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Query: UMLS:C0023890 (
cirrhosis
)
42,195
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In 10 patients with
hepatic cirrhosis
of various etiology both the insorption and the volume of distribution of tritiated water are determined. Indicator for the velocity of insorption is the time interval between the oral application of 200 mu-Ci THO distributed in 100 ml
tap
water and the appearance of a peak concentration of the isotope in the serum. In comparison with normal controls the insorption of THO is protracted in patients with
hepatic cirrhosis
from 37.0 plus or minus 4.4 min (S.E.) to a mean of 69.0 plus or minus 29.6 min. Individually the "insorption time" can be quite normal. The prolongation of the process of insorption is independent of the apparent volume of distribution of THO or of the etiology of
hepatic cirrhosis
. In the early phases of the insorption which are characterized by the main increase of the radioactivity in serum there is no difference between patients with
hepatic cirrhosis
and normal controls. Although an alteration of body fluid metabolism can not be excluded as a source of the prolonged equilibration, it is suggested that changes of the intestinal blood flow, of the tissue pressure and of the colloidosmotic pressure are due to a disturbance of the insorption of tritiated water in patients with
hepatic cirrhosis
.
...
PMID:[Insorption of tritiated water in hepatic cirrhosis (author's transl)]. 113 22
Zinc deficiency is a concomitant of both alcoholism and
cirrhosis
, as indicated by plasma and tissue measurements in man. The intracellular sites of zinc distribution, the site-specific nature of alcohol/
cirrhosis
-related depletion, and the alcohol exposure-zinc depletion time function have not been reported. Spague-Dawley rats (16) at 5 to 6 weeks were given normal chow and 20 per cent ethanol as sole water source. Control animals (14) had
tap
water. In rats killed at 2, 5, 9, and 14 weeks, zinc levels were measured by atomic absorption spectroscopy in plasma (p); muscle tissue (MT), cell sap (MCS) cell sap-free (MCSF), and mitochondria (MM); liver tissue (LT), cell sap (MCS), cell sap-free fraction (LCSF), And mitochondria (LM). Control zinc levels were stable in all tissues over the 14-week study; p = 108, plus or minus 10 mug per 100 ml., MT = 125 plus or minus 18, MCS = 30.3 plus or minus 3, MCSF = 70 plus or minus 6, MM = 209 plus or minus 17, LT = 198 plus or minus 29, LCS = 125 plus or minus 11.0, LCSF = 79.5 plus or minus 11.2, and LM = 291 plus or minus 30 mug per gram of dry tissue. Ethanol-fed rats showed marked decrease in all liver zinc fractions from the earliest (2 weeks) time, with the greatest depletion in LM to 35 per cent of control. MT and p zinc showed monotonic gradual declines at the rate of 3 per cent per week, becoming statistically different from control at 9 weeks in both tissues. Normal weight gain occurred in control animals: alcohol rats gained 52 per cent of control to 5 weeks, and showed no subsequent gain, weighing 62 per cent of control levels at 14 weeks. Liver mitochondria contain the highest zinc concentration, and are most rapidly depleted. MT and p declines follow hepatic zinc loss.
...
PMID:Distribution of zinc in skeletal muscle and liver tissue in normal and dietary controlled alcoholic rats. 117 Feb 68
Female Uje: WIST rats received thioacetamide (TAA) in the
tap
water (0.3 g/l) from the 4th to 6th months of life to produce experimental
liver cirrhosis
. Immediately, 2 and 7 days after TAA cessation it was investigated by means of in vivo (caffeine and metamizol elimination) and vitro methods (cytochrome P-450, 7-ethoxycoumarin and 7-ethoxyresorufin O-deethylation), whether this animal model represents the restricted cytochrome P-450-dependent biotransformation comparable to human
liver cirrhosis
. The total capacity of the liver was diminished immediately and 2 days after TAA cessation. After 7 days the capacity was unchanged compared to the controls or partly even enhanced. Therefore, this animal model reflects rather a short time than a stable alteration of biotransformation after TAA cessation comparable to human
liver cirrhosis
.
...
PMID:[Effect of 3 months of thioacetamide treatment on liver biotransformation in vivo and in vitro (various times after discontinuation)]. 209 75
Long term administration of thioacetamide (0.03% in
tap
water) results in a characteristic lesion in rat liver, which corresponds to
cirrhosis
-like patterns of micronodular
cirrhosis
type after treatment over 3 months. During its development a reproducible temporal course of biochemical and morphological changes can be recognized. After withdrawal of the toxic agent this lesion persists for about 2 months. Then the
cirrhosis
-like alterations recede and a proliferation of bile ducts predominates, which is associated with increasing portal fibrosis altering the pattern and relatively enhancing the total collagen content of the liver. Considering these peculiarities, the TAA-model is suitable for investigations into connective tissue metabolism in the fibrotic liver and
cirrhosis
-like patterns. Search for and test of therapeutic principles should be done during TAA-administration (prophylactic agents) or within 2 months after withdrawal of toxic agents (therapeutics).
