The Best Ways to Treat Fatty Liver Disease

Fatty Liver Diet Guide

In Dorothy Spencers guide she shares her methods for reversing fatty liver disease without taking harmful drugs, paying for expensive treatments, or undergoing surgery. Dorothys knowledge on the subject is impressive, and she notes case studies throughout to back up her assertions. Dorothy goes through a comprehensive list of what foods to take, what to eat in moderation, and what to avoid. She then provides you with sample meal plans for breakfast, lunch, and dinner, as well as snacks. She has created for you a seven-day meal plan that maximizes the antioxidant properties of the food you will eat to help heal your liver. According to the positive replies taken from customers all over the world, I believe that Fatty Liver Diet will continue to help a lot of readers succeed in getting rid of fatty liver disease and improve overall health within just a short period of time. More here...

Fatty Liver Diet Guide Overview

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Fatty Liver Solution

Fatty Liver Solution is a newly updated book that provides people with an effective treatment for liver damage, and a list of healthy foods to restore their liver function quickly. The book is created by Duncan Capicchiano, a medical researcher with over 10 years of experience in healing hepatic diseases naturally. The Fatty Liver Solution is the achievement of Duncan Capicchianos practial experience when treating his fatty liver patients. Through this guide, the creator brings to readers specific information about symptoms, root causes of fatty liver disease, and solutions to face with this obstinate disease. This treatment does not involve prescription drugs, or any harsh diet. More here...

Fatty Liver Solution Overview

Contents: Ebook
Author: Duncan Capicchiano
Official Website: www.thefattyliversolution.com
Price: $47.00

The Dangers of Alcohol and Other Drugs

Interferes with the natural breakdown of fats in the liver. When you drink excessively, fats accumulate in the liver, resulting in a condition known as fatty liver, the first step and the only reversible one in the continuum of alcoholic liver disease. The next phase, early fibrosis, happens when fibrous scar tissue appears around the central veins in the liver and impairs liver function. Continued heavy drinking rapidly produces the final two stages of liver disease alcoholic hepatitis and cirrhosis. Alcoholic hepatitis produces jaundice (a yellowing of the skin and eyes), appetite and weight loss, fever, an enlarged and inflamed liver, and accumulation of fluid in the abdomen. Permanent abstinence from alcohol is the only cure for alcoholic hepatitis. But the sexual problems that can arise after having a few drinks are mild compared with the effects of chronic alcoholism on your body. Alcoholism can obstruct the blood supply to the nerves in the penis, resulting in erectile...

Defining Abnormal Behavior

The overlap of the two types of disorders causes confusion among lay people as well as professionals. For example, cancer can cause severe depression, but it should be a ''mental disorder only if the physical illness has caused a dysfunction of the internal psychological mechanisms that control emotional behavior. If that is the case, then the individual has both a physical and mental disorder. The reverse can also occur. A mental disorder, such as alcohol abuse, can cause a physical disorder (i.e., liver damage). Physical and mental disorders can occur together or separately, but it is important to understand that they are different conditions. The relationship of the two conditions has instigated the growth and development of behavioral medicine and health psychology.

Tetrachlorodibenzopdioxin

TCDD is highly toxic on acute exposure. The oral LD50 in guinea pigs of either sex is 1 g kg. It induces a variety of adverse effects in experimental animals liver damage, porphyria, teratogenic effects, immune suppression and increased tumor incidence. It also causes enzyme induction. In man, the following effects have been reported (based on occupational exposures and industrial accidents) chloracne, porphyria, liver damage and polyneuropathies.

In Vitro Toxicological Models And Methods Commonly Used In Drug Discovery

Hepatotoxicity accounts for 15 among the toxicity profiles of drug candidates, second only to cardiovascular toxicity 1 . A plethora of assays have been used by investigators to study organ-specific toxicity mechanisms including hepatotoxicity. This can be conducted in an ex vivo fashion using cells from a specific target organ, followed by in vitro studies where cells from a specific target organ are treated by the toxic agents, and a series of measurements are made depending on the mechanism of interest. This typically falls into the investigative toxicological studies as opposed to the toxicological screening approaches listed above. The rationale for such a distinction is due to cost versus benefit (the cost of running all possible mechanistic assays for many compounds, as opposed to the benefit of having high confidence that a subset of such mechanisms is actually causal to the observed in vivo side effects). As an NCE enters the body and interacts with a variety of...

