Liver disease—Morphologic considerations

Pópper, Hans

doi:10.1016/0002-9343(54)90326-5

Cited by 39 publications

(8 citation statements)

References 65 publications

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“…Most patients whose serum bilirubin levels peaked earlier had mild jaundice while those in whom bilirubin levels peaked later tended to have higher levels (table 2). PREOPERATIVE (18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34) /xmolll (1-1-2-0 mg/100 ml)) in patients developing postoperative jaundice. Table 5 shows the postoperative features of patients with and without postoperative jaundice.…”

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confidence: 99%

Jaundice after open heart surgery: a prospective study.

Chu¹,

Chen²,

Liaw³

et al. 1984

Thorax

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One hundred and fifty four consecutive adult patients having cardiac surgery for a variety of cardiac lesions were evaluated prospectively for postoperative jaundice, those with a raised preoperative serum bilirubin concentration (greater than 34 ,mol/I or 2 mg/100 ml) being excluded. The incidence of early postoperative jaundice, as defined by a serum bilirubin concentration of 50 ,umoUl (3.0 mg/100 ml) or greater, was 23*4%. The jaundice was mild (bilirubin concentration 51-100 ,umoll (3-.06.0 mg/100 ml)) in 26 patients (16.9%) and moderate to severe (greater than 100 ,umol/I (6.0 mg/100 ml)) in 10 patients (6-5%). Important contributing factors were the preoperative severity of right heart failure (raised right atrial 'pressure at heart catheterisation) and hypotension or hypoxaemia and the amount of blood transfused during or shortly after surgery. Age, sex, underlying cardiac lesion, whether halothane was used, operative procedure, duration of cardiopulmonary bypass, and presence or absence of hepatitis B surface antigen were not predictive of postoperative jaundice.It has long been recognised that transient jaundice could appear after a surgical procedure' and that hepatic damage is particularly liable to follow cardiopulmonary bypass.23 In one retrospective study early jaundice was seen in 13% of 232 patients undergoing open heart operations.4 In a similar study 8.6% of 736 patients undergoing open heart surgery developed postoperative jaundice.5 There have, however, been only a few prospective inquiries into the incidence and causes of postoperative jaundice. The prospective study of Evans et a16 revealed a much higher incidence (21%) of postoperative jaundice in patients having major noncardiac operations. The true incidence of early jaundice after open heart surgery is therefore still unclear and awaits further study.Furthermore, all studies on jaundice after open heart surgery were reported more than 10 years ago, when the medical care of patients undergoing open heart surgery was not as good as today, and when the hepatitis B surface antigen (HBsAg) was not recognised.7 HBsAg carriers are now known to harbour various liver lesions,8 which might contribute to the development of postoperative jaundice.9 It seemed therefore pertinent to investigate this prob-

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confidence: 99%

Jaundice after open heart surgery: a prospective study.

Chu¹,

Chen²,

Liaw³

et al. 1984

Thorax

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“…By contrast, DF is not a feature of 'secondary' liver disease, for example metastatic carcinoma. In this circumstance, employing accepted criteria (Popper, 1954), convincing histological evidence ofliver cell regeneration, adjacent to the metastases, was not detected in a survey of postmortem material from 15 patients who had secondary carcinoma in the liver. Indeed, the dominant features in those hepatocytes adjacent to the expansile tumour deposit appeared to be degenerative in nature.…”

Section: Discussionmentioning

confidence: 90%

Dysfibrinogenaemia and liver cell growth.

Barr¹,

Allardyce²,

Brunt³

et al. 1978

J Clin Pathol

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“…Since the introduction of liver biopsy, the architectural distortion of the liver lobule has been discussed in terms of the progression of chronic hepatitis (CH) to liver cirrhosis (LC) . Its histological hallmarks involve fibrosis, such as periportal fibrosis, or fibrous septa or bridging fibrosis (BF), which are used in semiquantitative scoring systems for CH .…”

Section: Introductionmentioning

confidence: 99%

“…S INCE THE INTRODUCTION of liver biopsy, the architectural distortion of the liver lobule has been discussed in terms of the progression of chronic hepatitis (CH) to liver cirrhosis (LC). [1][2][3] Its histological hallmarks involve fibrosis, such as periportal fibrosis, or fibrous septa or bridging fibrosis (BF), which are used in semiquantitative scoring systems for CH. [4][5][6][7] We previously reported that the lobular angioarchitecture, which provides the basic framework of the lobule, showed various pathological changes at different foci, which were closely related to lobular architectural distortion in a case with CH.…”

Section: Introductionmentioning

confidence: 99%

Histological reassessment of the role of bridging fibrosis in the angioarchitectural features associated with lobular distortion of the liver in chronic viral hepatitis

Hano

Takasaki

Endo

et al. 2015

Hepatology Research

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Aim:To reassess the role of bridging fibrosis in the lobular distortion of the liver from an angioarchitectural aspect.Methods: Two tissue samples obtained from surgically resected livers with chronic hepatitis and one obtained from an autopsy case with chronic hepatitis were used for the threedimensional observation of angioarchitecture by histological reconstruction.Results: Samples showed bridging fibrosis with various degrees of severity, without cirrhotic changes. Two different types of portal-portal bridging fibrosis were found. In our samples, the type that developed in the bifurcation region of the portal tracts was more common than the type observed between the distal portions originating from different parent portal tracts. The angioarchitecture tended to be generally maintained in these lesions. Concerning portal-central bridging fibrosis, two types were observed. One type developed in the lesion with partial paucity of the third-step portal branches in the portal tract at a relatively early stage of chronic hepatitis. The other type developed in an advanced lesion with a complete loss of the normal angioarchitecture of the parenchymal portion of the portal veins. The former was likely developed after largescale necrosis, such as bridging necrosis, while the latter was presumed to be attributable to portal vein damage associated with long standing chronic inflammation. Conclusion:As has been previously noted regarding lobular angioarchitecture, portal-central bridging fibrosis clearly affects the lobular structure of the liver more than portal-portal bridging fibrosis. Therefore, portal vein damage may be a critical event in the eventual distortion of the lobular structure.

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Liver disease—Morphologic considerations

Cited by 39 publications

References 65 publications

Jaundice after open heart surgery: a prospective study.

Jaundice after open heart surgery: a prospective study.

Dysfibrinogenaemia and liver cell growth.

Histological reassessment of the role of bridging fibrosis in the angioarchitectural features associated with lobular distortion of the liver in chronic viral hepatitis

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