Serum levels of TSH, thyroxine-binding globulin (TBG), T4, T3 and reverse T3 (rT3) were measured in 36 patients with fatty liver disease, 11 patients wih chronic persistent hepatitis, 17 patients with chronic active hepatitis, and 29 patients with liver cirrhosis. TBG was significantly above normal levels in both groups of chronic hepatitis, the slight concomitant T4 and T3 increase was significant only for T4 in chronic persistent hepatitis. A significant decrease in T4 and T3 concentration was found in fatty liver disease and in hepatic cirrhosis. A shift in T4 conversion to rT3 could exclusively be demonstrated for the group of hepatic cirrhosis, reflected by a significant increase in rT3. As our findings indicate normal TSH levels and a lack of clinical signs of hypothyroidism in chronic liver disease, the possibility of diverse regulating changes must be considered.

Download full-text PDF

Source
http://dx.doi.org/10.1007/BF03349374DOI Listing

Publication Analysis

Top Keywords

liver disease
12
serum levels
8
levels tsh
8
chronic liver
8
fatty liver
8
chronic persistent
8
persistent hepatitis
8
hepatitis patients
8
hepatic cirrhosis
8
chronic
6

Similar Publications

Progressive systemic inflammation precedes decompensation in compensated cirrhosis.

JHEP 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).

View Article and Find Full Text PDF

Aim: Chronic hepatitis C virus infections can lead to liver fibrosis. Appropriate treatment of chronic hepatitis C may result in significant fibrosis reversal. The best method to assess liver fibrosis is an invasive hepatic biopsy.

View Article and Find Full Text PDF

Background: Adenocarcinoma of the esophagogastric junction (AEGJ) is a highly aggressive tumor that frequently metastasizes to the liver. Understanding the cellular and molecular mechanisms that drive this process is essential for developing effective therapies.

Methods: We employed single-cell RNA sequencing to analyze the tumor heterogeneity and microenvironmental landscape in patients with AEGJ liver metastases.

View Article and Find Full Text PDF

Background: There is no consensus regarding the optimal regimen for metastatic nasopharyngeal carcinoma (dmNPC). Locoregional intensity modulated radiotherapy (LRRT) following palliative chemotherapy (PCT) has been shown to prolong the overall survival (OS) and improve the progression-free survival (PFS) of patients with dmNPC, compared with PCT alone. However, patients with a high tumor burden do not benefit from additional LRRT, which inevitably results in toxicity.

View Article and Find Full Text PDF

CCL2, a pivotal cytokine within the chemokine family, functions by binding to its receptor CCR2. The CCL2/CCR2 signaling pathway plays a crucial role in the development of fibrosis across multiple organ systems by modulating the recruitment and activation of immune cells, which in turn influences the progression of fibrotic diseases in the liver, intestines, pancreas, heart, lungs, kidneys, and other organs. This paper introduces the biological functions of CCL2 and CCR2, highlighting their similarities and differences concerning fibrotic disorders in various organ systems, and reviews recent progress in the diagnosis and treatment of clinical fibrotic diseases linked to the CCL2/CCR2 signaling pathway.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!