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 68-year-old man, after having been diagnosed as having hepatic disease at about the age of 41 years, had been hospitalized frequently until his death. Blood sugar, iron, and copper had not increased during his illness. Although the diagnosis of liver cirrhosis had been made and he had been receiving therapy, various neurologic symptoms without disturbances of consciousness appeared six months before his death. Autopsy revealed hemochromatosis, liver cirrhosis, and pancreatic fibrosis. A large amount of iron had accumulated in the liver, the pancreas, and the thyroid gland, while considerable numbers of ceroid and lipofuscin pigment granules had accumulated diffusely in the brain. Abnormal astrocytes of the Alzheimer II type were diffusely distributed in the brain and contained no intranuclear glycogen which stained positive with the carmine stain. No spongy changes were seen in the deeper layers of the cerebral cortex. Chemical analyses for trace metals in the brain, liver, and kidneys revealed a large amount of iron and increased copper in the liver, and considerable quantities of copper, manganese, calcium, and mercury in the brain. Because of changes in the erythrocyte sedimentation rate and marked thymol turbidity seen before and after the occurrence of the neurologic symptoms, this man was suspected of having disorders of the trace-metal binding proteins and/or of their polymers.
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PMID:Hemochromatosis associated with brain lesions--a disorder of trace-metal binding proteins and/or polymers? 92 21

Serum apolipoprotein A-I measurement was compared in alcoholic patients according to presence or absence of chronic pancreatitis and liver fibrosis. Among alcoholic patients without liver disease, apolipoprotein A-I was significantly lower in patients with chronic pancreatitis (157 +/- 70 mg/dl) than in patients without pancreatitis (209 +/- 74 mg/dl, p less than 0.001). In cirrhotic patients, apolipoprotein A-I was lower in patients with chronic pancreatitis (82 +/- 35 mg/dl) than in patients without pancreatitis (102 +/- 45 mg/dl), but this difference was not significant. The decrease of serum apolipoprotein A-I was independent of nutritional parameters whether or not there was cirrhosis. Immunohistochemical study of pancreatic samples with chronic pancreatitis showed that apolipoprotein A-I was located in the pancreatic fibrosis whereas lobules were unstained. This study suggests that apolipoprotein A-I is trapped by the pancreatic extracellular matrix and that this sequestration might explain, in part, the decrease of the serum apolipoprotein A-I.
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PMID:Serum apolipoprotein A-I in alcoholic patients with chronic calcifying pancreatitis. 212 44

Seventeen high-risk critically ill patients with suspected cholecystitis underwent percutaneous transhepatic cholecystostomy between 1981 and 1986 using Hawkins' needle guide system for gallbladder intubation. Acute cholecystitis was documented in 15 patients, including 1 with common bile duct obstruction. Two other patients had common bile duct obstruction secondary to metastatic cancer (one patient) and chronic pancreatic fibrosis (one patient). There was rapid resolution of the signs and symptoms of cholecystitis, sepsis, or both in 16 of the 17 patients. One critically ill patient with positive findings on blood culture and an organism resistant to triple antibiotic therapy died soon after percutaneous cholecystostomy. In the entire group of 17 patients, there was no evidence of bile leaks or other catheter complications. Six patients subsequently underwent successful cholecystectomy and two underwent common bile duct exploration without complications. One patient underwent cholecystojejunostomy, and in three patients, the catheter was removed with no sequelae of cholecystitis. Two remaining patients had the catheter in place and were awaiting operation at last follow-up. Three of four patients who died within 30 days of percutaneous transhepatic cholangiographic cholecystostomy died either from the terminal malignant condition (two patients) or from arrhythmia (one patient with cirrhosis). This review suggests that percutaneous cholecystostomy is a safe and effective procedure for resolving acute cholecystitis in high-risk patients. In addition, the technique of percutaneous transhepatic cholangiographic cholecystostomy appears well suited for percutaneous dissolution of stones, sclerosis of the gallbladder, or both in selected high-risk critically ill patients.
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PMID:Percutaneous cholecystostomy for acute cholecystitis in high-risk patients. 379 87

To obtain a dynamic and non-invasive picture of hepatic fibrosis in pre-cirrhotic liver diseases we measured both the concentration of the N-terminal peptide of procollagen III, as a marker of collagen synthesis, and the activity of PZ-peptidase, an enzyme involved in collagen degradation, in the serum of alcoholic or chronic viral hepatitis patients. Peptide serum levels were similar in chronic persistent hepatitis and controls, but significantly higher in chronic active hepatitis. Chronic persistent hepatitis patients had PZ-peptidase levels higher than controls, but similar to chronic active hepatitis. The increase in collagen synthesis without a parallel increase in collagen degradation seen in chronic active hepatitis could be regarded as a sign of impending cirrhosis, whereas the unbalanced rise in PZ-peptidase observed in chronic persistent hepatitis is consistent with the non-progressive character of this disorder. In alcoholic hepatitis both peptide concentration and PZ-peptidase activity were elevated, thus suggesting that both collagen synthesis and degradation are activated. However, the greater increase in PZ-peptidase than in peptide serum levels seen in some patients seems to indicate a minor tendency to progressive fibrosis or a trend towards resolution. Unlike liver disease patients, normal peptide and PZ-peptidase levels were found in patients with pancreatic fibrosis. Since circulating inhibitors and activators of the PZ-peptidase activity can be excluded, as proved by this study, joint peptide and PZ-peptidase serum measurements would seem to offer a simple reliable non-invasive method for differentiating and monitoring progressive and non-progressive forms of hepatic fibrosis.
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PMID:Type III procollagen peptide and PZ-peptidase serum levels in pre-cirrhotic liver diseases. 388 56

