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)

Twenty patients with bilharzial periportal fibrosis (group I); 20 patients with post hepatitic cirrhosis (group II) and 20 normal controls were chosen to study the correlation between the serum level of human growth hormone (GH) and Somatomedin-C (Sm-C); and the anthropometric measurements; liver function tests and various haematological parameters. Group I showed no statistically significant difference in the mean values of serum GH before and after insulin induced hypoglycemia. The basal serum level of Sm-C showed a statistically significant decrease and highly significant decrease after insulin test. A statistically significant positive correlation was evident between the individual values of serum level of GH and Sm-C and the anthropometric measurements, haematological values and liver function tests (r = 0.41). The mean serum level of GH in group 2, showed statistically significant increase before and after insulin test. The mean serum level of Sm-C showed a statistically significant decrease before and after insulin test. A statistically significant negative correlation was found between the individual values of the serum level of GH and Sm-C and the anthropometric measurements, haematological values and liver function tests (r = 0.16).
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PMID:Correlation between the level of serum growth hormone; somatomedin-C; anthropometric measurements and the liver functions in chronic liver diseases. 203 95

Insulin-like growth factor II (IGF-II) levels in human plasma were measured in physiological and pathological conditions by radioimmunoassay (RIA) with biosynthetic IGF-II. This RIA was specific for IGF-II and cross-reactivity with IGF-I was 1%. The sensitivity was 15 pg/tube with 50% displacement at 50 pg/tube. The intra- and inter-assay coefficients of variation for IGF-II were 6.3 and 9.3%, respectively. The plasma IGF-II levels in normal adults, patients with hypopituitarism and patients with active acromegaly were 589.6 +/- 15.8, 800.9 +/- 45.6 and 330.3 +/- 24.3 ng/ml, respectively. After human growth hormone (hGH) treatment in hypopituitarism, IGF-II slightly increased, but not significantly. After adenomectomy in patients with acromegaly, IGF-II significantly decreased. These data indicate that IGF-II concentrations in plasma were partially GH dependent. This GH dependency was less than that of IGF-I. IGF-II was low in patients with anorexia nervosa and with liver cirrhosis and high in patients with renal failure. In two cases with extrapancreatic tumor-associated hypoglycemia, plasma IGF-II was increased to 1123.8 and 843.5 ng/ml, and returned to normal after tumor resection. These data showed that IGF-II was partly dependent on GH and nutritional conditions and that IGF-II was the most likely cause of some cases of hypoglycemia with extrapancreatic tumor. This specific and sensitive RIA of IGF-II would be useful in evaluating its physiological and pathological role in plasma and tissue.
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PMID:Radioimmunoassay for insulin-like growth factor II (IGF-II). 208 2

Hepatocellular carcinoma is a hormone-sensitive tumor. It has been reported that thyroxine and prolactin significantly stimulated hepatoma growth, whereas growth hormone failed to do so. To learn whether the growth hormone receptor is present in human hepatocellular carcinoma, we used radioreceptor assays in samples of human hepatocellular carcinoma. The liver tissues adjacent to hepatocellular carcinoma (mostly cirrhotic) and control liver tissues (taken during various surgical procedures) were also studied. The study results showed that the affinity constant and capacity of high-affinity growth hormone receptor in normal liver tissues were 6.6 +/- 2.0 x 10(10) mol/L-1 (mean +/- SE, n = 7) and 20.7 +/- 11.5 fmol/mg protein, respectively. The affinity constant and capacity of low-affinity growth hormone receptor in normal liver tissues were 8.9 +/- 3.3 x 10(9) mol/L-1 and 64.7 +/- 32.1 fmol/mg protein, respectively. The absence of growth hormone receptor in human hepatocellular carcinoma and cirrhotic liver samples may explain the absence of growth hormone in the stimulation of hepatoma growth and the decrease of somatomedin levels in cirrhosis.
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PMID:Absence of growth-hormone receptor in hepatocellular carcinoma and cirrhotic liver. 222 28

