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

The histopathology of acute and chronic infections associated with viral hepatitis is reviewed and illustrated. Particular attention is directed to changes that help to differentiate chronic persistent from chronic active viral hepatitis. Features that help to identify the intravenous drug abuser who has hepatitis, whether acute or chronic, include the presence of particulate birefringent material (usually talc) in reticuloendothelial cells, as well as tissue eosinophilia. Ground-glass hepatocytes are characteristic of the HBAg carrier. They may be present in chronic persistent and chronic active hepatitis and in cirrhotic livers with or without hepatocellular carcinoma. Ground-glass cells which contain the surface component of the HBAg, can be stained specifically by a number of stains that include aldehyde fuchsin and orcein. The cirrhotic liver of the HBAg-seropositive patient may show liver-cell dysplasia, a premalignant change.
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PMID:Light microscopic morphology of viral hepatitis. 80 46

Tetracyclines are active in vitro against most urinary tract pathogens, Chlamydia, Mycoplasma pneumoniae, Brucella, rickettsiae, and Nocardia. Chloramphenicol is used primarily for anaerobic infections, Haemophilus influenzae meningitis, and infections due to Salmonella typhi. Erythromycin is active in vitro against M. pneumoniae, Streptococcus pneumoniae, and group A beta-hemolytic streptococci. Erythromycin may be used as prophylactic therapy for subacute bacterial endocarditis and for recurrence of acute rheumatic fever in patients who are allergic to penicillin. Clindamycin should be used only for the treatment of anaerobic infections. Tetracycline may cause gastrointestinal upset; phototoxic dermatitis; hepatitis, especially in pregnant females; discoloration of teeth and bone dysplasia in the human fetus and children; and suprainfections, especially oral and anogenital candidiasis. Tetracycline should be used with caution in patients with renal insufficiency. The most important toxic effect of chloramphenicol is bone marrow suppression, which is dose related and idiosyncratic. The incidence of undesirable side effects associated with the use of erythromycin is low. Gastrointestinal irritation is the most common; cholestatic hepatitis may occur with erythromycin estolate. Pseudomembranous colitis is the most important toxic effect associated with clindamycin.
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PMID:Tetracyclines, chloramphenicol, erythromycin, and clindamycin. 90 15

The authors applied a silver colloid technique to identify Argyrophilic Organiser Region (AgNOR) to 8 groups of hepatic lesions: alcoholic hepatitis with dysplasia (3 cases); chronic active hepatitis with dysplasia (4 cases); cirrhosis with dysplasia (5 cases); focal nodular hyperplasia (4 cases) and hepatocellular carcinomas (3 cases of grade I, 3 cases of grade II and 5 cases of grade III of Edmondson). Four cases of non-specific reactive hepatitis were used as control. This work suggests the simplicity and utility of simultaneous application of clumps per cell, AgNORs per clump and total AgNORs counts in the evaluation of neoplastic and preneoplastic lesions of the liver. The results show, in hepatocellular carcinomas, a relationship between the number of clumps, the AgNORs per clump, the total number of AgNORs and the grading of Edmondson. The nodular lesions that can be considered in the differential diagnosis with carcinoma are sufficiently well discriminated using the two parameters AgNORs per clump and total number of AgNORs.
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PMID:Hepatocellular carcinoma and preneoplastic lesions of the liver: evaluation of argyrophilic nucleolar organizer regions (AgNORs). 133 18

We reviewed the laboratory parameters, clinical information including presence or absence of stool pigmentation, and ultrasonographic findings in 67 patients with neonatal conjugated hyperbilirubinemia and liver biopsies. Hepatobiliary nuclear scintigraphy was done in 14 of the patients. Final diagnoses included extrahepatic biliary atresia, neonatal hepatitis, cystic fibrosis, metabolic liver disease, alpha 1-antitrypsin deficiency, bile duct stenosis, Alagille syndrome (arteriohepatic dysplasia), choledochal cyst, panhypopituitarism, and miscellaneous causes of intrahepatic cholestasis. A single diagnostic criterion is insufficient to distinguish the various causes of neonatal jaundice. Clinical laboratory values varied widely among patients with medical and surgical causes of jaundice. Absence of stool pigmentation was not specific for biliary atresia and was found in patients with medical causes of jaundice. Conversely, two patients with biliary atresia had pigmented stools at presentation. Ultrasonography was diagnostic only for choledochal cyst and bile duct stenosis. Nonvisualization of the gallbladder by either ultrasonography or nuclear hepatobiliary scintigraphy was nonspecific in the discrimination of medical from surgical causes of jaundice. A multidisciplinary approach to the evaluation of neonatal jaundice is necessary, since no single test or imaging modality can reliably define the cause in all cases.
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PMID:Neonatal jaundice: clinical and ultrasonographic findings. 218 86

To characterize type and age distribution of malnutrition and to determine the usefulness of anthropometric indices in children with chronic liver disease (CLD), 56 children (aged 1 mo-10 y) with CLD underwent anthropometric evaluation when they were clinically stable. Mean-height Z score was depressed, whereas mean-weight Z score was closer to normal and mean-weight/height Z score was normal in patients with extrahepatic biliary atresia, idiopathic neonatal hepatitis, and other liver disorders. Patients with arteriohepatic dysplasia showed more severe depression of all three variables. In all patients, triceps skinfold (TSF) thickness Z scores were significantly more depressed than were weight/height Z scores. Depressions of midarm-circumference and midarm-muscle-area Z scores were intermediate. Mean-head-circumference Z score was depressed in children aged less than 24 mo. We conclude that acute (wasting) and chronic (stunting) malnutrition are common in childhood CLD and that weight/height values underestimate the degree of acute malnutrition compared with TSF thickness, most likely because of the inflated patient weight caused by organomegaly.
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PMID:Anthropometric evaluation of children with chronic liver disease. 237 85

