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 rise in plasma growth hormone (GH) after thyrotrophin-releasing hormone (TRH) and a striking reduction after dopaminergic drugs is present in acromegalic ('responder') patients. We have investigated the GH response to dopaminergic stimuli in two conditions of animals and man, which, like acromegaly, are characterized by a TRH-induced GH rise, i.e. rats with electrolytic lesions of the median eminence (ME) and patients with hepatic cirrhosis. In addition, we have studied the TRH-induced GH rise in rats with ME lesions, in the cirrhotic patients and in a group of 'responder' acromegalics before and after administration of dopaminergic drugs. In rats with ME lesions an infusion of dopamine (DA) neither modified baseline GH levels nor the TRH-induced GH rise. In five out of six cirrhotic patients oral administration of L-Dopa was followed by the usual rise in plasma GH. infusion of DA increased plasma GH levels in three out of seven cirrhotic patients and in four out of five subjects an earlier GH rise after TRH was seen. However, in the 'responder' acromegalics, the infusion of DA, besides lowering baseline plasma GH, was capable of reducing the TRH-induced GH rise. Collectively these data indicate that the TRH-induced GH rise emphasizes defects in the neurohormonal links between the central nervous system and the anterior pituitary. Instead, the paradoxical fall of GH after dopaminergic drugs appears to be a prerequisite of acromegaly and may be attributable to receptors for DA located on the tumorous tissue.
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PMID:Interaction between the thyrotrophin-releasing hormone-induced growth hormone rise and dopaminergic drugs: studies in pathologic conditions of the animal and man. 11 94

The plasma growth hormone (hGH) responses to an intravenous challenge of 400 micrograms of thyrotropin-releasing hormone (TRH) were evaluated in 14 normal controls and in 29 chronic alcoholic men. The normal controls had either a minimal or no hGH response to TRH, having basal hGH levels of 0.9 +/- 0.2 ng per ml and peak hGH levels of 2.0 +/- 0.5 ng per ml. In contrast, the chronic alcoholic men had a basal hGH level of 2.8 +/- 0.4 ng per ml, 3 times the basal level of the normal controls (P less than 0.01). The peak hGH response of the alcoholic men was 7.4 +/- 1.5 ng per ml (P less than 0.01). The 29 alcoholic men could be divided into two groups based upon the presence or absence of cirrhosis as determined by liver biopsy. The 16 alcoholic men with cirrhosis had greater basal hGH levels (3.5 +/- 0.6 ng per ml) and peak hGH levels (9.5 +/- 2.3 ng per ml) than did the 13 alcoholic men without cirrhosis (basal hGH 2.1 +/- 0.6 ng per ml, peak hGH 4.9 +/- 1.5 ng/ml). Plasma estradiol levels were similar in the normal controls and in the alcoholic men. In contrast, plasma estrone was greater in the alcoholic men (32.2 +/- 3.5 pg per ml) than in the normal controls (18.9 +/- 1.8 pg per ml) (P less than 0.05). However, when the plasma estrone levels of alcoholic men with cirrhosis were compared to those of the alcoholic men without cirrhosis no difference existed. Thus it is difficult to ascribe the increased hGH responses of the cirrhotic alcoholic men when compared to those of the noncirrhotic alcoholic men as being a result of increased basal estrogen levels.
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PMID:Thyrotropin-releasing hormone (TRH)-induced growth hormone (hGH) responses in cirrhotic men. 12 3

Basal plasma growth hormone (GH) and GH responses after the administration of thyrotropin releasing hormone (TRH) were studied in 9 male alcoholic patients with cirrhosis. Basal GH was significantly higher in cirrhotic patients than in normal men. Intravenous injection of synthetic TRH (400 microgram) caused a significant increase in plasma GH in 7 out of the 9 cirrhotic patients examined, while it did not increase GH levels in normal subjects.
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PMID:Elevated basal growth hormone levels and growth hormone response to TRH in alcoholic patients with cirrhosis. 40 28

