Fatty Liver Disease Alternative Treatments Ebook
Aspartate transaminase is also found in other tissues, including heart, muscle, pancreas and kidney. It is therefore not specific for liver damage. Alanine transaminase is only produced in the liver and is specific for liver disease. Both enzymes are released by damaged hepatocytes following injury by hypoxia, infection or drugs. Aspartate transaminase is cleared more rapidly from the circulation than alanine transaminase. Following acute injury, there may be a dramatic increase in concentration in plasma AST and ALT. However, in chronic diseases, plasma concentrations may be normal or only slightly increased.
Fatty liver disease is the most common reason for elevated serum liver enzymes and affects an estimated 20 of the U.S. population (Angelico et al., 2005). First described in obese diabetic females, fatty liver disease is widely recognized as a complication of obesity and is associated with the features of the metabolic syndrome. The spectrum of fatty liver disease ranges from nonalcoholic fatty liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH). Fibrosis and cirrhosis can develop in NASH, which has been linked to insulin resistance, as with metabolic syndrome (Choudhury and Sanyal, 2004). The increased insulin level likely causes fatty acid flux from adipose tissue to be deposited in the liver. Inflammatory cytokine release triggered by hyperinsulinemia contributes to the steatohepatitis and fibrosis.
Liver damage, tissue liver damage, lung problems, stroke, tissue damage, death from ruptured brain vessels weakness, depression, memory impairment, damage to cardiovascular and nervous systems, kidney damage, liver damage, increased blood levels can cause brain damage, sudden death
States and around the world, the consumption of alcohol is associated with numerous motor vehicle accidents. In addition, alcohol can be addictive and is the root of many social problems. Alcohol, in excess, is also associated with various health problems, including liver damage and damage to the fetus of women who consumed alcohol during
Deficiencies are uncommon but cats require a source of preformed vitamin A, which is only found in animal tissue, and thus theoretically could become deficient if fed a vegetarian diet. Vitamin A toxicity is fairly common in cats receiving a diet high in liver or following oversupplementation with cod liver oil, since these foodstuffs contain abundant amounts of preformed vitamin A. Clinical signs of vitamin A toxicity include liver damage and painful bone disease, especially of the cervical vertebrae and long bones of the forelimb.
Leflunomide inhibits dihydroorotate dehy-drogenase, an enzyme within the mitochondria that supplies T lymphocytes with the necessary components to respond to cytokine stimulation.26 Thus, leflunomide inhibits the T-lymphocyte response to various stimuli and halts the cell cycle. Its efficacy is similar to that of moderate doses of methotrexate or sulfasalazine.19 Because of its extended half-life, leflunomide therapy begins with a loading dose followed by a maintenance dose. Patients with pre-existing hepatic disease or a history of heavy alcohol ingestion should not receive leflun-omide26 Leflunomide may be used in combination with methotrexate, but the added efficacy comes with a dramatic rise in the risk of hepatotoxicity. Liver function tests must be followed closely to prevent or minimize liver damage.1 If therapy requires ab
Attempts to mediate some of the biochemical abnormalities with lipid therapy or dietary restriction of very long chain fatty acids and phytanic acid have been tried, but they do not normalize plasma levels of the fatty acids, phytanic acid, or red blood cell plasmologens. Ihe clinical effectiveness of these interventions has yet to be determined. Ursodeoxycholic acid has reduced levels of bile acid intermediates and has the potential to prevent liver damage. y Peroxisomal proliferators such as clofibrate do not induce formation of catalase-containing peroxisomes or improve clinical status.
When administered systemically is unknown. In mice injected intraperitoneally there is some evidence of liver damage.56 Arnon et al.51 examined the effects of the toxins in rhesus monkeys and noted that the animals apparently died from cessation of breathing. Death is not accompanied by the floppy paralysis characteristic of the botulinum and tetanus neurotoxins.
Hepatic overexpression of nSREBP-lc, the principal SREBP-1 isoform in the liver, produced a triglyceride-enriched fatty liver with no increase in cholesterol (Fig. 3). The fatty acid synthetic enzyme mRNA levels and the rates of fatty acid synthesis were similarly increased 4fold, whereas the mRNAs for cholesterol synthetic enzymes and the rate of cholesterol synthesis were unchanged (Horton et al. 2002). The ability of SREBP-lc to preferentially activate lipogenic genes provides a mechanism for the liver to increase fatty acid synthesis without altering cholesterol metabolism. Despite the increased rates of hepatic fatty acid synthesis, the plasma triglyceride levels were 40 lower in SREBP-lc transgenic mice compared to those in wild-type mice. Although the SREBP-la isoform is normally expressed at low levels in the livers of adult animals, the consequences of its overexpression were also studied in mice. nSREBP-la transgenic mice developed a massive fatty liver owing to the 6-fold...
