Takeo Madarame

Plasma abnormal prothrombin (PIVKA‐π): A new and reliable marker for the detection of hepatocellular carcinoma

We evaluated the clinical usefulness of a protein induced by vitamin K absence, antagonist‐prothrombin (PIVKA‐π), in detecting hepatocellular carcinoma (HCC) specifically in patients with liver cirrhosis, and the possible correlation between levels of PIVKA‐π and pathological features of HCC. Plasma levels of PIVKA‐π and α‐fetoprotein (AFP) were measured in 628 patients with various diseases, including 253 with liver cirrhosis and 116 with HCC. PIVKA‐π was detected (≥ 0.1 arbitrary unit/mL) in 54.3% of HCC and the concentration showed a positive correlation with the tumour size. As a screening test for the detection of HCC, PIVKA‐π produced values comparable with those of AFP with a sensitivity, specificity and validity of 52.8, 98.8 and 51.6% respectively. Sixteen of 45 patients (37%) with HCC who had low AFP (< 100 ng/mL) levels were positive for PIVKA‐π. No apparent relationship, however, could be found between the levels of PIVKA‐π and the aetiology or pathological findings of HCC. These results suggest that PIVKA‐π can be a reliable marker for detecting HCC in patients with liver cirrhosis.

Reduced cholecystokinin in the brain of LEC rats with hepatic encephalopathy

Levels of cholecystokinin (CCK) immunoreactivity and distribution of CCK immunoreactive cells were studied in the cerebral cortex of LEC (Long Evans Cinnamon) rats with hepatic encephalopathy. CCK immunoreactivity in water extract of cerebral cortex of LEC rats with hepatic encephalopathy (n = 7) was 41.5 +/- 2.6 (mean +/- S.E.M. pmol/g wet wt.) and that of LEC rats without encephalopathy (n = 8) was 67.1 +/- 6.9, the difference being significant (P less than 0.01). CCK immunoreactive cells assessed by immunohistochemistry were also markedly decreased in the cortex of LEC rats with hepatic encephalopathy of stage IV. Thus, CCK reduction was observed in the cerebral cortex of LEC rats with hepatic encephalopathy which are provided as a model for analysis of the pathogenesis of acute hepatic encephalopathy.

Decreased numbers of cholecystokinin-immunoreactive nerve cells in the cerebral cortex of LEC rats with a hereditary hepatitis.

The distribution of CCK-immunoreactive cells was investigated by the indirect fluorescence method in the cerebral cortex of LEC (Long-Evans Cinnamon) rats which have recently been introduced as a model of jaundice and hepatic encephalopathy. Reduction of CCK-immunoreactive nerve cells was observed in the brains of LEC rats with stage III to V hepatic encephalopathy in comparison with the rats without hepatic encephalopathy. These observations were confirmed by counting the CCK-positive nerve cells at magnification x 125. 3 microscopic fields per animal were immunostained and CCK-immunoreactive nerve cells counted. The number of CCK-immunoreactive cells per field was 28.5 +/- 0.7 (mean +/- SEM, n = 5) in rats without hepatic encephalopathy, and 14.1 +/- 2.0 (n = 3) in rats with stage III to V hepatic encephalopathy. Thus, the number of CCK-immunoreactive nerve cells was significantly less in rats with stage III to V hepatic encephalopathy (p less than 0.05). A decrease in CCK-immunoreactive nerve cells was not observed in the rats with stage I or II hepatic encephalopathy. This study shows that there is a relationship between the severity of hepatic encephalopathy and the number of CCK-immunoreactive nerve cells in the cerebral cortex.

Two cases of severe hepatitis B by familial transmission.

HBe抗体陽性キャリア妊婦から垂直感染し出生50日目に出生児が急性B型肝炎を発症し,さらに患児の発症から92日目に父親がB型劇症肝炎を発症し救命しえた家族内感染例を経験した.患児は発熱・哺乳力の低下で発症.GOT 11,380U, GPT 5,060Uと上昇しプロトンビン時間(PT)10%と著明な低下を示した.HBs-Ag陽性,anti HBc (200倍)74%であった.総ビリルビン(T. Bil)が漸増し32mg/dlとなり凝固能の改善がないため,プレドニゾロンを使用したところ改善し,急性肝炎重症型と考えられた.父親は嘔気・全身倦怠感で発症.T. Bil 14.7mg/dl, GOT 1,675U, GPT 4,690U, PT12%, HBsAg陽性,IgMHBc3.29と陽性.昏睡II度となりプレドニゾロン,グルカゴン-インスリン療法,特殊組成アミノ酸などの治療にて改善した.母親から出生児に垂直感染し,患児から父親に水平感染したと思われる.HBe抗体陽性キャリア妊婦からの出生児に対してもHBIGなどの対策が必要と考えられる症例である.