S-Space College of Medicine/School of Medicine (의과대학/대학원) Dept. of Medicine (의학과) The Seoul Journal of Medicine The Seoul Journal of Medicine Vol. 01 No.2 (1960)
유행성 Virus간염의 임상상과 간침생검 조직상에 관한 연구 제2편 급성기의 간침생검 조직선에 관한 연구
STUDIES ON CLINICAL, LABORATORY AND HISTOLOGICAL FINDINGS OF' LIVER BIOPSY IN EPIDEMIC VIRAL HEPATITIS Part II Studies on Histological Findings of Needle Biopsy in Acute Phase
- Issue Date
- 서울대학교 의과대학
- Seoul J Med, Vol.1 No.2, pp. 29-48
- This studies of infectious hepatitis in inpatients
of the Korean Army cover period of four and half
years. between April. 1956 to Sept.. 1960. Serial
biopsies have been done at appropriate intervals
on 98 out of 143 patients during the acute stage
of the 12 weeks after the onset of jaundice. Single
bIOpsIes were performed on the remaining 45 cases.
Incidence of the histological changes. pathogenesis.
histological course and final outcome were
studied. The histological picture of hepatitis was
compared with the histologic picture of several
groups of diseases which produce hepatic damage.
Following results were obtained:
1. Bile stasis was noted in the early stages
when serum bilirubin was elevated. the stasis was
more prominent in the fading stages of jaundice
Furthermore an appearance of bile plugs was
increased in number during fading stages of
2. As the intensity of jaundice increased. the
storage of cytoplasmic glycogen decreased. The
storage of cytoplasmic glycogen rose again after
recovery from jaundice.
3. The peak of inbibition of lipofuscin pigments in liver cells and Kupffer cells was in 4th week
after the onset of jaundice. As liver cell necrosis
increased, more lipofuscin pigment inbibition was
4. Eosinophilic bodies were frequently observed
during a month after the onset of jaundice, and
during the period, they were seen in a half of the
total cases, Ballooning cells were also prominent
in this period.
5. Single cell necrosis were peculiar, .and they
were seen within 4 weeks after the onset of jaundice.
Although the necrosis was noted in the central
zone of a lobule in νthe lst,week after the onset
of jaundice, it became more extensive in the .4th
week. Necrosis in peripheral zones were marked
in early stages, and the peak was in the 2nd week
after the onset of jaundice. Only 2 cases of massive
necrosIs were seen.
6. Mitosis appeared as regenerative phenomena
in early part of the 2nd week after the onset of
jaundice, multinucleated giant liver cells were noted
in the early stages, and multinucleated small liver
cells were noted in the later stages.
7. Kupffer cell proliferation was most striking
during 2nd and 4th week after the onset of jaundice,
and was noted in more than 80% of cases.
8. Inflammatory cellular infiltrations around
portal area were chiefly composed of monocytes in
the early stages, and lymphocytes in the later stages
with an occasional eosinophils and neutrophils.
The above picture were prominently observed
within one month after the onset of jaundice, and
chronic inflammatory mononuclear cells were
persistently observed in 77% out of the total cases
as late as 3 months after the onset of jaundice.
9. The pictures of bile duct proliferation chiefly
around the portal area were seen in later stages,
and these pictures persisted in over 60% of cases
2 to 3 months after the onset of jaundice.
10. Fibrosis after hepatitis took place chiefly
around the portal area, and its incidence of 11.1%
noted in the 1st week after the onset of jaundice,
increasing to 70.1% in the 12th week after the onset
of jaundice. Post-hepatitic fibrosis was a striking
part of the picture.
11. Serial histologic examination revealed that at
least 7 weeks were required for complete recovery
of severely damaged tissue. However, there was
one incidence in which 8 weeks elapsed from severe
state to moderate state showing no further recovery.
12. Histologic comparison was carried out with
44 liver biopsy specimens from patients suffering
with the following diseases; liver distosomiasls,
pulmonary tuberculosis, lobar pneumococcal pneumonia
, right sided hemothorax, post-typhoid
cholecystitis, passive cardiac congestion of liver,
acute bacterial hepatitis, acute cholecystitis and
chronic amebic colitis.