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)

In order to study the relationship between amiodarone-induced hepatic phospholipidosis and liver disease, liver biopsies obtained from 13 patients treated with amiodarone for 4 months to 15 years were investigated by light and electron microscopy. Light microscopy showed pseudoalcoholic liver lesions that were probably related to amiodarone in four cases, various alterations (i.e. cirrhosis, three cases; steatosis and fibrosis, two cases; chronic venous congestion, one case; acute hepatitis, one case) that could be explained by another cause than amiodarone in seven cases and normal liver in two cases. In all cases, electron microscopy showed intralysosomal myelin figures suggestive of phospholipidosis. These myelin figures were associated with intralysosomal electron-dense deposits. In the four cases in which analysis by electron microprobe was performed, it demonstrated large amounts of iodine in the electron-dense deposit-containing lysosomes, indicating the accumulation of amiodarone. These results show that hepatic phospholipidosis is constantly observed in amiodarone-treated patients, whether or not pseudoalcoholic liver lesions are present. This phospholipidosis, which could be only a morphological marker of intrahepatic accumulation of the drug, should not therefore be considered grounds for attributing liver disease to the drug.
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PMID:Amiodarone-induced hepatic phospholipidosis: a morphological alteration independent of pseudoalcoholic liver disease. 341 26

Portosystemic shunting was evaluated with rectal administration of iodine-123 iodoamphetamine (IMP) in seven patients without liver disease and 53 patients with liver cirrhosis. IMP (2-3 mCi [74-111 MBq]) was administered to the rectum through a catheter. Images of the chest and abdomen were obtained for up to 60 minutes with a scintillation camera interfaced with a computer. In all patients, images of the liver and/or lungs were observed within 5-10 minutes and became clear with time. In patients without liver disease, only liver images could be obtained, whereas the lung was visualized with or without the liver in all patients with liver cirrhosis. The portosystemic shunt index was calculated by dividing counts of lungs by counts of liver and lung. These values were significantly higher in liver cirrhosis, especially in the decompensated stage. Transrectal portal scintigraphy with IMP appears to be a useful method for noninvasive and quantitative evaluation of portosystemic shunting in portal hypertension.
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PMID:Portosystemic shunting in portal hypertension: evaluation with portal scintigraphy with transrectally administered I-123 IMP. 342 Feb 49

A total of 75 samples of body cavity fluids from 71 patients were analyzed by both flow cytometry (FCM), to detect cells with an abnormal DNA content (aneuploidy), and by conventional cytopathology. Samples included 27 pleural fluids, 35 peritoneal fluids, 11 peritoneal washings and 2 pericardial fluids. For cytologic examination, the samples were prepared using standard techniques. Samples for FCM analysis were centrifuged and exposed to a hypotonic solution containing detergent and propidium iodide, a DNA intercalating fluorescent stain. Aneuploidy as well as cytologic malignancy were found in 17 samples. Forty-seven samples had normal DNA histograms by FCM and were also cytologically negative. Four samples suspicious by cytology but normal by FCM were from patients with renal-cell carcinoma (two samples from the same patient), endometrial adenocarcinoma without metastasis and chronic lymphocytic leukemia. Three samples abnormal by FCM but negative by cytology were from patients with ovarian cystadenoma, cirrhosis and uterine leiomyoma. FCM showed aneuploidy in four cytologically negative samples from patients with histologically proven malignancy (lymphoma, colonic adenocarcinoma, cervical squamous cell carcinoma, and endometrial adenosquamous carcinoma). Based on these results, FCM analysis combined with conventional cytopathology yielded 100% sensitivity, 100% predictive value of a negative result and 94% specificity. This rapid and quantitative FCM analysis of body cavity fluids can be a very useful adjunct to conventional diagnostic cytopathology.
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PMID:Flow cytometric analysis and cytopathology of body cavity fluids. 346 44

