scholarly journals Drug Resistant Fetal Arrhythmia in Obstetric Cholestasis

2015 ◽  
Vol 2015 ◽  
pp. 1-4
Author(s):  
Nahide Altug ◽  
Ayse Kirbas ◽  
Korkut Daglar ◽  
Ebru Biberoglu ◽  
Dilek Uygur ◽  
...  
Keyword(s):  
Liver Disease ◽  
Bile Acid ◽  
Supraventricular Tachycardia ◽  
Preterm Labor ◽  
Fetal Distress ◽  
Intrauterine Death ◽  
Drug Resistant ◽  
Fetal Arrhythmia ◽  
Antiarrhythmic Treatment

Obstetric cholestasis (OC) is a pregnancy specific liver disease characterized by increased levels of bile acid (BA) and pruritus. Raised maternal BA levels could be associated with intrauterine death, fetal distress, and preterm labor and also alter the rate and rhythm of cardiomyocyte contraction and may cause fetal arrhythmic events. We report a case of drug resistant fetal supraventricular tachycardia and concomitant OC.Conclusion.If there are maternal OC and concomitant fetal arrhythmia, possibility of the resistance to antiarrhythmic treatment should be kept in mind.

scholarly journals Fetal Tachycardia in the Delivery Room: Fetal Distress, Supraventricular Tachycardia, or Both?

2020 ◽  
Vol 10 (04) ◽  
pp. e380-e385
Author(s):  
Satvinder Singh Bhatia ◽  
Wendy H. Burgess ◽  
Jonathan R. Skinner
Keyword(s):  
Heart Rate ◽  
Differential Diagnosis ◽  
Supraventricular Tachycardia ◽  
Fetal Distress ◽  
Emergency Cesarean ◽  
Rapid Heart Rate ◽  
Life Threatening ◽  
Antenatal Detection ◽  
Fetal Arrhythmia ◽  
Fetal Tachycardia

Abstract Background Supraventricular tachycardia (SVT) is seldom considered a cause for fetal tachycardia; commoner etiologies including maternal fever and fetal distress are usually envisaged. Fetal arrhythmia can be missed as a diagnosis, potentially leading to suboptimal management. Cases Three cases are described where detection of fetal tachycardia >200 beats per minute (bpm) at 36, 40, and 38 weeks gestation resulted in emergency cesarean section for presumed fetal distress. Retrospective review of the cardiotocograph in two cases revealed baseline heart rates 120 to 160 bpm, with loss of trace associated with auscultated rates over 200 bpm. The diagnosis of SVT was not initially considered and made later when the infants required cardioversion at the age of 3 weeks, 2 days, and 8 days, respectively. The 36-week infant required noninvasive ventilation for prematurity. Conclusion SVT should be actively considered in the differential diagnosis of fetal tachycardia. Unrecognized fetal SVT may result in avoidable caesarean for suspected fetal distress, with potential prematurity-related problems. The cardiotocograph can be helpful if showing contact loss associated with rapid heart rate auscultation. The antenatal detection of fetal SVT is important as it can allow anticipation and prevention of neonatal SVT, which is potentially life-threatening if not detected and treated promptly.

scholarly journals Role of FXR in Bile Acid and Metabolic Homeostasis in NASH: Pathogenetic Concepts and Therapeutic Opportunities

2021 ◽  
Author(s):  
Richard Radun ◽  
Michael Trauner
Keyword(s):  
Liver Disease ◽  
Bile Acid ◽  
Enterohepatic Circulation ◽  
Therapeutic Potential ◽  
Farnesoid X Receptor ◽  
Metabolic Homeostasis ◽  
Nonalcoholic Fatty Liver ◽  
Metabolic Dysregulation ◽  
Attractive Therapeutic Target