Pre-eclampsia complicates about 7 of all pregnancies in the UK, and is part of a spectrum of disease which includes HELLP syndrome, peripartum cardiomyopathy and possibly acute fatty liver of pregnancy. It is the second most common cause of maternal death after thromboembolic disease. Patients with pre-eclampsia are more likely to require anaesthetic expertise than mothers with uncomplicated pregnancies, and so you need to be aware of its important potential problems. If you have worked on a labour ward then you will have seen this condition, and your experience is likely to be more recent than many of the examiners, only a proportion of whom are obstetric anaesthetists. The viva, however, will concentrate much more on the basic science than on the practicalities of managing these sick mothers.
Women have lower rates of alcohol abuse and dependency than their male counterparts, 1.5 overall and 1.5 in older adult women (Mouton and Espino, 1999) (Box 49-7). Women generally enter treatment later than men and have more psychiatric symptoms. Women seem to develop many pathologic effects of alcohol more rapidly than men (Blume and Zilberman, 2005), including fatty liver, hypertension, anemia, malnutrition, GI hemorrhage, and peptic ulcer requiring surgery (Zweben, 2009). For women, five to seven drinks daily is sufficient to cause significant disease progression.
Taken together, the above evidence suggests that SREBP-lc mediates insulin's lipogenic actions in liver. This observation led to the discovery that SREBP-lc contributes to the development of hepatic steatosis or fatty liver associated with diabetes, obesity, and the metabolic syndrome. Hepatic steatosis is the most commonly encountered liver abnormality in the United States, owing to its strong association with obesity and insulin-resistant diabetes mellitus (Mokdad et al. 200l). Conservative estimates indicate that 40-60 of individuals with obesity or diabetes develop fatty livers. A subset of patients with fatty liver will subsequently develop fibrosis, cirrhosis, and liver failure. Data initially obtained in mice indicate that the fatty liver associated with insulin resistance is caused, in part, by increased SREBP-lc expression. The increased SREBP-lc expression occurs in response to the high insulin levels present in insulin-resistant states. Thus, SREBP-lc levels are elevated in...
The influence ofIL-18 on apoptosis through the increase in the FasL expression has been previously documented in somatic cells. High levels of IL-18 were found, e.g., in liver inflammation, which suggests that this cytokine may regulate apopto-sis of hepatocytes and may be a reason of liver damage. There were also some reports on the possibility of IL-18-exerted apoptosis on endothelial cells and this effect was mediated by members of TNF family or the Fas FasL system 155 , Some reports have described the IL-18's harmful effects on semen quality in infertile men with urogenital infections 71 , In in vitro conditions, a combination of IL-18 with IL-12 used together with leukocytes was linked with a significant increase in MDA concentrations 88 . It is possible that these inflammatory cytok-ines may cooperate with each other in apoptosis induction of mature spermatozoa (own unpublished data).
But in 1963, sporadic case reports in the anesthesia literature of unexplained massive liver damage following exposure to halothane caused concern within the anesthesia community.1 These cases of severe liver damage were seen after relatively minor surgery in healthy patients after having what seemed to be uneventful anesthesia. Because of these reports and the possibility that halothane was more toxic than previously thought, a study (the National Halothane Study) was undertaken to resolve the question.2 Charts of more than 850,000 anesthetics delivered between 1959 and 1962 were reviewed with the purpose of determining if cases of severe liver injury were caused by halothane or related to the multitude of other factors known to cause liver damage and hepatitis. The National Halothane Study concluded that although massive liver damage following halothane exposure can occur, it is exceedingly rare.3 The risk of this complication is greater with multiple exposures to halothane vapor...
