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Query: UMLS:C0023890 (
cirrhosis
)
42,195
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A 54-year-old woman with obesity, type II diabetes mellitus,
hyperlipidemia
, and massive hepatomegaly was found to have severe steatosis and
cirrhosis
on liver biopsy. Complete evaluation led to the diagnosis of fatty
cirrhosis
associated with obesity and diabetic mellitus. She underwent four months of fasting with a protein-carbohydrate and vitamin-mineral liquid supplement to control her weight and metabolic abnormalities and to evaluate the effect of this diet on her liver disease. She lost 40 pounds to ideal body weight, normalized her serum glucose and lipids, and decreased total liver height by one third. Liver biopsy at the completion of her diet showed inactive
cirrhosis
and complete resolution of steatosis. Supplemented fasting with only modest weight loss can safely resolve fatty liver in obese diabetics with nonalcoholic steatosis and
cirrhosis
. Aggressive dietary approaches to achieve long-term weight loss deserve study in this subgroup of diabetics with unexplained chronic liver disease.
...
PMID:Steatosis and cirrhosis in an obese diabetic. Resolution of fatty liver by fasting. 382 84
Ther are several main mechanisms that allow us to understand a number of the hepatic and metabolic effects of ethanol. Ethanol is oxidized in the liver to two products (hydrogen and acetaldehyde), to which many of the effects of ethanol can be attributed. The hydrogen generated alters the redox state, and though this effect is attenuated after chronic ethanol consumption, it may still be sufficient to explain alterations in lipid metabolism, possibly increased collagen deposition, and, under special circumstances, depression of protein synthesis. Acetaldehyde impairs microtubules, decreases protein secretion, and causes protein retention and ballooning of the hepatocyte. Acetaldehyde exerts toxicity also with regard to other key cellular functions, particularly in the mitochondria, and it may promote peroxidation of the cellular membranes. It is noteworthy that after chronic consumption of ethanol, there is increased acetaldehyde, in part because of decreased disposition in the mitochondria and partly because of induction of an alternative pathway of ethanol metabolism, namely the microsomal ethanol-oxidizing system. Indeed, this MEOS increases in activity after chronic ethanol consumption, with cross induction and acceleration of the metabolism of other drugs and increased lipoprotein production with
hyperlipemia
. There is also increased microsomal activation of hepatotoxic compounds (including drugs and possibly vitamin A). Fibrosis and
cirrhosis
can develop despite an associated adequate diet and even in the absence of alcoholic hepatitis. They are preceded by myofibroblasts and fibroblast proliferation. What eventually causes the increased number of myofibroblasts and promotes fibrosis is unclear, nor do we know the relative role of hepatocytes or mesenchymal cells in the process of fibroplasis. Possibly selective roles in this process of specific nutritional factors remain to be elucidated.
...
PMID:Alcohol, protein nutrition, and liver injury. 634 74
To study the effects of alcoholic liver injury on the ability of ethanol to promote hepatic fat accumulation and
hyperlipemia
, baboons were pair-fed liquid diets containing 50% of energy either as ethanol or as additional carbohydrate (controls) for 1 to 7 years. Alcohol consumption produced triacylglycerol accumulation in the liver, hypertriacylglyceridemia, and various degrees of liver injury, including
cirrhosis
. At the early stages of fatty liver (with or without perivenular fibrosis), there was increased activity of microsomal diacylglycerol acyltransferase and of both microsomal and cytosolic phosphatidate phosphohydrolase, with no changes in glycerol-3-phosphate acyltransferase. With progression of the liver injury and development of septal fibrosis and/or
cirrhosis
, the rate of hepatic triacylglycerol accumulation and the magnitude of the
hyperlipemia
decreased, despite continuous ethanol intake. These changes were associated with disappearance of the increases in microsomal diacylglycerol acyltransferase and cytosolic phosphatidate phosphohydrolase activities, whereas those of microsomal phosphatidate phosphohydrolase remained elevated and glycerol-3-phosphate acyltransferase was unaffected. Thus, changes in the activity of two enzymes of the triacylglycerol-synthesizing pathway, namely the microsomal diacylglycerol acyltransferase and the cytosolic phosphatidate phosphohydrolase, may contribute to the differences in the rate of hepatic triacylglycerol accumulation and the degree of
hyperlipemia
during progression of the alcoholic liver damage.
...