AbstractNonalcoholic fatty liver disease (NAFLD) has become the most prevalent cause of liver disease, increasingly contributing to the burden of liver transplantation. In search for effective treatments, novel strategies addressing metabolic dysregulation, inflammation, and fibrosis are continuously emerging. Disturbed bile acid (BA) homeostasis and microcholestasis via hepatocellular retention of potentially toxic BAs may be an underappreciated factor in the pathogenesis of NAFLD and nonalcoholic steatohepatitis (NASH) as its progressive variant. In addition to their detergent properties, BAs act as signaling molecules regulating cellular homeostasis through interaction with BA receptors such as the Farnesoid X receptor (FXR). Apart from being a key regulator of BA metabolism and enterohepatic circulation, FXR regulates metabolic homeostasis and has immune-modulatory effects, making it an attractive therapeutic target in NAFLD/NASH. In this review, the molecular basis and therapeutic potential of targeting FXR with a specific focus on restoring BA and metabolic homeostasis in NASH is summarized.

Bile Acid Synthetic Defects and Liver Disease

2000 ◽  
Vol 3 (1) ◽  
pp. 1-16 ◽  
Author(s):  
Kevin E. Bove ◽  
Cynthia C. Daugherty ◽  
Wes Tyson ◽  
Gary Mierau ◽  
James E. Heubi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Bile Acid

Bile acid conjugation in early stage cholestatic liver disease before and during treatment with ursodeoxycholic acid

1996 ◽  
Vol 248 (2) ◽  
pp. 175-185 ◽  
Author(s):  
Mario Fracchia ◽  
Kenneth D.R. Setchell ◽  
Andrea Crosignani ◽  
Mauro Podda ◽  
Nancy O'Connell ◽  
...  
Keyword(s):  
Liver Disease ◽  
Bile Acid ◽  
Ursodeoxycholic Acid ◽  
Early Stage ◽  
Cholestatic Liver Disease

Liver disease with altered bile acid transport in Niemann-Pick C mice on a high-fat, 1% cholesterol diet

2005 ◽  
Vol 289 (2) ◽  
pp. G300-G307 ◽  
Author(s):  
Robert P. Erickson ◽  
Achyut Bhattacharyya ◽  
Robert J. Hunter ◽  
Randall A. Heidenreich ◽  
Nathan J. Cherrington
Keyword(s):  
Liver Disease ◽  
Bile Acid ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Cholestatic Hepatitis ◽  
Diffuse Fibrosis ◽  
Acid Transport ◽  
High Fat ◽  
Bile Acid Transport ◽  
Niemann Pick

Cholestatic hepatitis is frequently found in Niemann-Pick C (NPC) disease. We studied the influence of diet and the low density lipoprotein receptor (LDLR, Ldlr in mice, known to be the source of most of the stored cholesterol) on liver disease in the mouse model of NPC. Npc1−/− mice of both sexes, with or without the Ldlr knockout, were fed a 18% fat, 1% cholesterol (“high-fat”) diet and were evaluated by chemical and histological methods. Bile acid transporters [multidrug resistance protein (Mrps) 1–5; Ntcp, Bsep, and OatP1, 2, and 4] were quantitated by real-time RT-PCR. Many mice died prematurely (within 6 wk) with hepatomegaly. Histopathology showed an increase in macrophage and hepatocyte lipids independent of Ldlr genotype. Non-zone-dependent diffuse fibrosis was found in the surviving mice. Serum alanine aminotransferase was elevated in Npc1−/− mice on the regular diet and frequently became markedly elevated with the high-fat diet. Serum cholesterol was increased in the controls but not the Npc1−/− mice on the high-fat diet; it was massively increased in the Ldlr−/− mice. Esterified cholesterol was greatly increased by the high-fat diet, independent of Ldlr genotype. γ-Glutamyltransferase was also elevated in Npc1−/− mice, more so on the high-fat diet. Mrps 1–5 were elevated in Npc1−/− liver and became more elevated with the high-fat diet; Ntcp, Bsep, and OatP2 were elevated in Npc1−/− liver and were suppressed by the high-fat diet. In conclusion, Npc1−/− mice on a high-fat diet provide an animal model of NPC cholestatic hepatitis and indicate a role for altered bile acid transport in its pathogenesis.

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