Recognizing and treating the cause of cirrhosis is paramount. Cirrhosis is irreversible treatments are directed at limiting disease progression and minimizing1 complications. The immediate treatment goals are to stabilize acute complications such as variceal bleeding and prevent SBP. Once life-threatening conditions have stabilized, the focus shifts to preventing complications and preventing further liver damage. Complication prevention involves both primary and secondary prophylaxis. To determine appropriate prophylactic therapy, a careful analysis of patient characteristics and disease history is mandatory. The sections that follow concentrate on treatment and prevention of cirrhotic complications. Lifestyle modifications can limit disease complications and slow further liver damage. Avoidance of additional hepatic insult is critical for successful cirrhosis treatment. The only proven treatment for alcoholic liver disease is the immediate cessation of alcohol consumption. Patients...
Acute fatty liver of pregnancy. Sem Perinatol 1998 22 134-40 41. Vigil-De Gracia P. Acute fatty liver and HELLP syndrome two distinct pregnancy disorders. Int J Gynaecol Obstet 2001 73 215-21 47. Maclean A, Almeida Z, Lopez P. Complications of acute fatty liver of pregnancy treated with activated protein C. Arch Gynecol Obstet 2005 273 119-21
The course of alcoholic liver disease moves through several distinct phases from development of fatty liver to the development of alcoholic hepatitis and cirrhosis. Fatty liver and alcoholic hepatitis may be reversible with cessation of alcohol intake, but cirrhosis itself is irreversible. Although the scarring of cirrhosis is permanent, main in body tissues, primarily the liver, producing hypoxic damage. High levels of ethanol saturate the ADH enzyme system when the ADH system is overwhelmed, the microsomal ethanol oxidizing system must take over the detoxification process. The microsomal ethanol oxidizing system is an inducible cytochrome P-450 (CYP 450) enzyme system it participates in phase 1 metabolism and also produces acetaldehyde as its end product. 4,25 Acetaldehyde exerts direct toxic effects on the liver by damaging hepatocytes, inducing fibrosis, and by directly coupling to proteins, interfering with their intended actions. Metabolism of large amounts of ethanol shifts...
And low platelets) Acute fatty liver of pregnancy (AFLP) TTP, thrombotic thrombocytopenic purpura HUS, hemolytic uremic syndrome HELLP, hemolysis, elevated liver enzymes, and low platelets AFLP, acute fatty liver of pregnancy. TTP, thrombotic thrombocytopenic purpura HUS, hemolytic uremic syndrome HELLP, hemolysis, elevated liver enzymes, and low platelets AFLP, acute fatty liver of pregnancy. Acute fatty liver of pregnancy Acute fatty liver of pregnancy affects one of every 5000-10 000 pregnancies and is most common in primagravidas during the third trimester39. The cause of the condition is unknown in the majority of instances, but some patients may have a long-chain 3-hydroxy-acyl CoA dehydrogenase (LCHAD) deficiency40. Acute fatty liver
Severe hepato- or splenomegaly is a relative contraindication to transperitoneal laparoscopic nephrectomy. An enlarged or fatty liver, which must be retracted to allow access to the kidney, adds to the complexity of the overall procedure. In these patients, a retroperitoneal approach is preferred.
Ill-effects as a result of chronic ingestion are most likely to occur as a result of drinking contaminated water. Health effects of long-term exposure include skin changes, e.g. pigmentation and lesions, peripheral neuropathy, liver damage, and circulatory effects. Arsenic has also been classified by the International Agency for Research on Cancer (IARC) as carcinogenic to humans.
For example, drugs such as general anesthetics, norepinephrine, cimetidine, propranolol, and calcium channel blockers (e.g., diltiazem) all can decrease hepatic blood flow and increase the elimination half-life of the amide-linked local anesthetics. Similarly, decreases in hepatic function caused by a lowering of body temperature, immaturity of the hepatic enzyme system in the fetus, or liver damage (e.g., cirrhosis) lead to a decreased rate of hepatic metabolism of the amide local anesthetics.
Liver damage is always associated with glutathione depletion. Unfortunately, glutathione itself does not enter cells readily and is only effective in extremely high doses. Glutathione precursors and related compounds, such as cysteine, acetylcysteine, cysteamine and methionine, prevent liver damage following paracetamol overdosage. Intravenous N-acetylcysteine is the treatment of choice but must be given within 10 h of ingestion of the overdose and is completely effective if given within 8 h. Oral acetylcysteine and oral methionine are less effective, probably because of the unreliability of oral absorption in the presence of nausea and vomiting (or before gastric aspiration). Transient allergic reactions have been reported rarely, but otherwise acetylcysteine appears devoid of serious side-effects.
