Stop Fatty Liver Today

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. More here...

Fatty Liver Remedy Summary


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Fatty Liver Hepatitis And Cirrhosis

Chronic alcohol consumption can cause the deposition of excess triglycerol in the liver leading to a condition known as 'fatty liver'. This damage can lead to hepatitis and, if severe enough, to cirrhosis. The damage is thought to be due to the high concentrations of ethanal within the cell and if severe enough will result in cell death. Cell damage and death trigger an inflammatory response, i.e. infiltration of lymphocytes and activation of an immune response. If this is not treated it will lead to the formation of fibrous tissue and a severe reduction in the functioning of the liver.

Transplantation and other treatment options

Transplantation remains the treatment of choice for a subgroup of patients with a poor prognosis. A variety of models have been developed, including assessment of liver volume (volumes below 700 cm3 resulting in transplantation), assessment of percentage necrosis on biopsy (complicated by sampling error), and a variety of prognostic models. These need to be simple to apply in the clinical setting and to achieve a high level of sensitivity and specificity in discriminating survivors and non-survivors. Two models are commonly used in Europe. In the first, criteria for poor outcome in non-acetaminophen-induced liver failure have been established as the findings of coma or confusion in association with a factor V level below 20 per cent of normal in patients less than 30 years of age, or below 30 per cent of normal in those aged 30 years or above. In the second, the criteria separate acetaminophen and non-acetaminophen patients. For acetaminophen, the criteria are an arterial pH below 7.3...

Pharmacological Interventions

In addition to their clinically useful metabolic benefits, TZD compounds are approved for treatment of type 2 diabetes, and have been shown to decrease hepatic steatosis in patients with nonalcoholic fatty liver disease 65 and result in pregnancy when given to women with PCOS 66 . In light of this appealing clinical profile, the possibility that these compounds might be particularly effective in reducing CVD, and preventing the development of type 2 diabetes in particularly susceptible individuals, that is, insulin resistant, but without known disease. At the present time there are no data indicating that the development of CVD can be decreased when a TZD compound is given to insulin-resistant, nondiabetic individuals, with no evidence of CVD. On the other hand, there is information concerning the use of insulin sensitizers in delaying the progression to type 2 diabetes of individuals classified as having prediabetes.

Hepatotoxicity of acetaminophen

The minimum dose of acetaminophen believed to cause hepatic damage is 125 mg kg (which is equivalent to 15 standard 500-mg tablets for a 60-kg person). Acetaminophen doses above 250 mg kg produce hepatotoxicity in 60 per cent of cases, and severe liver damage (serum aspartate aminotransferase (AST) above 1000 IU l) is inevitable when doses in excess of 350 mg kg are absorbed. The most common method of predicting the potential risk of an overdose is through plasma

Chemicalinduced Carcinogenesis

Nitrated compounds, polycyclic aromatic hydrocarbons, and carbon tetrachloride are established carcinogens used to assess mutagenicity in various experimental models. Anthocyanins have been reported to have antimutagenic activity toward these aforementioned compounds. Studies by Obi et al.97 revealed that anthocyanins extracted from the petals of Hibiscus rosasinensis protected against carbon tetrachloride-induced liver damage in rats. Carbon tetrachloride, a hepa-totoxin, is responsible for P450-induced trichloromethyl radical production and associated peroxidation of membrane lipids leading to extensive liver damage including liver cancer.97 Additionally, studies of the antimutagenic activity of fruit juices high in anthocyanins using the Ames test revealed blueberry juice to have one of the highest antimutagenic activities observed against polycyclic aromatic hydrocarbons.98 Furthermore, Tsuda et al.99 observed that the anthocyanin pelar-gonidin prevented the formation of nitrated...

IIA General Aspects of NO in the Liver

Cells in the liver can be divided into the hepatic parench-ymal cells (hepatocytes) and the hepatic nonparenchymal cells, which are further subdivided into endothelial cells, smooth muscle cells, Kupffer cells, and hepatic stellate cells. Both hepatic parenchymal cells and hepatic nonparenchymal cells can express iNOS, whereas eNOS is constitutively expressed in hepatic endothelial cells. Although iNOS is not thought to be expressed constitutively in healthy liver, it is readily upregulated in the liver under a number of disease conditions, including ischemia-reperfusion injury, cirrhosis, hepatitis, and liver regeneration (1-4). The iNOS is also upre-gulated in vitro in hepatocytes and Kupper cells in response to endotoxin, proinflammatory cytokines, such as tumor necrosis factor-a (TNF-a), interleukin-1 (IL-1 ), and interferon , as well as their combinations (5). These stimuli often act synergistically to induce iNOS expression however, IL-1 alone is an effective stimulator of iNOS...