Asphyxiating thoracic dystrophy is an autosomal recessive disorder characterised by an abnormally small thorax, variable shortening of the extremities, and pelvic anomalies. Renal and pancreatic symptoms are found in longer survivors, although most cases die in infancy of respiratory failure. Seven neonatal cases were studied at necropsy. These cases ranged in gestational age from 32 to 40 weeks. One was stillborn and the other six survived from 1 hour to 10 days. Two were sibs born to consanguineous parents. Dwarfing was not pronounced and the extremities were shortened in only one infant who also had polydactyly. All seven showed visceral changes in addition to abnormalities of bone. Endochondral ossification was irregular in sections of femur, vertebra, and rib. Pulmonary hypoplasia was associated with the small thorax typical of this disorder. Periportal fibrosis and bile duct proliferation were seen in sections of liver, and in one case cirrhosis was found. Pancreatic fibrosis was variable. These necropsy findings correlate with later clinical manifestations of the disease and emphasise the multisystem nature of this disorder.
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PMID:Necropsy findings in neonatal asphyxiating thoracic dystrophy. 398 24

Pancreatic fibrosis in patients with alcoholic dependence syndrome was studied histopathologically. In 30 of 41 autopsied patients with alcoholic dependence syndrome, fibrosis was observed despite the absence of clinical pancreatitis. The fibrosis was categorized into three types, according to Martin's classification: intralobular sclerosis in 15 cases, perilobular sclerosis in seven cases, and a mixed intralobular and perilobular sclerosis in the remaining eight cases. The type of the fibrosis was not related to the duration of alcohol abuse. Alcoholic liver cirrhosis was coexistent in 23 of the 30 cases of pancreatic fibrosis. These cases were also divided into categories according to the three types, as follows: intralobular sclerosis in 12 (80%) of 15 cases, perilobular sclerosis in four (57%) of seven cases, and mixed sclerosis in seven (88%) of eight cases. That is, intralobular and mixed sclerosis were frequently coexistent with alcoholic liver cirrhosis. When the pancreases from the 19 subjects with intralobular sclerosis and mixed sclerosis coexistent with liver cirrhosis in alcoholic dependence syndrome were compared with 20 pancreases from patients with nonalcoholic liver cirrhosis, periacinar (or intralobular) fibrosis was found in all cases of the former, but in none of the latter. Hence, it was concluded that periacinar fibrosis occurred as a result of alcohol abuse. Pancreatic fibrosis in patients with alcoholic dependence syndrome was distributed mainly in the intralobular areas and was frequently coexistent with alcoholic liver cirrhosis.
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PMID:Pancreatic fibrosis in patients with alcoholic dependence syndrome. 821 22

The distribution and clinicopathologic features of pancreatic fibrosis were studied histopathologically in 137 autopsy cases of chronic alcohol abuse. Fibrosis was observed in 90 of the cases and was classified as perilobular sclerosis (PS) and intralobular sclerosis (IS). Fibrosis of the PS type was irregular and sometimes patchy and extended into the intralobular area in advanced cases. In some advanced cases, complete replacement of the pancreatic tissue by extensive fibrosis was seen. Fibrosis of the IS type was uniformly distributed. The tissues in some cases showed prominently periacinar fibrosis. In these cases, the pancreatic parenchyma had not been completely replaced by extensive fibrosis. Clinicopathologic comparisons revealed the following results: accompanying liver cirrhosis was greater in the IS than in the PS of fibrosis. However, a higher frequency of protein plugs, pancreatic stones, extensive fibrosis replacement, peripancreatic fibrosis, splenic vein involvement, choledochus involvement, pseudocyst, and ductal hyperplasia was found in the PS type compared to the IS type. In conclusion, the findings on the perilobular and intralobular distribution of fibrosis and differences in various components or accompanying diseases in pancreatic fibrosis suggest that this entity shows two distinct pathologic patterns with differing mechanisms.
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PMID:Histopathologic study of coexistent pathologic states in pancreatic fibrosis in patients with chronic alcohol abuse: two distinct pathologic fibrosis entities with different mechanisms. 874 Apr 4

