Hilal Ermis

Protective and Therapeutic Effect of Apocynin on Bleomycin-Induced Lung Fibrosis in Rats

We aimed to investigate the preventive and therapeutic effect of apocynin (APO) on bleomycin (BLC)-induced lung injury in rats. Rats were assigned into groups as follows: control group; APO group, 20 mg/kg APO was given intraperitoneal for 29 days; BLC-1 and BLC-2 groups, a single intratracheal injection of BLC (2.5 mg/kg); APO+BLC-preventive group, 20 mg/kg APO was administered 12 h before the intratracheal BLC injection and continued for 14 days; BLC+APO-treatment group, 20 mg/kg APO was given on the 14th day after the intratracheal BLC injection and continued to sacrifice. The BLC-1 group was sacrificed on the 14th day of BLC administration to validate BLC-induced lung inflammation and fibrosis on the 14th of study initiation. All other groups were sacrificed on the 29th day after BLC administration. The semiquantitative histopathological assessment, tissue levels of malondialdehyde (MDA), superoxide dismutase, catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), total antioxidant capacity, total oxidant status (TOS), and oxidative stress index (OSI) were measured. An addition to the serum myeloperoxidase (MPO), the cell count and cytokines (IL-1β, IL-6, and IL-8) of bronchoalveolar lavage (BAL) fluid were assayed. BLC-provoked histological changes were significantly detected compared to the control group. APO restored these histological damages in different quantity in the treatment and prevention groups. BLC caused a significant decrease in GSH, CAT, and GPX, which were accompanied with significantly the increased MDA, TOS levels, and OSI in the lung tissue concomitant with increased levels of the cellular account and proinflammatory cytokines in the BAL fluid. Otherwise, APO administration, both before and after BLC, reversed all biochemical markers and cytokine as well as histopathological changes induced by BLC. Interestingly, APO treatment reversed MPO activity in serum increased by BLC. In this study, both protective and therapeutic effects of APO against BLC-induced lung fibrosis were demonstrated for the first time.

QT dispersion in patients with pulmonary embolism

ZusammenfassungHINTERGRUND: Verschiedene EKG Veränderungen sind mit der akuten Pulmonal-Embolie in Zusammenhang gebracht worden. Bezüglich möglicher Veränderungen des QT-Intervalls liegen allerdings keine Daten vor. Das Ziel unserer Studie war es, zu prüfen, ob es einen Zusammenhang zwischen Veränderungen des QT Intervalls und dem Schweregrad der Pulmonalembolie gibt. METHODEN: 129 Patienten mit Pulmonalembolie (mittleres Alter 58 ± 16.5 Jahre) mit einem EKG innerhalb der ersten 24 Stunden nach Spitals-Aufnahme wurden in die Studie inkludiert. Die Patienten wurden in Gruppen mit niedrigem, mit mittlerem und mit hohem Risiko eingeteilt. Retrospektiv wurden folgende EKG Parameter bei alle Gruppen gemessen: korrigierte maximale und minimale QT-Zeit (QTcmax und QTcmin) und korrigierte QT-Intervall Dispersion (QTcd, definiert als die Differenz zwischen QTcmax und QTcmin). Ausserdem wurde ein EKG score (bestehend aus Sinustachycardie, komplettem und inkomplettem Rechtsschenkelblock, T Inversion und S1Q3 Typ) erstellt. ERGEBNISSE: Der EKG score stieg vom niedrigem zu hohem Risiko der Pulmonalembolie an [3 (Interquartile Range, IQR: 2), 5 (IQR: 6) und 10 (IQR: 7) p < 0,0001]. Die QT Intervall Analyse zeigte, dass die QTcd in der Hoch Risiko Gruppe höher als in den Gruppen mit niedrigem und mittleren Risiko war (59,5 ± 23,4, 69,2 ± 21, 95,9 ± 33,2, p < 0,001 beziehungsweise p = 0,01). Patienten, die nach Diagnosestellung starben hatten signifikant höhere QTcd Werte bei der Aufnahme als die überlebenden Patienten (89,1 ± 45,5 to 65 ± 22,9, p = 0,001). Die Sensitivität eines QTcd von mehr als 71,5 ms in Bezug auf die Vorhersagefähigkeit bezüglich Mortalität war bei 71%. Die Spezifität bei 73% (p = 0,001). Wir beobachteten einen hoch signifikant Zusammenhang zwischen QTcd und den EKG score Werten (r = 0,69, p < 0,001). Der Pulmonalarterien Druck war auch – allerdings deutlich schwächer - mit den QTcd Werten korreliert (r = 0,27, p = 0,05). SCHLUSSFOLGERUNGEN: Die QTcd steigt bei Hoch Risiko Pulmonalembolie Patienten im Vergleich zu Patienten mit geringerem Risiko signifikant an. Außerdem ist die QTcd signifikant mit dem EKG score und dem Pulmonalarteriendruck korreliert.SummaryBACKGROUND: Various ECG patterns have been associated with acute pulmonary embolism. However, there is no data regarding the association between QT interval measurements and pulmonary embolism. We aimed to investigate the association between QT dispersion and the severity of pulmonary embolism (PE). METHODS: One hundred twenty-nine pulmonary embolism patients (mean age 58 ± 16.5 years) with ECGs obtained within the first 24 hours of hospital admission were included in the study. Patients were classified into low, intermediate and high-risk groups. We retrospectively measured ECG scores; maximum and minimum corrected QT intervals (QTcmax and QTcmin) and corrected QT interval dispersion (QTcd) in each risk group of patients. RESULTS: There was an increasing ECG score through from low to high-risk PE [3 (Interquartile Range, IQR: 2), 5 (IQR: 6) and 10 (IQR: 7) p < 0.0001]. QT interval analysis showed that QTcd was higher in high-risk group than in low and intermediate-risk groups (59.5 ± 23.4, 69.2 ± 21, 95.9 ± 33.2, p <0.001 and p = 0.01, respectively). Patients who died after diagnosis had significantly higher QTcd values at baseline compared with the QTcd values of surviving patients (89.1 ± 45.5 to 65 ± 22.9, p = 0.001). The sensitivity of QTcd > 71.5 ms for prediction of mortality was 71% with a specificity of 73% (p = 0.001). We observed a strong correlation between QTcd and ECG score values (r = 0.69, p< 0.001). There was also a correlation between QTcd values and pulmonary artery pressure (PAP) (r = 0.27, p = 0.05). CONCLUSION: QTcd is significantly increased in high-risk PE patients compared to intermediate and low-risk patients. In addition, QTcd is significantly correlated with ECG score and PAP.