Diffuse Liver Disease

Fatty liver (hepatic steatosis) may be associated with a variety of clinical disorders. US shows a diffuse or focal increase in the echogenicity of the liver. Increased fat content produces a decrease in mean hepatic CT attenuation value 26 . Milder degrees of diffuse fatty change can be diagnosed when the attenuation value of the liver is less than that of the spleen on plain study. Fatty liver may be more difficult to diagnose on scans obtained after administration of iv contrast material. Focal fatty infiltration frequently has a segmental or wedge-shaped configuration and characteristically produces no mass effect or bulging of the hepatic contour. In addition, it is simpler to diagnose when it occurs in typical locations such as adjacent to the gallbladder fossa. Normal coursing of hepatic vessels can often be seen in the affected area. MRI is extremely useful in providing definite diagnosis when the CT scan is equivocal. Proton chemical shift imaging tech

Antipyretic Analgesics

Antipyretic Mechanism Action

Acetaminophen (paracetamol) has good analgesic efficacy in toothaches and headaches, but is of little use in inflammatory and visceral pain. Its mechanism of action remains unclear. It can be administered orally or in the form of rectal suppositories (single dose, 0.5-1.0 g). The effect develops after about 30 min and lasts for approx. 3 h. Acetaminophen undergoes conjugation to glucuronic acid or sulfate at the phenolic hydroxyl group, with subsequent renal elimination of the conjugate. At therapeutic dosage, a small fraction is oxidized to the highly reactive N-acetyl-p-benzoquinonimine, which is detoxified by coupling to glutathione. After ingestion of high doses (approx. 10 g), the glutathione reserves of the liver are depleted and the quinonimine reacts with constituents of liver cells. As a result, the cells are destroyed liver necrosis. Liver damage can be avoided if the thiol group donor, N-acetylcysteine, is given intravenously within 6-8 h after ingestion of an excessive...

Drugs Used in the Treatment of Fungal Infections

Imidazole derivatives inhibit er-gosterol synthesis. This steroid forms an integral constituent of cytoplasmic membranes of fungal cells, analogous to cholesterol in animal plasma membranes. Fungi exposed to imidazole derivatives stop growing (fungistatic effect) or die (fungicidal effect). The spectrum of affected fungi is very broad. Because they are poorly absorbed and poorly tolerated systemically, most imidazoles are suitable only for topical use (clotrimazole, econazole oxiconazole, isoconazole, bifonazole, etc.). Rarely, this use may result in contact dermatitis. Mi-conazole is given locally, or systemically by short-term infusion (despite its poor tolerability). Because it is well absorbed, ketoconazole is available for oral administration. Adverse effects are rare however, the possibility of fatal liver damage should be noted. Remarkably, keto-conazole may inhibit steroidogenesis (gonadal and adrenocortical hormones). Fluconazole and itraconazole are newer, orally effective...

Toxicodynamic Interactions between Kepone and Carbon Tetrachloride

Lethal, toxicological interaction between Kepone (also known as chlordecone) and carbon tetrachloride (CCl4). Briefly, CCLt is a well-known hepatotoxin. Following free radical formation through the cytochrome P450 enzyme system, the toxicity of CCl4 is manifested through an accumulation of lipids (steatosis, fatty liver) and degenerative processes leading to liver cell death (necrosis). The toxicological interaction between Kepone and CCl4 was elucidated to be the Kepone-mediated impairment of the liver's regeneration process. These mechanistic studies were summarized in a number of publications 93-95 . Based on the described mechanism of interaction, El-Masri et al. 96 constructed a PBPD model, a conceptual version of which is shown in Figure 3.5. A computer implementation of this model was capable of providing time-course simulations of mitotic, injured, and pyknotic (dead) cells after treatment with CCl4 alone or with Kepone pretreatment. This implementation was further linked with...

