4 research outputs found
The neuroprotective effect of lamotrigine against glutamate excitotoxicity in SH-SY5Y human neuroblastoma cells
No full textProtective Effect of Artichoke (Cynara scolymus L.) Leaf and Receptaculum Extracts Against Hepatic Encephalopathy in Bile Duct Ligated Rats
No full textHepatic encephalopathy (HE), complication of liver dysfunction, leads to neurocognitive impairments. Artichoke (Cynara scolymus L.) has been traditionally used for its antioxidant, anti-inflammatory and hepatoprotective properties. This study evaluates artichoke leaf and receptaculum extracts in cholestasis and HE in a rat model. Wistar rats were divided into 6 groups: sham-control, bile duct ligation (BDL), and BDL with low/high-dose leaf or receptaculum extracts. After BDL, physiological saline and extracts (250/500 mg/kg) were administered orally for 28 days. Cognitive activity was evaluated using Morris water maze and novel object recognition tests on day 28. Artichoke extract regulated liver enzymes and bilirubin at high-doses and significantly increased antioxidant enzyme activities reduced by BDL. Elevated 8-Hydroxyguanosine (8-OHdG) levels decreased in liver and brain tissues. Similarly, artichoke extracts reduced cytokine and hydroxyproline (HP) levels elevated by cholestasis. Following BDL, Na+/K+-ATPase levels in brain and liver tissues decreased, while artichoke extract reversed this. Artichoke, particularly high-dose receptaculum, improved impaired performance and increased time in the target quadrant after BDL. Both artichoke leaf and receptaculum extracts improved recognition. Artichoke treatments, especially high-dose receptaculum, reduced hepatic and neuronal damage and improved histological appearance. These findings highlight the therapeutic potential of artichoke extracts for liver fibrosis and related neurocognitive disorders
Complete heart block in a patient with acute lymphoblastic leukaemia: Teicoplanin as a possible cause and review of literature
No full textSummary What is known and Objective: Teicoplanin is a glycopeptide antibiotic used against documented or presumed methicillin-resistant infections. We report a 31-month-old boy with acute lymphocytic leukaemia who developed permanent complete atrioventricular block (CAVB) necessitating pacemaker insertion after receiving teicoplanin for Staphylococcus epidermidis bacteremia. Case summary: Clinical assessment of the child revealed febrile neutropenia. After thorough assessment and work-up, the patient was started on teicoplanin intravenously after which he had sudden onset of bradycardia. Electrocardiography showed CAVB that eventually required permanent pacemaker insertion. Twenty-nine months from the incident, the patient is doing well. What is new and Conclusion: We report on a case of teicoplanin-associated CAVB in a child with acute lymphoblastic leukaemia (ALL). This is one of only two similar cases reported in the literature. Teicoplanin remains the most probable cause. The use of teicoplanin should be approached cautiously in the setting of immunosuppression. Whether VZV contributed and teicoplanin triggered remains speculative. Physicians should be aware of this possible complication. © 2012 Blackwell Publishing Ltd.Barbaric D, 2002, LEUKEMIA LYMPHOMA, V43, P2417, DOI 10.1080-1042819021000040161; Chatterjee K, 2010, CARDIOLOGY, V115, P155, DOI 10.1159-000265166; Elliott P, 2006, SEMIN ONCOL, V33, pS2, DOI 10.1053-j.seminoncol.2006.04.020; Enseleit F, 2008, INFECTION, V36, P291, DOI 10.1007-s15010-008-7424-5; ETTEDGUI JA, 1987, INT J CARDIOL, V14, P362, DOI 10.1016-0167-5273(87)90208-7; Ferreira A. L. A., 2008, Cardiovascular and Hematological Agents in Medicinal Chemistry, V6, P278, DOI 10.2174-187152508785909474; Katsuta T, 2011, PEDIATR INFECT DIS J, V30, P445, DOI 10.1097-INF.0b013e3182011286; Khare M, 2003, EXPERT OPIN PHARMACO, V4, P165, DOI 10.1517-14656566.4.2.165; Kilickap S, 2007, SOUTH MED J, V100, P262; Latour C, 2011, ARCH PEDIATRIE, V18, P877, DOI 10.1016-j.arcped.2011.05.017; Levine MC, 2010, CURR OPIN PEDIATR, V22, P278, DOI 10.1097-MOP.0b013e32833924d2; Nurnberg JH, 2002, KLIN PADIATR, V214, P113, DOI 10.1055-s-2002-30145; Prestor VV, 2000, PEDIATR HEMAT ONCOL, V17, P527; RICH R, 1993, AM J EMERG MED, V11, P602, DOI 10.1016-0735-6757(93)90011-Y; SHEA KW, 1995, MED CLIN N AM, V79, P833; Takemura G, 2007, PROG CARDIOVASC DIS, V49, P330, DOI 10.1016-j.pcad.2006.10.002; WOOLF PK, 1987, CLIN PEDIATR, V26, P480, DOI 10.1177-0009922887026009110
Real-life comparison of afatinib and erlotinib in non-small cell lung cancer with rare EGFR exon 18 and exon 20 mutations: a Turkish Oncology Group (TOG) study
No full textObjectives: To compare the survival of first- and second-generation tyrosine kinase inhibitors (TKIs) in patients with rare EGFR exon 18 and exon 20 mutation-positive non-small cell lung cancer (NSCLC). Materials and methods: We retrospectively evaluated survival characteristics of 125 patients with EGFR exon 18 and exon 20 mutated NSCLC who received erlotinib or afatinib as first line treatment between 2012 and 2021 from 34 oncology centres. Since exon 20 insertion is associated with TKI resistance, these 18 patients were excluded from the study. Results: EGFR exon 18 mutations were seen in 60%, exon 20 mutations in 16%, and complex mutations in 24% of the patients with NSCLC who were evaluated for the study. There were 75 patients in erlotinib treated arm and 50 patients in afatinib arm. Patients treated with erlotinib had progression-free survival time (PFS) of 8.0 months and PFS was 7.0 months in the afatinib arm (p = 0.869), while overall survival time (OS) was 20.0 vs 24.8 months, respectively (p = 0.190). PFS of exon 18 mutated arm was 7.0 months, exon 20 mutated arm was 4.3 months, and complex mutation positive group was 17.3 months, and this was statistically significant (p = 0.036). The longest OS was 32.5 months, seen in the complex mutations group, which was not statistically different than exon 18 and in exon 20 mutated groups (21.0 and 21.2 months, respectively) (p = 0.323). Conclusion: In this patient group, especially patients with complex mutations are as sensitive to EGFR TKI treatment similar to classical mutations, and in patients with rare exon 18 and exon 20 EGFR mutation both first- and second-generation EGFR-TKIs should be considered, especially as first- and second-line options. © 2022, The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature
