Fast Fatty Liver Disease Cure

Fatty Liver Remedy

The fatty liver remedy is a program that uses natural ways to treat diseases related to fatty liver. The creator of this program goes by the name of Layla Jeffrey and has for the better part of her life majored in the field of nutrition. This program is very secure and safe to use all the recommended methods in the guide because they have undergone testing and results have proven that they give 100% positive results. This program is worth trying as it involves zero-risk. Within 60 days after joining the program, a total money refund is guaranteed to any user who feels unsatisfied with the program. The program is a life changer as it will help you in the elimination of toxic elements in your body, help improve the level of efficiency of your liver. Also, help you save on the cost as you will use natural treatment methods and the program will free bonuses to help boost your health in a big way. Following all the benefits associated with this program, I highly recommend the fatty liver remedy program to everyone as it will enhance your healthy living permanently. Read more...

Fatty Liver Remedy Summary

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Reverse Your Fatty Liver Program

The Reduce Your Fatty Liver Program is a digital program designed to help work out the cause of fatty liver disease and what steps to take to reduce its symptoms. Through a variety of resources developed by author Susan Peters, who treated the condition herself when diagnosed with fatty liver disease, readers can reduce the fat build-ups in their livers that could be causing adverse effects to their personal health. As fatty liver disease comes with a host of unpleasant symptoms, such as weight gain, fatigue, skin breakouts, and even long-term liver ailments such as fibrosis or cirrhosis, the program aims to help those suffering from the disease to restore their liver to a natural and healthy condition. Resources included detailed medical information regarding fatty liver disease researched by Susan herself, along with a range of methods to naturally reduce fat in the liver, eliminating the disease entirely and enjoying the benefits of a healthy and functional liver. An in-depth dietary program is also included that aims to deal with the root cause, as poor diet is the leading cause of the condition, while suggestions for supplements, vitamins, minerals, and how to naturally detox the liver are all provided. Read more...

Reverse Your Fatty Liver Program Summary

Contents: Ebook
Author: Susan Peters
Official Website: www.reverseyourfattyliver.com
Price: $27.00

Nonalcoholic Fatty Liver Disease NAFLD

Nonalcoholic fatty liver disease (NAFLD) is a spectrum of histological changes in the liver in patients who drink < 20-30 g of alcohol per day, ranging from simple fatty infiltration (steatosis) to a pattern of injury characterized by inflammation, hepatocyte degeneration, and fibrosis, known as nonalcoholic steatohepatitis (NASH), and to frank cirrhosis. The histological changes in NAFLD are indistinguishable from those observed in alcoholic liver disease. Although the quantity of alcohol considered harmful is > 30 g day in men and > 20 g day in women, there is no consensus on the amount necessary to cause liver damage. Additionally, patients' self-reporting of alcohol consumption is frequently inaccurate. NAFLD has been increasingly recognized as an important public health problem. Since it is closely linked to obesity, its significance is expected to increase even further with the current obesity epidemic. NAFLD is seen most commonly in middle age in the fourth decade of life...

Fatty Liver

This is an abnormal accumulation of fat in the liver caused by alcohols, carbon tetrachloride, and several other agents. Excess synthesis or inadequate secretion of lipids from the liver may be responsible. Ethanol itself is believed to cause fatty liver, with up to 50 of the total liver mass becoming fat, by blocking the secretion from the liver of triglycerides. Other evidence, however, suggests that ethanol acts instead by increasing fatty acid synthesis. In the face of excess substrate (NADH that arises from the oxidation of ethanol) more lipoprotein product will be formed. This hypothesis is supported by the finding of low lipoprotein levels in the blood of chronic ethanol users who have fatty liver. Other hepatic toxins may act by inhibiting the synthesis of the protein moiety of very low density lipoprotein (VLDL). Without its protein moiety, VLDL particles could be trapped in the liver and contribute to fatty liver. Conversely, some act by limiting, not the synthesis of...

Box 21 Defects In The Urea Cycle

When we eat protein, nitrogen enters the body. The body uses some of the nitrogen but some of it needs to be eliminated. The protein ornithine trans-carbamylase carries out one of several critical steps in the urea cycle. In babies with a normal copy of the gene that makes the OTC protein, the urea cycle uses dietary nitrogen to produce urea and the extra nitrogen from the diet is thus excreted. A baby who has only damaged information for making OTC protein cannot use the urea cycle to turn nitrogen into urea to be excreted. These babies have problems that include accumulation of nitrogen-containing ammonia, which can be toxic. Excess ammonia can lead to problems such as brain damage, liver damage, coma and even death. How severe the problems are depends on whether the OTC protein is completely missing or whether the protein is damaged but still able to carry out its job at a low level. Defects in genes controlling the other steps in the urea cycle can cause similarly terrible...