Miscellaneous complications

Liver damage from drug abuse is often related to direct drug toxicity, allergic or idiosyncratic reactions, or various forms of hepatitis.4 Alcohol-induced fatty change, alcoholic hepatitis and cirrhosis are well-known entities which may exacerbate the effects of other drugs of abuse taken concomittantly. Hepatic damage from cocaine has been induced in laboratory animals5 but does not appear to occur in humans.1,6 Intravenous heroin addiction has been associated with a sometimes intense lymphoid infiltrate (occasionally with germinal centers) of the portal zones,7 often referred to as triaditis. This appears to be independent of viral hepatitis and may represent an immunologic phenomenon. These infiltrates are, however, not invariable with intravenous drug abusers and may be seen in apparently normal people (but usually to a lesser degree). Another nonspecific but fairly typical finding in heroin addicts is mild to moderate hepatosplenomegaly, sometimes associated with enlarged lymph...

Regulation Of The Jakstat Pathway Suppressors of Cytokine Signaling

Since SOCS-1 acts to inhibit cytokine signaling, mice lacking this protein would be expected to exhibit inappropriate or prolonged responses to cytokine stimulation. The phenotype of the SOCS-1 - - mice does not immediately indicate dysregulated responses to any particular cytokine. However, aspects of the disease seen in these mice, for instance, the specific depletion of B cells, suggest inappropriate signaling in response to an inhibitory cytokine. Indeed, overexpression of IFN-y in vivo has been seen to cause very similar defects, including liver damage and B-cell loss (71,72). Alternatively, it has been proposed that SOCS-1 (SSI-1) functions to inhibit expression of the pro-apoptotic molecule Bax (70). Loss of this regulation in SOCS-1- - mice has been suggested to lead to increased apoptosis possibly accounting for the depletion of lymphocytes (70). Further examination of the SOCS-1- - mice should help define which cytokine signal transduction pathways require regulation by...

Importance Of Nutrition In Alcoholic Liver Disease

Nutrition is of great importance in alcoholic liver disease, to the extent that some authors regard ethanol itself as nonhepatotoxic, and that the liver disease associated with chronic ethanol intake is caused purely by inadequate nutrition, in both animal models and human disease.20,21 Most authors now, however, regard ethanol as hepatotoxic and that the degree of hepatotoxicity is modified by nutritional factors.4,22 Not surprisingly for a disease associated with free-radical production, dietary antioxidant intake is of great importance in alcoholic liver disease. Particular interest has been shown in a possible relationship between vitamin E status and alcoholic liver disease. However a-tocopherol status of alcoholics has been variably reported as increased, decreased, or unchanged compared to controls (e.g., 23-25 , 26-28 ). These differences may be due to the degree of liver damage in the studied groups and or whether a-tocopherol levels are normalized to plasma lipid levels....

Iron Overload Depletes Hepatic Antioxidants

Iron has been used as a model substance in the studies of oxidative liver damage, since iron is known to increase the production of free radicals and enhance oxidative stress.24,25 In humans, the most common diseases with iron overload are genetic hemochromatosis and transfusional iron overload. Genetic hemochromatosis is an inherited disorder of iron metabolism in which excess iron is absorbed via the gut and deposited in parenchymal organs, predominantly the liver.26,27 With time, deposition of intracellular iron in hepatocytes results in lipid peroxidation of cellular membranes, impairment of mitochondrial functions, leakage of lysosomal enzymes, and finally iron-induced necrosis (called sideronecrosis).26 Once sideronecrosis has occurred, Kupffer cells and lipocytes will become activated and collagen synthesis increased,28 eventually leading to fibrosis, cirrhosis, and an increased risk for the development of hepatocellular carcinoma.29-31

Iron Potentiates Ethanolinduced Oxidative Stress

Iron may also act as a cofactor that increases the oxidative liver damage exerted by other hepato-toxins such as alcohol. Ethanol is metabolized by the enzyme cytochrome P4502E1 (CYP2E1). During this metabolism the CYP2E1 generates free radicals,42 and increased oxidative stress was found in livers exposed to ethanol.43 When iron is added to ethanol treatment, liver damage and indices of oxidative stress are greatly enhanced.44,45 We found that the combination of iron and ethanol significantly decreased the hepatic contents of reduced ubiquinone-9 and increased the serum aminotransferase activities, as compared with either substance given alone38 (Figure 23.2). In this respect, the free iron pool may play a major role in catalyzing oxidative damage exerted by ethanol.24 In the Fenton reaction, ferrous iron catalyzes the production of hydroxyl radicals from hydrogen peroxide. Indeed, chelating free iron by desferrioxamine reversed the increased levels of aminotransferases that were...

