Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient who developed fatal spontaneous bacterial peritonitis associated with cardiac ascites is reported. Spontaneous bacterial peritonitis most frequently occurs in patients with decompensated cirrhosis of alcoholic or nonalcoholic type. Although there are reports of spontaneous bacterial peritonitis occurring in patients with nephrotic syndrome, or with acute or chronic hepatitis, there appear to be no reports of spontaneous bacterial infection developing in cardiac ascites.
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PMID:Spontaneous bacterial peritonitis associated with cardiac ascites. 648 15

Kidney and liver sections were obtained from 75 consecutive autopsy cases with liver cirrhosis discovered at post-mortem. Mesangial IgA as the predominant immunoglobulin was found in 36% (27) cases, with accompanying IgM in 10, and IgG in three subjects. IgA deposits occurred more frequently in micronodular cirrhosis than in macronodular and mixed types. There was no direct correlation with alcoholism or HBs antigen-orcein positivity in livers. The IgA antigen-antibody complexes formed against infectious and/or dietary antigens may bypass the liver phagocytic system via collateral shunts and cause the mesangial IgA deposits. IgA-bearing plasma cells in the liver (80%) may also contribute to the deposits. In cases of liver cirrhosis, there was a variable glomerular morphology including normal appearance by light microscopy (32%), minor changes (38.7%), diffuse mesangial sclerosis (12%), diffuse mesangial cell proliferation, and infrequently membranous and diffuse proliferative glomerulonephritis with a 'lobular pattern'. Five (6.7%) cases showed focal and segmental mesangiolysis with glomerular aneurysms, probably caused by toxic and/or infective agents bypassing the liver reticuloendothelial phagocytic system and acting on the mesangium to cause rupture of anchor points and formation of capillary aneurysms. The cirrhotic glomerulonephropathy was usually clinically latent, but two biopsy cases with mesangiocapillary glomerulonephritis had developed a nephrotic syndrome.
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PMID:Heterogeneous IgA glomerulonephropathy in liver cirrhosis. 652 91

AT III substitution is indicated in patients with inherited antithrombin III deficiency if these patients suffer acute thrombosis, if they have to be treated surgically and in the case of pregnancy in women with AT III deficiency who have an abortion or thrombosis, as well as during and after delivery. In acquired antithrombin III deficiency such as in patients with liver cirrhosis or the nephrotic syndrome, AT III substitution may be necessary if thrombotic complications occur. AT III substitution has been propagated especially in patients with polytrauma, septicaemia, DIC, acute liver failure and in toxaemia. In AT III substitution initial doses of 1 U/kg body weight are used to reach a 1,5% rise in plasma AT III level. If AT III turnover is normal a rise above 80% of normal should be achieved. If AT III turnover is increased, much higher initial and maintenance doses may be needed to normalize plasma AT III levels and to block DIC.
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PMID:Substitution of antithrombin III. 652 16

Primary peritonitis accounts for 1 to 2 per cent of all paediatric abdominal emergencies and for about 15 per cent of diffuse peritoneal sepsis. The condition is still mainly seen in infants and in mid-childhood years, Most frequently in children four to eight years of age, with females outnumbering the males except among neonates where the males predominate. The mortality rate is about 50 per cent for infants, but drops to 10 to 15 per cent in older children. The origin of the infecting organism may be a haematogenous spread or ascension through the female genital tract, but transdiaphragmatic lymphatics and transmural migration through the gut wall may also be possible sources. The incidence of primary peritonitis is increased in children with nephrotic syndrome, postnecrotic cirrhosis with ascites and immunologic deficiency. Practically all kinds of pathogenic organisms are found, but a relative increase in staphylococcal and gram-negative infections has been noted.
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PMID:[Primary peritonitis]. 663 43

The distribution of detectable antibodies against antigen Dd has been studied in rheumatoid arthritis, goitre, nephrotic syndrome, cirrhosis, gastrointestinal tract diseases, neurological diseases, liver and gall bladder diseases, breast cancer, respiratory diseases and cardiovascular diseases. Except in rheumatoid arthritis, breast cancer and nephrotic syndrome, where the incidence of antigen Dd-reactivity did not differ much from that in the control group, in all other disease it was significantly lower.
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PMID:Antigen Dd reactivity in selected diseases. 668 Jun 63

Edema is a collection of fluid within the body's interstitial space which occurs when there is an alteration of the Starling forces which control transfer of fluid from the vascular compartment to surrounding tissue spaces. Generalized edema results when altered Starling forces affect all capillary beds, such as occurs in cardiac failure, cirrhosis, and nephrotic syndrome. Common to these conditions is the development of increased total body sodium and water content. The kidneys play an essential role in the retention of this sodium and water. In this article we shall discuss the signals the kidneys receive for sodium and water retention in these edematous disorders (afferent mechanisms). We shall also examine the means by which the kidney responds to these signals and retains sodium and water (efferent mechanisms). As shall become apparent these edematous states may share many of the same afferent and efferent mechanisms for sodium and water retention.
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PMID:Pathogenesis of sodium and water retention in edematous disorders. 675 Oct 72