Ionizing Radiation Roy E Albert MD

Rubin and Casarett's categorization of types of cells according to decreasing levels of radiosensitivity is still used (23). Category I includes the most radiosensitive these are cells like the basal cells of the epidermis that undergo regular cell division and show no differentiation between divisions. Category II cells are like myelocytes in the bone marrow that also divide regularly but do undergo some differentiation between divisions. Category III cells are relatively resistant like the hepatocytes in the liver that normally divide very infrequently but can be triggered into rapid mitosis In the case of the liver, this occurs with toxic liver damage or partial hepatectomy. Category IV has the most resistant cells, including muscle cells and the neurons of the central nervous system. These cells are highly differentiated, and it is questionable that they divide at all once the organism reaches maturity.

Safety issues 1241 In animals

Fatty liver while the 9c,11t isomer had little or no effect (Clement et al., 2002 Degrace et al., 2003). While adipose tissue mass was shown to decrease after feeding CLA for 6 days, plasma levels of leptin and adiponectin decreased after 2 days of feeding, and hyperinsulinaemia developed on day 6 (Poirier et al., 2005). CLA was shown to alter the capacity of pancreatic islets to secrete insulin and the increase in insulin secretion was correlated to an increase in beta cell mass and number, leading to liver steatosis (Poirier et al., 2005). Degrace et al. (2003) demonstrated using C57BL 6J mice that the steatosis was not due to an alteration of the liver lipoprotein production. A three-fold decrease in plasma triacylglycerol and induction of mRNA expression of low-density lipoprotein receptors suggest an increase in the lipoprotein clearance at the level of liver. Further work also indicated that the steatosis was not due to impaired fatty acid oxidation as in fact in the liver,...

Conformational Diseases

In a-1-antitrypsin deficiency, a mutation hinders the proper folding of the protein in the ER of liver cells. The misfolded protein tends to form oligomers that are targeted for degradation (Carrell and Lomas 2002). In heterozygous carriers and in homozygous patients with the lung form of the disease, the capacity of degradation components of the protein quality control system is sufficient to cope with the accumulated protein. However, owing to a yet unexplained decrease in the degradation capacity found in 10 -15 of ho-mozygous patients, the protein aggregates cannot be eliminated in the liver cells of such individuals and they develop cirrhosis-like liver damage and hepatocellular carcinoma (Wu et al. 1994).

Liver DiseasesA Variety of Conditions

Cirrhosis is not a disease in itself but a stage in the course of inflammatory liver diseases. Cirrhosis can be caused by liver damage resulting from alcoholism, hepatitis B and hepatitis C, drugs, metabolic disorders, prolonged cholestasis, etc. Cirrhosis is characterized by increased presence of fibrous tissue, destruction of the lobular architecture and sinusoidal network, and nodular degeneration. The hepatic synthesis of proteins such as albumin, prothrombin, and enzymes is decreased. Cirrhosis often gives rise to portal hypertension. In portal hypertension, the blood flow coming from the intestine through the liver via vena porta is reduced while the arterial blood flow is increased relative to the portal flow. Many cirrhotic patients have portacaval shunts, where a substantial fraction of the portal blood bypasses parenchymal tissue in the liver or enters directly into the superior vena cava via esophageal varices. A characteristic late sign of liver disease is ascites, an...

D Other Biological Activities

Turmeric and curcumin are beneficial as food additives for human health. These products have been shown to reverse the aflatoxin-induced liver damage produced by feeding AFB1 (5 g day for 14 days). In addition, aqueous extract of turmeric (10 mg ml) inhibits the toxin production by 99 . The concentration of the extracts needed for 50 inhibition of toxin production is approximately 2.5 mg ml. It is known that AFB1 produced by Aspergillus parasiticus induces extensive changes in liver fatty acid changes, granular degeneration, necrosis, and bile duct hyperplasia. In animals treated with AFB1, the presence of turmeric has almost completely reversed necrosis and there are only moderate fatty acid changes. Turmeric inhibits the production of toxins in foods, without inhibiting the growth of mycelium.118

Nsaids And Clinical Trials

And renal sensitivity and liver damage in elderly patients has clouded the results from these trials. A major concern, however, with the use of NSAIDs is the potential toxic-ity of these drugs associated with COX inhibition, such as gastric ulceration, liver and kidney damage (49), and the increased risk for cerebrovascular events. This concern was reflected in the recent announcement of suspension of the use of Naproxen (nonselective COX inhibitor) and Celecoxib (Cox-2 inhibitor), in the trial by NIH, called Alzheimer's disease Anti-inflammatory Prevention Trial (or ADAPT). The data from National Cancer Institute trial to test the effectiveness of celecoxib in preventing colon cancer and the early observations from the ADAPT trial indicated an apparent increase in cardiovascular and cerebrovascular events, probably associated with the inhibition of cytoprotective prostaglandins among participants. Because of the failure of NSAIDs, there is an unmet need to develop and test new...

