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)

Previous our studies showed that some steroid hormones, as pure crystalline Progesterone (pPc) and 17-alpha-hydroxyprogesterone capronate (17 alpha HPC) heightened the cirrhogenic action produced in rat liver by carbon tetrachloride. Medroxyprogesterone (MPA), however, did not appear to promote cirrhosis, but increased just steatosis. In the present paper, we have studied the above mentioned steroid hormones for their possible capability of inducing changes in plasma fibronectin concentration. For this purpose, the soluble plasma fibronectin level was measured in female rats 45 days after CCl4-induced cirrhosis, and it was compared with the insoluble fibronectin of liver (detected by immunostaining) and the collagen content in the organ. The results obtained show that, after treatment with CCl4 and MPA, both plasma and liver fibronectin content strongly increases, whereas liver collagen content lowers. However, after treatment with CCl4 alone or in association with the other two steroid hormones, any changes in fibronectin content is not observable, but, on the contrary, is evident a heightened collagen production associated with a cirrhotic change of liver.
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PMID:Changes in fibronectin production in rat liver during cirrhotic evolution due to treatment with CCl4 and steroid hormones: correlation with plasmatic fibronectin. 146 20

To estimate the diagnostic value of elastase output in the duodenal aspirates during a pancreozymin secretin test, elastase as well as amylase, chymotrypsin, trypsin, and lipase was determined in 46 controls and 61 patients with various disease. The elastase output decreased significantly in chronic pancreatitis (mild exocrine insufficiency 13 and advanced eight), pancreatic cancer (n = 10), and liver cirrhosis (n = 14) when compared with the controls. The outputs of the four other enzymes also decreased in chronic pancreatitis and pancreatic cancer, not in liver cirrhosis. Low elastase output was found in four of 13 chronic pancreatitis patients with mild exocrine insufficiency, whereas low outputs of the other enzymes were observed in only one or less of the 13. The ratio of elastase to amylase alone was significantly lower in the pancreatic diseases. The results suggest that elastase is the most susceptible enzyme to pancreatic dysfunction and that its output and its ratio to amylase output provide a valuable index to assess the enzyme secretory capacity in the pancreatic diseases.
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PMID:Elastase secretion in pancreatic disease. 384 84

We have studied the volume, protein concentration, total protein, and chymotrypsin and trypsin outputs in pure pancreatic juice (PPJ) following endoscopic cannulation of the pancreatic duct in 11 male and 2 female patients with advanced alcoholic cirrhosis (AC). Results were compared to those obtained from 21 nonalcoholic volunteers (NAV) and 26 chronic alcoholic (CA) patients without cirrhosis. Intravenous stimulation with secretin followed 10 min later by intravenous cholecystokinin-pancreozymin (CCK-PZ) resulted in highly significant increases in volumes during both phases of pancreatic stimulation in AC compared to NAV and CA. Protein concentration and total output during secretin stimulation was not different among the three groups. During CCK-PZ stimulation, CA exhibited a significant elevation in protein concentration and total output compared to NAV and AC. Although total chymotrypsin output was lower in secretin-stimulated CA than other groups, no other differences between the groups were observed in either of the hormone-stimulation phases. Marked elevations in trypsin output were observed in secretin-stimulated AC and in CCK-PZ-stimulated AC and CA. The high PPJ volume and the relatively low protein concentration observed in AC may effect a washout phenomenon resulting in a decreased tendency for ductal protein precipitation in these patients.
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PMID:Pancreatic secretion after secretin and cholecystokinin stimulation in chronic alcoholics with and without cirrhosis. 665 99

In spite of having been the object of a number of studies, the association of morphologic and functional alterations of the pancreas with liver cirrhosis is as yet controversial. Therefore, the authors have studied exocrine pancreatic function in 40 patients: 8 with alcoholic cirrhosis, 18 with non-alcoholic cirrhosis, and 14 without evidence of hepatobiliary and pancreatic pathology. Pancreatic function was studied by the fecal chymotrypsin test which is sufficiently sensitive and specific and has been preferred in view of its practicability and non-invasiveness. Analysis of the results showed pathologic values to be significantly more frequent in subjects with alcoholic cirrhosis (50%, p < 0.05) compared to non-alcoholic cirrhotics (11.11%) and to controls (7.2%). These findings go to show that pancreatic exocrine deficit is frequently associated with alcoholic cirrhosis, thus confirming what has already been known about the pathogenetic role of alcohol which is apt to provoke both hepatic and pancreatic damage. Finally, it should be pointed out that pancreatic exocrine deficit is a purely functional alteration without clinical manifestations.
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PMID:[Evaluation of exocrine pancreatic insufficiency in cirrhotic patients,using the fecal chymotrypsin test]. 800 34