Carbon Tetrachloride May Alter The Hepatic Contents Of Antioxidants

Chronic CCl4 administration is known to induce cell necrosis by increased oxidative stress,46 and repeated injections of CCl4 initiate the fibrogenic process in the liver and may result in cirrhosis.47 Administration of vitamin E prevents CCl4-induced liver necrosis and cirrhosis, which supports the role of reactive oxygen species in liver damage associated with CCl4.48 CCl4 is metabolically activated by cytochrome P450 to form CCl3 free radicals, which initiate lipid peroxidation in the cell and decrease cellular ubiquinol-10.49 Kishi et al. demonstrated that administration of ubiquinone supplement attenuated CCl4-induced cell necrosis.49 In a study in which rats were exposed to diethylnitrosamine (DEN) as initiator, followed by repeated injections of carbon tetrachloride (CCl4)

Hepatitis Induces Oxidative Dna Damage Of Importance For Hepatocarcinogenesis

Thus, experimental data strongly indicate that increased oxidative stress is an important pathogenic mechanism in hepatitis-induced liver damage, and these results are supported by clinical data on humans with hepatitis B and C. In these patients, plasma levels of vitamin E were decreased as compared with that of healthy controls, indicating depletion of antioxidants secondary to the hepatitis infection.21,23 Likewise, in an assay using the plasma ratio of oxidized and reduced ubiquinone as a marker of oxidative stress,20 patients with hepatitis were found to have a significantly increased ratio as compared with healthy controls.22 In a prospective randomized double-blind crossover study, patients with chronic hepatitis C refractory to alpha-interferon therapy were treated with high doses of vitamin E, which significantly reduced the serum activities of aminotransferases, indicating a reduction of the liver damage.50 These findings indicate that enhanced free radical production may be...

Interaction Between Iron Alcohol And Hepatotropic Viruses

These findings indicate that both iron- and ethanol-induced free radical production may enhance the virus-associated liver damage and cancer development, although the exact roles of these hepatotoxic compounds in virus-associated hepatocarcinogensis still has to be determined.

Classification Vitamin B complex

Side Effects GI N& V, diarrhea, peptic ulcer activation, abdominal pain. Dermatologic Flushing, warm feeling, skin rash, pruritus, dry skin, itching and tingling feeling, keratosis nigricans. Other Hypotension, headache, macular cystoid edema, amblyopia. NOTE Megadoses are accompanied by serious toxicity including the symptoms listed in the preceding as well as liver damage, hyperglycemia, hyperuricemia, arrhythmias, tachycardia, and dermatoses.

Therapeutic Phlebotomy

The indications for therapeutic phlebotomy are shown in Table 40.1. The most common of these conditions is idiopathic hemochromatosis. Periodic removal of red cells is essential in this condition in order to prevent iron damage to the parenchyma of the liver, heart, pancreas, and endocrine organs. A program of weekly to twice weekly, phlebotomy is commenced, as tolerated by the patient, until a prescribed amount of iron has been removed (1 unit 250 mg iron). The blood is removed in single whole blood units, although two-unit removal may be well tolerated based on experience with healthy donors. Blood collected from patients with hemochromatosis generally is discarded but could be used in theory as a red cell product for a transfusion recipient. There are several reasons not to use this product as an allogeneic red cell. First, patients with hemochromatosis may have subclinical liver damage and, thus, have elevated alanine aminotransferase (ALT) levels. In some blood centers, this will...

Aflatoxins occurrence and significance

The aflatoxins are produced by a small number of species of Aspergillus which currently includes A. flavus, A. parasiticus, A. nomius and a species originally isolated from Ivory Coast soil, A. ochraceoroseus (Bartoli and Maggi, 1978 Klich et al., 2000). A strain of A. tamarii has also been shown to produce afla-toxin (Klich et al., 2000), but this may be a brown spored form of A. flavus and is certainly very closely related. It should be emphasised that not all strains within a species are toxigenic. On a worldwide basis the majority of strains of A. parasiticus are aflatoxigenic but only about 35 of strains of A. flavus produce aflatoxins. Indeed some strains of A. flavus have been used to produce koji and the more widely used species A. oryzae is probably a domesticated form of this species (Cruikshank and Pitt, 1990). At the level of acute toxicity the aflatoxins cause liver damage and, in animals such as cattle, the farmer will initially see reduced feed consumption, depressed...