Exogenous Sphingolipids To Prevent Cancer In Vivo

Another sphingolipid derivative, safingol, the L-threo isomer of sphinganine, a potent inhibitor of protein kinase C, was developed to treat dermatoses and cancer. Topical application of safingol, however, caused liver damage that was more pronounced in female than in male rats possibly due to insufficient clearance of safingol by cytochrome P450 isozymes.51

Essential Fatty Acid Requirements

In patients receiving long-term parenteral nutrition without lipid, continuous glucose infusion results in high circulating levels of insulin that inhibit lipolysis and depress release of EFA from adipose fat stores (131). Development of EFAD in infants, children, and adults maintained on continuous fat-free or minimal-fat parenteral nutrition has been reversed by oral or intravenous administration of C18 2n-6 ( 151). Parenteral nutrition containing only amino acids and completely free of glucose does not produce evidence of EFAD (153). Clinical signs of EFAD include alopecia, scaly dermatitis, increased capillary fragility, poor wound healing, increased platelet aggregation, increased susceptibility to infection, fatty liver, and growth retardation in infants and children ( 153).

Ecogenetics The Study of Gene Environment Interactions Daniel W Nebert Amy L Roe PhD

Around 1930-1970, DMEs were considered as a liver detoxification system responsible for breaking down drugs and other hydrophobic environmental chemicals for excretion. It is now clear that (1) at least some of these DMEs are located in every eukaryotic cell, (2) almost all DMEs have endogenous compounds as their natural substrates, and (3) many of these DMEs have existed in evolution prior to the divergence of bacteria from eukaryotes, indicating that these DMEs have been responsible for critical life functions long before animal-plant divergence (8, 9). Since the late 1940s, it has been taught that drug and carcinogen metabolism is carried out by phase I (functionalization) and phase II (conjugation) reactions (Fig. 7.5). Originally, these two coupled reactions were regarded simply as a liver detoxification system. In the 1960s, some of these activities were then discovered in nonhepatic tissues such as lung, kidney, and gastrointestinal tract indicating that the activities were not...

Insulin Resistance Hyperinsulinemia and the IRS

Pathogenesis of the abnormalities and clinical syndromes that make up the IRS. To begin with, type 2 diabetes is the only clinical syndrome listed in Table 3 that is not associated with a significant degree of hyperinsulinemia. Obviously, in this instance, it is the failure of the pancreatic P-cell to adequately compensate for the insulin resistance that is responsible for the development of the clinical syndrome 16 . In the case of the other abnormalities and clinical syndromes listed in Tables 2 and 3, it is the relationship between insulin resistance, compensatory hyperinsulinemia, and the individual tissue response to the chronically elevated plasma insulin concentrations that is responsible for the observed pathophysiology. In this context, it is necessary to address the question of differential tissue insulin sensitivity, for if this phenomenon did not exist, there would be no IRS. For example, the ability of insulin to stimulate muscle glucose uptake and inhibit free fatty acid...

Formation Of A Chemically Reactive Intermediate

For a number of drugs that undergo metabolism, CRM will be formed irrespective of the dose of the drug (Pirmohamed et al., 1996). When a drug is taken in therapeutic dosage, any toxic metabolite formed will be detoxified by normal enzymatic or non-enzymatic cellular defence mechanisms. An imbalance between bioactivation and bioinactiva-tion leading to toxicity may however be created by taking a drug overdose. This will lead to the formation of large amounts of chemically reactive metabolites, overwhelming the cellular detoxica-tion capacity, and leading to cell damage. The clearest example of this is paracetamol, which causes hepatotoxicity when taken in overdosage, and still causes about 160 deaths per year in the United Kingdom (Bray, 1993). According to the conventional definition of adverse drug reactions, paracetamol hepatotoxicity should not be classified as an adverse drug reaction, since the hepatic injury occurs when the drug is used inappropriately. However, it is important...

