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)

Seventy-five morbidly obese patients underwent jejunoileal bypass between December 1968 and October 1975. The average weight of 45 patients who had had the bypasses for over two years stabilized at 62.4% of the maximum preoperative value. Postoperative complications included recurrent diarrhea in 11% (8/74) and serum electrolyte deficits in 64% (48/75), most of which were transient. Potassium and calcium deficiencies were usually correctable by oral supplementation, but hypomagnesemia persisted in 23% (16/71) despite supplementation. Nine percent (4/43) had biopsy-proved hepatic cirrhosis after one year. Other complications were polyarthralgia, bone demineralization, renal stones, and vasculitis. Three patients required reanastomosis to original bowel continuity; all rapidly regained weight. One died of vasculitis and hepatic failure attributable to the bypass. Jejunoileal bypass is suitable only in morbidly obese patients with particularly high motivation, whose risk factors outweigh those risks incurred through bypass.
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PMID:Jejunoileal bypass as a treatment of morbid obesity. 85 58

The clinical syndrome of portal-systemic encephalopathy is caused by far advanced cirrhosis of the liver in most cases; it is characterized by increasing drowsiness, disturbances of mentation, flapping tremor and hyperreflexia. An early diagnosis can be established by testing writing and drawing abilities. Increased occurrence of spider nevi, a dry, deep red tongue, and hemorrhagic lesions of skin and mucous membranes are symptoms of incipient hepatic insufficiency. The syndrome is initiated in most cases by excessive intake of protein or alcohol, by intestinal bleeding, by diuretics, or by intercurrent infections. Therapy has to include elimination of causes, reduced intake of protein, enemas with acetate buffer solution and oral medication with lactulose, bifidum milk, and certain amino acids in order to lower hyperammoniemia; in serious cases neomycin has to be given. At the same time a normalization of fluid and electrolyte balance has to be achieved; replacement of potassium is especially important, when hypokalemia and alcalosis are present. In general prognosis of portal-systemic encephalopathy however is serious, depending primarily upon the fact, whether or not sufficient functional hepatic parenchyma is present.
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PMID:[Clinical picture and therapy of portal-systemic encephalopathy (author's transl)]. 89 27

In 2 elderly patients with ascites due to hepatic cirrhosis, potassium excretion decreased during re-administration of potassium-sparing diuretics after recurrence of ascites following withdrawal of previous prolonged treatment. An exaggerated antikaliuretic response and a paradoxic rise in potassium excretion are "unpredictable" changes which may occur during administration of potassium-sparing diuretics at different times in the same patient treated with the same drug.
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PMID:Change in antikaliuretic response to potassium-sparing diuretics in patients with cirrhotic ascites. 93 97

Glomerular filtration rate and renal plasma flow may be normal, reduced or increased in cirrhosis. The mechanism of departures from normal is not known. Other renal functional changes in cirrhosis include avid sodium reabsorption, impaired concentrating and diluting abilities, and partial renal tubular acidosis. Fluid and electrolyte disorders are common. Sodium retention with edema and ascites should generally be treated conservatively because they tend to disappear as the liver heals and because forced diuresis has hazards. The indications for diuretics are (1) incipient or overt atelectasis; (2) abdominal distress; and (3) possibility of skin breakdown. Hyponatremia is common and its mechanism and treatment must be assessed in each patient. Hypokalemia occurs and requires treatment. Respiratory alkalosis and renal tubular acidosis seldom need therapy. The hepatorenal syndrome is defined as functional renal failure in the absence of other known causes of renal functional impairment. The prognosis is terrible and therapy is unsatisfactory. The best approach is not to equate the occurrence of renal failure in cirrhosis with the hepatorenal syndrome. Rather the physician should first explore all treatable causes of renal failure, eg, dehydration, obstruction, infection, heart failure, potassium depletion, and others.
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PMID:Fluid and electrolyte disturbances in cirrhosis. 96 15

