Hepatic necrosis and fibrosis after ethanol injection.

Kanzo ◽  
1989 ◽  
Vol 30 (1) ◽  
pp. 43-48
Author(s):  
Kenichiro MATSUZAKI ◽  
Yukio YOKOI ◽  
Hiroyuki KURODA
Keyword(s):  
Hepatic Necrosis ◽  
Ethanol Injection

Fine Structural Alterations in Thyroid Follicular Cells (FC) and Changes in Serum Thyroxine Produced by Feeding Polychlorinated Biphenyl (PCB) to Rats

1977 ◽  
Vol 35 ◽  
pp. 498-499
Author(s):  
W.T. Collins ◽  
Charles C. Capen ◽  
Louis Kasza
Keyword(s):  
Feed Efficiency ◽  
Polychlorinated Biphenyl ◽  
Serum Proteins ◽  
Skin Lesions ◽  
Hepatic Necrosis ◽  
Ultrastructural Changes ◽  
Lymphoid Tissues ◽  
Heat Transfer Fluids ◽  
Thyroid Follicular Cells ◽  
Peripheral Metabolism

The widespread contamination of the environment with PCB, a compound used extensively by industry in hydraulic and heat transfer fluids as well as plasticizers and solvents in adhesives and sealants, has resulted in detectable tissue levels in a large portion of the human population, domestic animals, and wildlife. Intoxication with PCB produces severe hepatic necrosis, degeneration of lymphoid tissues and kidney, skin lesions, decreased reproductive performance, reduced feed efficiency, and decreased weight gain. PCB also has been reported to reduce the binding of thyroid hormone to serum proteins and enhance the peripheral metabolism of thyroxine with increased excretion of thyroxine-glucuronide in the bile (Bastomsky, Endocrinology 95: 1150-1155, 1974).The objectives of this investigation were (1) to investigate the histopathologic, histochemical, and ultrastructural changes in thyroid FC produced by the acute (4 week) and chronic (12 week) administration of low (50 ppm) and high (500 ppm) doses of PCB to rats, (2) to correlate these alterations to changes in serum immunoreactive thyroxine concentration, and (3) to investigate the persistence of the effects of PCB on the thyroid gland.

Early Development of Drug-Induced Hepatic Necrosis

1971 ◽  
Vol 29 ◽  
pp. 576-577
Author(s):  
F. G. Zaki ◽  
E. Detzi ◽  
C. H. Keysser
Keyword(s):  
Early Development ◽  
Hepatic Necrosis ◽  
Screening Tests ◽  
Dense Matrix ◽  
Sprague Dawley ◽  
Electron Microscopic ◽  
Drug Induced ◽  
Hepatocellular Damage ◽  
Sprague Dawley Rats ◽  
Microscopic Studies

This study represents the first in a series of investigations carried out to elucidate the mechanism(s) of early hepatocellular damage induced by drugs and other related compounds. During screening tests of CNS-active compounds in rats, it has been found that daily oral administration of one of these compounds at a dose level of 40 mg. per kg. of body weight induced diffuse massive hepatic necrosis within 7 weeks in Charles River Sprague Dawley rats of both sexes. Partial hepatectomy enhanced the development of this peculiar type of necrosis (3 weeks instead of 7) while treatment with phenobarbital prior to the administration of the drug delayed the appearance of necrosis but did not reduce its severity.Electron microscopic studies revealed that early development of this liver injury (2 days after the administration of the drug) appeared in the form of small dark osmiophilic vesicles located around the bile canaliculi of all hepatocytes (Fig. 1). These structures differed from the regular microbodies or the pericanalicular multivesicular bodies. They first appeared regularly rounded with electron dense matrix bound with a single membrane. After one week on the drug, these vesicles appeared vacuolated and resembled autophagosomes which soon developed whorls of concentric lamellae or cisterns characteristic of lysosomes (Fig. 2). These lysosomes were found, later on, scattered all over the hepatocytes.

