should be aware of these complications if a patient presents with thrombosis of the caval vein or signs of pulmonary embolism.     

Angiographic lesion severity and subsequent myocardial infarction

We sought to determine the angiographic severity of coronary lesions leading to ST-segment elevation myocardial infarction (STEMI) and non-STEMI (NSTEMI) with a focus on determining the impact of interval from initial angiogram to subsequent clinical event. In the late 1980s angiographic data on lesion characteristics that culminated in STEMI and NSTEMI were obtained from angiograms obtained several months before MI. It is not clear whether the conclusions on lesion severity would be different if elapsed interval from baseline angiogram to clinical event was factored in the analysis. From 2003 through 2010, we identified 84 patients with NSTEMI and 41 patients with STEMI in vessels without previous intervention. These patients had ≥1 previous angiographic study at our center. Angiograms were reanalyzed with quantitative coronary angiography, and relevant clinical data were obtained from medical records. Similar to previous studies, 71% of patients with STEMI and 63% of patients with NSTEMI had <50% baseline stenosis at the culprit site when the interval from initial angiogram to MI was >3 months. Interestingly, lesions that led to STEMI ≤3 months after evaluation were more severe than those leading to STEMI in >3 months (59 ± 31% vs 36 ± 21%, p = 0.02) with 57% of lesions having >50% stenosis. Although most MIs occurred at sites that did not have significant obstruction when examined >3 months before MI, most baseline lesions showed significant luminal narrowing when examined ≤3 months before STEMI. In conclusion, high-grade coronary stenosis may be an important predictor of STEMI in subsequent months.     

Up-regulation of a HOXA-PBX3 homeobox-gene signature following down-regulation of miR-181 is associated with adverse prognosis in patients with cytogenetically abnormal AML

Increased expression levels of miR-181 family members have been shown to be associated with favorable outcome in patients with cytogenetically normal acute myeloid leukemia. Here we show that increased expression of miR-181a and miR-181b is also significantly (P < .05; Cox regression) associated with favorable overall survival in cytogenetically abnormal AML (CA-AML) patients. We further show that up-regulation of a gene signature composed of 4 potential miR-181 targets (including HOXA7, HOXA9, HOXA11, and PBX3), associated with down-regulation of miR-181 family members, is an independent predictor of adverse overall survival on multivariable testing in analysis of 183 CA-AML patients. The independent prognostic impact of this 4-homeobox-gene signature was confirmed in a validation set of 271 CA-AML patients. Furthermore, our in vitro and in vivo studies indicated that ectopic expression of miR-181b significantly promoted apoptosis and inhibited viability/proliferation of leukemic cells and delayed leukemogenesis; such effects could be reversed by forced expression of PBX3. Thus, the up-regulation of the 4 homeobox genes resulting from the down-regulation of miR-181 family members probably contribute to the poor prognosis of patients with nonfavorable CA-AML. Restoring expression of miR-181b and/or targeting the HOXA/PBX3 pathways may provide new strategies to improve survival substantially.     

Effects of captopril on factors affecting gastric mucosal integrity in aspirin-induced gastric lesions in Sprague-Dawley rats

Introduction

Captopril is an angiotensin-converting enzyme inhibitor, which is used as an antihypertensive agent and has shown antioxidant properties. This study aims at determining the effects of captopril on factors affecting gastric mucosal integrity in aspirin-induced gastric lesions.

Material and methods

Eighteen male Sprague-Dawley (200-250 g) rats that were given aspirin (40 mg/100 g body weight) were divided into three groups: the control, captopril (1 mg/100 g body weight daily) and ranitidine (2.5 mg/100 g body weight twice daily) groups. Ranitidine and captopril were given orally for 28 days. Rats in all groups were sacrificed and the parameters measured.

