[Herpes simplex virus encephalitis: report of 3 cases, and possibilities of early diagnosis].
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Biomedical subjects
Publications and source records attributed to T Higashi.
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Three cases of aneurysms of the anterior inferior cerebellar artery are reported. Two of the aneurysms were located in the cerebellopontine angle and one in the ventral portion of the pons. Through a suboccipital craniectomy, beck clipping was performed on one aneurysm, neck ligation on another, and coating on the third. A discussion of the surgical procedures and complications includes a review of previous reports.
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Generally, it is reported that the smallest tumor that can be detected with the 67Ga scintigram is limited to a diameter of approximately 3.0 cm. To surmount that limitation we have attempted to detect small lung cancer by means of quantitative external counting of 67Ga uptake rather than the qualitative scintigram. Seventy-two hours after 67Ga injection, the uptake counts of tumor (T) and a corresponding normal region in the opposite lung (N) were measured with scintillation camera. The 67Ga uptake ratio ((T-N)/N) could then be calculated. The 67Ga uptake ratio of 6 pulmonary adenocarcinomas was measured to be 0.05-0.22. In contrast, the 67Ga uptake ratio of benign lesions such as tuberculoma, pulmonary infarct, cyst, pneumoconiosis, mucoid impaction, hamartoma and chronic inflammatory lesion with calcification resulted in negative values (-0.01--0.77). From these results, it was possible to differentiated small adenocarcinoma of the lung tumor from these benign diseases. However, the 67Ga uptake ratios of 4 cases of active tuberculosis, 5 chronic inflammatory lesions and 1 granuloma were 0.01-0.41. The cases with more than 0.30 of 67Ga uptake ratios all represented active inflammatory lesions. However, there were some cases of inflammatory lesions where the values overlapped with adenocarcinoma.
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In 24 patients with and without cirrhosis of the liver, portal vein pressure was measured prior to and after hepatic resections of various magnitudes. In 6 patients who underwent resection of less than 20% of the liver portal pressure did not change although all patients had associated cirrhosis. On the other hand, a substantial rise in portal pressure was found in 17 of 18 patients who had resection of more than 30% of the liver irrespective of the presence or absence of cirrhosis. No significant difference was observed between the degree of portal pressure rise and the magnitude of hepatic resection. Also, there was no difference in the increase in portal pressure between the patients with and without cirrhosis of the liver. The present study may indicate that splanchnic sequestration associated with acute portal hypertension frequently occurs even in humans after resection of 30% or more of the liver even if the remaining liver is normal and anatomical dissection has been employed. Appropriate intra- and postoperative management is necessary to combat this difficult condition.
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Serum methionine levels increased to a greater extent in patients with severe liver diseases such as fulminant hepatitis and liver cirrhosis with and without hepatic encephalopathy. However, the concentrations remained unchanged in non-encephalopathic cirrhotic cases associated with hepatocellular carcinoma, and their serum methionine levels increased only moderately even at the time of encephalopathy. At least two different mechanisms of serum methionine elevations, possibly due to release from injured hepatocytes or diminished catabolisms of this amino acid in the damaged liver, could be differentiated; the former would be involved mainly in fulminant hepatitis and the latter in liver cirrhosis. A methionine-loading test performed in cirrhotic patients supported the validity of these considerations. No significant increase of serum methionine levels in cirrhotic patients with hepatocellular carcinoma was observed, possibly by remarkable consumption of this amino acid in hepatoma tissues. During the clinical course of several patients, serial determinations of serum methionine concentrations indicated that the levels varied depending upon alterations in the pathophysiological state of the damaged liver; much higher levels were observed concomitantly with decompensated signs such as ascites, jaundice and hepatic encephalopathy. These results suggest that monitoring of serum methionine levels would be very valuable, especially for judging prognosis and predicting hepatic encephalopathy in severe liver disease.
Hepatic encephalopathy in patients with severe liver disease was associated with marked elevation of either serum methionine or blood ammonia levels or with simultaneous moderate increases in both parameters. CSF methionine levels also increased in encephalopathic patients with fulminant hepatitis and liver cirrhosis. Increased influx of methionine into the brain over the theoretical values predicted from Pardridge's equation suggested that accelerated transport of serum methionine across the blood-brain barrier was observed in these cases with hepatic encephalopathy. Hepatic encephalopathy in acute carbon tetrachloride liver injury could be obtained experimentally following intraperitoneal injection of ammonium acetate in rats, which already received intragastric administration of methionine. However, similar encephalopathy could not be observed by the administration of glycine or leucine in place of methionine. These results suggest at least that methionine and ammonia act synergistically on inducing hepatic encephalopathy.
Insulin and glucagon concentrations in the peripheral and portal circulation were comparatively determined during 48 hours following partial hepatectomy and hepatotoxin treatment. Insulin and glucagon levels both in the peripheral and portal blood increased 24 hours after carbon tetrachloride (CCl4) and D-galactosamine administrations, when nearly maximum degree of liver injury has been occurred. Thereafter glucagon continued to rise further, but insulin diminished sharply at the 48th hour of the hepatotoxin treatment. In partially hepatectomized rats, glucagon levels both in the peripheral and portal blood increased to a greater extent but insulin only in the portal circulation slightly elevated. The liver under repaired process of acute CCl4 and galactosamine liver injuries can not uptake glucagon from the portal blood, but the regenerating liver following partial hepatectomy showed the increased uptake of glucagon as well as insulin. Different behaviors of glucagon uptake by the liver under these experimental conditions may support our previous observations that repair process of liver injury is pathophysiologically different from liver regeneration following partial hepatectomy.
Serum amino acid patterns in patients with different types of hepatic encephalopathy were investigated. Marked elevations in most of serum amino acids observed in untreated patients with acute type of fulminant hepatitis were not remarkable in the patients who have already treated; particularly branched chain amino acids (BCAA), phenylalanine and tyrosine were much lower in the latter group. However, elevation of serum methionine levels and lower ratio of BCAA/(phenylalanine + tyrosine) were similarly observed in both groups. In encephalopathic patients with decompensated cirrhosis, many amino acids such as phenylalanine, tyrosine and methionine were elevated with a slight depressed levels of serum BCAA. Highly significant decrease in serum BCAA levels and no elevation of phenylalanine and methionine with a minimal increase of tyrosine were observed in patients with chronic type of hepatic encephalopathy; other amino acids except for glutamine and arginine were much lower as compared to those in decompensated cirrhotics and even to the control values.
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