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Hepatic disorders in pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Ghassan M. Hammoud, Jamal A. Ibdah
Typically patients present with nausea and vomiting for several days, followed by jaundice and then progressive encephalopathy. Right upper quadrant pain and epigastric abdominal pain are common (50–80%) (72). Fever, headache, diarrhea, back pain suggestive of acute pancreatitis, and myalgias are occasionally initial presentation. Hepatic failure may ensue. Approximately 50% of patients may also have features of preeclampsia. Physical examination may reveal only right upper quadrant tenderness. Laboratory abnormalities include elevated serum aminotransferases usually 300 to 500U/L, moderate increase in serum bilirubin 5mg/dL and variable degrees of leukocytosis (73), DIC, hypoglycemia, hyperuricemia, and bacteremia. Patients may develop gastrointestinal hemorrhage, pancreatitis, and renal failure. Radiographic evaluations may suggest the diagnosis from steatosis seen by ultrasound, computerized tomography, or magnetic resonance imaging. However, this finding may not be universally present and normal studies do not exclude the diagnosis.
Gastroenterology
Published in Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan, Essential Notes for Medical and Surgical Finals, 2021
Kaji Sritharan, Jonathan Rohrer, Alexandra C Rankin, Sachi Sivananthan
Alcohol may cause a number of problems of increasing severity in the liver: Alcoholic steatosis – fatty change, reversible if patient stops drinking.Alcoholic hepatitis – may present acutely with jaundice, tender hepatomegaly, vomiting, fever and general malaise.Alcoholic cirrhosis.InvestigationsAbnormal LFTs: raised bilirubin, AST >ALT, GGT; raised serum ferritin.Liver biopsy.ManagementAbstinence from alcohol (and if acute presentation, treatment of withdrawal).Treatment of complications of cirrhosis.Surgery: consider liver transplantation in select cases.
The liver, gallbladder and pancreas
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Dina G. Tiniakos, Alastair D. Burt
A condition that is histologically similar to alcohol-related steatosis and steatohepatitis is increasingly encountered in obese patients; in such patient populations, there is a high incidence of type 2 diabetes mellitus and other features of the metabolic syndrome, a constellation of disorders related to adverse cardiovascular outcomes. Patients are usually discovered to have abnormal liver function tests, after blood testing for complaints of liver tenderness or tiredness without markers of other liver disease (viral, autoimmune, or drug induced). On imaging, they have evidence of fatty liver (‘bright liver’ on ultrasound). The underlying pathogenesis is thought to be related to an insulin-resistant state with oversupply of fatty acids, coupled with altered fatty acid metabolism. The accumulation of triglycerides in the fat droplets, leading to steatosis, is now considered an adaptive protective response, whereas lipotoxic metabolites of hepatocellular free fatty acids are considered major players in inducing steatohepatitis, the progressive form of non-alcoholic fatty liver disease that may lead to cirrhosis (Figure 11.11). Steatosis usually has a benign course but there are now well-documented instances of slow progression to cirrhosis. The importance of the condition is its increasing prevalence related to the obesity ‘epidemic’, its relationship to treatable or preventable conditions such as diabetes and obesity, and the necessity to ensure that patients are not falsely accused of secret excessive alcohol consumption and the attendant stigma associated with it.
Protective Effect of Nigella sativa and Onion Extract against 5-Fluorouracil-Induced Hepatic Toxicity
Published in Nutrition and Cancer, 2022
Sherif Mohamed Zaki, Dania S. Waggas
Microvesicular and macrovesicular steatosis is associated with 5-FU administration. Macrovesicular steatosis is caused by abnormal metabolism, synthesis, and transfer of lipids. (47). Microvesicular steatosis is a hepatic disease caused by faulty beta-oxidation of fatty acids (47). It is likely that steatosis is caused by lipid peroxidation since oxidative stress damages cellular membranes and membranes of its organelles (48). Such a conclusion is in line with the significant increases in MDA levels in the 5-FU-treated group. A 5-FU-treated liver cells had apoptotic, karyorrhectic nuclei with marginated nucleoli, while their cytoplasm was rarified. The damage is caused by oxidative stress because antioxidant markers (SOD, GSH and GSH/GSSG ratio) decreased, while oxidant markers (MDA and TBARS) increased.
Inactivation of the superoxide dismutase by malondialdehyde in the nonalcoholic fatty liver disease: a combined molecular docking approach to clinical studies
Published in Archives of Physiology and Biochemistry, 2021
Arash Arya, Nahid Azarmehr, Mahboubeh Mansourian, Amir Hossein Doustimotlagh
Scans were done by the operative who was blinded to clinical and laboratory results using an Esaote Medica apparatus equipped with a convex 3,5 MHz probe. Hepatic steatosis was determined based on the Hamaguchi criteria according to the brightness of vascular structures, hyperechogenicity (high level echoes) of liver tissue and modification in echogenicity between diaphragm and liver (Hamaguchi et al. 2007). Liver ultrasonography scanning was implemented to evaluate the grade of steatosis. Although, ultrasonography cannot define presenting of inflammation or fibrosis in the liver, it has a specificity of 100% and a sensitivity of 91.7% for distinguishing histological steatosis. The classification of liver steatosis was based on the following score of 0–6: 0, absent; 1, 2 mild; 3, 4 moderate; 5, 6 severe (Del Ben et al.2014).
Effects of anti-diabetic treatments in type 2 diabetes and fatty liver disease
Published in Expert Review of Clinical Pharmacology, 2021
Elizabeth M. Lamos, Megan Kristan, Maka Siamashvili, Stephen N. Davis
No singular pathophysiologic defect is associated with the development of NAFLD. The mechanisms for steatosis are multiple and include: increases in de novo lipogenesis, dietary intake of free fatty acids, decreases in free fatty acid oxidation and increased adipose lipolysis [2]. Muscle, adipose tissue, and insulin resistance, as well as possible genetic mutations (e.g. PNPLA3), play important roles in hepatic triglyceride accumulation in the pathogenesis of NAFLD [3–7]. These alterations in triglyceride metabolism result in a phenotype of proatherogenic dyslipidemia distinguished by elevated triglycerides, low HDL and small dense LDL particles [4]. Lipo-toxicity from lipids other than triglycerides also induce hepatocyte stress leading to NASH [8]. Furthermore, dysregulation of adiponectin, leptin, and bile metabolism, reduced growth hormone signaling in the liver [9], effects of gut microbiota [10], stimulation of immune cells (Kupffer cells) [10], dysregulation of nuclear receptors [11–13] and possible genetic [3] and molecular factors (i.e. single-nucleotide polymorphisms) [1] have all been studied as part of the complex interplay of hepatocellular and extra-hepatic interactions in NAFLD pathogenesis [2]. These factors play a role not only in the pathogenesis and disease progression of NAFLD but may be targets of drug treatment in the future. We refer the reader to recent excellent reviews of the pathophysiology of NAFLD [1,8,14].