Foods you can eat with Fatty Liver
Important role in lipid metabolism, and triglyceride synthesis occurs particularly in zone 3. Consequently, fatty liver is a common response to toxicity, often the result of interference with protein synthesis, and may be the only response as after exposure to hydrazine, ethionine and tetracycline, or it may occur in combination with necrosis as with carbon tetrachloride. It is normally a reversible response which does not usually lead to cell death, although it can be very serious as is the case with tetracycline-induced fatty liver in humans. Repeated exposure to compounds which cause fatty liver, such as alcohol, may lead to cirrhosis.
Acute fatty liver of pregnancy (AFLP) is a condition characterized by microvesicular fatty infiltration of the liver, developing in the latter half of pregnancy. The incidence is approximately 1 12,000 deliveries. Clinical disease severity varies with some patients having only mild right-upper quadrant discomfort associated with prodromal nausea and vomiting. Others develop fulminant liver failure leading to coma. A depressed level of consciousness may arise from either hypoglycemia or the onset of hepatic encephalopathy. Hypoglycemia is a common feature of AFLP and should alert the clinician to the possible diagnosis. More than 50 of affected patients will have mild hypertension and pro-teinuria, making the distinction from HELLP syndrome difficult. Jaundice is often present at the time of diagnosis. Liver enzymes are increased and transaminases may rise above 1000 IUl 1 in severe cases. Liver failure leads to severe coagulo-pathy and a prolonged partial thromboplastin time and INR....
With the onset of biochemical evidence of liver damage. The virus does not persist and chronic excretion of HAV does not occur. There is no evidence of progression to chronic liver disease. The incubation period of hepatitis A is 3-5 weeks, with a mean of 28 days. Subclinical and anicteric cases are common and, although the disease has in general a low mortality rate, patients may be incapacitated for many weeks. There is no evidence of progression to chronic liver damage.
Flows through the vessels surrounding the tubule because there will be a concentration gradient in the direction
One of the factors which affects excretion is the urinary pH. If the compound which is filtered or diffuses into the tubular fluid is ionized at the pH of that fluid, it will not be reabsorbed into the bloodstream by passive diffusion. For example, an acidic drug such as phenobarbital is ionized at alkaline urinary pH and a basic drug such as amphetamine is ionized at an acidic urinary pH. This factor is utilized in the treatment of poisoning with barbiturates and salicylic acid for example (see Chapter 7). Thus by giving sodium bicarbonate to the patient, the urine becomes more alkaline and excretion of acidic metabolites is increased. The pH of urine may be affected by diet high protein diet for instance causes urine to become more acid. The rate of urine flow from the kidney into the bladder is also a factor in the excretion of foreign compounds high fluid intake, and therefore production of copious urine, will tend to facilitate excretion. Factors which affect kidney function such...
Management of hepatitis C infection is difficult. The patients must be excluded from donating blood and should be advised about the known modes of transmission of the virus, particularly by the parenteral route. Alcohol may act synergistically with HCV in causing liver damage, and alcohol intake must be reduced to the absolute minimum, if any. Consideration of life style risks for other viral infections such as hepatitis B and HIV infection is essential.
Transfused blood contains citrate which binds the patient's ionised calcium. Usually this is not a problem as the healthy liver can metabolise (to bicarbonate) the citrate in one unit of blood in 5 minutes. Where transfusion rates are rapid, however, excessive calcium binding may itself lead to hypotension, and also to tetany. To avoid citrate toxicity it has been common practice to give Ig of calcium chloride (or4 g calcium gluconate) for every 4 units of blood administered. It is recommended, as belter practice, to avoid the administration of calcium unless there are clinical or biochemical indications (e.g. by the assessment of the ionised calcium levels).