Diseases and disorders

Liver damage is often caused by infections or drugs and may be acute or chronic. Acute liver disease can rapidly progress to liver failure, or can resolve, either spontaneously or with appropriate treatment. Chronic liver disease may cause cirrhosis, which is characterized by a variety of signs and symptoms and changes throughout the body, including the effects of hepatic portal venous hypertension.

Mechanisms of Viral Tumorigenesis

In the case of the HPVs (and other small DNA tumor viruses), the viral oncogene products inactivate both the Rb and the p53 tumor suppressor pathways (Nevins, 2001). Strikingly, these pathways are often crippled during the development of nonviral tumors as well. Inactivation of these tumor suppressor pathways not only provides a proliferative stimulus, but also elicits genetic instability, in part by decreasing the likelihood of growth arrest and or apoptosis in response to DNA damage (zur Hausen, 2002). The ensuing mutations in cellular growth control genes undoubtedly play a role in further carcinogenic progression. However, despite these accumulated mutations, the proliferation of HPV-induced cervical cancer cells requires continued expression of the viral E6 and E7 oncogenes (von Knebel Doeberitz et al., 1988 Hwang et al., 1993). The mechanisms of herpesvirus transformation are more complex and appear to involve modulation of cellular signaling and cell cycle control pathways by...

Additional Reading

Update on nonalcoholic fatty liver disease. J. Clin. Gastroenterol. 34 155-62, 2002. Alba, L. M. and Lindor, K. Review article Nonalcoholic fatty liver disease. Aliment Pharmacol. Ther. 17 977-86, 2003. Sanyal, A. J. (guest editor), and Gitlin, N. (consulting editor) Nonalcoholic fatty liver disease. Clinics Liver Dis. 8 481-734, 2004. Kleiner, D. E., Brunt, E. M., Van Natta, M., et al. Design and validation of a histological scoring system for nonalcoholic fatty liver disease. Hepatology 41 1313-21, 2005.

The Asymptomatic Iron

The patient was referred to a hematologist, who recommended a liver biopsy to confirm and quantify excess tissue iron deposition and to assess liver damage due to mildly elevated transaminases. Steatosis and mild portal inflammation, but no fibrosis or architectural abnormalities were seen on trichrome and reticulin stains. In addition, there was moderate periportal and pericanalicular iron deposition, primarily in the hepato-cytes. The total liver iron was reported as 4896 units (normal 200-2400) and the hepatic iron index was 1.3. Molecular diagnostic testing for the two most common HFE gene mutations associated with hereditary hemochromatosis was performed, and the patient was compound heterozygous for a mutation that coded for substitution of tyrosine for cysteine at amino acid 282 (C282Y), and a second mutation that coded for substitution of aspartate for histidine at amino acid 63 (H63D).

Answers and Discussion

Q1. (Answer b) Adriamycin, in common with virtually all chemotherapeutic agents, has high potential toxicity. In the case of this drug, the limiting toxicity is cardiac. More drug might have been beneficial in attacking the tumor but it would likely have been cardiotoxic. There was no mention in his history of chemical abnormalities nor of myocardial infarction during his treatment for the angiosarcoma. Q2. (Answer c) Alcohol is responsible for a range of liver pathology. Heavy drinking causes fatty liver that may progress to hepatitis that may progress to cirrhosis. Some small number of alcoholics develop liver cancer. The specific pathology resulting from alcohol is not predictable but it is certain that alcoholism correlates with risk of hepatic cancer. A history of alcohol abuse puts this patient in a higher risk category. Whether this is merely additive to the risk that arises from vinyl chloride exposure or whether it is greater than the additive risk predicted from each factor...

