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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical course and prognosis of hepatic coma were examined in 102 patients treated in the period from 1958 to 1975. The diagnoses included 9 fulminant hepatitis, 7 subacute hepatitis, 53 liver cirrhosis without liver carcinoma (40 cases of the acute type, 10 cases of the chronic type and 3 cases of another type, according to Sherlock's classification of hepatic coma) and 33 liver cirrhosis with primary liver carcinoma. Four of 9 fulminant hepatitis patients gained consciousness within 1 week and recovered completely. Seven subacute hepatitis patients died within 2 weeks after onset of hepatic coma. In the period from 1958 to 1969, 20% of liver cirrhosis patients with the acute type of coma recovered from coma, and in the period from 1970 to 1975, 45% of patients recovered. Seven of 10 patients with the chronic type of coma died between 4 months and 9 years after the onset of coma. Three other patients are presently still alive. The median survival time was 2.5 years. Nine primary liver carcinoma patients with coma were hospitalized from 1958 to 1969 and 24 from 1970 to 1975. Hepatorenal syndrome was present in 31 of 71 examined patients. Twenty-three patients with hepatorenal syndrome were in the period from 1970 to 1975.
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PMID:Clinical course and prognosis of one hundred and two patients with hepatic coma 1958 through 1975. 59 69

We assessed the bilirubin reduction capacity of three different types of devices in vitro: a high-permeable membrane column for double-filtration plasmapheresis (DFP) (Evaflux 2A, Kuraray, Japan), and non-coated charcoal column for hemoperfusion (HP) (N-180, Asahi Medical, Japan), and ion-exchange columns for plasma adsorption (PA) (BR-350, Asahi Medical, Japan, and B-001, Kuraray, Japan). A column for DFP reduced the concentration of low-molecular proteins effectively such as plasma bilirubin and bile acids in an albumin-dependent manner. A charcoal column adsorbed low-molecular substances preferentially. But in these two columns, the loss of fibrinogen is a limiting factor for determining the processing plasma volume. Ion-exchange columns for PA adsorbed bile acids, disconjugated bilirubin, and monoconjugated bilirubin more efficiently compared with delta-bilirubin and unconjugated bilirubin. Pretreatment of the column with heparin reduced the loss of fibrinogen to less than 10%. We applied the BR-350 ion-exchange column in vivo for treatment of three patients with hyperbilirubinemia. After treatment, an alcoholic hepatitis patient with the hepatorenal syndrome (HRS) recovered from acute renal failure. However, in a patient with primary biliary cirrhosis and in a patient with fulminant hepatitis, the decrease of serum bilirubin was transient and no obvious beneficial responses were noted. The capacity and ability of the BR-350 column to adsorb plasma bilirubin was shown sufficient to treat deeply jaundiced patients, because 4 liters of the plasma of a patient with 108 mg/dl of initial total bilirubin concentration was able to be processed continuously without an obvious decrease in bilirubin adsorption capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Assessment of bilirubin clearance capacity of a newly developed ion-exchange adsorption column and its possible use as a supportive therapy in hepatorenal syndrome. 234 58

We have evaluated the clinical and epidemiological features of hepatic cirrhosis in a retrospective study of 200 patients admitted to our Area Hospital from 1984 to 1987. 77% of patients were 40-69 years old and 74% were males, with a M/F ratio of 2.84. 56% were caused by high alcohol intake, 25% were cryptogenic and 13% post-hepatitis. 29.2% were diagnosed in a compensated stage of the disease. 52.2% presented with ascites, and 30.5% with upper gastrointestinal hemorrhage. We found superimposed hepatocellular carcinoma in 4.5% of patients, all of them males, with a mean age of 63.5 years. 18% died during their hospital admission, 50% from hepatic coma, 19.4% from hypovolemic shock and 16.6% from hepatorenal syndrome. Survival from the time of diagnosis in the patients who died was shorter than one year in 41.5%.
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PMID:[Clinical and epidemiological features of hepatic cirrhosis. Analysis of 200 patients]. 251 71