Data provided by 51 voluntary blood donors identified as asymptomatic HBsAg carriers five to ten years (mean = 7.5 years) before their inclusion in the study are analysed towards their long-term evolution. HBsAg clearance was estimated 2.5% yearly and 83.9% of those remaining positive showed the classical non-replicative serological pattern; another 12.9% were negative for both HBeAg-Anti HBe (seroconversion window?), one of them presenting raised ASAT-ALAT levels and enhanced histological activity (lobular chronic hepatitis). Neither alpha-fetoprotein seric levels (RIA) nor liver ultrasonography demonstrated hepatocellular carcinoma suspicion signs in 35 HBsAg positive cases to this methods; ASAT-ALAT levels raised over two fold the normal superior limit in only 11.4%, and neither aggressive chronic liver disease nor hepatocyte dysplasia was showed in 17 biopsied cases (70.6% normal; 23.6% chronic reactive or chronic persistent hepatitis; 5.8% chronic lobular hepatitis). One out of five patients biopsied with a seven years interval showed histologic worsening.
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PMID:[Long-term course in asymptomatic carriers of HBsAg in an area of low prevalence of hepatocarcinoma]. 248 74

We reviewed 40 liver biopsy specimens from 36 patients with non-A, non-B (NANB) hepatitis by light microscopy to characterize the histopathologic features associated with this condition. NANB hepatitis had been acquired from intravenous drug use (6 patients), transfusion (11 patients), sporadic (13 patients), and other routes (6 patients). The major pathologic diagnoses included acute hepatitis, chronic persistent hepatitis, chronic lobular hepatitis, chronic active hepatitis with or without cirrhosis, and hepatocellular carcinoma. Histopathologic changes seen in varied combinations in these specimens included acidophilic degeneration of hepatocytes (100%), fat (85%), formation of portal tract lymphoid aggregates or follicles (52%), bile duct damage (30%), and multinucleate giant hepatocytes (25%). Prominence of sinusoidal cells was variable, but often striking. Hepatocyte atypia (liver cell dysplasia) was noted in 17 specimens. These histologic parameters appear to be diagnostically useful when applied in appropriate clinical settings and will require reevaluation when serologic tests for NANB hepatitis become available.
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PMID:Non-A, non-B hepatitis: characterization of liver biopsy pathology. 250 Apr 77

A total of 123 patients with neonatal liver disease without extrahepatic bile duct obstruction or arteriohepatic dysplasia have been studied for six to 18 years. Idiopathic neonatal hepatitis, present in 73 babies, carried a high mortality due to liver failure (18%), septicaemia (6%), and associated defects (14%), especially in the first year of life (25%). Progression to chronic liver disease in non-familial idiopathic cases occurred in three of 40 reviewed patients. Only 12 of these children were completely healthy, the remainder having other permanent disabilities (57%). Four of nine familial cases of idiopathic neonatal hepatitis died in the first 12 months of life as did two of the four reviewed survivors. Progression to chronic liver disease or to death was a continuous process without any interval of recovery in all but one of these patients. Among patients with a presumed infective cause, cytomegalovirus infection caused a particularly benign form of neonatal hepatitis but was a frequent cause of brain damage or other disabilities. Babies who survived other infective liver diseases showed complete healing of the liver damage. Neonatal liver disease associated with alpha 1 antitrypsin deficiency progressed to death or chronic liver disease in three of nine patients and was not associated with a paucity of interlobular bile ducts.
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PMID:Long term prognosis for babies with neonatal liver disease. 299 Mar 56

Liver cell dysplasia (LCD) is a premalignant cytologic change of hepatocytes that has been statistically linked to cirrhosis, hepatocellular carcinoma (HCC), and chronic liver disease related to hepatitis B virus. The relationship of LCD to non-A, non-B (NANB) hepatitis is currently unknown. We studied liver biopsy and surgical resection specimens from 36 patients with NANB hepatitis, and identified LCD in 17 (42.5%) of 40 specimens, most often associated with cirrhosis. Dysplasia was present in individual hepatocytes, in clusters, and in a distinctive "spreading" pattern of hepatocytes about central veins. Three patients had HCC with a predominant giant cell pattern, as well as LCD. These findings suggest that LCD and HCC should be included among the potential pathologic sequelae of NANB hepatitis.
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PMID:Liver cell dysplasia and hepatocellular carcinoma in non-A, non-B hepatitis. 302 14

To the best of our knowledge this is the reported first case of the successive occurrence in the same patient of chronic active hepatitis and acquired pure red cell aplasia, both probably of autoimmune origin. The diagnosis of autoimmune hepatitis was based on the presence of characteristic lesions at the examination of the liver biopsy specimen, high titer of anti-smooth muscle antibodies in the serum, and remission obtained by steroid therapy. Erythroid aplasia, which appeared during the course of this treatment, was revealed by a regenerative anemia (4.4 g Hb/100 ml) and proved by bone marrow aspiration and biopsy. In vitro bone marrow culture was normal, suggesting the in vivo presence of an inhibitor of erythroblastic differentiation. Red cell aplasia was cured by cyclophosphamide (100 mg/day during 56 days). No recurrence was noted until the death of the patient, which occurred one year later, due to hepatic cholangiocarcinoma. Action of cyclophosphamide on the pure red cell aplasia suggested the immune origin of this disease. The liver and the bone marrow erythroid lineage have probably been the successive targets of immunologic dyscrasia.
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PMID:[Association of autoimmune chronic active hepatitis and acquired erythroblastopenia cured by cyclophosphamide]. 310 Mar 75


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