Because growth failure is a frequent complication of chronic liver disease in childhood, we examined the growth hormone/insulin-like growth factor type I axis and its relationship to growth disturbances, nutritional status, and carbohydrate metabolism in nine children (2.1 to 18.6 years of age) with chronic cholestatic liver disease. Seven had cholestasis associated with splenomegaly and histologic findings of cirrhosis; two patients had Alagille syndrome. Stature was less than or equal to 15th percentile in all except the youngest subject and less than 5th percentile in five subjects. Ten-hour, nocturnal, integrated serum concentrations of growth hormone were considerably higher in patients with cholestasis than in control subjects (mean +/- SD) 9.7 +/- 3.8 vs 4.7 +/- 1.9 ng/ml; p less than 0.02). Serum concentrations of insulin-like growth hormone type I were less than 95th percentile confidence intervals for age- and sex-matched norms in five patients and at the lower limits of normal in the remaining four patients. Insulin sensitivity, determined with the minimal model intravenous glucose tolerance test, was not decreased in five patients despite elevated levels of circulating growth hormone. The estimated mean caloric and protein intake exceeded the recommended dietary allowance and the weight-for-height index was greater than 90% for six of nine patients. Triceps and subscapular skin-fold thicknesses, indicators of body fat stores, were greater than 25th percentile for five of nine and eight of nine patients, respectively, suggesting deficient lipolytic action of GH. We conclude that children with cholestatic liver disease have a resistance to the growth-promoting, diabetogenic, and lipolytic properties of growth hormone.
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PMID:Resistance to the growth-promoting and metabolic effects of growth hormone in children with chronic liver disease. 239 94

The median plasma concentration of growth hormone (GH) in 63 women with liver cirrhosis was significantly elevated when compared with a control group (4.4 ng/ml vs 1.8 ng/ml, p less than 0.01). In 38% of the patients GH concentration was higher than 6.0 ng/ml. GH correlated significantly with the degree of decompensation of the cirrhosis (Child A-C). It was not influenced by the concentrations of estradiol, estrone, or testosterone. Thyrotropin releasing hormone (TRH) induced paradoxial GH increase (delta-GH) in 23 patients showed no significant difference to the data of the control group (2.7 ng/ml vs 0.8 ng/ml). The etiology of cirrhosis (alcoholic or non alcoholic) proved to be unimportant concerning the GH elevation. A missing correlation of GH to thyroid stimulating hormone (TSH), and of delta-GH to TRH induced increase of TSH (delta-TSH) argues against the hypothesis that latent hypothyroidism - often described in cirrhosis - might be responsible of the GH elevation.
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PMID:[Growth hormone in females with liver cirrhosis]. 250 56

Paradoxical growth hormone (GH) responses in 50 g or 75 g oral glucose tolerance tests (OGTT) have been demonstrated in 24 patients with hepatocellular carcinoma, whereas no significant changes in serum GH levels after OGTT were shown in 10 normal controls, 6 patients with cirrhosis of liver, and with chronic active hepatitis. There were no significant difference in the GH responses in OGTT as well as in the incidence of paradoxical GH responses between diabetic and non-diabetic patients with HCC. Informatively, the basal somatomedin C level was very low in all cases examined.
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PMID:[Clinical studies on the relation of abnormal growth hormone secretions to hepatic diabetes mellitus in patients with hepatocellular carcinoma]. 254 47

Binding proteins (BP) for growth hormone (GH) have recently been discovered in human plasma. The main BP is related to the GH receptor and probably corresponds to the extracellular portion of the receptor. The BP influence several aspects of GH homeostasis and action. Their level and activity in blood, therefore, become important variables in overall GH physiology. However, to date little is known about the regulation of GH-BP in health and disease. To gain initial information about this point, GH-BP activity was examined in the plasma of 124 subjects with various physiologic and pathologic conditions. The conditions were selected to provide basic physiologic data (men, women, children, age, pregnancy and to investigate key disease states attended by abnormal GH physiology (liver cirrhosis, uremia, infection, acromegaly). A standardized GH binding assay was used to measure BP activity as an index of BP levels. Both the principal, high affinity BP (peak II) and the minor, low affinity BP (peak I) showed considerable individual variation in all groups. Neonates had the lowest levels of both BPs, but by the age of 1 year the levels had increased and remained fairly stable through the seventh decade. In males but not females between the ages of 1 and 20 years, the main (peak II) BP showed a slight upward trend, whereas the minor (peak I) BP declined moderately. Patients with cirrhosis showed the most variation in both BP, and uremic patients demonstrated decreased peak II, but not peak I, binding. Neither BP was affected in acromegaly. We conclude that BP activity in plasma is well conserved in most conditions, but substantial individual variability exists. BP activity increases dramatically during the first year of life.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of plasma growth hormone-binding proteins in health and disease. 273 78

