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)

The purpose of the present study was to elucidate the interrelationship between pancreatic polypeptide (PP) and other pancreatic endocrine hormones. For this purpose, a radioimmunoassay (RIA) system of plasma PP was established and the changes in plasma PP, plasma immunoreactive insulin (IRI), plasma C-peptide reactivity (CPR) and plasma immunoreactive glucagon (IRG) following oral administration of glucose were examined in ten normal subjects and twenty-five patients with liver cirrhosis. Patients with liver cirrhosis were classified into a normal glucose tolerance group (NGT), an impaired glucose tolerance group (IGT), and a diabetes mellitus group (DM) on the basis of the glucose tolerance curves obtained after the oral administration of glucose. In the IGT and DM groups, fasting plasma PP levels were significantly elevated when compared with those in the control and NGT groups. Also oral administration of 75g glucose elicited an exaggerated rise in plasma PP in the IGT and DM groups when compared with the response in the control and NGT groups. On the other hand, PP response to glucose in the NGT group was similar to that in the control group. Plasma IRI increased markedly before and after oral administration of glucose in the IGT and DM groups when compared with the control groups. In these patients, plasma levels of CPR almost paralleled those of IRI. No significant difference was noted between the NGT group and the control group with regard to plasma IRI and CPR levels before and after oral glucose loading. Accordingly, insufficient insulin action was considered to exist in the IGT and DM groups. This insufficiency in insulin action was expressed in terms of the indices of increase in plasma IRI and CPR, delta IRI/delta BS and delta CPR/delta BS, which corresponded to the elevated blood glucose levels, being significantly lower in the IGT and DM groups than in the control and NGT groups 30 minutes after oral administration of glucose. No significant difference was noticeable between the NGT group and control group with regard to these indices. In the patients with liver cirrhosis, the delta PP value, obtained by subtracting the plasma PP level during fasting from the PP level 30 minutes after oral glucose loading, was inversely correlated with the values of both delta IRI/delta BS and delta CPR/delta BS.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pancreatic polypeptide response to oral glucose load in patients with liver cirrhosis--interrelationship between PP and other pancreatic endocrine hormones]. 329 51

A patient with biopsy-proved biliary cirrhosis and previous gastrojejunostomy and portacaval anastomosis experienced episodes of severe hypoglycemia. She was found to have hyperinsulinemia and hyperglucagonemia. An oral glucose tolerance test showed postgastrectomy hypoglycemia. Results of the intravenous tolbutamide test were diagnostic for insulinoma, but results of the intravenous glucagon test and prolonged fast (96 hours) were not. Failure, on two occasions, to suppress C-peptide normally during insulin-induced hypoglycemia led to a diagnosis of pancreatogenous hyperinsulinemia. The pancreas showed a 10-fold increase in islet volume, with intensely positive staining with anti-insulin and anti-glucagon antiserums in addition to anti-somatostatin and anti-pancreatic polypeptide antiserums. Incidental findings at pancreatic exploration were a mesothelioma, which did not stain with anti-insulin antiserum, and, at autopsy one year later, a hepatoma.
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PMID:Diagnosis of pancreatic islet hyperplasia causing hypoglycemia in a patient with portacaval anastomosis. 699 72

Basal plasma concentrations of human pancreatic polypeptide (PP) were measured in 14 patients with chronic renal failure (CRF), 13 patients with cirrhosis of the liver, and age-matched controls. PP was significantly higher in patients with CRF than in controls (817 +/- 183 vs. 157 +/- 118 pg/ml; P < 0.005). The degree of PP elevation in patients with CRF correlated well with the degree of their renal insufficiency (r = 0.85; P < 0.001). Fractionation of plasma over Sephadex G-50 columns revealed comparable elution patterns in patients with CRF and in normal controls. Hemodialysis had no effect on the PP concentration. We also determined arterial venous PP concentration differences and plasma blood flow across the kidneys and liver in 13 patients with cirrhosis and arteriovenous differences across of the liver in 13 controls with normal hepatic and renal functions. The mean PP concentration was significantly higher in arterial plasma than in renal venous plasma (143 +/- 24 vs. 123 +/- 23 pg/ml; P < 0.025). Renal fractional extraction was 17.2 +/- 6.6%, and renal clearance of PP was 151 +/- 47 ml/min. No significant extraction of PP occurred across the liver. It is concluded that the kidneys, but not the liver, are important sites for the metabolism of PP and that elevated PP concentrations in patients with CRF may contribute to their uremic syndrome.
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PMID:Human pancreatic polypeptide in chronic renal failure and cirrhosis of the liver: role of kidneys and liver in pancreatic polypeptide metabolism. 741 May 34

