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Query: UMLS:C0023890 (
cirrhosis
)
42,195
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In a double-blind, crossover study, 10 cirrhotic patients (Child B rating) with steatorrhoea (daily output of faecal fat greater than 8 g) and
dyspepsia
were placed on a controlled diet for 14 days. Patients then received 150 mg ursodeoxycholic acid (UDCA) or placebo twice daily for 14 days. Faecal fat excretion was reduced from 14.7 to 10.6 g/day by UDCA and
dyspepsia
symptom scores were also reduced. Serum aspartate aminotransferase concentrations declined significantly (P less than 0.02) following UDCA treatment, whereas serum bile acid levels increased from 35 to 40.5 microM and the percentage of UDCA increased to 22%. It is concluded that UDCA may be useful for many of the symptoms present in patients with
liver cirrhosis
.
...
PMID:Steatorrhoea in cirrhosis: effect of ursodeoxycholic acid administration. 222 76
Clinical studies show that patients with
liver cirrhosis
associated with portal hypertension have a high incidence of duodenal ulcer and duodenitis. However, little information is available concerning pathophysiological process of such duodenal diseases in
liver cirrhosis
. Hemodynamics of the duodenal mucosa was studied in cirrhotics with esophageal varices (68 cases) and in noncirrhotics with non-ulcer
dyspepsia
(37 cases) as well. In each group, hemoglobin concentration in the peripheral venous blood was measured, and mucosal hemodynamics was examined in 4 regions of the duodenum by endoscopic reflectance spectrophotometer. No significant intergroup difference was noted in the mean age or sex ratio. Hemoglobin concentration in the peripheral venous blood was significantly lower (p less than 0.01) in the cirrhotics. There were no significant intergroup differences in duodenal mucosal blood volume. However, the cirrhotics showed significantly lower oxygen saturation of hemoglobin in all regions of the duodenum (p less than 0.01). These results show that the cirrhotics with esophageal varices had relative increase in blood volume and decrease in oxygen saturation of hemoglobin in the duodenal mucosa. Such microcirculatory disturbances seem to predispose
liver cirrhosis
patients to duodenal injury.
...
PMID:Duodenal mucosal hemodynamics in patients with liver cirrhosis. 226 Apr 99
The aim of the present investigation was to study the clearance of 99mTc-p-butyl IDA in some acute and chronic liver diseases, it being considered that the typical parameters obtained with this method are as indicative as any of the others put forward for the study of liver function using radioisotopes. 46 subjects were examined: 6 with acute hepatitis, 10 with chronic hepatitis, 18 with
liver cirrhosis
and 12 with
dyspepsia
but otherwise normal haematochemical tests. Two basic 99mTc-p-butyl IDA clearance parameters, Tu (semi-take up time) and Te (semi-excretion time), were determined plotting the data obtained using a Gamma-Camera on semi-logarithmic paper. Mean Tu values were as follows: 5'06'' +/- 1'24'' in dyspeptics, 12'30'' +/- 6'31'' in subjects with acute hepatitis, 6'30'' +/- 1'45'' in subjects with chronic hepatitis and 13'30'' +/- 4'30'' in subjects with
cirrhosis
. The values were: 34'30'' +/- 4'30'' in dyspeptics, 49'54'' +/- 2'36'' in subjects with acute hepatitis, 42'24'' +/- 12'24'' in subjects with chronic hepatitis and 65'30'' +/- 39'36'' in subjects with
cirrhosis
. The Tu parameter was found to be delayed more significantly in cirrhotic patients and less in subjects with acute or chronic hepatitis, compared to dyspeptics with normal haematochemical parameters. Te was significantly delayed in subjects with
cirrhosis
and acute hepatitis, while there was no difference for subjects with chronic hepatitis. Of the routine haematochemical tests, the albumin/gamma-globulin ratio and unconjugated bilirubin were found to correlate significantly with the Tu parameter, whereas conjugated bilirubin was found to bear a significant correlation to the Te parameter.
...
