Description

As part of routine laboratory testing, numerous Liver Function Tests (LFT) are frequently used to assess hepatic or biliary diseases. Acute and chronic heart failure (HF) patients have been reported to have abnormal LFT, which is typically regarded as end-organ damage due to altered hepatic metabolism in HF patients. Transaminases, markers of hepatocellular injury or hepatocellular necrosis, hepatobiliary markers of obstructive or cholestasis disease, and markers of impaired hepatic protein synthesis function and hepatic fibrosis are the three types of LFT that are observed in HF patients. The pathophysiology of abnormal LFT in HF, the function of hepatic fibrosis markers in HF, and the anatomy and metabolism of hepatocytes and the liver will be the primary topics of this chapter. Abnormalities in liver function tests and how they affect HF patients' prognoses will also be the focus of this chapter.

Serious Perioperative Complications

An abnormal blood vessel called a porto systemic shunt connects the portal vein to the systemic circulation, allowing blood from the pancreas, spleen, stomach, and intestines to bypass the liver. As a result, the liver's portal perfusion is reduced, resulting in a poorly developed and dysfunctional liver. The majority of hepatobiliary system congenital disorders in dogs are porto systemic shunts, which affect 0.18 percent of all dogs and are more prevalent in purebred dogs. For clinically affected dogs, surgical management is thought to be the most effective treatment option because congenital PSSs typically only involve one vessel. Surgical management may provide a better quality of life and a longer survival time for dogs, whereas medically managed dogs can have long survival times and good QoL. However, surgery comes with a risk of serious perioperative complications that could have a negative impact on a dog's quality of life and survival time. Although the primary PSS may remain patent or multiple acquired PSS may develop, surgical attenuation aims to completely close the PSS, resulting in persistent porto systemic shunting of blood. Clinical outcomes, medical imaging and/or liver function tests can be used to assess PSS surgical attenuation's success. Although clinical outcome assessment may appear to be simple and inexpensive, it frequently does not accurately reflect the presence or absence of persistent shunting. Additionally, clinical signs may be ambiguous and nonspecific, or they may be caused by conditions other than PSS. When compared to allowing persistent shunting, various studies indicate that complete closure of the PSS results in more successful and sustained positive outcomes; despite ongoing shunting, partial surgical attenuation is associated with clinical improvement. A recent retrospective study revealed that surgical attenuation significantly improved the quality of life of dogs with congenital PSS and was either comparable to or superior to that of control dogs over time. Despite this, these dogs' PSS-associated clinical signs scores were still lower than those of the healthy control group following surgical PSS attenuation. However, because the surgical outcome—that is, the degree of surgical attenuation—for these dogs was not available, the inclusion of dogs with persistent portosystemic shunting may have contributed to the suboptimal quality of life. Doppler ultrasonography, port venography, computed tomography angiography, and scintigraphy determination of the shunt fraction are all described medical imaging techniques that can be used to follow up PSS that has been surgically treated. The quality of the images produced by Trans Splenic Portal Scintigraphy (TSPS) is significantly higher than that of Per Rectal Portal Scintigraphy (PRPS) and the dose of radioactivity administered is significantly lower. However, TSPS will miss rare PSS that originates caudally of the splenic vein. Since CTA can yield false-positive results, one study found that splenoportography is a superior method for determining PSS closure than CTA. Although Porto venography, CTA, and scintigraphy are regarded as extremely reliable, no reference standard has been established at this time due to the fact that none of these methods are 100% accurate. Liver function tests continue to be appealing alternatives due to the fact that the majority of medical imaging techniques call for specialized equipment, sedation or general anesthesia, expertise and the acquisition and interpretation of images.

Majority of Vertebrates

In 1817, Swedish chemist Jons Jacob Berzelius discovered selenium, which was initially thought to be toxic in the early 20th century. As an essential trace element in the human body, it is now widely acknowledged that selenium plays crucial roles in antioxidant properties, cancer prevention, and immune function. There are two types of selenium compounds: selenium, both organic and inorganic. Organic selenium is a great supplement for selenium because it is more bioavailable. Selenium's potential toxicity is frequently overlooked due to its widespread use in supplement form. For the majority of vertebrates, the concentrations of selenium that are beneficial and those that are harmful fall within a narrow range. Studies done in the past have shown that taking too much selenium supplements can have serious effects on humans. Selenium is frequently found in aquatic environments as selenite and selenate, with reported concentrations ranging from 10 g/L to 78.1 g/L (0.13–0.99 mM). The majority of the environment's selenium concentration is higher than the recommended limit of 1 g/L for protecting aquatic animals. Selenium could be released into aquatic water by human activities like mining, agriculture, and industry, which could have serious effects on the environment. Assessing the toxicity of selenium to aquatic animals is especially important now that regulators of water quality are paying more attention to selenium pollution. Selenium enters the liver after first being absorbed in the intestine when consumed by animals. Since the liver is the organ that is most sensitive to selenium supply, our primary focus was on selenium's hepatic toxicity in zebrafish embryos. The liver primarily metabolizes selenium in two ways: either enters the pathway for the synthesis of selenoproteins or is excreted as small molecules. Since the liver stores a lot of selenium, its content has a significant impact on liver development (Xu et al., 2014). Both animals and humans can suffer liver damage from excessive selenium. Congestion of the liver and kidneys, for instance, was a symptom of acute selenium poisoning. Deaths even occurred when liver selenium content reached a certain threshold. In humans, a higher risk of liver cirrhosis and steatosis is associated with a higher level of dietary selenium and blood selenium concentration. Non-alcoholic steatohepatitis, also known as simple steatosis, can progress into liver cirrhosis and even cancer. Additionally, previous research demonstrated that excessive selenium in mammals could increase the risk of metabolic disorders and chronic liver disease (CLD), such as non-alcoholic fatty liver disease and type 2 diabetes mellitus. As a result, concerns about the adverse effects of excessive selenium arise as a result of the worldwide rise in CLD mortality. Although there have been numerous reports of selenium-induced liver injury and metabolic disorders, not many studies have looked at the toxicity of selenium to aquatic animals' livers. In this study, we looked at how selenium affected the structure, histomorphology, subcellular structure, and key pathways of glucolipid metabolism of the liver.