PMID:Hepatic triacylglycerol synthesizing activity during progression of alcoholic liver injury in the baboon. 649 27
The technique of feeding ethanol as part of a totally liquid diet was invented two decades ago and its successful application for the intervening period is reviewed. This technique results in much higher ethanol intake than with conventional procedures. As a consequence, various complications observed in alcoholics were reproduced in animal models, including fatty liver,
hyperlipemia
, various metabolic and endocrine disorders, tolerance to ethanol and other drugs, physical dependence and withdrawal, the fetal alcohol syndrome and, in the baboon, liver fibrosis and
cirrhosis
. Variations of the liquid diet formulation are compared and three standardized basic formulas are being proposed for the rat: (1) a regular diet, comparable to the diet previously referred to as the "Lieber-DeCarli Formula" and suitable for most experimental applications, particularly those intended to mimic the clinical situation in which the various effects of alcohol occur in the setting of liver changes characterized by a fatty liver; (2) a low fat diet comparable in all respects to the preceding diet but with a lower fat content, intended to minimize the hepatic changes; and (3) a high protein formula particularly useful in those circumstances in which an oversupply of dietary protein might be recommended (i.e., pregnancy and lactation).
...
PMID:The feeding of alcohol in liquid diets: two decades of applications and 1982 update. 675 24
A review of the literature on the medical and nutritional use of medium-chain triglycerides (MCTs) since 1970 is presented with additional discussions on the various modifications and applications of the MCTs in the synthesis of certain structured lipids. The metabolism of MCTs in the liver and extrahepatic tissues is discussed along with further documentation of the use of MCTs in malabsorption and
hyperlipidemia
cases. Recent applications of MCTs and modified MCTs in hyperalimentation, deficiency in the carnitine system, epilepsy, obesity, and other special areas of application are cited. The use of medium-chain monodiglycerides for dissolving cholesterol gallstones is presented. The contraindications for the use of MCTs in ketosis, acidosis, and
cirrhosis
are also discussed. Suggestions for use of MCTs in a variety of medical and nutritional applications are presented.
...
PMID:Medium-chain triglycerides: an update. 681 31
Administration of ethanol to healthy subjects as well as those with alcoholic fatty livers has been noted to cause mild elevation of serum enzyme activities and alcoholic
hyperlipemia
. To see whether this effect is also manifested in alcoholics with advanced liver damage, the serum enzyme activities and lipid content after administration of i.v. ethanol (1.2 g/kg of body wt) over 90 min were compared in 5 alcoholics with hepatic fibrosis and/or alcoholic fatty liver and in 9 patients with alcoholic hepatitis with or without
cirrhosis
. Disappearance rate of ethanol from the serum was nearly the same in both groups. Serum activities of asparate aminotransferase, mitochondrial isoenzyme of asparate aminotransferase, and ornithine carbamyl transferase, measured at 9 and 12 hr after termination of the i.v. ethanol, were significantly elevated in alcoholics with alcoholic hepatitis (P less than 0.05). They were not elevated in alcoholics with fatty liver. By contrast, hyperlipemic responses, measured as the serum content of triacylglycerol 3 hr after ethanol were significantly greater in alcoholics with fatty liver than in alcoholics with alcoholic hepatitis (P less than 0.05). The observed difference in responses of serum enzyme activities and lipid content after ethanol represents an enhanced susceptibility of patients with alcoholic hepatitis and
cirrhosis
towards alcohol-induced injury.
...
PMID:Effect of an intravenous infusion of ethanol on serum enzymes and lipids in patients with alcoholic liver disease. 735 55
Nonalcohol-induced fatty liver is widely believed to be a benign condition with little or no risk of disease progression. There have been occasional reports of progression to
cirrhosis
but none in the absence of preexisting fibrosis on the index biopsy specimen even when co-existing hepatitis was present (steatohepatitis). From our histological database (1978 to 1985), we identified 161 patients with fatty liver seen at our institution and traced the case notes of 156. One hundred five patients were initially excluded as having an alcohol-induced cause, and the remaining 51 either were seen in the clinic (37) or had died, in which cases copies of their death certificates were obtained (14). A further 7 patients were excluded after clinic attendance gave evidence of alcohol excess and another 4 after review of their initial biopsy showed the presence of fibrosis or steatohepatitis. The apparent cause of the steatosis in the 40 included patients with strictly nonalcohol-induced pure fatty liver was obesity in 12, diabetes in 4 (1 obese patient), and cachexia associated with extrahepatic malignancy in 6. Four of the remaining 19 had serological evidence of an autoimmune disorder, but none of these had any clinical or histological features of autoimmune liver disease. Nine patients had evidence of
hyperlipidemia
, 3 of whom were also obese. At a median follow-up of 11 years (7 to 16), 12 of 26 living patients had abnormal results of liver blood tests and had repeat liver biopsies performed. None had progressed to steatohepatitis or
cirrhosis
; 1 obese patient had developed mild fibrosis 9.8 years after her index biopsy.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:The natural history of nonalcoholic fatty liver: a follow-up study. 748 79
Nonalcoholic steatohepatitis is a poorly understood disease that mimics alcoholic liver disease histologically. Its natural history is not well defined, although gradual progression to
cirrhosis
has been described. Most patients with this condition have been obese, with or without associated diabetes or
hyperlipidemia
. No known effective treatment exists for nonalcoholic steatohepatitis, although weight loss may have a beneficial effect. We report two cases of nonalcoholic steatohepatitis. One patient with well-established nonalcoholic steatohepatitis had
cirrhosis
with a complete loss of fat on subsequent liver biopsy despite a gain in weight, simulating cryptogenic
cirrhosis
. In another patient, the condition improved after use of ursodeoxycholic acid; this agent may be a potential therapeutic agent for the treatment of nonalcoholic steatohepatitis. We believe these two cases represent the spectrum of this condition: on the one end is a progressive liver disease that in some instances may be a cause of cryptogenic
cirrhosis
; at the other end, a potentially treatable liver condition.
