Does COVID-19 infection significantly affect liver transplantation? Results of liver transplantation in the COVID-19 era at a single, high-volume centre.

BACKGROUND: Liver transplantation is a proven management method for end-stage cirrhosis and is estimated to have increased life expectancy by 15 years. The COVID-19 pandemic posed a challenge to patients who were candid for a solid-organ transplant. It has been suggested that the outcomes of liver transplants could be adversely affected by the infection, as immunosuppression makes liver transplant candidates more susceptible to adverse effects while predisposing them to higher thrombotic events. MATERIAL AND METHODS: In this retrospective study, the cases who received liver transplants from January 2018 to March 2022 were assessed regarding early postoperative mortality rate and hepatic artery thrombosis (HAT) with COVID-19 infection. This study included 614 cases, of which 48 patients were infected. RESULTS: This study shows that the early COVID-19-related early postoperative mortality rates substantially increased in the elective setting (OR: 2.697), but the results for the acute liver failure were insignificant. The average model for end-stage liver disease score increased significantly during the pandemic due to new regulations. Although mortality rates increased during the pandemic, the data for the vaccination period show that mortality rates have equalised with the prepandemic era. Meanwhile, COVID-19 infection is assumed to have increased HAT by 1.6 times in the elective setting. CONCLUSION: This study shows that COVID-19 infection in an acute liver failure poses comparatively little risk; hence transplantation should be considered in such cases. Meanwhile, the hypercoagulative state induced by the infection predisposes this group of patients to higher HAT rates.

Idiopathic methicillin-susceptible Staphylococcus aureus associated tricuspid valve endocarditis and pneumothorax in a patient without apparent predisposing factor: a case report.

Pneumothorax following right-sided bacterial endocarditis is an infrequent medical complication usually reported in cases with a history of intravenous drug abuse. The following report describes the condition of a girl without congenital heart disease or a history of intravenous drug abuse who developed pneumothorax secondary to endocarditis.

Disseminated TB in an Immunocompetent Patient: A Case Report.

BACKGROUND: Tuberculosis considered as a chronic infectious disease caused by Mycobacterium tuberculosis, may invade all organs but mainly affects the lungs. Overall, disseminated TB is rare in immunocompetent patients and its association with seborrheic keratosis has never been reported. ; Case Presentation: We reported a 54-year-old man with a complaint prolonged fever, abdominal pain, weight loss and lymphadenopathy without any immunosuppression who was eventually treated based on the diagnosis of diffuse tuberculosis.

Influence of central nicotinic receptors on arachidonylcyclopropylamide (ACPA)-induced antinociception in mice.

The nicotinic cholinergic receptors have been reported to be involved in several actions of cannabinoids (e.g., bradycardia, hypothermia). However, the influence of central cholinergic system on cannabinoids antinociceptive effect has not been reported. This study investigated the possible part played by nicotinic cholinergic modulator drugs on the antinociceptive effect of central administration of arachidonylcyclopropylamide (ACPA) in mice. The antinociceptive effects of intracerebroventricular (i.c.v.) administration of ACPA using the formalin test have been studied in mice. The effects of nicotine or mecamylamine (a nicotinic cholinergic antagonist) on ACPA analgesia are also studied. i.c.v. administration of ACPA (0.004-1 microg/mice) induced antinociceptive effect in mice. i.c.v. administration of nicotine (0.1 or 0.5 microg/mice) or mecamylamine (2 microg/mice) potentiated or antagonized ACPA antinociceptive effects, respectively. It is concluded that ACPA-induced analgesia is influenced by central nicotinic cholinergic activity.