Survivors can experience significant short-term and long-term morbidities. Patients cannot be fed until the GI tract recovers, so they require parenteral nutrition and fluid. Although intravenous access is difficult in many infants, prolonged parenteral nutrition requires the placement of central venous catheters, which has attendant risks and complications of its own. Prolonged hyperalimentation and the absence of enteral nutrition can also cause liver damage with cholestasis. In addition, patients with significant disease can develop a stricture (narrowing of the bowel as it heals), which may require surgical intervention and which further compromises successful enteral feeding. Infants with extensive involvement of the GI tract are critically ill,
Between 1 and 3 h after dosing with carbon tetrachloride triglycerides accumulate in hepatocytes, detectable as fat droplets, and there is continued loss of enzyme activity in the endoplasmic reticulum. Cellular calcium accumulates and the rough endoplasmic reticulum becomes vacuolated and sheds ribosomes. The smooth endoplasmic reticulum shows signs of membrane damage and eventually contracts into clumps. At later timepoints lysosomal damage may become apparent when the centrilobular cells are damaged, cells may begin to show intracellular structural modifications and eventually the plasma membrane ruptures. It is now generally accepted that although metabolic activation to a reactive radical may be the first event, the production of lipid radicals and subsequent chain reactions leading to reactive products of lipid peroxidation are the important mediators of cellular toxicity. There may be many targets for these reactive products, but interference with calcium homeostasis seems to...
TTP is one of a spectrum of microangiopathic hemolytic conditions that include pre-eclampsia, hemolytic uremic syndrome (HUS), acute fatty liver of pregnancy and autoimmune conditions such as systemic lupus erythematosus. TTP is a condition in which multimers of von Willebrand factor, derived from the endothelium, accumulate in the circulation due to lack (either functional or absolute) of a specific metalloproteinase enzyme that breaks down the multimers. Von Willebrand factor binds platelets to the endothe-lium and high concentrations are associated with peripheral platelet consumption and the formation of platelet microthrombi. Von Willebrand factor is usually broken down by a specific metalloproteinase but may accumulate if this enzyme is deficient or if endothelial damage
Thus, the overall exposure to acetylhydrazine is greater in the slow acetylators. Another possible toxic metabolite is hydrazine itself which causes fatty liver and may cause liver necrosis in some animal species. This metabolite arises by metabolic hydrolysis of isoniazid, but the amount of isoniazid which is metabolized by this route is difficult to estimate as the other product of the hydrolysis, isonicotinic acid, can also arise from acetylisoniazid (figure 7.15). Hydrazine has been detected in the plasma of human subjects treated with isoniazid and was found to accumulate in slow, but not rapid, acetylators. The role of hydrazine in isoniazid hepatotoxicity, if any, remains to be clarified.
A maculopapular rash appears between 5 and 7 days after the onset of illness and is most marked on the buttocks, trunk and lateral aspects of the upper arms. Conjunctivitis is common. A tendency to bleed develops, particularly from the gums and from needle punctures, and severe bleeding into the gastrointestinal tract and elsewhere may occur. There is functional evidence of liver damage but clinical jaundice has not been reported. Renal damage occurs and is manifested by proteinuria, oliguria and viruria.
Maternal mortality associated with hypertensive disorders of pregnancy in Africa, Asia, Latin America and the Caribbean. Br. J. Obstet. Gynaecol., 99(7), 547-53. Duncan, R., Hadley, D., Bone, I., Symonds, E. M., Worthington, B. S. and Rubin, P. C. (1989). Blindness in eclampsia CT and MR imaging. J. Neurol. Neurosurg. Psychiatry., 52(7), 899-902. Hauser, W.A. and Kurland, L. T. (1975). The epidemiology of epilepsy in Rochester, Minnesota, 1935 through 1967. Epilepsia., 16(1), 1-66. Hogberg, U., Innala, E. and Sandstrom, A. (1994). Maternal mortality in Sweden, 1980-1988. Obstet. Gynecol. 84(2), 240-4. Kaplan, M. M. (1985). Acute fatty liver of pregnancy. N. Engl. J. Med., 313(6), 367-70.
Hepatic disease and damage clearly have the potential to be major factors in the metabolism of foreign compounds. Thus, in patients with liver necrosis due to paracetamol, the half-life of the latter was increased from 2 to 8 h and that of antipyrine from 12 to 24 h. Acute hepatic necrosis in animals caused by the administration of hepatotoxins resulted in the plasma half-lives of barbiturates, diphenylhydantoin and antipyrine being approximately doubled. However, there may be several factors operating such as displacement of a drug from plasma-protein binding sites by bilirubin. In liver damage, plasma-bilirubin levels may be high due to lack of conjugation with glucuronic acid. This may alter elimination of some drugs such as tolbutamide. The level of plasma albumin may often be reduced by liver disease as this is the site of synthesis of albumin, the hence binding to plasma albumin will tend to be reduced. However, the effects of liver disease can be somewhat unpredictable. For...
