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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently noted a hitherto undescribed hepatic hemosiderosis confined to endothelial cells of the portal tract in chronic viral hepatitis. In this study, this lesion was surveyed in 156 liver biopsy specimens from patients with chronic hepatitis C and in 21 liver biopsy specimens from patients with chronic hepatitis B. As controls, we examined 110 liver biopsy specimens from patients with primary biliary cirrhosis (PBC), 36 from patients with alcoholic liver injury, nine from patients with autoimmune hepatitis (AIH), and five from patients with primary hemochromatosis. Hemosiderin deposition was found in the endothelial cells of venous vessels in portal tracts regardless of the presence or degree of hemosiderin deposition in hepatic parenchyma. This phenomenon was observed in 65 of 156 cases (42%) of chronic hepatitis C and in eight of 21 (38%) cases of chronic hepatitis B. In controls, this lesion was frequent in AIH (78%), but infrequent in PBC (8.1%) and alcoholic liver injury (11%). The incidence of this lesion showed significant differences between chronic hepatitis C, B, and AIH, and between PBC and alcoholic liver injury. There was a positive correlation between the progression of disease and the incidence of this feature in chronic viral hepatitis; the incidence was 18.3% and 11.1% in milder chronic hepatitis C and B, respectively, and 61.2% and 58.3%, respectively, in more severe cases. However, this correlation was not evident in either PBC or alcoholic liver injury. This hemosiderin deposition was positively correlated with the degree of piecemeal necrosis in chronic hepatitis C, and to a lesser degree, the positive correlation was shown in chronic hepatitis B. These findings suggest that the progression of chronic hepatitis and the piecemeal necrosis in chronic hepatitis C and B, followed by the release of hepatocellular iron to portal and periportal areas, are directly or indirectly responsible for endothelial hemosiderosis. Further studies focusing on this peculiar phenomenon in relation to choice of therapy and evaluation of chronicity of viral hepatitis are encouraged.
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PMID:Hemosiderin deposition in portal endothelial cells: a novel hepatic hemosiderosis frequent in chronic viral hepatitis B and C. 755 40

This is the first reported case, to our knowledge, of hypoparathyroidism and hypothyroidism due to secondary hemochromatosis with onset during childhood. The patient was a boy with refractory aplastic anemia in whom primary hypothyroidism and hypoparathyroidism became apparent at the age of 10 and 11 years old, respectively. He had received a total of 100 L of transfused blood by the age of 10 years. The patient showed poor annual height gain due to primary hypothyroidism, together with hypocalcemia, cataract and intracranial calcification due to hypoparathyroidism. The early appearance of both thyroid and parathyroid dysfunction in this patient may have been due to the delay of initiation of iron-chelating agents and liver dysfunction due to hepatitis type C.
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PMID:Hypothyroidism and hypoparathyroidism in an 11 year old boy with hemochromatosis secondary to aplastic anemia. 757 61

Pathological iron deposition in liver is often found in various liver diseases. The deposited iron is thought to be one of the most important factor of liver cell injury, not only in hemochromotosis but also in cirrhosis following hepatitis virus B or C infection. To investigate the influence of the deposited iron on damage and regeneration of hepatocyte, primary cultured hepatocytes obtained from carbonyl iron-loaded rats were treated with carbon tetrachloride (CCl4) in the presence or absence of hepatocyte growth factor (HGF). Although the section of liver from carbonyl iron-loaded rats showed no necrosis and fibrosis, iron-loaded hepatocytes contained about twofold more iron than control. The damage of iron-loaded hepatocytes induced by CCl4 was more serious than that of control, and HGF decreased this injury only in iron-loaded hepatocytes but not in control. There is no difference in DNA synthesis stimulated by HGF between iron-loaded hepatocytes and control. These findings suggest that the pathological iron deposition induces the fragility of hepatocyte and that cytoprotective effect of HGF is induced by this pathological iron.
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PMID:[An experimental study on the protective effect of hepatocyte growth factor (HGF) for the primary cultured hepatocytes obtained from iron-loaded rats]. 774 74