Mediators of Hepatic Inflammation

Experimental data have demonstrated a critical role for proinflammatory cytokines (e.g., TNFa, IL-1, and IFNg in the development of liver injury. Although TNFa is required for normal hepatocyte proliferation during liver regeneration, it is also involved in inflammation. TNFa is known to induce the transcription factor nuclear factor-kappaB (NF-kB) which regulates many proinflammatory mediators (e.g., TNFa and IL-1). Overexpression of TNFa (from Kupffer cells or infiltrating neutrophils) has been shown to correlate with hepatotoxicity in endotoxemia, alcoholic liver disease, and viral hepatitis. Another cytokine noted for its involvement in liver injury is IFNg. In alcoholic hepatitis, overexpression of IFNg mediates liver injury. By contrast, in viral hepatitis it is a lack of functioning IFNg that permits the liver damage.

Older Sedativehypnotic And Anxiolytic Agents

Chloral hydrate (Noctec, Somnos) was developed in the late 1800s and is still used as a sedative-hypnotic agent. It is a hydrated aldehyde with a disagreeable smell and taste that is rapidly reduced in vivo to trichloroethanol, which is considered to be the active metabolite. It produces a high incidence of gastric irritation and allergic responses, occasionally causes cardiac arrhythmias, and is unreliable in patients with liver damage.

Proliferation And Apoptosis In Normal Cells Versus Cancer Cells

Now imagine that the animal receives an injury that slices away a small section of its liver. The injured area soon becomes inflamed and steeped in growth factors. These factors, produced by immune cells, released from the blood, or derived from other sources, cause various types of cells to proliferate. For example, blood vessel cells proliferate to replace those damaged in the injury, and liver cells are also stimulated to proliferate by these growth factors. In addition, the reduced cell-to-cell contact at the edge of the healthy liver tissue signals that new liver cells are needed. In response to the growth factors and signals from reduced cell-to-cell contact, stem cells or other poorly differentiated cells in the liver enter the cell cycle and proliferate. The entire repair process and all the cell proliferation that goes on in it is wondrously orchestrated so that once tissue repair is complete, no new tissue is produced.

Mary E Davis and Mark J Reasor

The discipline of toxicology considers the adverse effects of chemicals, including drugs, and other agents, such as biological toxins and radiation, on biological systems. Toxicity associated with drug action can generally be characterized as either an extension of the therapeutic effect, such as the fatal central nervous system (CNS) depression that may follow a barbiturate overdose, or as an effect that is unrelated to the therapeutic effect, such as the liver damage that may result from an acetaminophen overdose. This chapter focuses on the tissue response associated with the latter type of drug toxicity and on the toxicities associated with several important classes of nontherapeutic agents.

Pyrazolone Derivatives

Phenylbutazone (Butazolidin) is metabolized to oxy-phenbutazone (Phlogistol), and both compounds have all of the activities associated with the NSAIDs. Their use is accompanied by serious adverse reactions, such as anemia, nephritis, renal failure or necrosis, and liver damage. Because of their toxicity, they are prescribed only for the treatment of pain associated with gout or phlebitis or as a last resort for other painful inflammatory diseases resistant to newer and less toxic treatments. Interactions with a large number of other drugs (similar to those described for aspirin) occur, since phenylbutazone displaces several drugs from plasma protein binding sites.The drug is contraindicated in children and in the elderly with diminished renal function. The consequences of overdose occur slowly and can include liver damage, renal failure, and shock. There is no antidote for overdose. Supportive measures include ventilation, dialysis, and gastric lavage with activated charcoal, as well...


Ketones are the toxic elements in essential oils and these molecules can penetrate the blood-brain barrier causing damage to the nervous system and irreversible liver damage. The ketone most widely found in oils is thujone, a component in mugwort, sage, thuja, wormwood, and yarrow oils. Although sage oil has a high content of the ketone, it appears to have low toxicity and can be used by adults with caution. The toxic effects of ketones depend on how it is administered inhalation being the safest, followed by skin contact, vaginal, rectal, and oral ingestion.

