A rare case of alpha-fetoprotein (AFP)-producing early gastric cancer with liver cirrhosis is presented. A 61-year-old man was admitted to Shimane Medical University Hospital in 1988 because of abnormal liver function test results suggestive of liver cirrhosis with mild elevation of AFP. Liver cirrhosis was confirmed laparoscopically and histologically. Gastric cancer was found in fluoroscopic and endoscopic studies. After partial gastrectomy, the serum AFP level fluctuated transiently within normal limits, and then gradually increased soon after the operation. Therefore, complication of hepatocellular carcinoma was suspected, but no tumor in the liver was detected by any imaging examination, including angiography. Two years after the operation, swelling of abdominal periaortic lymph nodes was noted at a periodic checkup, but still no hepatic tumor was found. At this point, AFP-producing gastric cancer was suspected, and an AFP staining test was carried out on the tissue of the resected specimen. AFP-positive cells were recognized immunohistochemically. Thus, we diagnosed the condition as post-operative recurrence of an AFP-producing gastric cancer accompanying liver cirrhosis.

Scanning electron microscopy of a liver biopsy specimen from a patient 6 months after the onset of acute hepatitis revealed a normal appearing bile ductule. The bile ductule was 13 micron in outer diameter and 1.5-2.7 micron in inner diameter. The ductular lumen was surrounded by two ductular cells and ampullary dilated at the canalicular side. In the lumen, intracytoplasmic diverticles were observed with an orifice diameter of 0.9 micron. About 15 microvilli 0.4-0.6 micron in length and 0.1 micron in thickness were observed on 1 micron2 of luminal surface. The number of microvilli was calculated to be approximately 1,500 per ductular cell. A single cilium 0.15 micron in diameter at the base and 0.10 micron at the trunk, and 7-15 micron in length was found on each ductular cell. The cilium arose from a recess at the canalicular side of the ductular cell, and the free-end was on the bile-duct side. The cilia seemed to play an important role in bile flow to the duct. Sometimes between the ductular cells at the edge of the basal portion a cell was intercalated with thin processes. Such thin processes were not observed on ductular cells.

Kupffer cells were observed in liver biopsy tissues of 9 cases of liver diseases by scanning electron microscopy to prove Kupffer cell proliferation numerically. Kupffer cell count per 0.01 mm2 of cracked surface of liver lobule was 1.2 +/- 0.3 in the convalescent stage of a mild acute hepatitis case and 1.2 +/- 0.1 in a chronic persistent hepatitis case with slight inflammation. Whereas it was increased to 2.4-5.5 (P less than 0.01) in the convalescent stage of moderate to severe acute hepatitis cases, 1.8 +/- 0.1 (p less than 0.05) in a chronic active hepatitis case, 2.5 +/- 0.3 (p less than 0.001) in an alcoholic portal fibrosis case and 2.2 +/- 0.4 (p less than 0.001) in a liver cirrhosis case. Kupffer cell count per mm3 of liver lobule was estimated roughly 3,500 in the convalescent stage of a mild acute hepatitis case and in a mild chronic persistent hepatitis case and 7,000 to 16,000 in the convalescent stage of moderate to severe acute hepatitis cases.

Peritoneoscopy as an aid in intravenous injection of indocyanine green (ICG) was clinically evaluated. Hepatic parenchyma was stained after intravenous injection of ICG, while interstitial connective tissue, fatty deposition and hepatoma tissue were not. Regenerative hepatic cell mass including dark reddish patchy marking (Shimada's code No. 7) and semispherical areas of regeneration or nodules (Shimada's code No. 8) was well stained and clearly contrasted. There were some cases of chronic active hepatitis, in which liver surface showed spotty staining at sites expected to become regenerative nodules in the future, in contrast to being judged as "no abnormal findings" peritoneoscopically. On the other hand, periportal reddish marking (Shimada's code No. 4) representing piecemeal or bridging hepatic cell necrosis was not stained.

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