Clinical And Pathologic Characterization

Of muscle butyrylcarnitine in the controls. The mutant mice develop severe fatty liver with fasting, as well as excessive fat in the liver without fasting as compared to normal controls. Immunoprecipitation studies later showed that there was no detectable SCAD antigen produced in multiple tissues.8 Clinically, these mutants have remained consistently normal.3 We have challenged them with fasting,3 medium-chain triglyceride loading,3 as well as, sodium butyrate loading, sodium benzoate and salicylate loading in an attempt to overload the glycine conjugation pathway. We have also fed them a high fat diet (40 fat) composed of butter fat with a relatively high short-chain fatty acid content. Even after consuming this diet for over a month, these mice showed no clinical signs of disease with fasting. Pathological characteristics include predominately fatty liver and kidney3,9 ultrastructural studies demonstrated swollen, disorganized mitochondria in hepatocytes from fasted mutants with...

Transgenic Correction Studies In Vivo The Potential For Gene Therapy

We have explored the potential therapeutic effects of liver specific expression of a short-chain acyl-CoA dehydrogenase (SCAD) transgene in the SCAD deficient mouse model.24 Transgenic mice were produced with a rat albumin promoter enhancer controlling a mouse SCAD minigene (ALB-SCAD) on both the SCAD normal genetic background (C57BL 6J x SJL J-F1) and an SCAD deficient background. In three transgenic lines produced on the SCAD deficient background, recombinant SCAD activity and antigen in liver mitochondria increased up to 7-fold of normal control values. All three lines showed a markedly reduced organic aciduria and fatty liver, which are sensitive indicators of the metabolic abnormality seen in this disease found in children. We found no detrimental effects of high liver SCAD expression in transgenic mice on either background. These studies provide important basic and practical therapeutic information for the potential gene therapy of nuclear-encoded mitochondrial enzyme...

Viral hepatitis A virus

Infections caused by hepatitis A virus are most severe in adults. In children it is often asymptomatic and confers immunity. Symptoms appear 2 to 6 weeks after the initial infection and they consist of loss of appetite, fever, malaise, abdominal discomfort, nausea and vomiting. These are followed by signs of liver damage such as passage of dark urine, pale stools and jaundice. In older persons, the infection may cause long lasting liver disorder.

Toxic phenolic substances

Tannic acid has been necrosis and fatty liver. Safrole has been shown to cause liver tumors in rats. It is found in the oil of sassafras and in black peppers. Both coumarin and safrole are still allowed for food use in the European Community. They are prohibited in the US though, as they have been found to cause liver damage in rats.

Avascular Necrosis in Chronic Alcoholism

Osteonecrosis The Right Femoral Head

In the femoral head (Patterson et al. 1964). In a recent review Jones (2001) again emphasized the importance of alcohol-induced fatty liver as a major source of continuous or intermittent fat embolism that creates avascular necrosis. Radiographically detectable osteonecrosis was observed in the femoral head or the humeral head in all 30 chronic alcoholism patients he studied. The diagnosis was histologically confirmed in 19 patients. The mechanism was explained on the basis of endarterial occlusion created by repeated shower of fat emboli.

Pharmaceutical Industry and FDA Perspective

Which is a cytochrome P450-dependent oxidation step. Excessive formation of NAPQI in the liver can cause depletion of glutathione and may result in cell death and hepatotoxicity due to covalent binding to essential cellular macro-molecules and or other mechanisms such as oxidative stress. It has been shown in animal models that activators of PXR (PCN) or CAR (PB) can enhance the hepatotoxicity of APAP by the increased formation of NAPQI 87,88 . Notably, increased liver damage is not observed in CAR- or PXR-knockout animals, suggesting that receptor activation and enzyme induction play critical roles in the hepatotoxicity of APAP. In humans, several hormone nuclear receptors that are activated by many drugs and steroids play major roles in the induced expression of CYPs and other drug-metabolizing enzymes that are involved in APAP elimination and toxicity. For example, PXR plays a key role in the regulation of CYP3A4, CYP2C9, CYP2B6, and UGT1A1 as well as transporters such as MDR1....