Weight Loss

It has been clear for more than 30 years that overweight obese individuals are more likely to be insulin-resistant hyperinsulinemic, and that weight loss in these individuals will improve insulin sensitivity, associated with lower plasma insulin concentrations and an improved lipoprotein phenotype 39 . It is now well-recognized that a variety of metabolic abnormalities improve when overweight obese individuals lose weight, and that this intervention can lead to substantial clinical benefit. For example, it has been shown that weight loss leads to clinical improvement in patients with essential hypertension 40 , PCOS 41 , and nonalcoholic fatty liver disease 42 . Of greater relevance to this book is the finding that weight loss, in association


An enormous amount of new information relevant to the role of insulin resistance in human disease had appeared since the introduction of the concept of Syndrome X, and the abnormalities related to insulin resistance have broadened considerably. At the same time, it has become clear that the adverse clinical outcomes associated with insulin resistance extend far beyond type 2 diabetes and CVD. For example, in addition to type 2 diabetes and CVD, insulin-resistant individuals are at increased risk to develop essential hypertension, PCOS, nonalcoholic fatty liver disease, congestive heart failure,


It is possible that deficient bile production or secretion leads to the absorption of minute amounts of endotoxin, which may play a role in the induction of atherosclerosis. We showed in cholesterol-treated rabbits that endotoxin significantly increases the development of atherosclerosis 48 . Recently several authors recognized his fact 49-60 . Partial or temporary bile acid deficiency may occur for several reasons CCK deficiency, disturbance of bile secretion and deficient bile production due to liver damage, leading to endotoxin absorption. In turn, the absorbed endotoxin will act on sessile phagocytes fixed to the wall of blood vessels according to known pathways (e.g., endotoxin-binding protein and CD14 endotoxin receptor), which leads to the production of cytokines and other biologically active materials. These mediators, in conjunction with elevated cholesterol levels, could precipitate and initiate plaque formation. On this basis one may suggest that the systematic...


Regardless of etiology, much of the liver damage has often occurred by the time of presentation. However, this should not result in a failure to define the cause since the treatment options may vary. For example, liver transplantation would be inappropriate for a patient with malignant infiltration, while chemotherapy is indicated as early as possible for lymphoma. Thus the work-up and management of all patients with acute hepatic necrosis should address etiology. Investigations and imaging will be dictated by the clinical scenario, but may include some or all of those shown in Table, .

Renal management

Renal failure (urine output below 300 ml day and serum creatinine above 300 pmol l) despite adequate filling occurs in up to 70 per cent of patients with AHF. Hypovolemia and sepsis are important precipitating factors. In addition, altered levels of vasodilators and constrictors within the renal vasculature play an important role. Acetaminophen may cause direct renal toxicity as well as liver damage. The etiology of renal failure in AHF is usually multifactorial, comprising prerenal factors, hepatorenal failure, acute tubular necrosis, and direct nephrotoxicity.

ACTHproducing Tumors

The definitive treatment for Cushing's disease is surgery. For those in whom surgery is not possible or has failed, radiotherapy is usually given. This may be accompanied by adrenalec-tomy and steroid replacement. Adrenalectomy carries a 20 risk of Nelson's syndrome (pituitary hyperplasia and autonomous production of ACTH) and thus medical rather than surgical adrenalectomy is usually the first choice. The 11 p-hydroxylase inhibitor metyrapone is the most commonly used agent. Ketoconazole, which inhibits steroid production and release of ACTH, may also be used, or mitotane, which destroys adrenal tissue. All of these agents have potentially serious side-effects, particularly ketoconazole and mitotane, which my cause liver damage and hypercholesterolemia respectively. Another group of agents acts centrally by enhancing the activity of endogenous inhibitors, or by antagonizing endogenous ACTH stimulators. The most commonly used agents are bromocriptine (dopamine agonist), cyproheptadine...

Haemolytic Anaemia

Drug-induced haemolytic anaemia results from a type II immune reaction in which antibodies to the drug or its metabolite(s) attack blood cells. Antigens on the cell's surface combine with antibody and complement to stress the cell to the point of destruction. The cell damage causes anaemia. There is an increased production of bilirubin, although a healthy liver can excrete six times the normal load before unconjugated bilirubin accumulates in the plasma jaundice is therefore mild. Severe haemolysis can result in prerenal uraemia and renal failure. Other related immunological reactions are referred to below.

Intracellular FABPs

It has been known for some time that the expression of LFABP was increased by a seemingly heterogeneous group of compounds that caused the proliferation of peroxisomes,124,135-138 and that induction of hepatic peroxisomal P-oxidation capacity correlates strongly with the increase in LFABP levels.139 Indeed, when ethanol, which impairs mitochondrial P-oxidation and stimulates peroxisomal P-oxidation, was added to a high fat diet, LFABP was found to be expressed at levels up to 20 of soluble protein.140 Dicarboxylic acids, FA metabolites that are found under conditions of impaired mitochondrial P-oxidation or with high levels of FA flux, have also been shown to increase LFABP mRNA levels in cultured hepato-cytes.135,141 It is now known that these compounds, which include long-chain FA, bind to and activate PPARs. In mice null for PPARa, fasting induced a fatty liver accompanied by severe impairment of fatty acid oxidation, and LFABP expression was dramatically decreased in the the...