Neuromuscular transmission in hypoxemic patients with chronic obstructive pulmonary disease

Many studies have focused on the systemic effects of chronic obstructive pulmonary disease (COPD), but none has examined neuromuscular junction transmission (NMT). We evaluated NMT dysfunction using single-fiber electromyography (SFEMG) in patients with COPD. Twenty patients with COPD and 20 age-matched healthy controls were included in the study. All patients and controls underwent SFEMG. Abnormal NMT was found in seven of 20 patients (35%), but in none of the control subjects. The COPD patients were subgrouped according to the presence of hypoxemia. The patients with normoxemia were classified as Group 1, and the patients with hypoxemia were classified as Group 2. Abnormal NMT was found in six patients in Group 2 and in one in Group 1. While there was significant difference in terms of abnormal NMT between Group 2 and the controls, there was none between Group 1 and the controls. Our results show that NMT abnormalities can be present in hypoxemic patients with COPD.

Anticoagulant therapy for acute venous thromboembolism

Deep vein thrombosis (DVT) and pulmonary embolism (PE) are currently defined as venous thromboembolism (VTE) since they share pathophysiological features and the treatment is similar in many respects. It has been determined that more than 90% of PE cases originate from DVT in the legs. PE, which is difficult to diagnose, has a mortality rate of 12% when untreated. The worldwide increase in obesity, cancer diseases, and average survival time also contribute to the increase in the incidence of VTE. Traditional treatment of VTE includes heparin, low-molecular-weight heparin, and warfarin. Despite availability for oral use, warfarin has a narrow therapeutic range and a wide range of food interactions. After many years of research, new oral anticoagulant agents (NOACs) are expected to overcome these handicaps in treatment. In this review, the use of NOACs in the treatment of VTE is investigated in the light of current guidelines.

Pulmoner emboli için kazanılmış olası yeni bir risk faktörü: Kolonoskopi işlemi

Knowing the risk factors of PE contributes to the promptness of diagnosis and treatment. Although most patients with pulmonary embolism (PE) have acquired or hereditary risk factors, the cause of PE is unknown in one-quarter of patients. We describe a 66-year-old man who presented with chest pain, dyspnea, and hemoptysis one day after he had a colonoscopy performed due to chronic constipation complaints. The computed tomography pulmonary angiography revealed thrombus in the left peripheral pulmonary artery. He did not have any risk factors for PE, and a hypercoagulable workup was normal. Because of his development of PE one day after his colonoscopy and the absence of any risk factors, the colonoscopy could have caused the PE. PE may be caused by increased intra-abdominal pressure during this procedure. This is the first case of PE following a colonoscopy in the literature. We recommend that patients with idiopathic PE should be questioned aspect of invasive procedures such as colonoscopy.