Treatment Strategies And Outcomes Of Thoracic Aortic Blunt Injuries In Adults: A Systematic Review.

INTRODUCTION: Blunt thoracic aortic injuries (BTAI) once had mortality rates up to 32%, but the advent of thoracic endovascular aortic repair (TEVAR) has significantly improved outcomes. However, concerns persist regarding long-term devicerelated complications, device integrity in aging aortas, and the criteria for selecting patients for endovascular repair. We aimed to assess BTAI treatment strategies based on injury grade and their associated outcomes. METHODS: A systematic search of MedLine and Scopus databases was conducted to identify original articles published after 2013, which provided information on injury characteristics, outcomes, secondary effects, and reinterventions following BTAI. We classified aortic injuries following the SVS Clinical Practice Guidelines. RESULTS: We included 28 studies involving 1888 BTAI patients, including 5 prospective studies. Most patients were under 45 years old (86.4%), and grade III injuries were the most common (901 patients), followed by grades I and II (307 and 291 patients, respectively). TEVAR was performed in 1458 patients, mainly with grade III and IV injuries (1040 patients). Approximately half of the grade I injuries (153 of 307) were treated with TEVAR. Thirty-day mortality rate was 11.2%, primarily due to associated injuries. Aortic-related deaths were reported in 21 studies, with an overall rate of 2.2%, but none occurred beyond the first 30 days. Partial or complete coverage of the left subclavian artery was performed in 522 patients, with 27.9% requiring immediate or delayed revascularization. Aortic reintervention rates were relatively low (3.9%). CONCLUSION: TEVAR effectively treats BTAI grades III and IV, with potential benefit for some grade II injuries with more aggressive early intervention. Despite SVS guidelines suggesting conservative management for grade I injuries, there is a substantial rate of intervention with positive outcomes and low mortality. Long-term follow-up data, extending up to almost 20 years, reveal the durability of grafts, aortic remodeling, and minimal reintervention and complications.

Clinical and Forensic Aspects of Pharmacobezoars.

BACKGROUND: Pharmacobezoars are specific types of bezoars formed when medicines, such as tablets, suspensions, and/or drug delivery systems, aggregate and may cause death by occluding airways with tenacious material or by eluting drugs resulting in toxic or lethal blood concentrations. OBJECTIVE: This work aims to fully review the state-of-the-art regarding pathophysiology, diagnosis, treatment, and other relevant clinical and forensic features of pharmacobezoars. RESULTS: Patients of a wide range of ages and of both sexes present with signs and symptoms of intoxications or more commonly gastrointestinal obstructions. The exact mechanisms of pharmacobezoar formation are unknown but are likely multifactorial. The diagnosis and treatment depend on the gastrointestinal segment affected and should be personalized to the medication and the underlying factor. A good and complete history, physical examination, image tests, upper endoscopy, and surgery through laparotomy of the lower tract are useful for diagnosis and treatment. CONCLUSION: Pharmacobezoars are rarely seen in clinical and forensic practice. They are related to controlled or immediate-release formulations, liquid, or non-digestible substances, in normal or altered digestive motility/anatomy tract, and in overdoses or therapeutic doses, and should be suspected in the presence of risk factors or patients taking drugs which may form pharmacobezoars.

High density lipoprotein is an inappropriate substrate for hepatic lipase in postmenopausal women.