Acetaminophen, with a pKa of 9.5, is rapidly absorbed from the GI tract following oral administration. Peak plasma concentrations are observed within 30 minutes to 2 hours. Absorption is nearly complete following oral administration but varies with suppository forms of the drug. Acetaminophen is less plasma protein bound than the salicylates, although the amount bound varies from 20 to 50 . Following the use of normal therapeutic doses of acetaminophen, metabolism and conjugation to sulfate or glucuronides occurs, and clearance of these metabolites occurs in the kidney.A minor toxic metabolite is generated by the metabolism of acetaminophen via the P450 mixed-function oxidase system. This toxic metabolite is normally conjugated to glutathione in the liver and excreted via the kidney as conjugated cysteine and mercapturic acid. However, with the depletion of glutathione in certain disease states, such as liver cirrhosis and necrosis, and following chronic use of high doses of...


Naltrexone can induce hepatotoxicity at doses only five times the therapeutic dose and should be used with care in patients with poor hepatic function or liver damage. Side effects of the use of naltrexone are more frequently observed than following naloxone administration. Such side effects include headache, difficulty sleeping, lethargy, increased blood pressure, nausea, sneezing, delayed ejaculation, blurred vision, and increased appetite.

Organ failure

Extensive liver disease is required to cause hypoglycemia. This can happen with fulminant hepatitis, fatty liver from starvation or alcohol ingestion, and cholangitis with biliary obstruction. Hypoglycemia is unusual with common forms of cirrhosis or hepatitis, although glucose metabolism may be altered.


Ciproterone acetate has proved quite effective because of its antiandrogenic, antigonadotrophic, and progestational effects. (54 This agent blocks intracellular testosterone uptake as well as the intracellular metabolism of antiandrogens. As a consequence, it drastically reduces circulating testosterone and therefore reduces the paraphiliac's sexual drive. The oral dosage is usually 50 to 200 mg day but it is also available in an intramuscular form, requiring a dosage of 200 to 400 mg once every 1 or 2 weeks. Side-effects include liver damage, gynaecomastia (usually temporary and reversible), and reduction of sexual drive, fantasies, erections, frequency of masturbation, and sexual intercourse. This drug was first used in 1971, and a number of studies have shown it to be highly effective at reducing recidivism.(55) Ciproterone acetate is available throughout Europe and Canada, but is not available in the United States.

Wilson Disease

One of the important diagnostic features of Wilson disease is the Kayser-Fleisher ring caused by deposition of copper in the cornea. Patients with early onset of the disease usually display predominantly hepatic symptoms, whereas those with a late onset mostly display neurologic symptoms 15 . Liver dysfunction symptoms which include jaundice and fatigue and other conditions include asymptomatic cirrhosis, subacute hepatitis and hepatitis resembling autoimmune hepatitis 16 . The mechanism of liver damage in Wilson disease is thought to be oxidant stress 17 . Levels of antioxidants such as vitamin E are low 18 . Accumulation of copper is most likely the source of activated oxygen species (superoxide O-, hydrogen peroxide, and hydroxyl radical). Studies using primary cultures of rat hepatocytes show that copper generates more activated oxygen species and causes more lipid peroxidation than cadmium 19 . Generation of peroxides and hydroxyl radicals leads to nuclear damage.

Figure 352

Tance in the metabolism of ethanol in humans, it may be involved in some of the reported interactions between ethanol and other drugs that are also metabolized by this system. Microsomal mixed-function oxidases may be induced by chronic ethanol ingestion. Because ethanol is metabolized in the liver, it can interfere with the metabolism of other drugs by blocking microsomal hydroxylation and demethylation. Drug classes whose metabolism is most affected include the barbiturates, coumarins, and anticonvulsants, such as phenytoin. Liver damage resulting from chronic abuse of ethanol can impair metabolism of a variety of drugs.

Treatment of Anemia

Anemia is a common finding in patients with CIMF and is frequently multifactorial. Iron deficiency, ineffective erythro-poiesis, red cell sequestration, hemodilution due to plasma volume expansion consequent on splenomegaly, and hemolysis are major mechanisms, whereas folate and or vitamin B12 deficiency is uncommon. Androgen therapy improves marrow function in approximately 40 percent of patients, with optimal responses occurring in individuals with normal karyotypes and lack of massive splenomegaly. Oxymetholone is the drug of choice and should be prescribed for at least 3 to 6 months to identify responsive patients. Careful monitoring of liver function and periodic ultrasound imaging is recommended to detect liver damage or the development of hepatic tumors. Danazol, a synthetic steroid derived from ethisterone, has been used successfully in some patients and may also reduce the degree of thrombocytopenia. A number of patients with nor-mochromic normocytic anemia have a reduced red...