Twenty patients with biopsy proved liver disease, and roentgenologic features of hypertrophic osteoarthropathy have been studied, and the literature has been reviewed. The syndrome is a rare association of many chronic liver diseases, including primary biliary cirrhosis, bile duct carcinoma, benign bile duct stricture, chronic active hepatitis, posthepatitic cirrhosis and alcoholic cirrhosis. Patients may be asymptomatic, although bone pain, arthralgia or arthritis may be presenting symptoms. Ninety per cent of the patients are clinical jaundiced at the time of diagnosis, and 95 per cent have digital clubbing. The distal tibia and fibula are the first bones to become involved, although wrist, foot bones, femurs, hand bones and humeri may be affected in order of frequency. There is no correlation between the presence of esophageal varices or surgical portacaval shunts and the extent of the syndrome, neither is there a correlation with the degree of liver function impairment. Serum calcium and phosphate levels are normal, as is urinary hydroxyproline and estrogen excretion. There was no evidence to implicate elevated levels of growth hormone or overdosage of vitamin A. Although the majority of patients tested had mild arterial hypoxemia, increased cardiac output and evidence of right to left shunting, these were also present in disease-matched control subjects without osteoarthropathy. For screening purposes, patients with chronic liver disease and clubbing should have roentgenologic studies of the lower tibias and fibulas, to select those patients suitable for a more extensive skeletal survey.
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PMID:Hypertrophic hepatic osteoarthropathy. Clinical, roentgenologic, biochemical, hormonal and cardiorespiratory studies, and review of the literature. 46 21

Porphyria cutanea tarda (PCT) has a known increased incidence of diabetes mellitus and hepatic involvement. We investigated glucose tolerance and glucoregulatory hormone alterations in seven patients with PCT and correlated these results with hepatic histology by percutaneous liver biopsy. Abnormal glucose tolerance was observed in six of the seven patients (87%). Fasting serum insulin levels were normal range, and normal glucose and growth hormone responses to standard, exogenous intravenous insulin were observed. Fasting serum glucagon and urine free cortisol levels were normal in those patients in whom they were measured. While varying degrees of abnormalities were found on histopathologic exam of the liver biopsies, no patient met the criteria for cirrhosis, and none of the patients demonstrated abnormal levels of insulin counterregulatory hormones commonly seen in cirrhosis. Thus, liver disease may not be the sole cause of the observed glucose intolerance and hyperinsulinemia in PCT patients.
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PMID:Carbohydrate metabolism in porphyria cutanea tarda. 46 44

Ten male patients with cirrhosis of the liver (three with portacaval anastomosis [PCA]) and eight sex- and age-matched controls underwent an arginine infusion test followed by an intravenous glucose tolerance test. Plasma glucose and growth hormone (GH) levels were measured during a period of three hours. In the normal subjects, the peak GH response to arginine occurred 60 minutes after the start of the infusion and was followed by a progressive decline in GH concentration; dextrose injection resulted in a further rapid fall in GH concentration. In cirrhotic patients, both fasting and postarginine GH concentrations were significantly higher than in controls; in addition, the dextrose injection, after causing a transitory drop in plasma GH levels, resulted in a marked increase in plasma GH concentration. In the patients with PCA, the plasma GH increase after arginine and after dextrous was more marked. In these cirrhotic patients, the plasma GH levels correlated directly with the magnitude of the portal hypertension and inversely with the serum albumin concentration, suggesting that the abnormality of GH secretion was a reflection of the derangement in liver function.
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PMID:Altered control of growth hormone secretion in patients with cirrhosis of the liver. 48 48

Serum somatomedin (SM) activity, measured as sulphation factor on chick embryo cartilage, and growth hormone (GH) levels were measured in peripheral, hepatic and renal veins of 23 patients with a alcoholic cirrhosis. SM activity (mean +/- SEM) was 0.65 +/- 0.05 U/ml in peripheral vein, 0.59 +/- 0.04 U/ml in hepatic vein, and 0.74 +/- 0.07 U/ml in renal vein. Mean GH levels were respectively 2.8, 2.5 and 3.1 ng/ml. Compared to peripheral vein, SM increase in renal vein was 19% (P less than 0.05). Serum SM activity was significantly lower in 13 patients with alcoholic hepatitis associated with cirrhosis than in other 10 patients (P less than 0.02 in hepatic blood and P less than 0.05 in peripheral blood). The decrease of SM activity seems related to cytolysis and hepato-cellular insufficiency. At last, in patients with alcoholic hepatitis, SM activity was lower in the hepatic vein than in the peripheral vein (P less than 0.05). The cause of this difference remains under discussion, no SM inhibitors being found in the serum samples used in this study.
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PMID:Serum somatomedin activity measured as sulphation factor in peripheral, hepatic and renal veins of patients with alcoholic cirrhosis. 58 Nov 14