As it is one of the portals of entry to the tissues of the body, the liver is exposed to many potentially toxic substances via the gastrointestinal tract from the diet, food additives and contaminants, and drugs and is frequently a target in experimental animals. In man, liver damage is less common and only around 9 of adverse drug reactions affect the liver. By virtue of its position, structure, function and biochemistry the liver is especially vulnerable to damage from toxic compounds. Substances taken into the body from the gastrointestinal tract are absorbed into the hepatic-portal blood system and pass via the portal vein to the liver. Thus, after the gastrointestinal mucosa and blood, the liver is the next tissue to be exposed to a compound, and as it is prior to dilution in the systemic circulation, this exposure will often be at a higher concentration than that of other tissues. The liver, the largest gland in the body, represents around 2-3 of the body weight in man and other...
Isoniazid and iproniazid are chemically similar drugs having different pharmacological effects they may both cause liver damage after therapeutic doses are given. Isoniazid is still widely used for the treatment of tuberculosis, but iproniazid is now rarely used as an antidepressant.
Halothane is a very widely used anaesthetic drug which may cause hepatic damage in some patients. It seems there are two types of damage, however. One is a very rare, idiosyncratic, reaction resulting in serious liver damage with an incidence of about 1 in 35 000. The other form of hepatotoxicity is a mild liver dysfunction which is more common and occurs in as many as 20 of patients receiving the drug. The two different types probably involve different mechanisms.
Excess energy intake and positive energy balance are promoted by readily available, energy-dense foods and sedentary lifestyles 11 . The consequences of excess energy and obesity are well described in children 12 . Obesity-related co-morbidities include type-2 diabetes, hyperlipidemia, hypertension, hyperandrogenism in girls, sleep disorders, respiratory difficulties, nonalcoholic fatty liver disease, gallbladder disease, orthopedic problems, and idiopathic intracranial hypertension. Serious psychosocial problems including poor self-esteem and depression also are common. Childhood obesity and its co-morbidities have a significant likelihood of persisting throughout adolescence and into adulthood.
A hepatotoxic solvent which causes centrilobular necrosis and fatty liver liver cirrhosis and tumours and kidney damage after chronic exposure. It is metabolized in liver by cytochrome P-450 by reduction to a free radical which causes lipid peroxidation which destroys membranes and produces toxic aldehydes such as 4-hydroxynonenal. The rough endoplasmic reticulum is damaged, hence protein synthesis is disrupted and this may cause the fatty liver. The free radical also binds to protein and lipid. Cytochrome P-450 (1A2) is also selectively destroyed and so a small dose protects against the hepatotoxicity of a subsequent large dose. Isoniazid and iproniazid. These substituted hydrazine drugs may both cause liver damage after therapeutic doses. With isoniazid a mild hepatic dysfunction may occur in 10-20 of patients and a more severe type in less than 1 . Both isoniazid and iproniazid yield hydrazine metabolites (acetylhydrazine and isopropylhydrazine respectively)...
Few areas have been as confusing to clinicians as is the perplexing array of adverse drug reactions affecting the liver. Given the central role that the liver plays in drug metabolism, it is not surprising that many drugs are converted to compounds that cause liver damage. In fact, liver injury has been estimated to be the principal safety reason for terminating clinical trials during drug development and for withdrawing marketed drugs (9). Traditional classifications of drug hepatotoxicity, such as that shown in Table 16.2, have been based on descriptions of observed histopathol-ogy rather than on an understanding of the basic mechanism involved (10). We focus the discussion here on representative adverse reactions that damage the liver either through covalent binding of a reactive metabolite or through an idiosyncratic mechanism. A major advance in our understanding of the role of covalent binding of reactive metabolites in causing hepatotoxic drug reactions was provided by Brodie...
The serum folate level rises in severe cobalamin deficiency because of blockage in conversion of methyl THF, the major circulating form, to THF raised levels have also been reported in the intestinal stagnant loop syndrome, acute renal failure and active liver damage. (High levels are also obtained when the patient is receiving folic acid therapy, when the serum is contaminated with folate or folate-producing bacteria or, if a sample is haemolysed, because of the high concentration of folate in red cells.)