Blood flow obstruction in the sinusoids is the likely cause of liver distension, subcapsular hemorrhage, and hepatic rupture, the most feared complication of HELLP (Wej_n_s_t_ein_.1982). Increased hepatic artery resistance to blood flow has been demonstrated in pre-eclampsia with or without HELLP and is not implicated in the development of the syndrome. Some liver biopsy specimens have shown fat within hepatocytes an overlap with acute fatty liver has been described, but clinical and histological findings can distinguish this syndrome from HELLP (Barton.eLai 1992).

Lifestyle and health

The effects on health of behaviours such as smoking(22) and high alcohol use(23) are well documented. There is overwhelming evidence that smokers not only are much more likely to die from lung cancer and other cancers but also have much higher rates of cardiovascular disease and chronic respiratory disorders, particularly emphysema and chronic bronchitis. Moreover, the disease risk is dose related in that higher levels of smoking are more strongly associated with all these diseases. With sustained high levels of alcohol use a different but equally unpleasant spectrum of health problems can be seen. Drinking is a major cause of accidents particularly motoring accidents and can cause liver damage as well as having detrimental effects on brain functioning. (1)


Most patients with primary bone tumors are managed by tertiary referral hospitals and may present for major resection following chemotherapy and or radiotherapy. Side-effects from both these treatments vary from minor inconvenience to life threatening. Myelosuppression is common and may result in anemia, leukopenia, and thrombocytopenia. There is an increased association between malignancy and deep vein thrombosis. Cardiomyopathy, pulmonary fibrosis, and renal and liver damage are associated with various chemotherapeutic agents and should be sought.


Adverse reactions particularly associated with the trivalent antimonials are coughing, occasional vomiting, myalgia, arthralgia, and changes in the electrocardiogram. Sodium stibogluconate occasionally causes rashes, pruritus, abdominal pain, diarrhea, and anaphy-lactoid collapse. Liver damage with jaundice is a rare side effect. Toxic reactions are more common with repeated courses of treatment. Biochemical evidence of pancreatitis is usual (97 ), but severe or fatal pancreatitis is extremely infrequent.

Urinary bilirubin

When bilirubinuria is present the urine is usually a dark brown color. The presence of bilirubin in the urine is easily tested for by a test strip impregnated with a diazo reagent. This test is easy to perform at the bedside and is sensitive to bilirubin levels of 1 to 2 mmol l (0.06-0.12 mg 100 ml). It can establish the presence of liver damage before frank jaundice is clinically apparent. In jaundiced patients, the absence of bilirubinuria usually implies that the hyperbilirubinemia is unconjugated and thus suggests a hemolytic cause (Table 1).

Yellow Fever

Causative Agents

Viral liver damage results in jaundice and decreased production of clotting proteins, and injury to small blood vessels produces petechiae, tiny hemorrhages, throughout the body. The virus affects the circulatory system by directly damaging the heart muscle, by causing bleeding from blood vessel injury in various tissues, and by causing disseminated intravascular coagulation (DIC). Kidney failure is a common consequence of loss of circulating blood and low blood pressure. biological vector, p. 491 disseminated intravascular coagulation, p. 720

Hepatitis C

What Anti Hcv Means

Screening tests to determine the levels of anti-HCV antibodies are conducted using commercial tests, whereas HCV-RNA is detected via PCR. Usually a PCR is conducted to quantify the viral-load , which provides the number of circulating HCV genomes. A positive finding is followed by HCV geno-typing. Characteristically, the transaminases progress in an often unsteady and fluctuating manner, and the discovery of normal levels is not unusual. A liver biopsy is usually not necessary and should only be performed if there is any reason to suspect significant liver damage or as a means of ruling out other liver diseases.

Liver Constitution

Endothelial Cell Liver

Intrahepatic lymphocytes comprise 25 percent of non-parenchymal cells in the normal liver (Figure 1). In contrast to peripheral blood, the major lymphoid population in the normal liver are pit cells (i.e., NKT cells, 30 ), then T cells (20 TCR-ab and 10 TCR-gS), NK cells (20 ), and very few B lymphocytes (5 ). Natural killer T cells are a unique population of cells that express both CD3 and NK1 on their cell surface, secrete IL-2, IL-4, and IFNg, and recognize antigen in association with CD1. After NKT cells, the predominant intrahepatic T cells are CD8+. Notably, this predominance of CD8+ T cells in the liver differs from the CD4+ T cell majority observed in peripheral blood and spleen. CD8+ T cells, NKT cells, and NK cells all possess cytotoxic activity. Activated CD8+ T cells can be retained by the liver via their interaction with sinusoidal endothelial cells. These trapped activated T cells can then cause liver injury by releasing inflammatory cytokines and by apoptos-ing....


