Intrahepatic cholestasis in subclinical and overt hyperthyroidism: two case reports

<p>Abstract</p> <p>Introduction</p> <p>Non-specific abnormalities in liver function tests might accompany the clinical course of hyperthyroidism. Hyperthyroidism can cause the elevation of hepatic enzymes and bilirubin. Jaundice is rare in overt hyperthyroidism, especially in subclinical hyperthyroidism. On the other hand, the use of anti-thyroid drugs has rarely been associated with toxic hepatitis and cholestatic jaundice.</p> <p>Case presentation</p> <p>Here we present two cases of cholestasis that accompanied two distinct forms of clinical hyperthyroidism. The first patient had a clinical presentation of severe cholestasis in the absence of congestive failure related to hyperthyroidism. The second case had developed intrahepatic cholestasis in the presence of subclinical hyperthyroidism, and improved with rifampicin treatment.</p> <p>Conclusion</p> <p>Hyperthyroidism should be a consideration in non-specific liver dysfunction.</p

The use of chemotherapy regimens carrying a moderate or high risk of febrile neutropenia and the corresponding management of febrile neutropenia: an expert survey in breast cancer and non-Hodgkin's lymphoma

The use of chemotherapy regimens with moderate or high risk of febrile neutropenia (defined as having a FN incidence of 10% or more) and the respective incidence and clinical management of FN in breast cancer and NHL has not been studied in Belgium. The existence of a medical need for G-CSF primary and secondary prophylaxis with these regimens was investigated in a real-life setting.Journal ArticleMulticenter StudyResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe

American Thyroid Association Guide to Investigating Thyroid Hormone Economy and Action in Rodent and Cell Models

Background: An in-depth understanding of the fundamental principles that regulate thyroid hormone homeostasis is critical for the development of new diagnostic and treatment ap-proaches for patients with thyroid disease. Summary: Important clinical practices in use today for the treatment of patients with hypothy-roidism, hyperthyroidism, or thyroid cancer, are the result of laboratory discoveries made by scientists investigating the most basic aspects of thyroid structure and molecular biology. In this document, a panel of experts commissioned by the American Thyroid Association makes a se-ries of recommendations related to the study of thyroid hormone economy and action. These recommendations are intended to promote standardization of study design, which should in turn increase the comparability and reproducibility of experimental findings. Conclusions: It is expected that adherence to these recommendations by investigators in the field will facilitate progress towards a better understanding of the thyroid gland and thyroid hormone dependent processes

Expression of thyroid hormone transporters during critical illness

Objective: Prolonged critically ill patients have low circulating thyroid hormone (TH) levels Without a rise in TSH. it condition labeled 'the low tri-iodothyronine (T-3) syndrome'. Currently, it is not clear whether this represents all adaptive response. We examined the role of TH transporters monocarboxylate transporter 8 (MCT8, also known its SLC16A2) and MCT10 in the pathogenesis of the low T-3 syndrome in prolonged critical illness. Methods: A clinical observational study in critically ill patients and all intervention study in all ill vivo animal model of critical illness. Gene expression levels of MCT8 and MCT10 were measured by real-time PCR. Results: In prolonged critically ill patients. we measured increased MM'S but not MCT10 gene expression levels in liver and skeletal muscle as compared with patients undergoing acute Surgical stress. In it rabbit model of prolonged critical illness, gene expression levels of MCT8 ill liver and of MM 0 in skeletal muscle were increased as compared with healthy controls. Treatment of prolonged critically ill rabbits with TH (thyroxine + T-3) resulted in a downregulation or gene expression levels of MCT8 ill liver and of MCT10 ill muscle. Transporter expression levels correlated inversely with circulating TH parameters. Conclusions: These data Suggest that alterations in the expression of TH transporters do not play a major role in the pathogenesis of the 'low T-3 syndrome' but: rather reflect a compensatory effort ill response to hypothyroidism