After an incubation period of some 5 to 8 days, the disease manifests itself suddenly, with shivering, headache, body pains, and high temperature. Nausea and vomiting are occasionally present. The spleen and liver are enlarged and tender bronchitis is present in 40 to 60 percent of cases and jaundice in 20 to 60 percent. In cases with a favorable outcome, there is a crisis of 1 to 2 hours or longer within 3 to 9 days, followed by a fall in temperature. Relapse, shorter and less severe than the primary attack, follows in 11 to 15 days. A diminishing proportion of patients suffer up to four relapses. Not all cases relapse, however, and in some epidemics no more than 50 percent of the patients suffer relapse. Death is due to liver damage, lobar pneumonia, subarachnoid hemorrhage, or rupture of the spleen.
I t is useless to attempt to cure a patient whose eyes have a yellow hue a reflection of either liver damage or the destruction of red blood cells , whose fingernails have no white crescents at the bottom, whose hands are wholly anesthetic, whose palm or sole bleeds, whose eyeballs are ulcerated, whose penis is putrified, whose hands or feet are clawed, whose skin is spotted with black, whose fingers have melted off leaving frog-foot shaped ends, whose body hairs fall off, whose nose is gone, whose bones are poisoned and putrified. (Skisnes 1973)
If you undergoing multiple anesthetics, some of the newer anesthetic vapors are better choices than halothane. Forane has largely replaced halothane as the anesthetic gas of choice for adults. Forane has been available since the 1980s, undergoes minimal metabolism in the liver, and has not been shown in any well-conducted study to cause liver damage directly related to any effect of the vapor. Sevoflurane (Ultane) is replacing halothane as the anesthetic agent of choice in pediatrics. In many hospitals, however, the high cost of Sevoflurane makes halothane the only anesthetic vapor available for pediatric anesthesia.
Probably the most common cause of persistently elevated unexplained aminotransferases is fatty infiltration of the liver. Less common causes of mildly elevated aminotransferases with ALT AST include autoimmune hepatitis, hemochromatosis, alpha-1 antitrypsin disease, Wilson's disease, metastatic disease, and cholestatic liver disease. Mild aminotransferase elevations with AST ALT are more suggestive of alcohol-related liver disease, but can also occur with cirrhosis and fatty liver. With alcoholic hepatitis, AST levels typically are approximately twice ALT levels, but the AST levels rarely are greater than 300 U L. Marked elevations (greater than 15 times upper limit of normal) of AST and ALT suggest significant necrosis, such as seen in acute viral or drug-induced hepatitis, in ischemic hepatitis, or as can occur with acute biliary obstruction (Green and Flamm, 2002). However, the magnitude of elevation of the amino-transferases does not necessarily correlate...
This B-vitamin is also involved in energy-producing reactions in the cells that convert food to energy. In addition, niacin helps maintain healthy skin, nerves, and your digestive system. In some instances, you can use large doses of niacin as a cholesterol-lowering medication. However, you should only do this under the supervision of your doctor. Megadoses can cause hot flashes, itching, ulcers, high blood sugar, and liver damage.
Hepatitis C is a serious disease in that a high proportion of cases develop permanent liver damage. In spite of the paucity of our knowledge about this disease, it is almost unique among viral infections in being treatable. Alpha interferon results in dramatic improvement of hepatitis C liver disease. Unfortunately, the disease often recurs when treatment stops, and the treatment is both expensive and accompanied by unpleasant side effects.
Hepatitis literally refers to any inflammation of the liver. Even when restricted by the term infectious, it has many causes, including malaria and many viruses including that of yellow fever. By convention, however, infectious hepatitis usually refers to a small group of diseases caused by several unrelated viruses, whose most obvious and most consistent symptoms are due to liver damage. Because these diseases are unrelated, except in liver involvement, they will be treated individually. Only their early undifferentiated history can be reviewed in general terms.
Because good recovery of hepatic and neurological function is possible in most patients, treatment must be instituted quickly. Ihe goal of therapy is to reduce copper intake by means of a low-copper diet and increase copper excretion. D-Penicillamine is the chelating agent most often used its side effects are potentially serious but preventable. Ihese include nephrotic syndrome, fever, thrombocytopenia, dermatitis, vitamin B 6 deficiency, seizures, and zinc deficiency, which causes impairment of taste and smell. Pyridoxine should be administered along with penicillamine. Some investigators suggest using tetrathiomolybdate, a drug that both blocks copper absorption and binds to bloodborne copper, as an initial therapy. In addition, zinc acetate may be used as a maintenance therapy because of its low potential for serious side effects other than gastrointestinal effects. Dietary education about foods containing high levels of copper should be undertaken, and specific...