BACKGROUND: HDL antiatherogenic effects would not only depend on its concentration but also on its biological quality. Hepatic lipase (HL) action on HDL acts in one of the last steps of reverse cholesterol transport. Cardiovascular risk increases after menopause, however HDL does not decrease even when HL is increased. We evaluated HDL capacity as a substrate of HL in healthy postmenopausal women (PMW). METHODS: We studied 20 PMW (51-60 y) and 20 premenopausal (PreMW) (26-40 y). In fasting serum, lipid-lipoprotein profile and HDL composition were assessed. Optimal assay conditions for HDL/HL ex vivo incubation were established. Increasing HDL-triglyceride concentrations (0.015 to 0.20 mmol/l) were incubated with post-heparin plasma obtained from a single healthy donor as a source of HL. Free fatty acids were measured and kinetic parameters calculated: K(m)(app), inverse to enzyme affinity, and V(max). RESULTS: HDL composition in PMW exhibits triglyceride enrichment (p<0.001). Kinetic analysis revealed higher K(m)(app) in PMW [130 (40-380) vs 45 (20-91) mmol/l, p<0.0001)] correlating directly with HDL-triglycerides (r=0.7, p=0.0001). Catalytic efficiency, V(max)/K(m)(app) was reduced when compared to controls (p=0.0001). CONCLUSION: Triglyceride-enriched HDL from PMW constitutes a poor substrate for HL suggesting that this particle may not exert efficiently its antiatherogenic function, regardless of plasma concentration.

Expresión de oncogenes y estado de integración del Papilomavirus Humano (HPV) como posibles marcadores de progresión maligna en pacientes con lesiones cervicales: estudio preliminar en la ciudad de Buenos Aires / Viral oncogene expression and integration status of the human papillomavirus as possible markers of malignant progression in patients with cervical lesions

Introducción: el Papilomavirus Humano (HPV) ha sido identificado como agente causal del cáncer cervical, induciendo lesiones cervicales de bajo grado que, eventualmente, se malignizan debido a distintos factores. La expresión de oncogenes virales y el estado de integración viral son necesarios para el desarrollo de neoplasias, por lo que podrían utilizarse como marcadores de progresión maligna en éste tipo de lesiones. Objetivo: evaluar la expresión de los oncogenes virales E6/E7 de HPV16 y 18 y el estado del genoma viral como posibles marcadores de progresión maligna. Materiales y métodos: se evaluaron muestras de lesiones cervicales (n = 27 controles (Ctrl), n = 18 CIN I, n= 24 CIN II/III y n = 32 Carcinomas invasivos (CC) derivadas del Hospital Gral. de Agudos C. Durand, CABA. Se evaluó la presencia de genoma consenso HPV y específico HPV16 y 18 mediante dPCR. Se determinó la expresión de oncogenes virales E6/E7 de HPV16 y HPV 18 y el estado de integración viral se analizó mediante PCR-APOT. Resultados: se observó un aumento significativo de presencia de genoma viral en correlación con el grado de lesión analizada CIN I: 77,8 %, CIN II/III: 83,3 % y CC: 100 % en comparación con el grupo control (25,9 %, p<0,001). La infección con HPV16 fue significativamente mayor en todos los grupos (vs. HPV18, p<0,001), encontrándose coinfección en varios casos. La expresión de los oncogenes virales de HPV16 fue significativamente mayor en comparación con HPV18 (p<0,0001). El estado físico de los genomas virales mostró una tendencia a la forma integrada en correlación con el grado de lesión analizada, encontrándose mayor presencia de genomas integrados en CC (vs. Episomal y/o episomal e integrado p<0,02) de HPV16. Para HPV18, sólo pudimos observar genomas integrados en CIN II/III (100 %) y CC (50 %). Sólo el 12,5 % de los genomas HPV 18 fueron detectados episomal e integrado. Conclusiones: observamos altas frecuencias de infección con HPV16 en comparación con HPV 18...

