Background: Bacterial hepatic abscess usually is acute and progressive, often resulting in sepsis, impairment of liver function and disseminated intravascular coagulation. The mortality rate was as high as 80% in the past. For the purpose of early diagnosis and differential diagnosis of this disease, we probed the imaging manifestations and their characteristics in bacterial hepatic abscesses by CT scan.
Methods: Twenty-four lesions from 21 patients with bacterial hepatic abscesses that were confirmed by clinical features, puncture and culture were reviewed for CT manifestations. Fourteen patients were male and 7 were female, with an average age of 56.2 years. All lesions underwent CT plain scan and three-phase enhanced scan and 15 patients underwent delayed-phase imaging. Three senior radiologists read the films in accordance with a standard.
Results: Among 24 lesions, 18 (75%) were situated in the right liver with diameters of 1.4-9.3 cm (average 4.5 cm). Nineteen (79.2%) lesions were round or sub-round in shape, and 22 (91.7%) had smooth, uninterrupted and sharp edges. All lesions showed low attenuation of less than 20 Hu. Twenty-two enhanced lesions (91.7%) had rim-shaped enhancement in the abscess wall, and 13 (54.2%) showed single or double-ring signs. Eighteen (75%) displayed honeycomb-like, grid-like or strip-like enhancement. Eighteen (75%) were regionally enhanced in the surroundings or upper or lower layers. Only 2 (8.3%) displayed a gas-liquid surface sign.
Conclusions: The CT findings of bacterial hepatic abscess are usually typical, and the diagnosis of the abscess is not difficult. To precisely diagnose atypical cases, it is necessary to combine CT with clinical observations and follow-up.
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J Med Food
January 2025
Department of Infectious Diseases and Liver Diseases, Ningbo Medical Centre Lihuili Hospital, Affiliated Lihuili Hospital of Ningbo University, Ningbo, China.
Disturbances of the intestinal barrier enabling bacterial translocation exacerbate alcoholic liver disease (ALD). GG (LGG) has been shown to exert beneficial effects in gut dysbiosis and chronic liver disease. The current study assessed the combined effects of LGG and metformin, which play roles in anti-inflammatory and immunoregulatory processes, in alcohol-induced liver disease mice.
View Article and Find Full Text PDFJHEP Rep
February 2025
Department of Gastroenterology and Hepatology, Hospital Universitario Ramón y Cajal, Instituto Ramon y Cajal de Investigación Sanitaria (IRYCIS), Universidad de Alcalá, Madrid, Spain.
Background & Aims: Systemic inflammation is a driver of decompensation in cirrhosis with unclear relevance in the compensated stage. We evaluated inflammation and bacterial translocation markers in compensated cirrhosis and their dynamics in relation to the first decompensation.
Methods: This study is nested within the PREDESCI trial, which investigated non-selective beta-blockers for preventing decompensation in compensated cirrhosis and clinically significant portal hypertension (CSPH: hepatic venous pressure gradient ≥10 mmHg).
EClinicalMedicine
February 2025
Faculty of Medicine, University of Queensland, Australia.
Background: Small Intestinal Bacterial Overgrowth (SIBO) has been implicated in the pathophysiology of chronic liver disease (CLD). We conducted a systematic review and meta-analysis to assess and compare the prevalence of SIBO among CLD patients (with and without with complications of end stage liver disease) and healthy controls.
Methods: Electronic databases were searched from inception up to July-2024 for case-control studies reporting SIBO in CLD.
Arthritis Rheumatol
January 2025
Assistant Professor of Pathology and of Microbiology and Microbiology and Immunology, Stanford University, Stanford, CA, 94305.
Humans develop hyperuricemia via decreased urate elimination and excess urate production, consequently promoting monosodium urate crystal deposition and incident gout. Normally, approximately two thirds of urate elimination is renal. However, chronic kidney disease (CKD) and other causes of decreased renal urate elimination drive hyperuricemia in most with gout.
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