Basal T4, T3, TSH, prolactin and growth hormone levels were determined in several groups: patients with postnecrotic cirrhosis with hepatocellular carcinoma (n = 14); patients with postnecrotic cirrhosis but without hepatocellular carcinoma (n = 26); cholangiolar carcinoma (n = 9); and normal controls age-matched to within 5 yr of the liver disease subjects studied. In addition, TRH stimulation (400 micrograms TRH) was performed; TSH, prolactin and growth hormone responses over a 180-min time interval were evaluated for each subject. The responses observed varied between liver disease groups. The presence or absence of hepatocellular carcinoma was found to determine, at least in part, the type of response observed. Similarly, the presence or absence of hepatic encephalopathy determined, and/or reflected, at least in part, the type of response observed. Finally, for purposes of continuity, basal and TRH-stimulated levels of TSH, prolactin, growth hormone, T4 and T3 are compared in 3 settings of cirrhosis: alcoholic, nonalcoholic postnecrotic cirrhosis, and postnecrotic cirrhosis with hepatocellular carcinoma.
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PMID:Thyroid and pituitary hormone responses to TRH in advanced nonalcoholic liver disease. 303 51

Patients with cirrhosis of the liver often have insulin resistance and elevated circulating growth hormone levels. This study was undertaken (a) to evaluate glucose intolerance, insulin resistance and abnormal growth hormone secretion and (b) to determine if GH suppression improves insulin resistance. Glucose tolerance tests (GTT), intravenous insulin tolerance tests (IVITT), arginine stimulation tests (AST) and glucose clamp studies before and during GH suppression with somatostatin were performed in a group of patients with alcohol-induced liver cirrhosis. During GTT cirrhotic subjects had a 2-hour plasma glucose of 200 +/- 9.8 ng/dl (N = 14) compared to 128 +/- 8.0 ng/dl in normal controls (N = 15), P less than 0.001. Basal GH was elevated in cirrhotic patients and in response to arginine stimulation reached a peak of 17.0 +/- 5.4 ng/ml (N = 7), compared to a peak of 11.3 +/- 1.8 ng/ml in 5 normal controls (P = NS). During IVITT patients with cirrhosis had a glucose nadir of 60.0 +/- 4.0 mg/dl (N = 9), compared to 29.0 +/- 7.0 mg/dl in controls (N = 5), P less than 0.001. Peak GH levels during IVITT were not significantly different in cirrhotics and controls. Glucose utilization rates in 4 patients with cirrhosis of the liver before somatostatin mediated GH suppression was 3.1 +/- 0.5 mg/kg/min and 6.5 +/- 1.5 mg/kg/min during somatostatin infusion, P less than 0.025. We conclude that patients with alcohol induced cirrhosis have sustained GH elevations resulting in insulin resistance which improves after GH suppression.
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PMID:Growth hormone and carbohydrate intolerance in cirrhosis. 305 69

Basal plasma concentrations of thyroxine (T4), 3,3',5-triiodothyronine (T3), free T4 index (TF4I), free T3 index (FT3I) reverse T3, 3,3',5-triiodothyronine (rT3), resin T3 uptake (TR3U), thyroxine-binding globulin (TBG), thyrotropin (TSH), prolactin (PRL) and growth hormone (GH) as well as thyrotropin releasing hormone (TRH) stimulated TSH, PRL and GH were investigated in 31 consecutive male patients (mean age 41 years) with chronic alcoholism. According to the histology of their liver biopsies the patients were divided into three groups: patients with normal livers, steatosis and cirrhosis. The control group consisted of 30 healthy males. The patients had abstained from alcohol for at least one week when studied, and they were on a nutritionally adequate diet. All had consumed a daily minimum of 52 g ethanol for at least 5 years. None of the patients had severe or decompensated liver disease. The patients had significantly reduced T3 and rT3 plasma levels compared to normals. Patients with cirrhosis of the liver had increased TBG and normal RT3U levels, while those without cirrhosis had increased RT3U and normal TBG levels. Plasma concentrations of basal as well as TRH-stimulated TSH and PRL were unchanged in alcoholic patients, whereas basal as well as stimulated GH levels were increased in cirrhotic alcoholics. It is concluded that alcohol per se influences T3 levels, but not the part of the hypothalamic-pituitary axis studied, and that the binding proteins are mostly determined by the degree of liver disease.
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PMID:Pituitary-thyroid function and thyrotropin, prolactin and growth hormone responses to TRH in patients with chronic alcoholism. 309 23


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