"Refractory" ascites was drained off by combinations of antialdosterone (spironolactone, canrenone) and pseudoantialdosterone (triamterene, amiloride) drugs inducing as high sodium excretion as 100 mEq per day in two patients with liver cirrhosis kept on a 9 mEq Na diet. Potentiation of the natriuretic effects of the two types of antikaliuretic drugs occurred by real synergism rather than addition. Although natriuretic acitivity showed a typical dose-related pattern, potassium excretion was unpredictable. Significant increase in potassium excretion (reversal of the suppression) occurred when 300 mg triamterene was combined with 200 mg canrenone in one of the two patients and when the dose of spironolactone or canrenone was increased from 200 mg to 600 mg within the combinations with 300 mg triamterene or 20 mg amiloride in the other. Parallel increase in sodium and potassium excretions might be caused by a proximal tubular effect or by inhibition of potassium reabsorption along with sodium in Henle's loop. The vasopressin (DDAVP) refractory distorsion of the relationship between osmolal clearance and free water reabsorpton (induced by pseudo-antialdosterone agents and potentiated by antialdosterone drugs) observed in all the 6 cases of the present patient material favoured the "loop hypothesis".
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PMID:Reversal of the suppressed potassium excretion during treatment with combinations of antikaliuretic drugs (spironolactone, canrenone, triamterene, amiloride) in patients with liver cirrhosis. 100 53

The factors involved in renin release have been extensively evaluated. The primary determinants are the transmural pressure at the afferent arteriole, sodium delivery to the macula densa, and the activity of the adrenergic nervous system. Other possible factors include circulating catecholamines, the serum and cerebrospinal fluid sodium concentration, serum potassium concentration, angiotensin II concentration, and antidiuretic hormone release. There is no convincing evidence that the renin-angiotensin system mediates renal autoregulation. Plasma renin activity is altered in a number of clinical settings. This parameter is elevated in most patients with cirrhosis and the nephrotic syndrome as well as in individuals with severe congestive heart failure. Despite inappropriately large weight gains, plasma renin suppresses normally with increased salt intake in edematous patients who have a normal glomerular filtration rate. The mechanisms of the alteration in the renin-angiotensin system in Bartter's syndrome is still not clear.
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PMID:Renin and the kidney. 110 Oct 89

Orthotopic allogenic liver transplantations were carried out on 39 pigs. The length of survival time ranged from a few hours until 179 days. The clinical and biochemical laboratory findings as well as the macroscopical, light microscopical and electron microscopical findings established by biopsy and autopsy in the period after the transplantation are described and discussed with regard to their diagnostic significance and pathogenesis. The causes of death are generalized haemorrhages (15 cases), post-operatively bleeding gastric ulcers (12 cases), infections (7 cases), and early or late complications connected with the surgical interventions (5 cases). Observations of liver homografts over a long period after healing-in without complications and during sufficient function of the transplant show (without immunosuppressive treatment) the development of alterations in accordance with the features of chronic aggressive hepatitis and subsequent liver cirrhosis. Complications resulting from this account for some of the established causes of death. According to the results of experiments in animals surviving for a longer time after transplantation there are a general adaptive activation of metabolism and focal alterations in the outer cell membrane of the parenchymal cells in the transplanted liver. This alteration in the cell membrane of the liver epithelial cells causes an abnormal permeability and may lead to partial peripheral lysis and to total lytic necrosis (colliquation necrosis) of these cells. The main cause of these changes is ischaemia or hypoxia brought about by a variety of factors and the cytolytic effect of specifically sensitized lymphocytes ("killer", lymphocytes, immunocytes, effector cells) of the host organism which is the basis of the actual immunologic rejection process. The observed increase of glutamic oxalacetic transaminase (GOT) and lactate dehydrogenase (LDH) as well as potassium in the blood serum may be regarded as a sign of a progressive (developing) rejection or a chronic insufficience of blood circulation of the transplant. Long-term observations show the tendency for a slow continuous reduction in number of the erythrocytes and leucocytes in the host animals. The behaviour of the macrophages (Kupffer cells) in the liver transplant in relation to erythrocytes, thrombocytes and also lymphocytes of the host organism requires particular attention.
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PMID:[Light microscopical, electron microscopical and clinical findings in orthotopic allogenic porcine liver homografts (author's transl)]. 110 5