Two contrasting cases of amiodarone hepatotoxicity are described. In one, perivenular collections of swollen cells, probably macrophages, with granular cytoplasm in an otherwise nearly normal liver were observed. Transmission electron microscopy showed that the cytoplasmic granularity was due to lysosomal bodies of various sizes. X-ray energy and wavelength spectroscopic analysis showed a high iodine content in these lysosomal bodies, good presumptive evidence of the presence of amiodarone or one of its metabolites. In the second case there was a micronodular cirrhosis, and similar granular cells also containing iodine were seen in the fibrous connective tissue. These cases seem to represent the very early and late stages of amiodarone hepatotoxicity. In a patient taking this drug aggregates of swollen granular cells may be a sensitive and histopathologically useful marker of early amiodarone toxicity.
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PMID:Granular cells as a marker of early amiodarone hepatotoxicity: a pathological and analytical study. 358 85

The influence on the parameters of the thyroid gland BEI, T3-, T4- and TSH-serum level by the iodine-containing oral bile X-ray contrast remedy Falignost is demonstrated. Following a peripheral conversions inhibition from T4 to T3 by the contrast remedy the thyroid hormones in the serum are changed in different kind and duration. This influence is more expressed in patients with liver cirrhosis and continues. The risk of an iodine-induced hyperthyroidism is discussed. In the judgment of a possible disturbance of the function of the thyroid gland anamnestically is always to be asked the question about previous applications of iodine-containing drugs and it must be accordingly be taken into consideration.
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PMID:[Modification of the diagnosis of thyroid gland function by iodine-containing roentgen contrast media]. 372 45

Diatrizoate, iopamidol and ioxaglate were compared in five normal dogs and in five dogs with presinusoidal cirrhosis and portal hypertension for arterial portography. After selective injection of 40 ml of each contrast agent in iodine concentrations of 320 mg per ml into the superior mesenteric artery, portal vein blood samples were collected in 2-second intervals and the iodine concentrations determined using x-ray energy spectrometry. The highest iodine concentrations in the portal blood were found in both normal portal pressure and portal hypertension with ioxaglate, followed by iopamidol and diatrizoate in this order. Compared with diatrizoate, ioxaglate and iopamidol increased the peak portal blood iodine concentrations 45% and 22%, respectively. The use of ioxaglate in arterial portography should show the portal system at least as well as when a conventional contrast agent is used together with a vasodilator such as tolazoline.
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PMID:Comparison of diatrizoate, iopamidol, and ioxaglate for arterial portography. An experimental study in normal dogs and dogs with portal hypertension. 404 82

The metabolism of human fibrinogen labeled with radioactive iodine was studied in 50 patients with documented cirrhosis of the liver and in 35 healthy control subjects. Results in cirrhotic subjects were the following: plasma volume 47 +/- 10 ml/kg; plasma fibrinogen concentration 250 +/- 102 mg/100 ml; total plasma fibrinogen pool 118 +/- 59 mg/kg, representing 0.73 +/- 0.10 of the total body pool; fibrinogen half-life 2.99 +/- 0.59 days; fractional catabolic rate 0.34 +/- 0.09 of the plasma pool per day; absolute catabolic rate 39 +/- 20 mg/kg per day; fractional transcapillary efflux rate 0.82 +/- 0.30 of the plasma pool per day. Results in the control subjects were the following: plasma volume 42 +/- 7 ml/kg; plasma fibrinogen concentration 284 +/- 71 mg/100 ml; total plasma fibrinogen pool 119 +/- 40 mg/kg, representing 0.72 +/- 0.07 of the total body pool; fibrinogen half-life 4.14 +/- 0.56 days; fractional catabolic rate 0.24 +/- 0.04 of the plasma pool per day; absolute catabolic rate 28 +/- 9 mg/kg per day; fractional transcapillary efflux rate 0.60 +/- 0.26 of the plasma pool per day.A significant difference between cirrhotics and controls was observed for plasma volume, fibrinogen half-life, fractional and total catabolic rates, and transcapillary efflux rate. During heparinization of 10 cirrhotic patients the fibrinogen half-life was prolonged from 3.15 +/- 0.69 to 4.59 +/- 0.79 days. This was associated with a rise in plasma fibrinogen in six out of eight patients. Heparinization did not influence the fibrinogen half-life in five control subjects. Inhibition of the fibrinolytic system in 17 patients resulted in prolongation of the plasma radioactivity half-life of more than 1 day in only three patients, an incidence comparable with that in five control subjects. These results strongly support the concept of accelerated fibrinogen consumption by a process of disseminated intravascular coagulation in cirrhosis of the liver.
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PMID:Metabolism of fibrinogen in cirrhosis of the liver. 516 79

