RESUMO
Gastrointestinal bleeding is a frequent symptom, with increasing age as a risk factor. Upper, middle and lower gastrointestinal bleeding are differentiated depending on the location, whereby only upper and lower gastrointestinal bleeding are elucidated in this article. The symptomatology varies depending on the localization of the bleeding. German and international clinical guidelines currently exist for the preclinical and clinical management of gastrointestinal bleeding. The main focus of the article is on pre-endoscopic management of upper gastrointestinal nonvariceal and variceal bleeding, including the risk stratification, transfusion and coagulation management as well as the initial pharmacological treatment. In addition, current developments in endoscopic and interventional treatment of gastrointestinal bleeding are highlighted.
Assuntos
Varizes Esofágicas e Gástricas , Hemorragia Gastrointestinal , Humanos , Hemorragia Gastrointestinal/diagnóstico , Hemorragia Gastrointestinal/etiologia , Hemorragia Gastrointestinal/terapia , Varizes Esofágicas e Gástricas/complicações , Fatores de Risco , Endoscopia/efeitos adversosRESUMO
INTRODUCTION: Coronavirus disease 2019 (COVID-19) can lead to many extrapulmonary manifestations. In this case series, we report on 7 patients developing secondary sclerosing cholangitis (SSC) after severe COVID-19 with intensive care treatment. METHODS: Between March 2020 and November 2021, 544 patient cases with cholangitis treated at a German tertiary care centre were screened for SSC. Patients found to be suffering from SSC were assigned to COVID-19 group if SSC presented after a severe course of COVID-19 and to non-COVID-19 group if not. Peak liver parameters as well as intensive care treatment factors and data generated from liver elastography were compared between both groups. RESULTS: We identified 7 patients who developed SSC after a severe course of COVID-19. In the same period, 4 patients developed SSC due to other causes. Mean values of gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP) were higher in the COVID-19 group than in the non-COVID-19 group (GGT: 2,689 U/L vs. 1,812 U/L and ALP: 1,445 U/L vs. 1,027 U/L), whereas intensive care treatment factors were comparable in both groups. Only the mean duration of mechanical ventilation was shorter in the COVID-19 group than in the non-COVID-19 group (22.1 days vs. 36.7 days). Liver elastography indicated a fast progression to liver cirrhosis with a mean liver stiffness of 17.3 kilopascals (kPa) in less than 12 weeks in the COVID-19 group. CONCLUSIONS: Our data suggest a more severe course of SSC when caused by SARS-CoV-2. Reasons for this are probably multifactorial, including a direct cytopathogenic effect of the virus.
Assuntos
COVID-19 , Colangite Esclerosante , Humanos , Colangite Esclerosante/complicações , Colangite Esclerosante/diagnóstico por imagem , Colangite Esclerosante/terapia , COVID-19/complicações , SARS-CoV-2 , Cirrose Hepática/complicações , Fosfatase AlcalinaRESUMO
BACKGROUND AND RATIONALE: Acute and chronic heart failure (HF) may affect the liver, but the underlying mechanisms that lead to progressive liver damage are poorly understood. The hepatic cytokeratin-18 (CK18) epitopes M65 and M30 have been reported to distinguish between overall (necrotic) and apoptotic cell death, respectively. We aimed to evaluate the predominant hepatic cell death pattern in acute vs. chronic heart failure and examined if these assays predict the course of the disease. MAIN RESULTS: In a prospective study comprising 21 patients with acute HF (AHF) and 18 patients with chronic HF (CHF) serum levels of M65 and M30 were assessed. Compared with CHF, M65 levels were significantly increased in patients with AHF (CHF: 1,283 ± 591.6U/l vs. AHF: 20,912 ± 15,132U/l, p < 0.001). In addition, M30 levels were significantly increased in AHF (CHF: 642.2 ± 177.4U/l vs. AHF: 3,844 ± 5,293U/l, p < 0.05), but the M30/M65 ratio was significantly higher in CHF (CHF: 0.54 ± 0.15 vs. AHF: 0.20 ± 0.19, p < 0.001), indicating a greater contribution of apoptotic cell death in CHF. AHF patients with higher M30 values had a worse prognosis. CONCLUSIONS: The ratio of CK18 M30/M65 is a potential marker to discriminate AHF from CHF induced LF and M30 might be a prognostic marker for survival in AHF induced liver injury.