...
PMID:Thioacetamide-induced cirrhosis-like liver lesions in rats--usefulness and reliability of this animal model. 285 79
To investigate whether paracentesis could be an alternative therapy for ascites, 117 cirrhotics with tense ascites were randomly allocated into two groups. Fifty-eight patients (group 1) were treated with paracentesis (4-6 L/day until disappearance of ascites) and intravenous albumin infusion (40 g after each
tap
). Fifty-nine patients (group 2) were treated with spironolactone (200-400 mg/day) plus furosemide (40-240 mg/day). Patients from group 2 not responding to diuretics were treated with a LeVeen shunt. After disappearance of ascites, patients from both groups were discharged from hospital and were instructed to take diuretics. Patients developing tense ascites during follow-up were readmitted to hospital and treated according to their initial schedule. Paracentesis was effective in eliminating the ascites in 56 patients from group 1 (96.5%) and did not induce significant changes in renal and hepatic function, plasma volume, cardiac index, peripheral resistance, plasma renin activity, plasma norepinephrine and antidiuretic hormone concentration, and urinary excretion of prostaglandin E2 and 6-keto-prostaglandin F1 alpha. Diuretics were effective in eliminating the ascites in 43 patients from group 2 (72.8%) (p less than 0.05). Ten patients in group 1 and 36 in group 2 developed complications during their first hospital stay (p less than 0.001). This difference was due to the significantly higher incidence of hepatic encephalopathy, renal impairment, and electrolyte disturbances occurring in patients treated with diuretics. The duration of hospital stay was 11.7 +/- 1.5 days for patients from group 1 and 31 +/- 2.8 days for patients from group 2 (p less than 0.001). The two groups did not differ significantly with respect to the probability of requiring readmission to hospital during follow-up, reasons for readmission, survival probability after entry into the study, and causes of death. These results indicate that paracentesis associated with intravenous albumin infusion is a fast, effective, and safe therapy for ascites in patients with
cirrhosis
.
...
PMID:Comparison of paracentesis and diuretics in the treatment of cirrhotics with tense ascites. Results of a randomized study. 329 7
It has recently been shown that repeated large-volume paracentesis associated with intravenous albumin infusion is a rapid, effective, and safe therapy of ascites in
cirrhosis
. To investigate whether intravenous albumin infusion is necessary in the treatment of cirrhotics with large-volume paracentesis, 105 patients with tense ascites were randomly allocated into two groups. Fifty-two patients (group 1) were treated with paracentesis (4-6 L/day until disappearance of ascites) plus intravenous albumin infusion (40 g after each
tap
), and 53 (group 2) with paracentesis without albumin infusion. After disappearance of ascites, patients were discharged from the hospital with diuretics. Patients developing tense ascites during follow-up were treated according to their initial schedule. Paracentesis was effective in eliminating the ascites in 50 patients from group 1 and in 48 from group 2, with the duration of the hospital stay being approximately 11 days in both groups. Paracentesis plus intravenous albumin did not induce significant changes in standard renal function tests, plasma renin activity, and plasma aldosterone. In contrast, paracentesis without albumin was associated with a significant increase in blood urea nitrogen, a marked elevation in plasma renin activity and plasma aldosterone concentration, and a significant reduction in serum sodium concentration. One patient from group 1 and 11 from group 2 developed renal impairment or severe hyponatremia after treatment, or both (chi 2 = 9.19; p less than 0.01). The development of these complications could not be predicted by clinical and laboratory data before treatment. Although the probability of survival after entry into the study was similar in patients from both groups, a multivariate analysis identified the development of hyponatremia or renal impairment, or both, following the first paracentesis treatment and the occurrence of other complications during the first hospitalization (encephalopathy, gastrointestinal bleeding, and severe infection) as being the only independent predictors of mortality. These results indicate that intravenous albumin infusion is important in avoiding renal and electrolyte complications and activation of endogenous vasoactive systems in cirrhotics with ascites who are treated with repeated large-volume paracentesis. The development of such complications may impair survival in these patients.
...
PMID:Randomized comparative study of therapeutic paracentesis with and without intravenous albumin in cirrhosis. 336 Feb 70
A three year old child with
cirrhosis of the liver
and ascites caused by alpha-1-antitrypsin deficiency, developed severe abdominal pain with diarrhea and fever. Spontaneous bacterial peritonitis was diagnosed by demonstrating a purulent ascitic fluid with gram-positive cocci in the smear which were identified as pneumococci in the bacterial culture. The peritonitis subsided under antibiotic treatment without complications. Spontaneous bacterial peritonitis in children with
cirrhosis of the liver
is mentioned in the literature, but up to now, however, only three cases were reported in detail. In order to establish the diagnosis, abdominal
tap
should be tried rather than explorative laparotomy, the demonstration of gram-positive cocci is diagnostic of spontaneous bacterial peritonitis. With early antibiotic therapy, prognosis of the disease is favourable. Newborns and children with nephrotic syndrome, however, are particularly at risk.
