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  • Wang Fischer posted an update 20 days ago

    86), nor postoperative course differed between patients with and without biliary complications. Risk factors for mortality within 1 year were cirrhosis caused by entities other than viral hepatitis (P=0.017), cardiac comorbidities (P=0.019), re-transplantation (P=0.032), and reduced organ weight (P=0.002). Biliary complications, postoperative hemorrhage, primary nonfunction, and repeated surgery worsened outcome; moreover, serum bilirubin trough in the first 30 days after transplantation might be prognostic for mortality (P=0.043). CONCLUSIONS Biliary complications adversely affect outcome after liver transplantation. Neither frequency nor outcome of biliary complications was improved by intensified endoscopic evaluation. Patients on the waiting list for liver transplants should also be closely monitored for cardiac comorbidities.BACKGROUND Amiodarone is an anti-arrthymic drug used to treat and prevent several types of dysrhythmias. This drug is known for multiple-organ toxicity. Lung toxicity occurs in about 1% to 5% of cases. A wide variety of lung manifestations have been described, from mild to severe forms. Pulmonary toxicity can be acute, sub-acute, or chronic. Amiodarone-induced lung toxicity is a diagnosis of exclusion. The main treatment is discontinuation of the drug. Lung disease may progress initially due to the prolonged half-life and the accumulation of amiodarone in adipose tissue. Regarding the prognosis, lung toxicity can be reversible, but in some cases, it is irreversible and is sometimes fatal. The risks associated with its use must always be considered. Amiodarone should only be used for short periods. CASE REPORT The authors present a case of a 71-year-old female patient, taking amiodarone 200 mg/day for 18 months. The patient presented with amiodarone-induced lung toxicity. After drug withdrawal, without corticosteroid therapy, we observed clinical, functional, and radiological improvement. CONCLUSIONS This case shows that not all cases of amiodarone-induced lung toxicity require corticosteroid therapy, and highlights that is important to consider this diagnosis in patients on amiodarone therapy with respiratory symptoms.In December 2019, pneumonia of unknown cause broke out, and currently more than 150 countries around the world have been affected. Globally, as of 5 46 pm CET, 6 November 2020, the World Health Organization (WHO) had reported 48 534 508 confirmed cases of COVID-19, including 1 231 017 deaths. The novel coronavirus disease (COVID-19) outbreak, caused by the SARS-CoV-2 virus, is the most important medical challenge in decades. Previous research mainly focused on the exploration of lung changes. selleck inhibitor However, with development of the disease and deepening research, more and more patients showed cardiovascular diseases, even in those without respiratory symptoms, and some researchers have found that underlying cardiovascular diseases increase the risk of infection. Although the related mechanism is not thoroughly studied, based on existing research, we speculate that the interaction between the virus and its receptor, inflammatory factors, various forms of the stress response, hypoxic environment, and drug administration could all induce the development of cardiac adverse events. Interventions to control these pathogenic factors may effectively reduce the occurrence of cardiovascular complications. This review summarizes the latest research on the relationship between COVID-19 and its associated cardiovascular complications, and we also explore possible mechanisms and treatments.An editorial decision has been made to retract this manuscript due to breach of publishing guidelines, following the identification of non-original and manipulated figures.ReferenceYong Xiong, Yi-Jia Xiong, Dong-Yang Liu, Rong-Rong Shen Pancratistatin Inhibits the Growth of Colorectal Cancer Cells by Inducing Apoptosis, Autophagy, and G2/M Cell Cycle Arrest.Med Sci Monit 2019; 256015-6022. 10.12659/MSM.916116.Hypertrophic pachymeningitis (HP) is a rare clinical entity which uncommonly occurs in rheumatoid arthritis (RA) patients. We describe the case of a rheumatoid factor and anti-citrullinated protein antibody positive RA male that was diagnosed with HP and multiple mononeuropathy. Although histological evaluation was not performed, after excluding infectious and neoplastic causes, it was possible to determine a probable inflammatory etiology. He was treated with glucocorticoids and rituximab with a good clinical evolution. This case represented a challenging differential diagnosis but the need for an accurate diagnosis should not delay the introduction of an effective therapy for a potentially lethal disease.

    Thiols are crucial anti-oxidant agents that contain a sulfhydryl group; they play an important role in defence against reactive oxygen species. We aimed to determine the thiol/disulphide homeostasis in rheumatoid arthritis (RA) patients in conjunction with its association with disease activity, preclinical atherosclerosis, and other disease-related indices.

    We enrolled 64 RA patients without known cardiovascular (CV) disease or risk factors and 46 healthy controls. Disease activity was evaluated using the Disease Activity Score 28-erythrocyte sedimentation rate (DAS28-ESR). Thiol/disulphide homeostasis was evaluated using a novel automated method, and serum native thiol (NT), total thiol (TT), and disulphide(SS) levels were recorded. The carotid intima media thickness (CIMT) was measured using carotid ultrasound to evaluate preclinical atherosclerosis.

    The NT and TT levels were significantly lower in RA patients than in controls (231.7 ± 52.3 vs. 293.6 ± 74.8 µmol/L, p < 0.001; 271.6 ± 52.1 vs. 331.3disulphide homeostasis for CV risk stratification and risk prediction in RA patients.

    RA patients without known CV disease or risk factors exhibited increased CIMT values and decreased thiol levels; moreover, thiol levels were found to be correlated with disease activity. Further studies are needed to detect the value of thiol/disulphide homeostasis for CV risk stratification and risk prediction in RA patients.

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