Diabetes mellitus is more frequently found in pateints with hepatic cirrhosis (about 10%) than in subjects without liver disease. Cirrhosis has been the main subject of interest in this respect. Very few studies have been made in viral hepatitis or steatosis. In about 40% of cases, the diabetes is identified before the cirrhosis. More often (in about 60% of cases) the diabetes is discovered at the same time as or after the finding of cirrhosis. This "post-cirrhosis diabetes" shows no clinical peculiarity. In about 80% of patients with liver cirrhosis when fasting blood glucose is normal, abnormalities of carbohydrate metabolism are to be found by the oral glucose tolerance test. Approximately 50% show an abnormal response to intravenous glucose and 30% to intravenous tolbutamide. The "mechanism" of these metabolic abnormalities in liver cirrhosis is unknown. The following abnormalities are observed: 1) With similar glycaemic response to a glucose challenge, plasma insulin levels are higher than in patients without liver disease, suggesting insulin unresponsiveness. Resistance to exogenous insulin can be demonstrated. 2) Plasma free fatty acid levels are often elevated. 3) Plasma growth hormone levels are often raised. 4) Plasma glucagon levels are high when porto-caval shunting is present. 5) Potassium is often depleted. These metabolic abnormalities, in association with porto-caval shunting and hepatocyte insufficiency may explain the insulin resistance which characterises liver cirrhosis, and the diabetes which it may precipitate in predisposed persons.
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PMID:[Diabetes mellitus secondary to liver diseases. A review (author's transl)]. 79 27

Most forms of liver disease are probably associated with impaired gluconeogenesis, although hypoglycaemia is rarely an important clinical feature. Blood concentrations of the gluconeogenic precursors, lactate, glycerol and alanine are elevated although, in certain situations, alanine levels may be decreased. Abnormal glucose tolerance is present in both acute and chronic liver disease, but is usually not of clinical importance. The mechanism of glucose intolerance remains uncertain, with diminished hepatocyte mass, portal diversion and insulin resistance the major postulates. Indeed, the importance of the liver in disposing of an oral glucose load, is still questioned. Both hyperinsulinism and hypoinsulinism are found in liver disease, with hyperinsulinism common in cirrhosis and acute viral hepatitis. This is accompanied by insulin resistance. The hyperinsulinism is probably due to defective hepatic clearance of insulin rather that to over-production. The cause of the insulin resistance remains to be established. Glucagon levels are raised and may contribute to this resistance. Growth hormone levels are also increased but are associated with low somatomedin levels and the role of growth hormone in insulin resistance is therefore questionable. Future developments include use of new animal models, studies of biopsy specimens and studies of hepatic hormone receptors.
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PMID:Carbohydrate metabolism in liver disease. 79 84

Derangements in glucose, amino acid and protein metabolism in patients with liver cirrhosis were examined with special reference to plasma levels of human growth hormone (HGH). Changes in blood glucose, IRI (immunoreactive insulin), HGH, FFA (free fatty acid) and plasma free amino acid levels were determined in controls and patients following either oral glucose load, protein feeding or intravenous arginine infusion. 1) In patients with liver cirrhosis, incidence of glucose intolerance after glucose tolerance test (GTT) was high and IRI levels were elevated in the fasting state as well as after glucose, protein or arginine loads. 2) Fasting levels of blood HGH were significantly higher in liver cirrhosis than in controls. GTT revealed that blood HGH levels decreased slightly during the rising phase of blood glucose, and conversely, increased during the falling phase of glucose (180 minutes after the glucose load) both in controls and in patients. In cirrhotic patients, marked increases in HGH levels were observed both 120 minutes after the protein load and 60 minutes after the arginine infusion. 3) Fasting levels of serum FFA were significantly higher in liver cirrhosis than in controls. Both controls and patients, however, showed a similar pattern of change in FFA levels following GTT or protein ingestion, i.e. a minimum value 120 minutes after the load and a gradual increase thereafter. 4) Fasting levels of plasma free amino acids were significantly higher in cirrhotic patients than in controls. After the glucose load, however, slight decrease was noted in some amino acid levels. All the amino acid levels examined were elevated following protein ingestion, particularly in cirrhotic patients. 5) A positive correlation was demonstrated in cirrhotic patients between total plasma free amino acids and maximal HGH responses following protein ingestion. Similar significant correlations were observed between the maximal HGH response and the plasma level of several amino acids such as His., Ser., Gly., Thr., Ala., and Ileu., respectively. 6) In cirrhotic patients, negative correlations were demonstrated between fasting levels of serum albumin and total plasma free amino acids or maximal HGH responses, respectively, after the protein ingestion. From these results it was inferred that derangements in the metabolism of protein and amino acids in cirrhotic patients may result in an increase in plasma free amino acid level which in turn stimulates HGH secretion. It was surmised that the HGH levels so elevated in the patients may cause FFA mobilization which in effect results in the glucose intolerance.
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PMID:[Studies on glucose, amino acid and protein metabolism in patients with liver cirrhosis in relation to plasma levels of human growth hormone (author's transl)]. 81 50


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