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1.
The Liver and Celiac Disease.
Rubio-Tapia, A, Murray, JA
Clinics in liver disease. 2019;(2):167-176
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Abstract
Celiac disease is a multisystem disorder. Celiac hepatitis characterized by gluten-responsive mild elevation of transaminases is the more common liver manifestation of celiac disease. Celiac disease may also be associated or coexist with other chronic liver disorders. Shared genetic risk and increased intestinal permeability have been suggested to be the most relevant events in the pathogenesis of liver injury in celiac disease. The aim of this article is to review the full spectrum of liver disorders in patients with celiac disease.
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The Relevance of Toxic AGEs (TAGE) Cytotoxicity to NASH Pathogenesis: A Mini-Review.
Sakasai-Sakai, A, Takata, T, Takino, JI, Takeuchi, M
Nutrients. 2019;(2)
Abstract
Non-alcoholic fatty liver disease (NAFLD) is currently the most common feature of chronic liver disease. Non-alcoholic steatohepatitis (NASH) is a severe form of NAFLD, and one of its risk factors is hyperglycemia. The chronic ingestion of excessive amounts of high-fructose corn syrup is associated with an increased prevalence of fatty liver. Under hyperglycemic conditions, advanced glycation end-products (AGEs) are generated through a non-enzymatic glycation reaction between the ketone or aldehyde groups of sugars and amino groups of proteins. Glyceraldehyde (GA) is a metabolic intermediate of sugars, and GA-derived AGEs (known as toxic AGEs (TAGE)) have been implicated in the development of NASH. TAGE accumulates more in serum or liver tissue in NASH patients than in healthy controls or patients with simple steatosis. Furthermore, the TAGE precursor, GA, causes cell damage through protein dysfunctions by TAGE modifications and induces necrotic-type hepatocyte death. Intracellular TAGE may leak outside of necrotic-type cells. Extracellular TAGE then induce inflammatory or fibrotic responses related to the pathology of NASH in surrounding cells, including hepatocytes and hepatic stellate cells. This review focuses on the contribution of TAGE to the pathology of NASH, particularly hepatic cell death related to NASH.
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Literature review of liver injury induced by Tinospora crispa associated with two cases of acute fulminant hepatitis.
Huang, WT, Tu, CY, Wang, FY, Huang, ST
Complementary therapies in medicine. 2019;:286-291
Abstract
INTRODUCTION Species of Tinospora are used as herbal remedies for the treatment of various diseases with very few toxic effects having been reported. Tinospora cordifolia (TCF) has been reported to effectively prevent hepatotoxicity. However, there are an increasing number of cases revealing that Tinospora crispa (TCP) might have the negative effect of inducing hepatotoxicity. Because of the similar leaves, people may mistake TCP for TCF, and consume it with the purpose of protecting liver function. OBJECTIVE Find out the misusing level of TCP and TCF and which chemical compound in TCP might induce hepatotoxicity. METHODS We report two cases of acute fulminant hepatitis associated with chronic use of TCP. Given that the two herbs were misidentified in these two reports, we investigated the frequency of erroneous identification by using three keywords ("Guduchi", "Tinospora cordifolia", "Tinospora crispa") to search images from the Google Images database. To further clarify the influence of liver function between TCP and TCF, we searched PubMed (up to 29 July 2018) for relevant publications on clinical trials or case reports. RESULTS Based on web review, over 35 percent of websites failed to accurately identify these two herbs. The different effects on liver function between TCP and TCF were compared through literature review. It indicated that TCF exerted liver protection, TCP had a contrary effect, suggesting its cis-Clerodane-type furano-diterpenoids might be an important factor of inducing hepatotoxicity. CONCLUSIONS We concluded that people might cause hepatic injury or even death without correctly identifying these two Tinospora species.
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4.
Autoimmune Hepatitis A Case Report and Literature Review.
Hong, AS, Desta, M, Hong, JM, Ohning, GV, Pillinger, MH, Saxena, A, Modjinou, DV
Bulletin of the Hospital for Joint Disease (2013). 2019;(2):146-152
Abstract
INTRODUCTION Autoimmune hepatitis (AIH) is a cause of chronic liver disease. It is usually suspected based on clinical presentation and laboratory findings, but the diagnosis relies on the presence of specific autoantibodies and characteristic histology. Other unexplained findings should always prompt investigation for coexisting syndromes. CASE PRESENTATION The patient is a 60-year-old Hispanic female with a history of mild asthma presented with exertional and pleuritic chest pain with weight loss, arthralgia, subjective fever, and night sweats for the last 3 months. Given the nonspecific nature of the presentation, further workup was pursued. Laboratory results indicated pancytopenia, elevated INR, and positive autoimmune panel including ANA, anti-chromatin, anti-histone, and rheumatoid factor as well as abnormal C3 and C4. Subsequent liver biopsy with interface hepatitis lead to a diagnosis of AIH with concurrent systemic lupus erythematosus suspected. CONCLUSION The diagnostic work up for AIH is multimodal and aims to differentiate other etiologies such as congestive hepatopathy, iron overload, viral hepatitis, and other autoimmune liver diseases. In this particular case, unusual clinical and laboratory findings led to diagnosis of the overlap syndrome. Treatment for both was necessary to prevent further progression of disease.
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5.
Macronutrients and the Adipose-Liver Axis in Obesity and Fatty Liver.