The effects of chronic administration of methamphetamine on pancreatic tissues were histopathologically studied in experimental models. Methamphetamine (1 ml/kg body weight/day) was subcutaneously injected into 14 five-week-old male Wistar Kyoto rats (WKY) for 12 weeks. Age and sex matched 5 WKY rats served as controls. With light microscopy, some scattered edematous lesions and moderate vacuolization were demonstrated in the pancreas of 8 of the methamphetamine treated rats. However, in 4 of the rats, severe regional hemorrhage, partial acinal cell necrosis, destruction of the acinal cells, neutrophile infiltration, interstitial vessel dilatation, interstitial edema and fatty cell invasion were observed after the injections of methamphetamine. In 2 other animals, fibrosis and cirrhosis-like lesions with destruction and degeneration of the acinal cells were observed the small vessels had a slight degeneration of the endothelial cells. In the control animals, no lesions, except for some edematous lesions were found. In all cases, there were no nesidioblastosis-like lesions or necrosis of the Langerhans's islets. In the immunohistochemical study using anti- alpha 1-chymotrypsin antibody, more positive reactive cells were demonstrated among the interstitial and inter acinal cells, both in number and degree, in the methamphetamine treated rats. In addition to the animal model, there were 4 autopsy cases of sudden death in chronic methamphetamine abusers. The autopsies demonstrated a severe acute necrotic hemorrhagic pancreatitis, with only scattered slight hemorrhaging in the brain and lungs. These findings indicate that chronic administration of methamphetamine to rats evoked significant changes in pancreatic tissues including some degeneration of the endothelial cells of the small vessels in this hypoxia-vulnerable organ.
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PMID:A histopathological study of pancreatic lesions after chronic administration of methamphetamine to rats. 933 52

Zinc absorption in alcoholism was studied by a combination of zinc tolerance tests in 382 male patients with alcoholism (more than 140 g/day of ethanol) who had alcohol-induced disease of the liver or pancreas. In study 1, the serum zinc level was measured in all patients, and serum zinc and fecal chymotrypsin levels were compared in various disease groups. In study 2, 14 patients with liver cirrhosis (LC), 15 with chronic pancreatitis (CP), 7 with LC + CP, and 7 controls underwent oral zinc tolerance and zinc dipicolinate tolerance tests, zinc absorption and disorders of pancreatic exocrine functions were examined. In study 1, the serum zinc concentration was significantly lower in the CP and LC groups than in the control group, and the fecal chymotrypsin activity was significantly lower in the CP than in the control groups. In study 2, during the oral zinc tolerance test, the serum zinc concentration 3 hours after administration was significantly lower in the LC, CP and LC + CP groups than in the control group. In these groups, the serum zinc concentration was significantly lower in the abnormal fecal chymotrypsin group than in the control group at 2 and 3 hours after administration of zinc sulfate. In the oral zinc dipicolinate tolerance test, the serum zinc levels 2 and 3 hours after administration were significantly elevated in the control and all disease groups; there were no significant differences between the control and each disease group. These results suggest that reduction of pancreatic exocrine functions by alcohol and chronic reduction of synthesis of ligands such as picolinic acid in the liver are involved in the reduction of serum zinc in alcoholism.
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PMID:Evaluation of pancreatic exocrine function and zinc absorption in alcoholism. 965 43

Alpha-1-antitrypsin (alpha1-AT) is a member of the serine protease inhibitor family regulating numerous proteolytic processes. The genetic disorder, alpha1-AT deficiency, is well known as a cause of hereditary pulmonary emphysema and liver cirrhosis. To create an animal model of human alpha1-AT deficiency, we disrupted the major murine isoform PI2, which is similar to human alpha1-AT and is one of 7 alpha1-AT isoforms found in the mouse. The ability of the serum to inhibit the activities of human leukocyte elastase (HLE) and human chymotrypsin (CYT) was significantly lower in heterozygous mice (alpha1-AT/PI2 -/+) than wild-type (alpha1-AT/PI2 +/+) mice (73.2% vs. 100% for HLE and 67.8% vs.100% for CYT, respectively; P<0.05). The distribution of genotypes among F(2) progeny was not in accordance with Mendelian distribution (P<0.01), as the percentages of wild-type, heterozygotes and homozygotes were 47.8%, 37.3% and 14.9%, respectively. Thus, it is likely that impairment of the protease inhibitor had a critical effect on fetus development. The alpha1-AT/PI2 deficient mouse will be a useful animal model for elucidating the function of alpha1-AT in fetal development, studying the mechanisms of chronic inflammatory disease and evaluating therapeutic candidates for the treatment of inflammatory disease.
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PMID:Disruption of the murine alpha1-antitrypsin/PI2 gene. 1551 92