PMID:[Hepatic clearance of 99mTc-p-butyl HIDA in liver diseases. Correlations with routine hematochemical parameters of liver function]. 608 7
Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer
dyspepsia
), and in 19 patients with proven
liver cirrhosis
of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with
liver cirrhosis
, but statistical significance was not attained for patients with nonulcer
dyspepsia
. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.
...
PMID:Gastric secretion, gastroduodenal histological changes, and serum gastrin in chronic alcoholic pancreatitis. 707 77
A prospective case controlled study was conducted to evaluate the value of real time ultrasound in establishing the diagnosis and the etiology of portal hypertension. Patients attending the outpatient department of a tertiary care centre were included. There were 324 consecutive patients with portal hypertension due to
cirrhosis
(n = 229), non cirrhotic portal fibrosis (NCPF: n = 64) and extrahepatic portal venous obstruction (EHPVO: n = 31). During this period, 146 patients with
dyspepsia
, 35 with splenomegaly and 32 with ascites due to varied causes served as negative and positive controls. Real time ultrasonography using a 3.5 MHz linear array scanner was performed in a fasting state in all subjects. Portal and splenic vein diameter greater than 10 mm, splenomegaly, hepatic and splenic hilar collaterals were suggestive of portal hypertension. Non visualization of the portal vein which was replaced by a cavernoma had a diagnostic accuracy of 98% in EHPVO. Splenic infarcts and absence of ascites were features of non cirrhotic portal hypertension (NCPF and EHPVO). Sonography had an overall diagnostic accuracy of 80%. A stepwise logistic regression with multivariate analysis using discriminate function showed that collaterals at the hepatic and splenic hilum, hepatomegaly, ascites and splenic infarcts were independent markers to differentiate cirrhotic from noncirrhotic causes of portal hypertension. The discriminate equation generated had a mismatch of 9.8%. Correlations between the sonographic signs demonstrated that the variceal grade correlated positively with the presence of splenic hilar collaterals and the liver size inversely correlated with presence of ascites. It was concluded that real time ultrasonography is an accurate method to establish the presence and etiology of portal hypertension.
...
PMID:Sonographic signs in portal hypertension: a multivariate analysis. 878 73
Many patients with
liver cirrhosis
have dyspeptic complaints. Peptic ulcer, gallstones and oesophagitis are the most common causes of
dyspepsia
. Functional dyspepsia is infrequently investigated in
liver cirrhosis
. Sixty-two patients with
liver cirrhosis
and
dyspepsia
were submitted to endoscopic and sonographic investigation. In 28 of them no organic finding was detected. These cases were considered as having functional
dyspepsia
. 36% were of dysmotility-like type, 28% were ulcer- and reflux-like, each, and 7% were of idiopathic type. Aerophagia could not be taken in consideration as functional
dyspepsia
, due to portal hypertension. In comparison with a group of 30 patients with functional
dyspepsia
without
liver cirrhosis
, functional
dyspepsia
in
liver cirrhosis
is more frequent in men than in women and occurs about a decade later. In 12 subjects the gastric emptying of a semifluid meal estimated by sonography was normal. Functional dyspepsia is a reality in
liver cirrhosis
. Gastric emptying seems not to have a major role in the etiopathogenesis of such complaints.
...
PMID:[Functional dyspepsia in liver cirrhosis]. 896 53
Helicobacter pylori (H. pylori) is the most common cause of peptic ulcers, and is considered as carcinogenic with respect to gastric cancer and MALT lymphoma. The role of H. pylori in other gastroduodenal diseases like atrophic gastritis and functional
dyspepsia
has been investigated in hundreds of works, but little is done about what role H. pylori may play in non gastric diseases. Gastro-esophageal reflux disease does not seem to be related to H. pylori but Barrett's esophagus might be. Inflammatory bowel diseases tend to be reverse correlated with H. pylori. In coronary heart disease some studies have shown a connection, others not. Diabetes is not likely to be H. pylori-associated and nor do liver diseases with exception for
cirrhosis
, where a correlation is possible. Respiratory diseases are little examined but bronchiectasis might have a correlation with H. pylori. A small series of children, who had died in sudden infant death, showed a high rate of H. pylori infection.