Chronic liver disease is usually secondary to chronic alcohol abuse or chronic viral hepatitis. Alcoholic liver disease is most common and begins with the accumulation of fat vacuoles within hepatocytes and hepatic enlargement. There is a decrease in cytochrome P450 content per weight of tissue, but this is compensated for by the increase in liver size so that drug metabolism is not impaired (18). Alcoholic fatty liver may be accompanied or followed by alcoholic hepatitis, in which hepatocyte degeneration and necrosis become evident. In neither of these conditions is there significant diversion of blood flow past functioning hepato-cytes by functional or anatomic shunts.
Ii Increased synthesis of lipid or uptake. Increased synthesis of lipid may be the cause of fatty liver after hydrazine administration as this compound increases the activity of the enzyme involved in the synthesis of diglycerides. Hydrazine also depletes ATP and inhibits protein synthesis however. Large doses of ethanol will cause fatty liver in humans and it is believed that this is partly due to an increase in fatty acid synthesis. This is a result of an increase in the NADH NAD ratio and therefore of the synthesis of triglycerides. Changes in the mobilization of lipids in tissues followed by uptake into the liver can also be another cause of steatosis.
As already mentioned many compounds are toxic following metabolism to reactive metabolites. These reactive metabolites may then initiate one or more primary events. For example, paracetamol and bromobenzene-induced liver damage results from metabolic activation, discussed in more detail in Chapter 7. In other cases metabolic activation is not necessary, and the parent compound or a stable metabolite initiates the primary event. For example, cyanide is cytotoxic as a result of inhibition of crucial enzymes and carbon monoxide deprives the cell of oxygen (see Chapter 7 for more details). The major primary events are
Various parameters may be measured in plasma. Thus determination of the enzymes aspartate transaminase (AST) and alanine transaminase (ALT) is the most common means of detecting liver damage, the enzymes being raised several-fold in the first 24 h after damage. However, there are a number of other enzymes which may be used as markers. Plasma bilirubin can also be measured, being increased in liver damage, and plasma albumin is decreased by liver damage (although also by renal damage). Liver function may be determined using the hepatic clearance of a dye such as sulphobromophthalein.
Antibody and cell-mediated immune responses to various types of antigens are induced during acute infection however, not all these are protective and, in some instances, may cause autoimmune phenomena that contribute to disease pathogenesis. The immune response to infection with HBV is directed toward at least three antigens HBsAg, the core antigen, and the e antigen. The view that hepatitis B exerts its damaging effect on hepatocytes by direct cytopathic changes is inconsistent with the persistence of large quantities of the surface antigen in liver cells of many apparently healthy carriers. Additional evidence suggests that the pathogenesis of liver damage in the course of hepatitis B infection is related to the immune response by the host.
A protease-specific model has also been reported in which a replication-defective adenovirus encoding an NS3 protease-SEAP fusion protein is injected into mouse tail veins, resulting in expression of the fusion protein in the liver 82, 83 . Protease activity can be detected both by measuring activity of liberated SEAP or by protease-induced liver damage. Protease activity was found to be reduced by administration of protease inhibitors. This model can be used to show that candidate inhibitors have adequate pharmacokinetic properties in mice to function in the intended target organ, but it is not a true disease model.
Comprehensive release planning includes transitional housing, continued access to discharge medications and immunizations, and coordination and case-management of long-term specialized care for persons with chronic conditions. Persons diagnosed with chronic HBV infection can benefit from counseling related to preventing transmission to household, sexual, and drug-use contacts. Susceptible contacts of persons diagnosed with chronic HBV infection benefit from hepatitis B vaccination. Persons with chronic hepatitis B or chronic hepatitis C can benefit from (1) counseling regarding ways to reduce further liver damage, (2) referrals to substance abuse treatment and other IDU programs if indicated (http www.cdc.gov idu substance.htm), and (3) medical referrals to specialists for future treatment.
Carbon tetrachloride, widely used as a solvent, has been implicated in liver damage. The primary effect is accumulation of fatty deposits within liver cells followed by cellular necrosis. Various elements of the cells are damaged by carbon tetrachloride. Although the exact mechanisms are unclear, it appears that a reactive metabolite of carbon tetrachloride attacks cellular macromolecules, interfering with cellular function and potentially resulting in cell death. Other halogenated alkanes and alkenes (e.g., PCA, DCA, TCA, TCE) seem to follow similar mechanisms of action, albeit with different levels of response. However, all of these compounds produce reactive metabolites and are thus implicated in varying degrees with car-cinogenesis as well.