A Comparison of the Ultrastructural Morphology of Hepatic Necrosis in BDF1 Mice

1981 ◽  
Vol 39 ◽  
pp. 586-587
Author(s):  
Becky Jackson
Keyword(s):  
Endoplasmic Reticulum ◽  
Smooth Endoplasmic Reticulum ◽  
Preliminary Investigation ◽  
Hepatic Necrosis ◽  
Hepatic Tissue ◽  
Pronounced Increase ◽  
Glycogen Store ◽  
Ultrastructural Morphology ◽  
Mitochondrial Integrity ◽  
Glycogen Stores

Preliminary investigation has indicated similarity in hepatic ultrastructural morphology in nutritional deprivation, and cyanide induced hepatic necrosis. Analysis of hepatic tissue has indicated disruption of intracellular membranes, specifically, reduction in rough endoplasmic reticulum (RER) mitochondrial integrity, and glycogen stores. An increase in smooth endoplasmic reticulum (SER) portion was observed.To further investigate the apparent equivalence of necrotic morphology, ultrastructura1ly, BDF1 mice were subjected to senescence, nutritional deprevation, potassium cyanide (KCN) induced toxemia, and acetaminophen induced toxemia. Controls were utilized to ellucidate non-necrotic hepatocellular normals. U1trastructura1 investigation of controls (Fig. 1) shows densely granular RER, abundant glycogen stores, and morphologically normal mitochondria. Subjects with acetaminophen induced necrosis exhibit reduced normal RER with increased levels of dialated, vesicular RER in apparent conversion to SER (Fig. 2), loss of mitochondrial integrity, and glycogen store reduction. Senescent subjects exhibit a pronounced increase in SER and loss of glycogen store. (Fig. 3). Investigation of the senescent SER at high magnification (Fig. 5) indicates that the SER is arising from degranulating and vesiculating RER.

Intraoperative abdominal ultrasonography-guided large volume ethanol injection for hepatocellular carcinoma

2001 ◽  
Vol 120 (5) ◽  
pp. A482-A482
Author(s):  
R MONDRAGONSANCHEZ ◽  
A GARDUOLOPEZ ◽  
H MURRIETA ◽  
M FRIASMENDIVIL ◽  
R ESPEJO ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Large Volume ◽  
Abdominal Ultrasonography ◽  
Ethanol Injection

Nonsurgical Therapies for Hepatocellular and Cholangiocellular Carcinoma

Swiss Surgery ◽  
1999 ◽  
Vol 5 (3) ◽  
pp. 116-121 ◽  
Author(s):  
Schmassmann
Keyword(s):  
Current Trend ◽  
Percutaneous Ethanol Injection ◽  
Cholangiocellular Carcinoma ◽  
Multidisciplinary Therapy ◽  
Term Survival ◽  
Ethanol Injection ◽  
First Choice ◽  
Tumor Stages ◽  
Choice Of Treatment ◽  
Advanced Stages

Surgical resection is the first choice of treatment for patients with hepatocellular (HCC) and cholangiocellular carcinomas. Prolongation of survival is, however, the only realistic goal for most patients, which can be often achieved by nonsurgical therapies. Inoperable patients with large or multiple HCCs are usually treated with transarterial chemoembolization (TACE) with lipiodol in combination with a chemotherapeutic drug and gelfoam. Three-year survival depends on the stage of the disease and is about 20%. Patients with earlier tumor stages (one or two tumor nodules less than 3cm in size) are suitable for treatment with percutaneous ethanol injection (PEI) alone or in combination with TACE. Several studies have shown that in these early stages, the 3-year survival rate is approximately 55%-70% in the actively treated patients which is significantly higher than in untreated patients. In advanced stages of the disease, TACE and PEI have no effect on survival and should not be performed. Some of these patients have been successfully treated with octreotide. Patients with inoperable cholangiocellular carcinoma are treated by endoscopic or percutaneous stent placement. If stenting does not achieve adequate biliary drainage, multidisciplinary therapy including internal / external radiotherapy or photodynamic therapy should be considered in patients with potential long-term survival. In conclusion, nonresectional therapies play an essential role in the therapy of inoperable hepato- and cholangiocellular carcinomas as they lead to satisfactory survival. Multidisciplinary therapy appears to be the current trend of management.

Percutaneous ethanol injection for benign cystic and mixed thyroid nodules

2018 ◽  
Author(s):  
Aysenur Ozderya ◽  
Kadriye Aydin ◽  
Naile Gokkaya ◽  
Sule Temizkan
Keyword(s):  
Thyroid Nodules ◽  
Percutaneous Ethanol Injection ◽  
Ethanol Injection
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