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

Histomorphological changes of the liver are demonstrated in 120 biopsy samples of 104 patients with clinically and serologically proven Bang's disease. A granulomatous hepatitis was found in 1/3 of the patients in addition to a non-specific mobilisation of the active mesenchyma and a reactive hepatitis of changing intensity. The nodules are not looking like tuberculous granulomas, but consist of a disseminated accumulation of small lympho-histiocytic cells. Furthermore, the relatively high percentage of steatosis of the parenchyma (50%), lipofuscinosis (40%), and circumscribed hepatocellular siderosis (26%) can be considered as important lesions of parenchymal cells.
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PMID:[Bioptic liver changes in brucellosis (author's transl)]. 56 93

The authors studied serum neopterin in 106 patients with beta thalassaemia major. A good correlation was found between neopterin values and glutamic pyruvic transaminase (GPT) mean values of the last 6 months, whereas no correlation was found between neopterin values and some siderosis indexes (iron/body weight, total accumulated iron). A statistically significant correlation was found between neopterin values (greater than 10 nM/L vs. less than 10 nM/L) and histological liver findings (chronic hepatitis vs. siderosis). Neopterin values were also statistically different between splenectomized and not splenectomized patients. Moreover serum neopterin was higher in HCV-Ab positive than in HCV-Ab negative patients, and 91.6% of the HCV-Ab positive group also showed histological signs of chronic hepatitis. These data suggest that increased serum neopterin might help to identify chronic C hepatitis in thalassaemic patients.
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PMID:Neopterin as a marker of C hepatitis in thalassaemia major. 164 87

Laminated iron concretions were noted in the liver of an aged siamang (Hylobates syndactylus) that had granulomatous enteritis and hepatitis due to Mycobacterium avium intracellulare infection. Preexisting hepatic siderosis, iron sequestration in macrophages, and compromised macrophage function due to mycobacterial infection are proposed as the basis for the abundance and size of the concretions. Similar siderophilic bodies and concomitant siderosis occurred in other siamangs. The concretions are similar to Schumann bodies and Michaelis-Gutmann bodies associated with granulomatous disease in other species.
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PMID:Siderophilic bodies associated with hemosiderosis and atypical mycobacterial infection in an island siamang (Hylobates syndactylus). 192 Mar 83

Three children of a mother with biopsy-confirmed posttransfusional hepatitis of undetermined etiology (non-A, non-B hepatitis) died in utero or in infancy. All had liver disease of intrauterine onset. The two liveborn children died of the consequences of severe hepatic insufficiency manifest at birth and met clinicopathologic criteria for neonatal hemochromatosis. Although hepatic architecture in the stillborn fetus was markedly disordered, with hepatocyte giant cell transformation, extrahepatic siderosis was not present and hepatic siderosis was minimal. These findings indicate that in some cases of neonatal hemochromatosis, extrahepatic siderosis may be caused by hepatic injury rather than primarily due to excessive transport of iron from mother to fetus and support speculation that in some instances an infective agent may be responsible.
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PMID:Fetal liver disease may precede extrahepatic siderosis in neonatal hemochromatosis. 211 Sep 17

131 patients thought to have diffuse liver disease underwent ultrasonography and percutaneous liver biopsy. The ultrasonographic criteria examined were hepatic echogenicity compared to that of the renal cortex, homogeneity of hepatic parenchyma, and regularity of hepatic outline. On the basis of histologic examination of liver biopsies, several groups of pathologic lesions (not diagnostic entities) were established. Evaluation of ultrasound and histology was double blind. When the lobular architecture of the liver was respected histologically (normal liver, granulomatosis, siderosis, hepatitis), the ultrasound was normal in 86% of cases. The sensitivity of ultrasound was 0.9 for detection of fatty liver and 0.6 for cirrhosis. An abnormal ultrasound predicted structural modifications or a fatty liver in 93% of cases. Ultrasound proved incapable of differentiating between fatty liver and cirrhosis.
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PMID:[The role of ultrasonography in the diagnosis of diffuse liver disease]. 351 4