Whole body potassium measurements were performed on 55 cirrhotic patients in different stages of the disease. They included 34 with alcoholic cirrhosis, 10 with cryptogenic cirrhosis, eight with chronic active hepatitis, and three with haemochromatosis. Serial measurements were carried out in 21 patients. The findings of this study indicate that: (1) the aetiology of the cirrhosis is important in determining the potassium status of cirrhotics, most alcoholics being depleted; (2) ascites and decompensation are usually associated with potassium depletion but compensated cirrhotics may also be depleted even when not receiving diuretics; (3) the initial potassium status, whether a cirrhotic be decompensated or not, is difficult to alter in the short term (six months). Marked changes in potassium status can occur in alcoholic patients studied over longer periods.
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PMID:Potassium status of patients with cirrhosis. 126 87

The purpose of this article is to present detailed data on the nutritional assessment in cirrhotic patients. The exact frequency and types of malnutrition, its associations with the aetiology of liver disease, liver dysfunction and clinical staging in liver cirrhosis are unknown. A new classification system is presented which may help to suggest some interventional guidelines. Physical (anthropometry, 24-h urinary creatinine excretion, bioelectrical impedance analysis (BIA), total body potassium counting, ultrasound examination) and metabolic (indirect calorimetry) assessment of nutritional status was therefore performed in 123 patients with liver cirrhosis, who were considered as potential candidates for liver transplantation. Data were related to the clinical, biochemical, histological and prognostic data of liver disease. Of our patients 65% showed some signs of protein-calorie malnutrition as indicated by low body cell mass, reduced serum albumin concentrations or abnormal skinfold thickness. Of these 34% were considered as "kwashiorkor-like" (normal body composition, serum albumin less than 35 g/l), and 18% were "marastic" (reduced body weight, body cell mass, and fat mass). However, 49% of the malnourished group had reduced body cell mass in association with increased fat mass and frequently presented with a normal body weight ("mixed" or "obese" type). Protein-calorie malnutrition did not correlate with the aetiology of the disease and biochemical parameters of liver function. Malnutrition was observed at all clinical stages but was more frequently seen at advanced stages. We conclude that malnutrition associated with liver cirrhosis is not a clear phenomenon. Its clinical presentation is heterogenous and not reflected by the histological or biochemical parameters of liver disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protein-calorie malnutrition in liver cirrhosis. 139 15

Duodenal and jejunal absorption of a nutrient solution at two different caloric loads (1.32 and 3.96 kcal/min = 5.6 and 16.8 kJ/min) was compared in chronic alcoholics without malnutrition, liver cirrhosis, obvious small-bowel dysfunction, and exocrine pancreatic insufficiency and in an age-matched control group, by means of the intestinal perfusion technique. In chronic alcoholics duodenal net absorption of water (p < 0.025), sodium (p < 0.02), potassium (p < 0.005), total nitrogen (p < 0.02), carbohydrates (p < 0.05), and lipids (p < 0.05) was lower than in controls when both caloric loads were administered, but jejunal absorption rates were not decreased. Biliopancreatic secretion did not differ between alcoholics and controls. Higher serum protein leakage in alcoholics was indicated by an increased (p < 0.01) duodenal alpha 1-antitrypsin clearance under low caloric load infusion. It is concluded that the absorptive function of the duodenum is impaired in alcoholics, whereas the upper jejunum is not affected.
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PMID:Absorption of a nutrient solution in chronic alcoholics without nutrient deficiencies and liver cirrhosis. 147 18


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