Endoscopic sclerotherapy is an effective method of controlling variceal hemorrhage, but complications frequently occur. Recent studies have shown that sclerotherapy may induce transient alterations in gastrointestinal motility. It has been suggested that these complications result from vagal nerve injury due to sclerotherapy. We have tested this hypothesis by measuring pancreatic polypeptide secretion in response to insulin-induced hypoglycemia (insulin 0.1 U/kg i.v.), a well-known stimulus for vagal nerve function. We studied six patients with cirrhosis and variceal bleeding (group A, mean age 52 years) on two occasions, before and 3 days after the first sclerotherapy. In addition six other patients with cirrhosis (group B, mean age 51 years) 6 months after successful repeated sclerotherapy for esophageal varices and 12 control subjects (mean age 50 years) were investigated. Basal plasma pancreatic polypeptide concentrations were not significantly different between group A patients before sclerotherapy (28 +/- 4 pM) or after sclerotherapy (24 +/- 6 pM), group B patients (40 +/- 9 pM) and controls (29 +/- 4 pM). Although the plasma pancreatic polypeptide peak increment in response to insulin hypoglycemia was reduced in group A patients after sclerotherapy (90 +/- 35 pM) compared to pre-sclerotherapy (120 +/- 18 pM), to group B patients (146 +/- 20 pM) and to controls (143 +/- 7 pM), this difference was not significant. Nor did sclerotherapy significantly reduce the integrated pancreatic polypeptide secretion between or within groups. However, in two group A patients a transient and reversible reduction in pancreatic polypeptide secretion was observed directly after sclerotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of endoscopic sclerotherapy of esophageal varices on vagus nerve integrity. 789 Aug 85

Unlike other carcinomas, hepatocellular carcinoma (HCC) metastasizes to distant organs relatively rarely. In contrast, it routinely metastasizes to liver vasculature/liver, affecting portal veins 3-10 times more often than hepatic veins. This portal metastatic predominance is traditionally rationalized within the model of a reverse portal flow, due to accompanying liver cirrhosis. However, this intuitive model is not coherent with facts: 1) reverse portal flow occurs in fewer than 10% of cirrhotic patients, while portal metastasis occurs in 30-100% of HCC cases, and 2) portal vein prevalence of HCC metastasis is also characteristic of HCC in non-cirrhotic livers. Therefore, we must assume that the route for HCC metastatic dissemination is the same as for other carcinomas: systemic dissemination via the draining vessel, i.e., via the hepatic vein. In this light, portal prevalence versus hepatic vein of HCC metastasis appears as a puzzling pattern, particularly in cases when portal HCC metastases have appeared as the sole manifestation of HCC. Considering that other GI carcinomas (colorectal, pancreatic, gastric and small bowel) invariably disseminate via portal vein, but very rarely form portal metastasis, portal prevalence of HCC metastasis appears as a paradox. However, nature does not contradict itself; it is rather our wrong assumptions that create paradoxes. The 'portal paradox' becomes a logical event within the hypothesis that the formation of the unique portal venous system preceded the appearance of liver in evolution of chordates. The analysis suggests that the appearance of the portal venous system, supplying hormones and growth factors of pancreatic family, which includes insulin, glucagon, somatostatin, and pancreatic polypeptide (HGFPF) to midgut diverticulum in the early evolution of chordates (in an Amphioxus-like ancestral animal), promoted differentiation of enterocytes into hepatocytes and their further evolution to the liver of vertebrates. These promotional-dependent interactions are conserved in the vertebrate lineage. I hypothesize that selective homing and proliferation of malignant hepatocytes (i.e., HCC cells) in the portal vein environment are due to a uniquely high concentration of HGFPF in portal blood. HGFPF are also necessary for liver function and renewal and are significantly extracted by hepatocytes from passing blood, creating a concentration gradient of HGFPF between the portal blood and hepatic vein outflow, making post-liver vasculature and remote organs less favorable spaces for HCC growth. It also suggested that the portal vein environment (i.e., HGFPF) promotes the differentiation of more aggressive HCC clones from already-seeded portal metastases, explaining the worse outcome of HCC with the portal metastatic pattern. The analysis also offers new hypothesis on the phylogenetic origin of the hepatic diverticulum of cephalochordates, with certain implications for the modeling of the chordate phylogeny.
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PMID:A hypothesis on paradoxical privileged portal vein metastasis of hepatocellular carcinoma. Can organ evolution shed light on patterns of human pathology, and vice versa? 3101 Apr 87