The differential diagnosis of seizure activity in pregnancy is extensive and includes epilepsy, systemic lupus erythematosus, acute fatty liver of pregnancy (hepatic encephalopathy), thrombotic thrombocytopenic purpura, amniotic fluid embo-lus, cerebral venous thrombosis, herpes encephalitis, malaria and cocaine intoxication (Clark et al., 1995 Hauser and Kurland, 1975 Towers et al., 1993). Late postpartum eclampsia (seizures first developing between 48 h and 4 weeks after delivery) require neuroradiological investigation to exclude alternative diagnoses (Douglas and Redman, 1994 Lubarsky etal., 1994 Tetzschner andFelding, 1994).
An hepatotoxic analogue of methionine causing fatty liver (accumulation of triglycerides). Chronic exposure causes cirrhosis, bile duct proliferation and heptatocellular carcinoma. It forms S-adenosyl ethionine which traps adenosyl leading to ATP depletion which reduces triglyceride export from the liver. It also leads to ethylated bases in DNA.
TABLE 7.2 Mean plasma concentration and half -life of unchanged paracetamol in patients with and without paracetamolinduced liver damage No liver damage (18) 2.9 0.3 Liver damage (23) 7.2 0.7 primarily centrilobular hepatic necrosis, but this may also be accompanied by renal damage and failure. By measurement of the blood level of paracetamol in overdose cases it is possible to estimate the likely outcome of the poisoning, and hence determine the type of treatment. Measurement of the blood level of paracetamol and its various metabolites at various times after the overdose showed that the half-life was increased several-fold (table 7.2), and the patients who sustained liver damage had an impaired ability to metabolize paracetamol to conjugates (figure 7.8). FIGURE 7.9 Species differences in the dose-response relationship for paracetamol-induced liver damage. Data from Potter et al., Pharmacology (1974) 12, 129 and Mitchell et al., J.Pharmacol. Exp. Ther. (1973) 187, 185. FIGURE 7.9...
Chemical estimation is the gold standard but can be inaccurate if fibrosis is present. Levels 15 mg g dry weight have been associated in DFX-treated patients with a high risk of cardiac disease, liver fibrosis and cirrhosis. Levels between 7 and 15 mg g dry weight are associated with liver damage only if there is also hepatitis C infection and have been considered relatively safe from cardiac disease but associated with damage to the endocrine organs. Levels less than 7 mg g are found in carriers of haemochromatosis.
The half-life will be independent of the dose provided that the elimination is first order and therefore should remain constant. Changes in the half-life, therefore, may indicate alteration of elimination processes due to toxic effects because the half-life of a compound reflects the ability of the animal to metabolize and excrete that compound. When this ability is impaired, for example by saturation of enzymic or active transport processes, or if liver or kidneys are damaged, the half-life may be prolonged. For example, after overdoses of paracetamol, the plasma half-life increases several-fold as the liver damage reduces the metabolic capacity, and in some cases kidney damage may reduce excretion (see Chapter 7).
Because of the liver's many functions, contaminants can act in a variety of ways to cause liver injury. The principal types of liver damage are necrosis (tissue destruction), cirrhosis (hardening of tissue), and the accumulation of abnormal amounts of fat. A particularly important function of the liver from the standpoint of poisons is the detoxification of compounds by transforming them into a more water-soluble form. Whereas this is an important protection mechanism for some compounds, others that are relatively benign in their administered form can be transformed into more toxic species. This process, known as metabolic activation,
It is a very lipid-soluble compound and is consequently well distributed throughout the body, but despite this its major toxic effect is on the liver, irrespective of the route of administration. It should be noted that it does have other toxic effects, and there are species and sex differences in toxicity. Chronic administration or exposure causes liver cirrhosis, liver tumours and also kidney damage. The reason for the liver being the major target is that the toxicity of carbon tetrachloride is dependent on metabolic activation by the cytochromes P-450 system. Therefore, the liver becomes the target as it contains the greatest concentration of cytochromes P-450, especially in the centrilobular region which is where the damage is greatest. Low doses of carbon tetrachloride cause only fatty liver and destruction of cytochromes P-450. Interestingly, a low dose of carbon tetrachloride protects the animals against the hepatotoxicity of a subsequent larger dose due to...