The autopsy data at the University of Southern California Liver Unit was studied during a 6-year period to investigate the relationship of fibrinous pericarditis with liver diseases. We found 18 cases of fibrinous pericarditis in 220 patients with alcoholic liver disease but none in 32 patients with fulminant and subacute hepatitis without alcoholism or in 39 patients with nonalcoholic cirrhosis. Although all the 18 patients with pericarditis had azotemia, 3 patients had pericarditis develop only in mild renal function impairment. These findings suggest that chronic alcoholism may precipitate pericarditis during the hepatorenal syndrome.
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PMID:Fibrinous pericarditis in alcoholic liver disease. 292 90

Hospitalized patients with hepatic insufficiency often suffer from severe catabolic states and are in urgent need of nutritional support during their acute illness. Protein intolerence, however, remains a significant problem with respect to the provision of adequate nutrition, either enterally or parenterally. The following report is an anecdotal series of 63 consecutive patients in a large urban hospital treated prospectively with nutritional support using a prototype high branched-chain amino acid solution (FO80) given by technique of total parenteral nutrition by the subclavian or internal jugular route with hypertonic dextrose. Sixty-three patients, of which 42 had chronic liver disease (cirrhosis) with acute decompensation and 17 with acute hepatic injury as well as four with hepatorenal syndrome, are the subject of this report. All required intravenous nutritional support and were either intolerant to commercially available parenteral nutrition solutions or were in hepatic encephalopathy at the time they were initially seen. The cirrhotic patients had been hospitalized for a mean of 14.5 +/- 1.9 days before therapy, had a mean bilirubin of 13 mg/100 ml, and had been in coma for 4.8 +/- 0.7 days despite standard therapy. Patients with acute hepatitis had been in the hospital for 16.2 +/- 4.1 days before therapy, had a mean bilirubin of 25 mg/100 ml, and had been in coma 5.2 +/- 1.6 days before therapy. Routine tests of liver function, blood chemistries, amino acids, EEGs, and complex neurological testing including Reitan trailmaking tests were used in the evaluation of these patients. Up to 120 grams of synthetic amino acid solution with hypertonic dextrose was tolerated in these patients with improvement noted in encephalopathy of at least one grade in 87% of the patients with cirrhosis and 75% of the patients with hepatitis. Nitrogen balance was achieved when 75 to 80 grams of synthetic amino acids were administered. Survival was 45% in the cirrhotic group and 47% in the acute hepatitis group. Encephalopathy appeared to correlate with individual amino acids differentially in the various groups and with the ratio between the aromatic and the branched-chain amino acids. Ammonia did not correlate with either the degree of encephalopathy or improvement therefrom. In 24 Patients therapy for hepatic encephalopathy was limited to infusion of the branched-chain enriched amino acid solution only, with wake-up in 66% of this group. The results strongly suggest that in protein intolerant patients requiring nutritional support, infusion with branchedchain enriched amino acid solutions is well tolerated with either no worsening of or improvement in hepatic encephalopathy coincident with the achievement of nitrogen equilibrium and adequate nutritional support.
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PMID:Infusion of branched-chain enriched amino acid solution in patients with hepatic encephalopathy. 628 73

Renal disorders complicating liver disease are a frequent finding. Extrahepatic causes like intoxications and circulatory dysfunction or diseases that simultaneously affect both the liver and the kidney, like multisystem or viral diseases (hepatitis B) have to be differentiated from clinical entities in which, like in liver cirrhosis or in fulminant hepatitis, the manifestation of renal disease has to be understood as a consequence of the hepatic disorders. Functional disturbances like the increases in tubular sodium reabsorption or the hepatorenal syndrome have been thoroughly investigate because of their clinical importance. Substantial research dealing with the consequences of the increased intrahepatic vascular resistance on systemic and renal hemodynamics and with vasoactive substances, either arising from the liver or accumulating due to poor inactivation by the liver, have led - in the last years - to a better understanding of the pathophysiology of renal involvement in liver disease. However, the exact pathophysiologic role of factors like the effective blood volume, the sympathoadrenergic tonus, the activation of the renin-angiotensin-aldosterone system, changes of kinin activity or in prostaglandin release and the accumulation of "false" neurotransmitters and endotoxins still remains to be established.
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PMID:[Kidney involvement in liver diseases. Pathophysiology and clinical course]. 664 4