The material comprises 34 patients with anicteric biliary diseases, 20 with obstructive jaundice, 8 with hepatic cirrhosis, and 3 with haemochromatosis. The intestinal contents were aspirated in four subsequent periods of 20 minutes each after ingestion of a standard meal. The volume, pH, and the concentration of alpha-amylase, trypsin, chymotrypsin and lipase were determined in the collections. The concentration of lipase was more markedly reduced than concentrations of amylase and of trypsin in patients with anicteric biliary diseases and in patients with hepatic cirrhosis. Concentrations of enzymes below the lowest normal value throughout the period of digestion represented an uncommon finding. The exocrine pancreatic function is rarely found to be reduced in patients with biliary or with hepatic disorders.
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PMID:pH and concentration of pancreatic enzymes in aspirates from the human duodenum during digestion of a standard meal in patients with biliary or hepatic disorders. 2018 82

In the past, chronic pancreatitis has been regarded as a fairly uniform and largely untreatable disorder that most commonly affects patients who both lack gainful employment or adequate insurance coverage and have a tendency to smoke and drink. Large clinical trials suggest that this perception is not only misguided and discriminatory but also not based on facts. We forgot that the perception of chronic liver disease was similar before World War II, and just like liver cirrhosis the fibrosis and cirrhosis of the pancreas--i.e. chronic pancreatitis--is the end result of a range of environmental, inflammatory, infectious and genetic disorders. A growing number of these have only recently been recognized as a distinct entity and several of which are becoming truly treatable. A large proportion of the risk for developing pancreatitis is conveyed by genetic risk factors, and we estimate that less than half of those have been identified so far. The same holds true for protective factors that can prevent pancreatitis, even in the face of excessive alcohol abuse. Various gene mutations and polymorphisms appear to determine an individual's susceptibility for developing pancreatic disease, for the severity of the disease, and for the disease progression. The spectrum of genotype/phenotype associations ranges from straightforward autosomal dominant traits with near-complete penetrance, as for the most common mutations in the cationic trypsinogen gene (PRSS1), to moderate risks factors without mendelian inheritance patterns, as for SPINK1 and CFTR mutations, to very subtle risk associations and disease modifiers that can only be identified in large cohort studies, as for the chymotrypsin C, calcium-sensing receptor and the anionic trypsin (PRSS2) mutations. Only a better understanding of the disease mechanisms that underlie these changes will make an individualized therapy of pancreatic disorders a realistic option.
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PMID:Advances in the etiology of chronic pancreatitis. 2081 6

Nonalcoholic fatty liver disease (NAFLD) includes a spectrum of diseases ranging from simple fatty liver to nonalcoholic steatohepatitis, (NASH) which may progress to cirrhosis and hepatocellular carcinoma. NASH has been independently correlated with atherosclerosis progression and cardiovascular risk. NASH development is characterized by intricate interactions between resident and recruited cells that enable liver damage progression. The increasing general agreement is that the cross-talk between hepatocytes, hepatic stellate cells (HSCs) and macrophages in NAFLD has a main role in the derangement of lipid homeostasis, insulin resistance, danger recognition, immune tolerance response and fibrogenesis. Moreover, several evidences have suggested that hepatic stem/progenitor cell (HPCs) activation is a component of the adaptive response of the liver to oxidative stress in NAFLD. HPC activation determines the appearance of a ductular reaction. In NASH, ductular reaction is independently correlated with progressive portal fibrosis raising the possibility of a periportal fibrogenetic pathway for fibrogenesis that is parallel to the deposition of subsinusoidal collagen in zone 3 by HSCs. Recent evidences indicated that adipokines, a class of circulating factors, have a key role in the cross-talk among HSCs, HPCs and liver macrophages. This review will be focused on cellular cross-talk and the relative molecular networks which are at the base of NASH progression and fibrosis.
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PMID:Role of hepatic progenitor cells in nonalcoholic fatty liver disease development: cellular cross-talks and molecular networks. 2411 87


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