Medications for High Cholesterol

If you're taking a statin, your blood should be tested for signs of liver damage at regular intervals if liver tests become abnormal (at least twice the upper limit of normal), withdrawal of the offending drug and its replacement by another of the same class often is effective, and no clinical liver toxicity results.

Blood at the Scene

Natural deaths may be associated with abundant blood near or away from the body. Chronic alcoholics may have such advanced disease that they may bleed from the mouth or the rectum or both. This is caused by liver damage (cirrhosis) in which blood begins to back up in the veins of the esophagus and the rectum. These thick and swollen veins are called varices. Varices have a tendency to rupture, and when they do, the bleeding may be quite extensive. The decedent may die within minutes, although the time is usually longer. There may be abundant blood in the toilet, bathtub, on towels, or in cups.

Cocaethylene

Ited, allowing higher levels of cocaine to remain in the body. A portion of this cocaine undergoes hepatic microsomal transesterification and is converted to cocaethylene (Andrews, 1997 Jatlow et al., 1991). Cocaethylene has very similar behavioral and toxicological effects to cocaine, but these effects last much longer (cocaethylene's plasma half-life is three to five times that of cocaine Jatlow et al., 1991). Cocaethylene causes significant sustained increases in heart rate and blood pressure, myocardial infarctions, arrhythmias, and decreases in heart functioning, possibly due its inhibitory effects on potassium channels in the heart (O'Leary, 2002). In addition, cocaethylene is associated with seizures, liver damage, and immune compromise in adults (Andrews, 1997). Additional toxicological aspects, such as the effects on the exocrine pancreas, remain unexplored (Jatlow et al., 1991).

Methotrexate

Methotrexate was used extensively a couple of decades ago for various inflammatory processes (Jeffes et al. 1995, Cronstein 1996). Within dermatology, the drug has gone out of fashion by the misconception of dose restriction at a cumulative dose of 1.5-2 g because of possible liver damage and fibrosis. It is not clear if rheumatologic patients show different incidences of methotrexate-related liver disease than patients with psoriasis. Blood cell counts, liver enzyme levels, and fibrotic processes (procollagen III peptide at biannual intervals) should be monitored regularly.

Background

The BALB cByJ mice are direct descendents of the BALB cBy strain maintained originally by Donald Bailey at the Jackson Laboratory through a subline removed from his research colony in 1975 and put in the Jackson Laboratory production colony 2 these became the BALB cByJ subline, now known to have SCAD deficiency. In later studies based on PCR analysis of the BALB cByJ-fld mutants,6 it was determined that the Acads mutation occurred sometime between 1981 and 1982. This study also established that the mutation for fatty liver dystrophy (fld) was not the same as SCAD deficiency, although fatty liver is found in both. Having been separated since 1935,7 BALB cByJ are more distantly related to the other common BALB cJ mouse strain also available from the production colony of the Jackson Laboratory. BALB cJ mice have a very aggressive, hyperactive behavior as compared to the relatively reserved BALB cByJ mice. We initially speculated that the BALB cByJ mice were mentally retarded as a result...

Eruptive Xanthoma

Eruptive Xanthomas And Lipemia Retinalis

Chylomicron remnants return to the liver via apolipoprotein E receptors for metabolic breakdown. VLDL particles originate within the liver, contain relatively more cholesterol than triglyceride, yet perform a similar function, delivering triglycerides to the peripheral tissues and returning to the liver for breakdown. These lipids are usually markedly elevated in the serum as a directly inherited consequence of faulty lipid metabolism such as lipoprotein lipase or apolipoprotein C-II deficiency or as an indirect mechanism following heavy ethanol consumption (3). As the liver is critical to the metabolism of lipoproteins, ethanol and various medications including miconazole and retinoic acid that are similarly metabolized within or are affected by the status of the liver may result in lipid abnormalities (4,5). Similarly, serious endocrinologic disturbances, such as hypo-thyroidism or diabetes mellitus, or intrinsic liver disorders, such as the condition of fatty...

General Statement

The choice of the anti-infective depends on the nature of the illness to be treated, the sensitivity of the infecting agent, and the client's previous experience with the drug. Hypersensitivity and allergic reactions may preclude the use of the agent of choice. Contraindications Hypersensitiv-ity or allergies to the drug. Side Effects The antibiotics and anti-infective agents have few direct toxic effects. Kidney and liver damage, deafness, and blood dyscrasias are occasionally observed.

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