Hepatitis C affects more than 300 million people worldwide and 4 million people in the United States. At least six genotypes and 100 subtypes have been identified (Bukh, 2000). The diagnosis is established with serum testing for HCV RNA antibodies although an antibody is induced, it is not protective against disease contraction and progression. Transmission occurs via blood or body fluid contamination through IV and intranasal drug use, blood transfusions, and in health care workers (e.g., needle stick or skin disruption with contaminated instrument). Data on sexual transmission and though tattooing have been inconsistent. Co-infection with human immunodeficiency virus (HIV) increases the risk of transmission sexually, as well as vertically mother to child. In patients with chronic hepatitis C, alcohol use rapidly accelerates liver damage and cirrhosis. Many experts believe lifelong abstinence from alcohol and IV and intranasal drugs should be immediate on diagnosis and enforced...
The failure to excrete bilirubin gives rise to yellowish discolouration of the whites of the eyes, the skin and nails, and mucosal membranes, which is called jaundice. Jaundice is essentially a sign of liver failure. Several toxic compounds, such as some pesticides, solvents such as carbon tetrachloride, and dry-cleaning fluids, damage the liver cells and prevent them from functioning normally to bind the bilirubin to the glucuronide. There are many drugs used in the treatment of disease which also damage the liver cells and are termed hepatotoxic. For example, high levels of the common drug paracetamol can cause liver damage, liver failure, and jaundice. Another common and important cause of damage to liver cells which often results in liver failure is excessive alcohol (ethanol) consumption.
Cirrhosis and chronic liver failure rank as the 12th leading cause of death in the United States, accounting for 27,555 deaths (9.2 per 100,000 population) in 2006, with a slight male predominance (NCHS, 2009). The vast majority of cirrhosis-related morbidity and mortality is secondary to excessive alcohol consumption, hepatitis B and C, and obesity (nonalcoholic fatty liver disease NAFLD ), and is theoretically preventable. The term cirrhosis refers to a progressive diffuse, fibrosing, and nodular condition that disrupts the entire normal architecture of the liver. Portal hypertension ensues with multiple long-term complications. Approximately 40 of patients are asymptomatic, with cirrhosis often discovered during a routine examination, including laboratory and radiographic studies (Figs. 38-13 and 38-14), or often at autopsy. Mortality rates in patients with alcoholic liver disease are considerably higher than in those with other forms of cirrhosis.
Short-bowel syndrome, bacterial overgrowth and translocation, and sepsis. Patients may exhibit increased liver transaminases, increase alkaline phosphatase and gamma-glutamyl transferase concentrations, and mainly increased bilirubin concentrations with jaundice. The most sensitive marker of cholestasis is an increased serum conjugated bilirubin concentration of 2 mg dL (34.2 imol L) or more.38 Cholestasis generally is reversible if PN is discontinued before permanent liver damage occurs. Serum liver enzyme concentrations may take up to 3 months to return to normal after discontinuing PN. Steps to prevent cholestasis associated with PN include early initiation
Beriberi and, 46 cirrhosis and, 79-81 diabetes and, 91 heart disease and, 160 lead poisoning from, 186-88 osteoporosis and, 237 tetany and, 329 alcoholic fatty liver, 80-81 Aleppo boil, 192 alimentary toxic aleukia, 133 alkali poisoning, 218 alkalosis, 329 alkaptonuria, 141 Allodermanyssus sanguineus, 285 allopurinol, 154 fatty-liver disease (kwashiorkor), 261-63
Xanthine oxidase catalyzes the oxidation of hypoxanthine to xanthine and uric acid in a reaction that involves a one-electron transfer to oxygen to yield superoxide. The source of xanthine oxidase is not completely clear, but increased cholesterol levels, liver damage, inflammation, and hypoxia may stimulate the release of the enzyme from the liver and other organs into the circulation. This circulating xanthine oxidase binds to endothelial cells to produce superoxide 20 . Endothelial cells themselves can express xanthine oxidase 21 .
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