Porphyria Cutanea Tarda

Porphyria cutanea tarda (PCT) is a defect of uroporphyrinogen decarboxylase that can be acquired or inherited through autosomal dominant transmission. This disorder becomes active only after additional liver-specific precipitating factors, such as alcohol, drugs, or viral infections (hepatitis, HIV) are present. Among the precipitating factors of hepatic porphyria, estrogens also play an important role estrogen-containing contraceptives have been implicated in the manifestation of PCT in young women. It is known that all of these factors either inhibit uroporphyrinogen decarboxylase or lead to liver damage as a result of direct or indirect deposition of iron in the liver. Perimenstrual improvement of PCT has been explained by menstrual bleeding, which, similar to therapeutic bloodletting, leads to a reduction of iron (36).

The effects of alcohol on the brain and addiction

Because alcoholics break down the alcohol more quickly than other people, they may appear to be sober even when they have had several drinks (that is, until they sustain liver damage, when they may be more affected than the average person). Can alcoholism be treated Apart from simple abstinence and drug treatment to alleviate the withdrawal symptoms, there is a drug, antabuse, which helps alcoholics to stop drinking by making the effects of the alcohol unpleasant.

Variability in the effects of alcohol sex and race

Studies in twins have suggested that genetic factors may be important in the development of alcoholic liver damage. While there are differences in the various enzymes involved with alcohol metabolism, some of the differences are not consistent or large enough to account for differences in susceptibility. Genetic differences in protective mechanisms and genes involved with inflammation have also been linked to susceptibility to alcohol-induced liver disease.

Nucleoside reverse transcriptase inhibitor NRTI

A set of serious side effects of NRTI drugs is now being called metabolic toxicity. This set of side effects is probably the result of mitochondrial toxicity. mitochondria are the cell's power organs that supply the energy needed for normal cell growth. Anti-HIV nucleoside analogs impair the production and function of mitochondria in the body, in many cases altering the mitochondria. This impairment can lead to increased acid levels in the blood and an enlarged, fatty liver. Clinical features that can usually be seen in patients with genetic mutations of mitochondrial DNA, such as polyneuropathy, myopathy, cardiomyopathy, fatty liver, lactic acidosis, pancreatitis, vomiting, pancy-topenia (low blood counts), and renal proximal tubular dysfunction, also occur in NRTI-related toxicities. Thus some have hypothesized that all adverse effects of NRTIs can be attributed to mito-chondrial toxicity. However, why toxicity related to NRTIs develops differently in different patients has not been...

Characterization of hazard in vitro

Primary cells are typically cells from the liver, as these are the most easily obtained and the majority are the same type of cell, whereas those from most other organs are a mixture of types of cells. Primary liver cells are the most likely to be representative of the organ in the whole animal. These cells however, will indicate the effects (if any) that the chemical has only on the liver. They do not necessarily predict the effects on other organs or tissues. Furthermore, research has shown that the way in which isolated cells in the laboratory respond to chemicals is not always the same as the way they respond in the animal or human. They are often less sensitive, sometimes requiring a concentration of chemical many times higher than that which causes an effect in the live whole animal. For example, when isolated human liver cells are exposed to paracetamol, toxic effects are observed only if a concentration of paracetamol is used that is at least ten times higher than the level...

Liver function tests 287

Alanine aminotransferase (ALT) ALT is an enzyme produced within the cells of the liver. Any form of liver damage can result in an elevation in the ALT. The ALT level may or may not correlate with the degree of damage or inflammation. ALT is the most sensitive and commonly used marker for liver cell damage. Aspartate aminotransferase (AST) AST is not as specific for liver function as the ALT ratios between ALT and AST are useful to physicians in assessing the possible cause of liver enzyme abnormalities. Gamma glutamic transpeptidase (GGT) Certain GGT levels, as an isolated finding, reflect rare forms of liver disease. Medications commonly cause GGT to be elevated. It is an enzyme that is also produced by the bile ducts, so it may reflect problems there. Alkaline phosphatase This is an enzyme that is associated with the biliary tract. If the alkaline phosphatase is elevated, biliary tract damage and inflammation should be considered.

Asymptomatic infection

Known side effects of atazanavir include diarrhea and elevated levels of bilirubin, a liver enzyme. Diarrhea was experienced by about 30 percent of research subjects. Bilirubin is the liver enzyme that causes jaundice. A person with high levels of bilirubin may experience a yellowing of the eyes, nails, and skin. The high bilirubin levels were not associated with any liver damage in patients. Research has shown that patients with HBV or HCV coinfection did not suffer liver problems from the rise in bilirubin levels. In some studies hyperbilirubinemia was experienced by 50 percent of the patients.