We report the incidence of normal (50.4%), increased (46.7%), and decreased (2.9%) anion gap among hospitalized patients in a retrospective study. The mean and range of increased anion gaps were 25 and 19-28 mmol/L. Values exceeding 30 mmol/L were uncommon and may indicate either acidosis or laboratory error. The most common causes of the increased anion gap among patients were chronic renal failure, congestive heart failure, malignant neoplasm, and diabetes mellitus. Increased anion gap in this study may be due to excess acids along with decreases in sodium, chloride, and carbon dioxide. The mean and range of decreased anion gap were 6 and 3-8 mmol/L. Anion-gap values less than 3 mmol/L were uncommon (one of 500 cases), and a high incidence of such values may indicate laboratory error. Nephrotic syndrome, liver cirrhosis, intestinal obstruction, and severe hemorrhage were the common disorders associated with decreased anion gap, which resulted from hypoalbuminemia and hyponatremia. Although most patients with decreased anion gap had hypoalbuminemia, hypoalbuminemic patients did not necessarily have decreased anion gap.
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PMID:Value of the anion gap in clinical diagnosis and laboratory evaluation. 682 31

Risk for renal insufficiency (RI) resulting from nonsteroidal anti-inflammatory drugs (NSAID) exists in cirrhosis with ascites, nephrotic syndrome, decompensated congestive heart failure, and chronic renal disease. We saw seven cases of NSAID RI that demonstrate important additional clinical risk factors. These include advanced age (mean, 76 years), use of diuretic drugs (6/7 patients), and evidence of renal vascular disease as suggested by long-standing hypertension, diabetes, or atherosclerotic cardiovascular disease (7/7 patients). Analysis of past case reports of NSAID RI also showed these features. Treatment of acute gouty arthritis was the most common precipitating event. Evolving NSAID RI was suggested by rising serum urea nitrogen, serum creatinine, and serum potassium levels, and body weight gain associated with low fractional excretion of sodium. We conclude that since NSAID RI is preventable and reversible, it is important to recognize and monitor the conditions of those patients at risk.
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PMID:Identification of risk for renal insufficiency from nonsteroidal anti-inflammatory drugs. 686 44

A three year old child with cirrhosis of the liver and ascites caused by alpha-1-antitrypsin deficiency, developed severe abdominal pain with diarrhea and fever. Spontaneous bacterial peritonitis was diagnosed by demonstrating a purulent ascitic fluid with gram-positive cocci in the smear which were identified as pneumococci in the bacterial culture. The peritonitis subsided under antibiotic treatment without complications. Spontaneous bacterial peritonitis in children with cirrhosis of the liver is mentioned in the literature, but up to now, however, only three cases were reported in detail. In order to establish the diagnosis, abdominal tap should be tried rather than explorative laparotomy, the demonstration of gram-positive cocci is diagnostic of spontaneous bacterial peritonitis. With early antibiotic therapy, prognosis of the disease is favourable. Newborns and children with nephrotic syndrome, however, are particularly at risk.
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PMID:[Spontaneous bacterial peritonitis in cirrhosis of the liver caused by alpha-1-antitrypsin deficiency (author's transl)]. 698 Oct 63

In three different disease entities associated with acquired antithrombin III (AT III) deficiency some of the pathogenetic mechanisms were studied. In liver cirrhosis (23 patients) the AT III level was closely correlated to the activity of hepatocellular synthesized clotting factors, indicating decreased AT III synthesis. In glomerular proteinuria (20 patients not on steroid therapy) the plasma level of AT III correlated inversely to the renal AT III clearance. In contrast to liver cirrhosis and proteinuria, in septicaemia (33 patients) the ratio between AT III antigen (radial immunodiffusion) and functional AT III (heparin cofactor assay using a chromogenic substrate) demonstrated an excess of AT III antigen probably due to inactive AT III-enzyme complexes. Therefore consumption of AT III appears to be an important cause of AT III deficiency in septicaemia. There was an inverse correlation between this ratio and the plasma AT III activity. It is well documented that congenital AT III deficiency predisposes to deep venous thrombosis (DVT) and sometimes to disseminated intravascular coagulation. A similar clinical relevance may be assumed for an acquired AT III deficiency, though so far a relationship between AT III deficiency and DVT has been only established in the nephrotic syndrome.
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PMID:[Pathogenetic mechanism and clinical relevance of acquired anti-thrombin III deficiency in internal medicine (author's transl)]. 702 26


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