Introduction: Human Papillomavirus (HPV) has been identified as causal agent of cervical cancer, inducing cervical low grade lesions that, eventually, maligniza due to different factors. Viral oncogene expression and integration status are necessary for neoplasic development, and they could be used as malignant progression markers in these types of lesions. Aim: Evaluate HPV16 and 18 (E6/E7) viral oncogene expression and genome integration status as possible malignant progression markers. Materials and methods: Cervical samples derived from Hospital GA C. Durand (CABA) were evaluated (n = 27 healthy controls -Ctrl-, n = 18 CINI, n = 24 CIN II/III abd b = 32 Invasive Carcinomas (CC). HPV consensus and HPV16 and 18 specific genomes were evaluated by PCR. Viral oncogene expression (E6/E7) of HPV16 and HPV18 was determined, as well as viral integration status was determined by means of PCR-APOT. Results: A significant increase in viral genome presence was observed in correlation with the degree of the lesion analyzed CIN I: 77,9%, CIN II/III: 83,3% y CC: 100% in comparison to control Group (25,9% p<0,001). The infection with HPV16 was significantly greater in all the groups in comparison with HPV18 (p<0,001); co-infection was detected in several cases. HPV 16 oncogene expression was greater than the one showed by HPV-18 (p<0,0001). The physcal state of the viral genomes showed a tendency to the integrated form in correlation with the degree of analyzed lesion, detecting most of integrated HPV16 genomes in CC group (vs. episomal and/or episomal and integrated, p<0,02), FORM II/III (100%) and CC (50%). Only a minor fraction of HPV18 genomes in CC where found to be, both, episomal and integrated (12,5%). Conclusions: We have detected higher HPV16 infection frequencies in comparison with HPV18 in all analyzed groups. On the other hand, we observed an increase in HPV-16 onocogene expression in comparison to HPV18 ones. HPV16 was found predominantly integrated...

Impaired high density lipoprotein antioxidant activity in healthy postmenopausal women.

The high incidence of atherosclerosis in women after menopause is associated with a risk pattern including an increase in low density lipoprotein (LDL), even though high density lipoprotein (HDL) cholesterol levels tend to be maintained or slightly decreased. Since estrogens are considered potent antioxidants, an increase in lipid peroxidation and formation of reactive oxygen species would be expected after menopause. If HDL becomes oxidized, the ability to protect LDL against oxidation may be impaired. In postmenopausal women there are scarce reports concerning HDL oxidability and no data about its antioxidant activity. We studied copper-induced oxidation and conjugated dienes formation in HDL isolated from 58 women, 30 postmenopausal (PMW) and 28 premenopausal (PreMW). None presented diabetes or cardiovascular disease and none was receiving hormonal, hypolipidemic or antioxidant therapy either. In order to evaluate the effect of HDL on LDL oxidation we isolated LDL and HDL from the same subject and assessed copper-induced LDL oxidation in the presence of HDL, followed by thiobarbituric acid-reactive substances determination. Relationships with HDL chemical composition, alpha-tocopherol content, cholesteryl ester transfer protein (CETP) and paraoxonase activity (PON) were investigated. HDL chemical composition in PMW exhibited triglyceride enrichment when compared to PreMW (p <0.05). alpha-Tocopherol content and CETP activity were similar in both groups. However, CETP activity correlated positively with HDL triglyceride and negatively with HDL cholesterol percentage (r=0.44, p <0.01 and r=-0.32, p <0.05, respectively). Paraoxonase activity did not show differences between PMW and PreMW. When evaluating HDL oxidability, PMW revealed a shorter lag time in comparison to PreMW, even after adjustment for age, p <0.05. Moreover, when the effect of HDL on LDL oxidation was evaluated, HDL from PMW showed a reduction in its ability to inhibit LDL oxidation, compared to PreMW (p <0.05). In addition, the extent of inhibition of LDL oxidation by HDL was positively correlated with HDL resistance to oxidation (r=0.27, p <0.05). After women classification by paraoxonase phenotype, HDL ability to protect LDL against oxidation remained reduced only in PMW belonging to the PON QR phenotype, in comparison to PreMW QR. These results suggest that HDL from PMW exhibits impairment in its antioxidant ability, which is associated to a decreased HDL resistance to oxidation. In turn, this was related to triglyceride enrichment of HDL particles. All these alterations were independent from HDL cholesterol plasma levels.