After rapid changes in transfusion practice over the past few years, blood conservation techniques have become standard in modern perioperative management. As a result, the amount of homologous blood products transfused has been markedly reduced in some types of surgical procedures. Provided that skillful surgical technique is applied and the use of blood products is restricted, autologous transfusion techniques (predonation of autologous blood, preoperative plasmapheresis, acute normovolaemic haemodilution, and intra- and postoperative blood salvage) can be performed with an acceptable risk for patients. In addition, stimulation of erythropoiesis with recombinant human erythropoietin, supplemental iron therapy, and improving haemostasis by aprotinin may further reduce homologous blood requirements. All patients undergoing elective surgery have to be informed about the side effects of transfusion of homologous blood products and the possibility of blood-saving methods. An individual blood conservation plan, based on the patient's status and surgery, the equipment available, and personal experience should be worked out by the responsible anaesthesiologist, whereby a combination of different methods may be most effective. If storage is necessary, autologous blood products should be preparated like homologous products. The feasibility of predonation and retransfusion of autologous blood in patients with infectious diseases like hepatitis or acquired immune deficiency syndrome and the amount of labaratomy testing are still under discussion. Although blood conservation programs are time-consuming and more expensive, they reduce the various risks of using homologous blood products.
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PMID:[Reduction in the use of donated blood in surgical medicine]. 859 69

Following the pioneer report of Di Luzio (Physiologist 6, 169-173, 1963) concerning the prevention of the acute ethanol-induced fatty liver by antioxidants, many observations have shown that ethanol-induced liver injury may be linked, at least partly, to an oxidative stress resulting from increased free radical production and/or decreased antioxidant defence. The disturbances induced in the major hepatic enzymatic and non-enzymatic antioxidant systems following experimental acute and chronic ethanol administration are reviewed, emphasizing the important role of dietary alpha-tocopherol in modifying the induction of oxidative stress and its usual expression as increased lipid peroxidation. Adaptative increases in some elements of the hepatic antioxidant defence partly counteract the enhanced generation of prooxidant free radicals following chronic ethanol intake. By contrast, lipid peroxidation is favoured when ethanol is administered together with a fat-rich diet and/or various xenobiotics. Chronic ethanol feeding has also been reported to potentiate the oxidative stress resulting from an acute ethanol load. By generating potent chemoattractants for human neutrophils and/or by stimulating the expression of genes involved in collagen biosynthesis, liver lipid peroxidation may play an important role in the progression of steatosis to hepatitis and cirrhosis. Oxidative stress has been shown not to be restricted to the liver, but also to affect, under some experimental conditions of ethanol administration, extrahepatic tissues, such as the central nervous system, the heart and the testes. This stress can be partly prevented by vitamin E supplementation. Ethanol-induced antioxidant disturbances have also been reported in clinical studies in blood and liver biopsies. Pharmacological antioxidants could have beneficial effects in reducing the incidence of ethanol-induced changes in cellular lipids, proteins and nucleic acids. The antioxidants considered could act by reducing free radical production (e.g. chelators of redox-active iron derivatives), trapping free radicals themselves, interrupting the peroxidation process or reinforcing the natural antioxidant defence.
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PMID:Alcohol and antioxidant systems. 781 35

Seventy-nine subjects (19 women and 60 men) with chronic viral hepatitis were studied to determine the role of hepatic iron and its biochemical correlates in determining response to interferon alpha therapy. Each subject was treated for 6 months with interferon alpha. A total of 45 (57%) subjects achieved either a full or partial response. No differences between responders and non-responders were evident for the type of hepatitis, age, initial alanine aminotransferase, serum iron, total iron binding capacity, %sat, or ferritin. In contrast, the hepatic iron content of non-responders was almost twice that of responders (1156 +/- 283 micrograms/g dry weight vs. 638 +/- 118; p < 0.05). Hepatic iron correlated with total iron binding capacity (r = 0.435) and ferritin (r = 0.585). This study showed that: 1) the hepatic iron content of responders is less than that of non-responders, 2) the relationships of hepatic iron with %sat and ferritin in patients with viral hepatitis are weak, and 3) hepatic iron content predicts a response to interferon therapy.
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PMID:Response to interferon alpha therapy is influenced by the iron content of the liver. 801 55