...
PMID:Two cases from the spectrum of nonalcoholic steatohepatitis. 776 92
The RRR-alpha-tocopherol (vitamin E) content in plasma from 46 patients with liver diseases and 23 healthy controls was determined by high performance liquid chromatography and electrochemical detection. Patients were divided into three groups: alcoholic liver diseases (n = 17; group A), hemochromatosis (n = 17; group B) and Wilson's disease (n = 12; group C). Lipid-standardized alpha-tocopherol levels were determined to neutralize differences due to
hyperlipemia
. The ratio of serum vitamin E to serum lipids (cholesterol, triglycerides, phospholipids) was highest in healthy controls and in patients in group A with
cirrhosis
and normal transaminases and bilirubin. Patients in group A with acute or chronic ethanol intoxication and high bilirubin levels had a 37% lower lipid-standardized vitamin E level than controls. Patients in group B with hemochromatosis, showing high serum iron (> 180 micrograms/dl), a low free iron binding capacity (< 8 mumol/l) and high ferritin-levels (< 450 micrograms/l), had a 34% lower vitamin E/lipid ratio than healthy controls. No significant lowering of the vitamin E/lipid ratio was observed in the other patients in group B. A significant decrease (37%) in the vitamin E/lipid ratio was only detectable in patients with Wilson's disease (group C) showing high free serum copper (> 10 micrograms/dl). The data support a role for free radicals in the pathogenesis of active liver diseases.
...
PMID:Low vitamin E content in plasma of patients with alcoholic liver disease, hemochromatosis and Wilson's disease. 781 21
A new non-linear mathematical model was constructed in order to perform in vivo quantification of the RES phagocytic function. This method is based on the same technical facilities as used for the routine liver-spleen scintigraphy with radiocolloids [1, 2]. But kinetic modeling of dynamic Tc-99m-sulfur colloid data produced estimations of the functional RE-parameters: the clearance rate of the colloidal particles, the rate of phagocytosis, and the RES functional volume, which can not be obtained by classical approaches. This non-linear model was designed on the basis of the principal characteristics of particulate material interaction with macrophages (attachment, phagocytosis, digestion) [3, 4, 5]. The theoretically examined behavior of this in vivo mathematical model corresponds with the experimental behavior of the RES. The mathematical expression of the dynamics is the system of non-linear differential equations with constant coefficients that have no analytical solution. Fitting of the normalized heart blood time-activity curve was obtained to identify the unknown model parameters via non-linear regression. For this purpose general interactive PASCAL procedure IDPAR for a PDP-11/34 computer was used (an IBM PC version is also available). Two to three iterations were needed to estimate the set of unknown parameters for any patient study (1-1.5 min). A very good fitting was obtained between experimental and model curves in every case of different pathologies (error of the approximation is about 2-3%). Studies were performed using an in vivo bolus injection of 3.6 mg/80 kg commercially available colloid KOREN labeled with 3m-Ci 99m-Tc (analog of TCK-1). Our method was used to determine the RES functional parameters for patient groups with different levels of the RES dysfunction. Obtained results illustrate the possibilities of our technique to quantitatively estimate not only great pathology (portal cirrhosis), but also small changes of the RE-function (case of
hyperlipidemia
and ulcer gaster). In all patient groups marked changes of Tc-99m-sulfur colloid turnover were observed. In general, tracer clearance from the circulation was decreased, and the rate of phagocytosis and the RES volume were diminished compared with controls. The effect of a reduction of phagocytosis increases when the RES dysfunction becomes stronger. It can be shown that a non-parametric Wilcoxon-Mann-Whitney test gives a significant difference (P95%) for these patient groups. Further, we represent the possibility of using the model for monitoring changes of the RES-function parameters during and after therapy. The quantitative test of the RES function can significantly enhance the diagnosis and management of different diseases. Serial colloidal studies may document changes in the RES-function for the tumors,
cirrhosis
,
hyperlipidemia
, reticulosis, hepatitis, thrombosis, infection, AIDS, burn injury, shock and trauma patients. The technique may be useful for the different RES investigations with laboratory animals. Created computer software can be used as a tool for kinetic models, simulation, and unknown parameters identification.
...
PMID:A non-linear mathematical model for the in vivo evaluation of the RES phagocytic function. 859 76
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