Results

Captopril reduced gastric acidity, and increased gastric glutathione (GSH) and prostaglandin E₂ (PGE₂) significantly in comparison to the control group. Captopril also reduced malondialdehyde (MDA) and gastric lesions insignificantly compared to the control group. Ranitidine healed the lesions significantly compared to the control group. There was no difference between ranitidine and captopril on the severity of lesions, gastric acidity, MDA and GSH. Captopril increased PGE₂ compared to ranitidine (p < 0.05).

Conclusions

Captopril has desirable effects on the factors affecting gastric mucosal integrity (acidity, PGE₂ and GSH) and is comparable to ranitidine in ulcer healing.     

Molecular characteristics of extended-spectrum beta-lactamases among gram-negative isolates collected in Cairo University Hospital

Phenotyping is commonly used for detection of extended-spectrum beta-lactamase (ESBL) production in gram-negative isolates. ESBLs are mainly coded for by four important genes, namely bla (TEM), bla (SHV), bla (CTX-M), and bla (OXA). Our aim in this study is to assess use of a multiplex PCR as a rapid method to identify four common genes responsible for ESBL production in different gram-negative isolates. All 793 clinical isolates are subjected to both screen and confirmatory testing for ESBL production using double disc synergy testing (DDST). Two hundred isolates with the ESBL phenotype are subjected to multiplex PCR for detection of the four genes bla (TEM, SHV, CTX-M, and OXA). The isolates were obtained from various clinical specimens: 68 (34 %) were isolated from urine cultures, 43 (21.5 %) from sputum, 26 (13 %) from wounds, 34 (17 %) from blood culture, 20 (10 %) from stool of healthy carrier and nine (4.5 %) from bronchoalveolar lavages. In this study, 83 isolates (41.5 %) were from outpatients (urine and stool specimens only), and the remaining 117 isolates (58.5) were from inpatients. By PCR technique, 181 isolates were found to be ESBL producers. blaTEM was the commonest genotype (39.2 %), followed by blaSHV (32.5 %) and blaCTX-M (30.9 %), either alone or in combination. Acinetobacter baumannii isolate had none of the ESBL genes. Eighteen (9.9 %) out of 181 isolates carried more than one type of beta-lactamase genes. Our study demonstrated rapid detection of bla (TEM, SHV, CTX-M, and OXA) in isolates belonging to Enterobacteriaceae and other nonfermenting clinical isolates using multiplex PCR. This genotypic method provided a rapid and efficient differentiation of ESBLs in the laboratory.     

Serum neutrophil gelatinase-associated lipocalin and cystatin C as markers of renal function in patients with stages 2–5 chronic kidney disease

Individuals with reduced glomerular filtration rate (GFR) are at greater risk for cardiovascular disease and other comorbidities. Creatinine-based equations are used to estimate GFR, identify patients with potential kidney disease, and classify them into different stages since serum creatinine is insensitive to changes in the GFR. The aim of our work was to evaluate diagnostic performance of serum cystatin C and neutrophil gelatinase-associated lipocalin (NGAL) as markers of kidney function in patients with reduced GFR. Fifty cases at different stages of renal impairment and 30 healthy control subjects were tested. Only serum NGAL and cystatin C were higher in stage 2 chronic kidney disease (CKD) when compared to the control group (p?<?0.05). For stages 3–5 the median levels of cystatin C, NGAL, and creatinine were found to be significantly higher than the control group. ROC curve constructed to differentiate stage 2 patients from the controls showed AUC for NGAL 0.795, sensitivity 86%, and specificity 63.3%; AUC for cystatin C 0.957, sensitivity 86%, and specificity 90%; and AUC for creatinine 0.738. Frequency of cases that tested positive for NGAL and cystatin C in stage 2 was higher than those in control group (p?<?0.05) with an OR of 10.364 (95% CI 1.099–97.686) for NGAL and OR 54 (95% CI 4.7–613) for cystatin C. NGAL and cystatin C exhibited higher sensitivity than creatinine for diagnosis of stage 2 CKD. Their use as adjunctive diagnostic tools in patients with mildly reduced GFR may be justified on the long term to diagnose early renal insult.