560 patients with hepatic coma were treated during the years 1958 to 1982 in Homburg and Bad Kissingen . 82 patients had an endogeneous and 478 an exogeneous hepatic coma. Endogeneous hepatic coma was caused most frequently by fulminant virus hepatitis, intoxication, and hepatorenal syndrome accompanying serum hepatitis. Exogeneous hepatic coma in patients with cirrhosis of the liver was caused in most cases by gastrointestinal bleeding, by a diet too high in protein, or by excessive diuresis. Early clinical symptoms are changes in writing tests and ability to concentrate, whereas hepatic foetor occurs in coma stage III and IV. Clinical chemistry findings pointing to imminent hepatic coma are increase of arterial ammonia in exogeneous hepatic coma, and increase of free phenols in endogeneous hepatic coma. The increase of prothrombin time is prognostic for imminent hepatic coma in both types. Prognosis of endogeneous hepatic coma is still rather bad; 87% of the patients suffering from it died; in exogeneous hepatic coma prognosis has improved for stage I and II in the last 23 years, whereas however the total prognosis for all 4 stages is still unchanged, letality being 55%.
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PMID:[Causes and diagnostic criteria of hepatic coma--an analysis of 560 cases]. 667 13

Patients with liver disease have increased morbidity and mortality following general anesthesia and surgery when compared with the general population. The increase in mortality appears to be directly related to the severity of hepatic parenchymal cell failure and to the magnitude and duration of the surgical procedure. The importance of preoperative detection of subclinical liver disease by use of a variety of blood tests has been emphasized. However, with the exception of hepatitis B and non-A non-B hepatitis, a precise diagnosis of the exact cause of liver disease is usually less important to the anesthesiologist than is a full characterization of the severity of hepatic dysfunction. Recognition and understanding of the central metabolic role played by the liver in maintaining carbohydrate, fat, and protein homeostasis can help in predicting and managing abnormalities which may complicate the preoperative, interoperative, and postoperative periods. Liver failure after anesthesia and surgery is treated by the same management principles used for liver failure with acute hepatitis. The incidence of postoperative renal failure may be increased in patients who have severe hyperbilirubinemia and its occurrence should be differentiated from the hepatorenal syndrome. It should be understood that complications of portal hypertension may develop in the absence of overt hepatic parenchymal cell failure and that liver failure may occur without gross evidence of portal hypertension. Either situation must be recognized and treated as far in advance of surgery as possible. In general, elective surgery in the patient with liver disease should be delayed until consequences of hepatic parenchymal cell dysfunction and portal hypertension are optimally corrected.
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PMID:Medical evaluation of the patient with liver disease prior to surgery. 701 90

Chronic alcoholism is accompanied by systemic involvement of the internal organs. Clinico-morphological forms of chronic alcoholism are distinguished on the basis of the prevailing organ pathology, Morphological data are presented, and pathogenesis of the lesions of the liver, heart, pancreas, and kidneys in patients with chronic alcoholism is analysed. The hepatic form may present alcoholic dystrophy, hepatitis or cirrhosis which are stages of progressing hepatopathy. The toxic and metabolic effect of ethanol is important in the pathogenesis of liver lesion. The cardiac form is characterized by the development of alcoholic myocardiodystrophy. In addition to the toxic influence of ethanol, hormonal and electrolyte changes and microcirculatory disorders play a role in its pathogenesis. Chronic calcifying pancreatitis in chronic alcoholism is associated with the effect of ethanol on the mediatory system. The renal form any present necronephrosis, hepatorenal syndrome, glomerulonephritis or pyelonephritis. Their pathogenesis is determined by toxicity of ethanol, circulation of immune complexes in the blood, or immunosuppression.
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PMID:[Morphology and pathogenesis of visceral manifestations of chronic alcoholism]. 711 39

Renal disease occurs frequently along with diseases of the liver. In autopsy material of patients with liver cirrhosis, half of the patients have morphological signs of secondary type IgA nephropathy. In this paper we report on the renal changes observed in patients with diseases of the liver, such as hepatic glomerulosclerosis, secondary IgA nephropathy, glomerulonephritis with viral hepatitis, systemic disease with hepatitis (mixed cryoglobulinemia and polyarteritis nodosa) with renal affection, renal changes after liver transplantation and the hepatorenal syndrome. The morphological changes of the kidney are emphasized.
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PMID:[Renal changes in liver diseases]. 812 96


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