Clearly there are many different types of toxicity which can be assessed and form the basis of the study of a dose-response relationship (see also Chapter 6). Thus toxic effects may be direct or indirect, local or systemic, immediate or delayed and reversible or irreversible. For example a strong acid may have a direct, local toxic effect on skin which is immediate but reversible. Paracetamol (see Chapter 7) has a direct but systemic effect leading to liver damage, which is somewhat delayed. Alternatively penicillin (see Chapter 7) has an indirect and sometimes immediate systemic effect on several body systems which is reversible. Cancer caused by chemicals, such as dimethylnitrosamine or benzo a pyrene, is a response which may be local or systemic and is generally irreversible and often very delayed, but usually it is the result of a direct effect on a particular organ (see Chapter 7). An effect may be reversible if damage to a tissue can be repaired or an inhibited enzyme...
Acute oral iron poisoning produces a severe necrotizing gastritis and enteritis, followed by metabolic acidosis and, after a day or two, cardiovascular collapse and evidence of liver damage. DFX should be given both orally and parenterally. The instillation of 5 g into the stomach after a 1 sodium bicarbonate gastric lavage (to reduce further absorption) and an injection of 1-2 g i.m. may be tried. If a large number of tablets have been taken, an i.v. DFX infusion up to a maximum dose of 80 mg kg in 24 h should be used. Deferiprone has not yet been used in this setting.
J., Weits, J., Vellenga, E. and Huisjes, H.J. (1986). A syndrome of liver damage and intravascular coagulation in the last trimester of normotensive pregnancy. A clinical and histo-pathological study. Br. J. Obstet. Gynaecol., 93(2), 145-55.
Ethionine is a hepatotoxic analogue of the amino acid methionine (figure 7.41). Ethionine is an antimetabolite which has similar chemical and physical properties to the naturally occurring amino acid. After acute doses ethionine causes fatty liver but prolonged administration results in liver cirrhosis and hepatic carcinoma. Some of the toxic effects may be reversed by the administration of methionine. The effects may be produced in a variety of species, athough there are differences in response. The rat also shows a sex difference in susceptibility, the female animal showing the toxic response rather than the level. Initially the fat droplets accumulate on the endoplasmic reticulum in periportal hepatocytes and then in more central areas of the liver. Some species develop hepatic necrosis as well as fatty liver, and nuclear changes and disruption of the endoplasmic reticulum may also be observed. Chronic administration causes proliferation of bile duct cells leading to hepatocyte...
Liver failure may arise from conditions that mimic pre-eclampsia such as thrombotic throm-bocytopenic purpura and acute fatty liver of pregnancy (see below) (Atlas et al., 1982 Kaplan, 1985). Obstetric cholestasis and viral hepatitis may also enter the differential diagnosis in milder cases of HELLP syndrome. Distinguishing between these conditions may be difficult but the hallmark Coagulopathy is an uncommon feature of HELLP syndrome but thrombocytopenia and impaired platelet function both give rise to impaired coagulation. Prolonged partial thromboplastin times and INRs are more likely to occur in association with acute fatty liver than HELLP syndrome. Hypoglycemia may occur in some cases but is more characteristic of acute fatty liver of pregnancy.
Other indirect estimates have included modelling the frequency dependence of attenuation in liver according to equation (4.37) used for solids in Section 4.3.4 (Narayana & Ophir 1983b) and the matching of changes which take place in the levels of absorption, backscattering and attenuation when tissues decay or are fixed histochemically (Bamber 1979). Ophir's analysis assumes that ms is proportional to f4 and provides an estimate of the value of the coefficient B in equation (4.37) that is required to produce the frequency dependence of m in liver demonstrated by published data. Resulting values for ms m come to about 1 in normal liver and 8-13 in fatty liver, over a 1-5 MHz frequency range. Bamber's analysis assumes that during tissue decay, neither the absorption coefficient nor the angular distribution of scattering vary significantly. For fixation in formalin, changes in the absorption coefficient (Lele & Senapati 1977) were included. Resulting values for ms m, again for liver,...
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