Novel therapeutics targeting the trail cell death pathway

The absence of detectable apoptosis activity in normal cells after treatment with soluble TRAIL has been shown for primary cells from the lung, bone, liver, endothelium breast, brain, and kidney (12,47). Importantly, short-term treatment of mouse, monkey, and chimpanzee with soluble, recombinant, Zn2+-stabilized TRAIL has demonstrated the tolerabil-ity of the ligand. No detectable toxicities were observed in these nonclinical safety studies. Earlier forms of TRAIL were generated with epitope tags (126). These epitope tagged forms also enhanced the toxicity of TRAIL on normal cells. HIS-tagged, leucine-zipper or antibody crosslinked forms of TRAIL have demonstrated the ability to induce apoptosis in normal hepatocytes in vitro (49,127). TRAIL can induce apoptosis in bacterially activated hepatocytes, in stellate cells from the liver and pancreas, or in mouse models of hepatitis or pancreatitis (50,128). Membrane-bound TRAIL has been shown to induce liver damage in...

The Spanish toxic oil syndrome

The disease appeared after a latent period of at least one to two weeks, longer in some cases, and an apparent relationship between the extent of use of the oil and the effect (a dose-response relationship) was noted in one report. The syndrome had an initial phase lasting one to two months, with effects mainly on the respiratory system and the accumulation of fluid in the lungs. There were many deaths at this early stage from respiratory failure. In the next phase (two to four months) there was muscle pain and liver damage. In the final phase there was muscle wasting and weight loss and the skin was affected (see box).

Definition of Alcoholic Liver Disease

Alcoholic liver disease (ALD) includes three conditions hepatic steatosis or fatty liver, alcoholic hepatitis, and cirrhosis.1,2 Heavy alcohol abuse, even for as little as few days can lead to hepatic steatosis, the earliest stage of ALD and the most common alcohol induced liver disorder. This condition can be reversed when alcohol consumption stops. Heavy use of alcohol for longer periods of time may lead to the development of the more severe and potentially lethal alcoholic hepatitis.3 Only 10-15 of abusers actually progress to acute alcoholic hepatitis however, up to 70 percent of all alcoholic hepatitis patients eventually may go on to develop cirrhosis.4 In 2000, ALD was the fourth most common cause of death in males between the ages of 45 and 54.5

Consequences of the metabolic syndrome

The metabolic syndrome is associated with increased risk of a variety of disease outcomes, including diabetes, peripheral arterial disease (the association with cardiovascular disease is discussed in Chapter 10), fatty liver and non-alcoholic steatohepatosis (discussed in Chapter 11), polycystic ovary syndrome (discussed in Chapter 12), gallstones, asthma, sleep apnoea and selected malignant diseases.

How alcohol is broken down and how it affects the liver

In addition to requiring an enzyme, the breakdown of alcohol requires a co-enzyme called NAD, which is converted into NADH when the alcohol is metabolized. The large increase in the level of NADH at the expense of NAD, and the lack of utilization of other sources of energy such as carbohydrate, leads to an increase in the production of fat, some of which accumulates in the liver after a heavy bout of drinking. This 'fatty liver', if maintained by regular and excessive drinking, seems to be a necessary stage in the eventual development of liver disease, like hepatitis and cirrhosis, which occurs in some alcoholics. The presence of the fat impairs the ability of the liver to function. The other effect of the change in the proportions of the coenzymes is that glucose is not produced, and this is made worse if the heavy drinker does not eat a normal diet from which glucose might be obtained. Blood glucose levels can therefore be dangerously low.

The development of an antidote

The outcome, however, can depend on the individual patient. The recommended dose of paracetamol is 1 to 2 tablets (500 mg each) but the size of dose necessary to cause damage depends on the individual. The average individual who is not taking other drugs regularly, may have to take about twenty tablets to suffer liver damage, but with some individuals as few as ten tablets can have the same effect. There is individual variability in the sensitivity to paracetamol due to variation in the metabolism. A major factor is the use of alcohol and certain other drugs such as barbiturates (see case notes).

Common disorders

Viral hepatitis is common throughout the world. Liver abscesses, caused by amoebae, bacteria and parasites, are common in some parts of the world. Drugs and toxins, including medications, also commonly affect the liver and the most important of these is alcohol. Chronic damage may cause scarring and lead to cirrhosis. Overwhelming liver damage, either acutely or chronically, causes liver failure. Although primary liver cancer is rare, metastatic cancers are common (see Chapters 33, 38, 41 & 42).