...
PMID:[Spontaneous bacterial peritonitis in cirrhosis of the liver caused by alpha-1-antitrypsin deficiency (author's transl)]. 698 Oct 63
The relationship between
liver cirrhosis
and the pathogenesis of black pigment stones has not been clarified. We attempted to induce black pigment stone formation in the gallbladders of hamsters. Male golden hamsters were divided into a
cirrhosis
group and a control group.
Liver cirrhosis
was induced by administering drinking water containing thioacetamide. The control group was given
tap
water. Gallstones at 48 weeks after treatment were examined by stereoscopic microscopy and scanning electron microscopy. The copper content of the black pigment stones was analysed by atomic absorption spectrophotometry. Black pigment stones in the gallbladder were detected in 25% of the
cirrhosis
group. Their surface and cross-section appeared amorphous. Black pigment stones contained copper. We confirmed the formation of gallstones in an animal model of
cirrhosis
by thioacetamide. Our findings may contribute to the clarification of the relationship between the pathogenesis of black pigment stones and the pathophysiology of
liver cirrhosis
.
...
PMID:Formation of black pigment gallstone in a hamster model of experimental cirrhosis. 937 63
Copper can induce acute and chronic intoxications in humans. Copper in
tap
water has caused a series of severe systemic diseases in Germany in recent years (copper induced
liver cirrhosis
). Besides
cirrhosis
, another type of disease with predominantly gastrointestinal symptoms has occurred which likewise appeared to be induced by copper in
tap
water. - In a retrospective investigation we looked for additional indications and proof that chronic copper poisoning has been the cause of the observed gastrointestinal diseases. All patients suffering from this type of disease had copper plumbing in their houses. - The patients (children and adults) suffered from nausea, vomiting, colic, and diarrhoea. In the group of infants, one refused formula milk (prepared with
tap
water) and the others suffered from persistent restlessness, unexplainable screaming (especially at night) and/or long lasting diaper rash. - We accept the diagnosis of chronic copper intoxication as the cause of the gastrointestinal symptoms when at least one of the following criteria were fulfilled: 1. first manifestation, remission and relapse of the disease depend on intake and a non-intake of water containing copper, respectively. 2. hypercupric state of the patients (i.e. pathological high concentrations of the non-ceruloplasmin-bound copper in serum and/or elevated copper levels in urine) 3. signs of systemic copper intoxication in the same patient 4. signs of systemic copper intoxication or hypercupric states in members of the patient s family or in his neighbourhood (non-relatives) - We found that the disease can even be caused by copper concentrations below the allowed concentration given by the German Guidelines for Drinking Water (Trinkwasserverordnung). - The data prove that copper in drinking water can cause gastrointestinal diseases and not only the better known systemic diseases (i.e. copper induced
liver cirrhosis
). Copper poisoning must be considered as a possible cause of chronic gastrointestinal diseases in those countries in which copper plumbing is common.
...
PMID:Chronic poisoning by copper in tap water: I. Copper intoxications with predominantly gastointestinal symptoms. 1057 26
During the past 20 years there has been much discussion about copper in connection with a form of Early Childhood
Liver Cirrhosis
(ECLC) known as Non Indian Childhood
Cirrhosis
(NICC). NICC is similar to Indian Childhood
Cirrhosis
(ICC) which occurs in India, and has already been known for many years. ICC is attributed to the excessive intake of copper derived from milk or water stored in copper and brass vessels. To determine precisely a possible connection between the amount of copper in
tap
-water and the risk of early childhood liver disease, an attempt was first made, through an epidemiological survey, to determine the extent of excessive concentrations of copper in the
tap
-water of households with copper pipes. To achieve this, water samples from 956 households were tested for copper, and the state of health of the infants in these households was documented. Infants who had been fed using water with a copper concentration of 0.8 mg/l or more received a paediatric examination with a blood check so as to rule out any possibility of liver damage. A copper level greater than 0.8 mg/l was found in only 2% of the households examined. Eight infants were examined by a paediatrician and received blood checks. (These infants had either been breast-fed up until their 12th week or had received more than 200 ml of
tap
water per day during their first 12 months). None of the infants examined showed any signs of liver malfunction. From the results of the study, no indication of a hazard due to copper pipes connected to public water supplies could be found.
...
PMID:Determination of the extent of excessive copper concentrations in the tap-water of households with copper pipes and an assessment of possible health hazards for infants. 1058 3
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