This paper, which is the first part of four, deals with the potential risks of homologous blood transfusion as well as with normovolemic hemodilution, an autologous transfusion method, which is easily to be applied and not expensive. Although the various methods of autologous transfusion are well known for many years the public discussion on the "AIDS-topic" has led to a growing interest in blood-saving measures. However, in contrast to the so-called "AIDS-topic" the potential risks of a transfusion-transmitted hepatitis as well as the immunologic effects of homologous blood are of much greater importance. Moreover, high-court-sentences give the legal background for intensifying autologous transfusion and to offer it to the patients. So far there are four autologous transfusion methods to be applied routinely: 1. normovolemic hemodilution (NHD); 2. intra- and/or postoperative blood salvage (I/PBS) with or without autologous direct-retransfusion (ADR); 3. preoperative autologous plasmapheresis (PPH); 4. preoperative autologous blood donation (ABD). Moreover, drug-induced stimulation of the erythropoiesis by means of erythropoietin and the additional (intravenous) administration of iron may become a further component among autologous transfusion methods. Normovolemic hemodilution means exchange of autologous blood versus an artificial colloid. To make sure for normovolemia is to be considered a "conditio sine qua non" for "functioning" of normovolemic hemodilution.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The present possibilities for routine use of blood-saving measures from the anesthesiologic point of view--theoretical basis and clinical practice. I. Potential risks of homologous transfusion; normovolemic hemodilution]. 814 16

Mild microcytic anemia (without changes in mean corpuscular hemoglobin concentration, MCHC) was discovered 6-14 weeks after a single s.c. administration of 4 mg of particulate glucan to C57BL/10ScSnPh mice serologically positive for murine hepatitis (MHV). The anemia was associated with granulocytosis, decreased body weight and spleen hypertrophy. The overall intensity of erythropoiesis was measured by 59Fe-incorporation into the heme of erythropoietic organs. The localization of erythropoiesis became markedly redistributed--heme production was suppressed in the bone marrow while a several-fold increase was recorded for the spleen. A new steady state was also discovered in ferrokinetics: an iron pool localized away from the blood, erythropoietic organs and the liver was significantly elevated, and hypoferremia was detected. Anemia and wasting of mice were not observed in the same mouse strain free of MHV. A single administration of particulate glucan resulted in late impairment of red blood cell formation in the C57BL/10ScSnPh mouse strain infected with the mouse hepatitis virus. The anemia shares a number of features with those observed for the anemia of chronic diseases.
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PMID:Microcytic anemia and changes in ferrokinetics as late after-effects of glucan administration in murine hepatitis virus-infected C57BL/10ScSnPh mice. 815 May 55

Among 450 thalassemic patients treated in the Hematologic Department, 50 patients who were disease-free 4-6 years after allogeneic bone marrow transplantation were sequentially studied by liver biopsy. The patients received marrow from siblings who were genotypically HLA identical at A, B, C and DR loci. For evaluation of siderosis and associated lesions, each patient underwent liver biopsy before, and again 6 months and yearly for 4 to 6 years after bone marrow transplant. Spontaneous reversibility of liver iron overload, once the need for transfusions ceased when a functioning graft had been established, was observed in the youngest patients, aged 1-8 years, whereas iron excess remained at the end of follow-up in many patients aged 9-15 years. Hypotheses about the mechanism of the iron decrease are discussed. Several cases also obtained improvement of associated pathologies such as hepatitis, probably through modifications in the mechanisms controlling their immunological status.
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PMID:Bone marrow transplantation in thalassemia: modifications of hepatic iron overload and associated lesions after long-term engrafting. 817 25

The involvement of free radical reactions in the pathogenesis of liver injury has been investigated for many years in a few defined experimental systems using carbon tetrachloride, excess iron or ethanol as prooxidant agents. More recently, the hepatotoxicity of several other free radical-generating compounds has been characterised mainly in the rat hepatocyte model. In particular, the mechanisms by which drugs like paracetamol, halothane, paraquat or conditions such as ischemia-reperfusion exert their damaging activity to the liver have mostly been clarified. Since we are not trying to cure diseases occurring only in rats, the likely relevance of free radical reactions also in the genesis and progression of human liver injury has been carefully considered. Increasing evidence of free radical involvement is reported for chronic ethanol intoxication and iron overload, but the most striking proof of a causative role of ree radical chain reactions, namely lipid peroxidation, in the acute lethal damage of the hepatocyte has been obtained so far in ischemic hepatitis.
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PMID:Liver damage due to free radicals. 822 Oct 26


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