Biotin

Three of the four biotin-dependent carboxylases are mitochondrial propionyl-CoA carboxylase, methylcrotonyl-CoA carboxylase and pyruvate carboxylase the fourth, acetyl-CoA carboxylase, is found in the mitochondria and the cytosol. Pyruvate carboxylase is a key enzyme in gluconeogenesis, so impairment as a result of biotin deficiency may lead to fasting hypoglycaemia. Work with chicks showed a fatal hypoglycaemia called 'fatty liver-kidney syndrome' was due to impaired gluconeogenesis caused by deficient activity of pyruvate carboxylase. Several workers have suggested that biotin deficiency may cause sudden infant death syndrome (SIDS) by an analogous pathogenic mechanism (Mock, 1999). The hypothesis was supported by demonstrating that hepatic biotin concentrations were significantly lower in infants who died from SIDS than those dying from other causes. Further work is needed to confirm this finding. There are no reports of biotin toxicity in amounts up to 10 mg day.

Toxic tea

A study in two hospitals in South Africa identified twenty children suffering from this type of liver disease which was thought to be due to the use of traditional remedies. Most of the children had fluid in the abdominal cavity and an enlarged liver, indicating liver damage and dysfunction. There was a high level of illness and mortality, and in those who survived the disease progressed to liver cirrhosis. In four cases pyrrolizidine alkaloids were detected in the urine of the children.2

Flucytosine 185

Fluconazole An antifungal drug that is approved for fungal infections, primarily those caused by Candida albicans (thrush or candidal esophagitis) and cryptococcus neoformans (cryptococcal meningitis), a severe complication of HIV infection. Another fungal infection, coccidioidomycosis, can also be treated with fluconazole. Fluconazole can be taken by mouth or vein. Side effects are unusual. occasional problems are abdominal discomfort, nausea, rash, or signs of liver damage. Fluconazole has many drug-drug interactions with a wide variety of agents, including those frequently taken concurrently by people with HIV For exam

Hepatitis A

HCV disease may progress more rapidly in people with HIV. Studies conducted before the use of haart showed that HIV could speed HCV disease progression. But HAART's boost to the immune system may help to slow HCV-related liver damage. Coinfected people usually have higher HCV viral loads than people with HCV alone, but much controversy remains about HCV disease progression in coinfection. Further research is needed to confirm whether HCV does make HIV disease worse.

Wilsons Disease

A genetic disorder that involves the nervous system and liver function, causing problems metabolizing copper. As copper builds up in the liver and in specific places in the nervous system, it causes tremors, uncoordination, falling, slurred speech, stiffness, and seizures. psychiatric problems also can occur, together with severe liver damage. Treatment includes medications that bind copper.

Nitrosamines

By far the most significant toxicological effect of nitrosamines is their carcinogenicity, which may result from exposure to a single large dose or from chronic exposure to relatively small doses. Different nitrosamines cause cancer in different organs. The first nitrosamine extensively investigated for carcinogenicity was dimethylnitrosamine, once widely used as an industrial solvent. It was known to cause liver damage and jaundice in exposed workers, and studies starting in the 1950s subsequently revealed its carcinogenic nature. Dimethylnitrosamine was found to alkylate DNA, which is the mechanism of its carcinogenicity (the alkylation of DNA as a cause of cancer is noted in the discussion of biochemistry of carcinogesis in Section 7.8).

Drugs and toxins

The most common liver-damaging toxin is alcohol, which causes metabolic damage to hepatocytes, partly by interfering with energy metabolism, resulting in fatty liver, and also by inducing inflammation, when it can cause alcoholic hepatitis. Sustained excess drinking can cause cirrhosis.

Sterilization 459

Steatosis The collection of excessive amounts of fats inside liver cells, which can also be referred to as fatty liver. By itself the condition is not threatening, though it usually indicates other problems. Causes of steatosis include hepatitis, alcoholism, malnutrition, pregnancy, and drug toxicities. Treatment involves eliminating the cause of the fat buildup, and prognosis is good if the condition is recognized and the problem has not continued over many years.