The liver not only processes nutrients but must detoxify all the harmful substances the villi were unable to prevent from being absorbed into the bloodstream. Other situations that can tax the liver considerably include overeating and eating foods that are refined. Refined foods are missing the nutrients they need to be properly metabolized. If the liver can no longer filter and cleanse the blood, or properly metabolize nutrients, or take care of its own health, it is because liver cells are damaged or begin to die. Liver damage is not easily detected by conventional testing and its condition may not be known until dysfunction becomes apparent through illness. Symptoms may range from headache, diarrhea, constipation, food sensitivities, flatulence, sleeplessness, and aching joints to cirrhosis and hepatitis.

Hormonal agents

Medroxyprogesterone acetate is the primary hormonal agent that has been used in the United States, since initially reported by Heller et al.(56 Its effect results from the acceleration of testosterone-A-reductase in the liver which accelerates testosterone metabolism and thereby reduces testosterone levels. Medroxyprogesterone acetate also reduces plasma testosterone through the pituitary axis. It is not an antiandrogen. Significant side-effects have included liver damage, fatigue, weight gain, hot and cold flushes, headaches, gallbladder disease, diabetes, and thrombophlebitis. Historically, the dose was 300 to 400 mg of the injectable form of medroxyprogesterone acetate, but in recent years lower doses have been found to be equally effective without causing so many side-effects that the medication is discontinued by the paraphiliac. An alternative to injectable medroxyprogesterone acetate can be administered orally. Generally doses of less than 200 mg daily by mouth are effective at...


At the opposite spectrum of malnutrition and wasting is obesity. As the prevalence of obesity increases in the general population, it is also increasing in the liver disease population. Specifically, there is a rise in the incidence of obesity and NAFLD. NAFLD is a syndrome ranging from steatosis to cirrhosis it affects 10-25 of people in the U.S. 18-20 . Nonalcoholic steatohepatitis (NASH) is the most severe form of NAFLD it is characterized by fatty liver, inflammation, necrosis and fibrosis and occurs in 50 of the obese population, but in only 3 of lean individuals 20 . Like many other chronic diseases, NASH is associated with metabolic syndrome 21, 22 . Obesity, dyslipidemia, hypertension, diabetes mellitus, hyperinsu-linemia and insulin resistance are common problems linked with the metabolic syndrome and NASH. Treatment of NAFLD includes diet changes, weight loss and insulin-sensitizing drugs 23 .

Human Studies

The sixth study was a two-year, unblinded, uncontrolled, pilot study on 10 patients with inoperable pancreatic cancer.216 This study by Nicholas Gonzalez, M.D., and Linda Isaacs, M.D., was a continuation of work originally started by Dr. John Beard and others in the early 1900s and later carried on by William Kelly, a dentist from Texas.229,230,231 Dr. Gonzalez became interested in the effects of proteolytic enzymes and other modalities after reviewing the work of Dr. Kelly. In this study, patients were treated with an intensive program of diet, oral supplementation of nutrients and enzymes, and routines such as coffee enemas (for the purpose of liver detoxification). The proteolytic enzymes are the proposed anticancer element in the program, while the other components are considered supportive in nature. The daily dose of pancreas enzymes (derived from pigs) was 25 to 40 grams, which was spread out over multiple doses throughout the day and night. Although the exact protocol has not...

Biochemical markers

Other more sophisticated enzyme tests measure serum myoglobin or troponin. These smaller molecules are released much earlier and can be used to diagnose infarction on admission when the ECG is equivocal. Bedside kits are now available. These may help to make a diagnosis of myocardial necrosis, particularly if the ECG is unhelpful because of previous infarctions or bundle branch block. However, these methods still involve some delay which may hinder proper administration of thrombolytic treatment. In practice, they have not yet proved clearly superior to clinical evaluation by the more traditional methods outlined above, except in the case of small infarctions when the value of reperfusion is less clear. Nevertheless, they may be useful as markers of early reperfusion or, more importantly, as markers of failure to reperfuse in the first 60 to 90 min, and so act as pointers for further intervention. Markers arising solely from the myocardium, such as the CK-MB and troponins, are quite...

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