...
PMID:Non-gastric effects of H. pylori infection: a literature review with respect to non gastric diseases which might be associated with H. pylori infection. 1002 62
Excessive consumption of alcoholic beverages may be associated with gastrointestinal symptoms, including
dyspepsia
and diarrhoea. It is not clear whether or not chronic alcohol ingestion damages the mucosa of the small intestine. We investigated the effect of chronic alcohol abuse on the duodenal mucosa, and particularly on its extracellular matrix (ECM) network. Duodenal biopsy specimens were obtained during upper gastrointestinal endoscopy from 50 chronic alcoholics without
cirrhosis
and 10 healthy subjects. Morphological studies were performed by routine histology, immunohistochemistry and electron microscopy. Morphometry of duodenal tissues was performed with a computerized image analyser. No significant duodenal epithelial changes were found in alcoholics, despite an evident reduction in the enterocyte turnover. Myofibroblast-like cells were significantly increased in the villus stroma of alcoholics in comparison to controls. These cells stained positively for desmin, alpha-smooth muscle actin and for several ECM components. In alcohol abusers the thickness of the mucosal basement membrane was greater and the staining for collagen I and III was enhanced both in the basement membrane and in the villus stroma. A higher expression of tenascin was also seen at the base of villi of alcoholics. Chronic alcohol abuse may induce fibrosis of duodenal villi which is associated with a transformation of villus juxta-parenchymal cells into active subepithelial myofibroblast-like cells able to produce different ECM components.
...
PMID:Ethanol-induced alterations of matrix network in the duodenal mucosa of chronic alcohol abusers. 1007 Dec 47
Herbal drugs are widely used and often contain highly active pharmacological compounds. Recently, reports have mounted about hepatotoxicity of herbal remedies which ranges from mild liver enzyme alterations to chronic liver disease and liver failure. Hepatotoxicity of Chinese herbs has been recognized, e.g. during treatment of patients with atopic eczema. However, the toxic compounds remain to be determined. Hepatic veno-occlusive disease may result from pyrrolizidine alkaloids which are contained in numerous plants worldwide. Teucrium chamaedrys, commonly referred to as germander, may cause hepatitis and even
liver cirrhosis
. Significant hepatotoxicity has also been observed after the ingestion of chaparral. Recently, greater celandine, which is widely used for biliary disorders and
dyspepsia
, was identified as a cause of cholestatic hepatitis. Hepatotoxic reactions have also been observed after the ingestion of Atractylis gummifera, Callilepsis laureola, Senna, Kavapyrone and Pulegium. The aim of this review is to summarize potentially hepatotoxic herbal remedies, to further elucidate their mechanisms of toxicity and thereby underline the likelihood of plants to be the cause of liver damage.
...
PMID:[Liver toxicity of drugs of plant origin]. 1132 40
The role of Helicobacter pylori in dyspeptic, cirrhotic patients remains unclear. This prospective outpatient study, conducted to assess the relationship of gastroduodenal disease and H. pylori as determined by the (13C) urea breath test, enrolled 109 consecutive cirrhotic patients with
dyspepsia
. All patients underwent upper-gastrointestinal endoscopy, which revealed respective prevalences of peptic ulcer, gastric ulcer, and duodenal ulcer of 41.3%, 23.9%, and 22.9%; H. pylori infection was found in 52.3%. The rate of peptic ulcer disease in the H. pylori-positive (45.6%) and -negative (36.5%) groups was not significantly different; neither was the prevalence of H. pylori in patients with or without portal hypertensive gastropathy and with or without esophageal varices. The relationship between peptic ulcer disease and H. pylori in dyspeptic patients with
cirrhosis
appears to be weak. Likewise, no significant relationship was evident between H. pylori and portal hypertensive gastropathy or esophageal varices. This organism may not be a major pathogenetic factor in gastroduodenal diseases in dyspeptic patients with
cirrhosis
.
...
PMID:Role of Helicobacter pylori in cirrhotic patients with dyspepsia: a 13C-urea breath test study. 1157 26
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