The Liver

Toxic effects to the liver are studied under the topic of hepatotoxicity, and substances that are toxic to the liver are called hepatotoxins. Much is known about hepatotoxicity from the many cases of liver toxicity that are a manifestation of chronic alcoholism.6 Liver injury from excessive alcohol ingestion initially hampers the ability of the organ to remove lipids, resulting in their accumulation in the liver (fatty liver). The liver eventually loses its ability to perform its metabolic functions and accumulates scar tissue, a condition known as cirrhosis. Inability to synthesize clotting factors can cause fatal hemorrhage in the liver. Steatosis, commonly known as fatty liver, is a condition in which lipids accumulate in the liver in excess of about 5 . It may result from toxicants that cause an increase in lipid synthesis, a decrease in lipid metabolism, or a decrease in the secretion of lipids as lipoproteins. An example of a substance that causes steatosis is valproic acid,...

Cognex

Tacrine is not a cure, its effects are slight, and there are unfortunate side effects. Tacrine increases an enzyme that can cause liver damage, and about half the patients stop taking the drug due to side effects. It will not help those with very advanced cases. The most significant side effect is an elevation of liver enzymes that, if untreated, could cause liver damage. This condition was reversed in all cases when therapy was reduced or discontinued. Weekly blood tests are required in order to detect the problem. Other side effects include nausea, vomiting, diarrhea, abdominal pain, indigestion, and skin rash.

Karnofsky index

Ketoconazole An antifungal medication, available in pill, cream, and liquid forms, that is effective against a variety of fungal infection such as oral, vaginal, and esophageal thrush and cryptococcosis. Ketoconazole requires acid in the stomach to be absorbed into the system, if taken orally. other medicines that neutralize stomach acids should therefore not be taken until at least two hours after taking ketoconazole. It is not currently prescribed as frequently as it was in the past for HIV patients. It is used predominantly in its cream form and in over-the-counter shampoos. Possible side effects, when it is taken orally, include nausea, vomiting, hormonal problems (menstrual problems and reduced sex drive), rash, headaches, and liver damage. (The brand name is Nizoral.)

Beer and paracetamol

A 43-year-old man was admitted to hospital suffering hallucinations. He had fallen off his bike, fractured a bone in his shoulder, and was prescribed one to two tablets of Tylenol (paracetamol plus codeine) every four to six hours for two days. He continued to suffer occasional hallucinations and vomiting and from jaundice. Once in hospital liver function tests on his blood indicated that he had liver damage. He died in a hepatic coma thirty hours after being admitted to hospital. It was later revealed by relatives that the patient had also treated himself with nine Tylenol tablets plus ten tablets of another preparation after the bicycle accident. Another important factor was that he regularly drank half a case (twelve bottles) of beer each day.2

Copper toxicity

Tions which are still in place.39 Acute toxicity results, initially, in symptoms such as abdominal pain, nausea, vomiting and diarrhoea. These gastrointestinal effects are often sufficiently severe and prompt to prevent systemic toxicity which, like chronic copper poisoning, is associated with liver damage. Chronic toxicity has most often been caused by contaminated water supplies, and occasionally by contamination of haemodialysis equipment by copper parts.40

Paracetamol overdose

In 1966 a young man, an inmate of a mental institution, was admitted to hospital in Edinburgh. He had taken a quantity of paracetamol tablets, his estimate being 150, along with a quarter of a pint of vodka, some seven hours earlier. During the next twenty-four hours he was reported to be well but obstreperous. On the second day in hospital he complained of pain in the abdomen and nausea. On the third day he was breathing abnormally (hyperventilating) and appeared jaundiced. On the fourth day his condition worsened, and he died 80 hours after admission. At post-mortem the liver was found to have signs of extensive damage as did the tubules of the kidneys. The levels of paracetamol in the blood were found to be very high, consistent with an overdose of the drug. The victim died as a result of liver damage and probably kidney failure. Although the patient had been taking and was given other drugs, paracetamol was the only one taken at an abnormally high dose. This case of fatal liver...

Hccccccch

Other than ethanol, the xenobiotic chemical best known to cause steatosis is carbon tetrachloride, CCl4. This compound was once widely used in industry as a solvent, and even in consumer items as a stain remover. As discussed in some detail in Chapter 16, it is converted by enzymatic action in the liver to Cl3C- radical, then by reaction with O2 to Cl3COO- radical, which reacts with unsaturated lipids in the liver to cause fatty liver.

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