A method for the simultaneous measurement of gastrointestinal protein loss and total albumin turnover entailing the use of a combination of (125)iodine- and (51)chromium-labeled albumin is described. Albumin turnover was calculated by the measurement of albumin-(125)I plasma decay and cumulative urinary excretion, and the results obtained agreed closely with previous studies utilizing albumin-(131)I. Gastrointestinal catabolism was calculated from the rate of fecal excretion of (51)Cr and the specific activity of plasma albumin-(51)Cr, and these data were related to the calculated albumin turnover results. During the period of 6-14 days after administration, the ratio of specific activties of albumin-(125)I and -(51)Cr in plasma and in extravascular spaces or gastric and biliary secretions remained almost identical. Fecal excretion of (51)Cr was also quite stable at this time. In six normal subjects gastrointestinal catabolism accounted for less than 10% of total albumin catabolism. Excessive gastrointestinal protein losses did not contribute to the low serum albumin in three patients with cirrhosis or in two adults with the nephrotic syndrome. Multiple mechanisms leading to hypoalbuminemia were demonstrated in other subjects with a variety of gastrointestinal disorders.
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PMID:Use of 125-I- and 51-Cr-labeled albumin for the measurement of gastrointestinal and total albumin catabolism. 563 Apr 19

Plasma-to-peritoneal transport rate of albumin (TERperit.space) was determined in eighteen patients with decompensated cirrhosis by sampling ascitic fluid after i.v. injection of 125I-labelled serum albumin. Median TERperit.space was 0.30% of the intravascular albumin mass (IVM) per hour (range 0.10-0.59). The transport rate of albumin from ascitic fluid back to plasma was measured in eight patients by plasma sampling after intraperitoneal injection of 131I-labelled serum albumin. After correction for tracer re-extravasation this back transport (median 0.31, range 0.07-0.44% IVM/h-1) was not significantly different from the simultaneously determined TERperit.space, indicating steady state with respect to albumin flux. Analysis of errors of the method was performed from experiments in pigs, and it is concluded that especially a high content of non-protein bound iodine and even minor bleeding from the abdominal puncture may lead to overestimation of TERperit.space, whereas systematic understimation seems less likely. This may besides differences in patient selection and unsteady state, account for the discrepancy between the present relatively low value and earlier reports on much higher values of TERperit.space in cirrhosis.
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PMID:Determination of albumin transport rate between plasma and peritoneal space in decompensated cirrhosis. 671 19

The value of performing arterial portography during reactive hyperemia was investigated in four dogs with presinusoidal cirrhosis, stable portal hypertension in excess of 20 cm of water, and extensive porto-systemic venous collaterals, and compared to tolazoline (1 mg/kg) and control studies. With SMA balloon occlusion the maximum decrease in portal flow and pressure occurred between 1 and 2 minutes. During reactive hyperemia following immediately the release of a 2-minute SMA occlusion, portal flow and pressure increased from pre-occlusion values (mean +/- 1 SE, n:4) of 15 +/- 2 ml per min per kg and 25 +/- 1 cm H2O to 32 +/- 5 ml per kg and 40 +/- 2 cm H2O. With reactive hyperemia both significant higher peak iodine concentrations in the portal blood and significant improvement in visualization of the portal system and porto-systemic venous collaterals occurred when compared to tolazoline or control angiograms. With reactive hyperemia both peak blood iodine concentrations and maximum opacification of the portal vein occur 2 to 3 and 4 to 6 seconds earlier than with tolazoline or in controls, respectively. Compared to controls, tolazoline increased peak iodine concentrations in portal vein significantly and improved visualization of the portal system and collaterals in 7 of 12 examinations. Judged from the experience in peripheral arteriography, performance of angiography during reactive hyperemia appears to be a very safe procedure. However, the use of balloon catheters carries additional risks particularly when not properly used.
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PMID:Improved arterial portography in portal hypertension during reactive mesenteric hyperemia induced by preceding 2-minute balloon occlusion of the superior mesenteric artery. 707 49


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