The present study was done to determine the additional influence of daily ethanol intake (15% in drinking water ad libitum) on long-term toxic effects of a single administration of dibutyltin dichloride (DBTC, 8 mg/kg b.w. i.v.) in pancreas and liver of rats. Pathohistological changes in pancreas, bile duct and liver as well as pathobiochemical parameters of pancreatitis (amylase and lipase activity), liver lesions (alkaline phosphatase activity and bilirubin) and fibrosis (hydroxyproline and hyaluronic acid) were measured 1 day and 1 to 24 weeks after DBTC- and DBTC/ethanol administration. DBTC alone induced in rats an acute interstitial pancreatitis as well as acute bile duct and liver lesions in the early experimental phase. Later on, the acute inflammatory processes in pancreas and liver took a chronic course resulting in pancreatic fibrosis and liver cirrhosis. Ethanol increased the toxic effects of DBTC on pancreas and liver during the acute and chronic course. In the acute phase lasting 1 day to 2 weeks, ethanol enhanced the DBTC toxicity on acinar cell and bilio-pancreatic duct epithelium as well as the formation of obstructive ductal plugs by necrotic cell debris. The obstruction and cholestasis in the DBTC/ethanol-group were significantly stronger as in the DBTC-group. The significant increase of hydroxyproline in urine and hyaluronic acid in serum of the DBTC/ethanol treated rats after 12 to 24 weeks was connected with a more severe chronic inflammatory fibrosis in pancreas and liver in comparison to the DBTC-treated group.
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PMID:The influence of ethanol on long-term effects of dibutyltin dichloride (DBTC) in pancreas and liver of rats. 958 82

Magnetic resonance (MR) imaging and MR cholangiopancreatography are useful, noninvasive techniques for the assessment of pancreatic and hepatobiliary complications in cystic fibrosis. Abnormalities of the pancreas in cystic fibrosis are typically characterized by fat deposition, which has increased signal intensity on T1-weighted MR images, and pancreatic fibrosis, which has low signal intensity on both T1- and T2-weighted images. Pancreatic cysts are a relatively common finding; these cysts are typically quite small but are well demonstrated at MR imaging and MR cholangiopancreatography. Pancreatic duct abnormalities are also occasionally seen. Hepatic manifestations range from hepatomegaly and diffuse fatty infiltration to severe cirrhosis with fibrotic change, regenerative nodules, and portal hypertension. Splenomegaly is often characterized by siderotic nodules that manifest as multiple focal areas of abnormal low signal intensity within the spleen. Biliary manifestations include cholelithiasis, stricturization, and narrowing or dilatation of intra- and extrahepatic bile ducts. Gallbladder abnormalities including microgallbladder are also readily demonstrated. MR cholangiopancreatography can be used to help determine the presence and severity of biliary complications without resorting to more invasive procedures and, in conjunction with MR imaging, may prove useful in the assessment of patients with cystic fibrosis who present with abdominal symptoms that suggest hepatobiliary involvement.
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PMID:Hepatobiliary and pancreatic manifestations of cystic fibrosis: MR imaging appearances. 1083 27

Di-n-butyltin dichloride (DBTC) induced thymus atrophy, bile duct lesions, pancreatitis, and liver lesions in rats. Depending on dose [6 and 8 mg/kg intravenous (i.v.) DBTC] and time (1-24 weeks), the lesions in pancreas developed to a pancreatic fibrosis and the lesions in liver to liver cirrhosis. A single i.v. administration of 4 mg/kg DBTC induces a mild interstitial pancreatitis after 2-4 days followed by a restitutio ad integrum after 21-28 days. In the present study, the lesions of biliopancreatic duct, pancreas, and liver of rats after repeated administration of 4 mg/kg DBTC i.v. at intervals of 3 weeks have been investigated. The histopathological changes of pancreas and liver were examined by light microscopy 1,4, and 7 days and 2,3,4,6,9, and 12 weeks after administration of DBTC. Furthermore, pathobiochemical parameters of pancreatitis (amylase and lipase activity in serum), liver lesions (alkaline phosphatase activity and bilirubin in serum), and of fibrosis (hyaluronic acid in serum) were studied. Repeated administration of rats with DBTC (4 mg/kg i.v.) at intervals of 3 weeks induced an acute interstitial pancreatitis and after 9-12 weeks, a pancreatic fibrosis and liver lesions (intrahepatic bile duct hyperplasia, inflammation in periportal tract, and necrosis). In serum, elevated levels of alkaline phosphatase, bilirubin, and hyaluronic acid were found. This study demonstrates that the organotin compound induces toxic effects on pancreas and liver of rats by repeated administration of lower doses at long intervals. The risk of exposure to organotin at long intervals should be considered.
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PMID:Repeated administration of a mild acute toxic dose of di-n-butyltin dichloride at intervals of 3 weeks induces severe lesions in pancreas and liver of rats. 1172 88


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