Duwaerts, CC, Maher, JJ
Cellular and molecular gastroenterology and hepatology. 2019;(4):749-761
Abstract
Macronutrient metabolism is a highly orchestrated process, with adipose tissue and liver each playing central roles in nutrient uptake, processing, transport, and storage. These 2 tissues form an important metabolic circuit, particularly as it relates to lipids as the primary storage form of excess energy. The function of the circuit is influenced by many factors, including the quantity and type of nutrients consumed and their impact on the overall health of the tissues. In this review we begin with a brief summary of the homeostatic disposition of lipids between adipose tissue and liver and how these processes can become dysregulated in obesity. We then explore how specific dietary nutrients and nutrient combinations can exert unique influences on the liver-adipose tissue axis.
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General advice in ultrasound based elastography of pediatric patients.
Dietrich, CF, Ferraioli, G, Sirli, R, Popescu, A, Sporea, I, Pienar, C, Kunze, C, Taut, H, Schrading, S, Bota, S, et al
Medical ultrasonography. 2019;(3):315-326
Abstract
Ultrasound elastography including transient elastography (TE), point shear wave elastography, (pSWE) and two (three)- dimensional shear wave elastography (2D-SWE) have been introduced mainly for the evaluation of the liver. All the techniques are also feasible for the examination of spleen, whereas pSWE and 2D-SWE can be used for the assessment of the pancreas, kidney, gastrointestinal tract and other organs. Strain elastography also plays a role for non-liver applications. The aim of the current report is to highlight unique features and techniques for the elastographic examinations in children and to report initial results in non-liver applications.
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7.
Hepatic fat as clinical outcome and therapeutic target for nonalcoholic fatty liver disease.
Pelusi, S, Valenti, L
Liver international : official journal of the International Association for the Study of the Liver. 2019;(2):250-256
Abstract
Nonalcoholic fatty liver disease (NAFLD) is rapidly becoming the leading cause of advanced liver disease in Western countries. NAFLD is defined in the presence of increased hepatic fat content, which is mainly stored under the form of neutral lipids within intracellular droplets and is not explained by at risk alcohol intake. In order to understand the pathogenesis, monitor the progression and find novel treatments for this condition, previous research efforts mainly addressed the role of inflammation. However, very recent data seem to suggest that hepatic lipid accumulation may be involved in NAFLD pathogenesis by driving secondary inflammation and fibrosis progression. Here, we will briefly review the novel results derived from natural history, genetics, imaging studies and therapeutic trials that support the notion that hepatic fat accumulation may represent a major clinical outcome and therapeutic target for NAFLD. Indeed, prospective and genetic data are consistent with hepatic fat being a driver of NAFLD progression. Furthermore, new technologies will render possible to monitor hepatic fat content without the need of invasive assessment, thereby allowing to identify patients at higher risk, and to monitor the response to drugs that act by decreasing hepatic lipid accumulation.
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8.
Signaling from Intestine to the Host: How Bile Acids Regulate Intestinal and Liver Immunity.
Biagioli, M, Carino, A
Handbook of experimental pharmacology. 2019;:95-108
Abstract
Primary bile acids (BAs) are generated in the liver as the end products of cholesterol catabolism; they are then conjugated and accumulated in the gallbladder. After a meal ingestion, BAs are reversed into the duodenum to facilitate the lipid absorption. At the intestinal level, the 95% of BAs are reabsorbed and redirected into enterohepatic circulation; indeed only a small amount of them are then subjected to chemical modifications by the intestinal microbiota, which plays a very important role in the generation of secondary bile acids and in regulating host's metabolism and activity of the immune system. Behind their role in nutrients absorption, bile acids act as signaling molecules, activating several receptors, known as bile acid-activated receptors (BARs), including the farnesoid-X-receptor (FXR) and the G protein-coupled bile acid receptor 1 (GPBAR1 or Takeda G-protein receptor 5). Both receptors appear to contribute to maintain the tolerogenic state of the liver and intestine immunity. In particular, FXR and GPBAR1 are highly expressed in cells of innate immunity including intestinal and liver macrophages, dendritic cells, and natural killer T cells. In this chapter, we provide an overview on mechanisms through which FXR and GPBAR1 modulate the signaling between microbiota and intestinal and liver innate immune system. This overview could help to explain beneficial effects exerted by GPBAR1 and FXR agonists in the treatment of metabolic and immuno-mediated diseases.
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9.
Kidney-liver pathophysiological crosstalk: its characteristics and importance.
Capalbo, O, Giuliani, S, Ferrero-Fernández, A, Casciato, P, Musso, CG
International urology and nephrology. 2019;(12):2203-2207
Abstract
The kidney plays a crucial role in controlling the blood volume and pressure, electrolyte and acid-base balance, erythropoietin secretion, as well as renin-angiotensin-aldosterone system activity. All these renal activities have important repercussion in the organism, explaining why morbidity and mortality rates are high in patients with significant renal dysfunction. In this sense, there are renal-induced liver damages in acute kidney injury, as well as liver-induced renal damages in hepatic disease. Ischemia, reperfusion, cytokine outflow, pro-inflammatory cascades, metabolic acidosis, oxidative stress, and changes in enzymatic and metabolic pathways provide the bases for this bidirectional kidney-liver damage. In conclusion, knowing the characteristics of this kidney-liver crosstalk is crucial for handling the complications induced by this vicious circle.
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10.
Updates on hepatic homeostasis and the many tiers of hepatobiliary repair.
Monga, SP
Nature reviews. Gastroenterology & hepatology. 2019;(2):84-86