Liver function has been evaluated in 74 patients (aged 9 months to 19 years) with beta-thalassemia major. They were selected from 212 patients because their transaminase levels were three times higher than normal for over three months. In 36 of these subjects BSF clearance test was performed. In the majority of patients (70%) average GPT serum values were increased (66.33 +/- 35.41 U/L) while only a few of the youngest age group exhibited normal values. The transaminase level showed a direct relationship with age, ferritin level and transfusional iron. Furthermore a direct correlation was found between iron and gamma globulin levels both being related to age. Test for viral hepatitis markers showed that 60% of all the subjects studied had had HBV infection. Twenty-six of the 36 patients who underwent BSF test had normal values in the first part of the clearance curve, 8 others showed moderate changes while only the 2 remaining revealed severe alterations. The second part of the curve was abnormal in 34 and markedly altered in 2 subjects. Mean GPT serum values correlated with the first part of BSF clearance curve and BSF 45' values correlated with transfused iron. Siderosis, fibrosis, chronic inflammatory infiltration and vacuolar degeneration were seen at liver biopsy. Histological findings of chronic aggressive hepatitis were shown in two patients with high transaminase and gammaglobulin levels who had markedly abnormal BSF curve.
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PMID:[Hepatic pathology in beta-thalassemia major]. 372 17

To evaluate the effective role of hepatitis viruses in thalassemic (Th) liver disease, we carried out a long-term study in 42 subjects with nontransfusion-dependent Th minor hospitalized for an episode of acute viral hepatitis. 10 patients had serologic evidence of hepatitis A, 23 of hepatitis B and 9 of hepatitis non-A, non-B. In the follow-up chronic hepatitis was detected histologically in 5/23 patients with hepatitis B and 5/9 with hepatitis non-A, non-B. All hepatitis A patients recovered completely. The prevalence in 7 out of 10 patients with chronic hepatitis of piecemeal necrosis and of inflammatory changes over hepatic siderosis and fibrosis evidenced a determinant role of chronic viral infection in the development of liver damage in these patients. Thus, heterozygous nontransfusion-dependent Th patients seem to have a high risk of developing a chronic inflammatory liver disease especially after an episode of non-A, non-B hepatitis. Therefore, in our geographical area, chronic hepatitis of viral origin should be taken into account, among other pathogenetic factors, in many cases of cryptogenic thalassemic liver disease.
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PMID:Chronic viral hepatitis in thalassemic liver disease. A long-term study in patients with acute hepatitis with nontransfusion-dependent thalassemia minor. 640 56

Serum ferritin, liver iron stores, and liver histology were studied in 38 children with thalassaemia major who were being treated by regular blood transfusions. There was no correlation between serum ferritin levels and either the number of transfusions or the amount of iron deposited in the liver. However, for a given level of iron stores, ferritin levels were higher in patients with chronic hepatitis (including chronic aggressive and chronic persistent forms) than in those with hepatic siderosis only. We conclude that serum ferritin reflects tissue iron deposits in regularly transfused thalassaemic patients, only in the absence of hepatitis.
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PMID:Serum ferritin, liver iron stores, and liver histology in children with thalassaemia. 737 16

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

We report the case of a 34-year-old woman with recurrent pure red cell aplasia and evidence of hepatitis B and C infection. Review of the English literature identified 19 prior cases in which pure red cell aplasia was associated with hepatitis. This case is the first in which serologic evidence of hepatitis C infection was documented. This patient also had porphyria cutanea tarda and marked hepatic siderosis but no active hepatitis or cirrhosis. Treatment with cyclophosphamide and prednisone produced complete remission of the pure red cell aplasia. Erythroid colony formation (colony-forming unit-erythroid and erythroid burst-forming unit) was reduced in cultures of bone marrow obtained during relapse but was normal in remission marrow. However, addition of the patient serum, whether collected during relapse or remission, inhibited erythroid colony formation by her bone marrow. These observations, and the known extrahepatic immunologic manifestations of hepatitis C infection, suggest that the pure red cell aplasia occurred because of autoimmune mechanism provoked by the infection.
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PMID:Pure red cell aplasia associated with hepatitis C infection. 925 13


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