[Diagnosis of hepatocellular carcinoma using tumor Doppler signals].
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Biomedical subjects
Publications and source records attributed to N Ban.
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A case of liver cirrhosis with large portacaval shunt from the superior mesenteric vein is reported. The portal blood flow was diagnosed as reversed on admission, but normalized with treatment. Blood flow was measured noninvasively and repeatedly using an ultrasonic Doppler duplex system. The reversed portal flow led to the superior mesenteric vein, right (and some left) internal inguinal vein, and inferior vena cava. This rare collateral pathway was clearly demonstrated by percutaneous transhepatic portalgraphy. A link between shunt and an appendectomy carried out 22 yr ago is considered, and the possibility of the temporarily reversed portal blood flow on admission being due to deteriorated hepatic hemodynamic conditions is discussed.
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The portal hemodynamics were studied in ten patients with portal hypertension, including three patients who had interposition mesocaval shunt (IMCS), three patients who had distal splenorenal shunt (DSRS), one patient who had gastrocaval shunt (GCS), and three patients who had splenectomy. Portal blood flow was measured by an ultrasonic Doppler duplex system, and portal venous pressure was measured by portal catheterization before, during, and after operation. The portal blood flow, and especially the splenic venous blood flow, was less during operation than before operation. Blood flow through the IMCS was greater than that through the DSRS, and the shunt flow had a tendency to increase after operation. The portal venous pressure measured during operation was slightly higher than that measured percutaneously before operation. In the patients who had the shunt operation, the portal venous pressure tended to decrease after operation. Study of portal hemodynamics, especially with the ultrasonic Doppler method, is useful in analysis and follow-up of patients who have shunt operations since the same method can be used before, during, and after operation.
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In order to clarify the natural transmission route of human T-cell leukemia virus type I (HTLV-I) from mother to child, we have followed two groups of children with ages of 1 to 3 years who were nourished either with HTLV-I-infected breast milk, or with non-infected milk from sero-positive, HTLV-I carrier mothers. Tests for the presence of antibody against HTLV-I revealed that 4 of 6 children in the former group developed HTLV-I infection, while only 1 of 14 children in the latter group became infected. The difference in HTLV-I infection rate for the children in the two groups was statistically significant (P less than 0.01 by chi-square). Furthermore, 2 of 4 elder siblings in the former group developed HTLV-I infection, whereas only one of 8 elder siblings in the latter group became infected. The overall rate of HTLV-I infection of breast-fed children born to HTLV-I-carrier mothers was 25% (8/32) by 3 years of age. Five of 6 mothers with HTLV-I-infected cells in the milk also possessed infected cells in their peripheral blood. Conversely 5 of 6 mothers without infected cells in the peripheral blood possessed no infected cells in their breast milk, suggesting that HTLV-I-infected cells in the peripheral blood can enter the breast milk. None of the 8 breast-fed children born to carrier mothers whose peripheral blood and breast milk-borne cells were negative, developed HTLV-I infection, suggesting that HTLV-I transmission from mother to child is dependent upon the number of HTLV-I-infected cells in carrier mothers.
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Using an ultrasonic Doppler duplex system, we investigated the portal hemodynamics of two patients with portal thrombosis after splenectomy and esophageal transection for portal hypertension accompanied by liver cirrhosis. In both cases, the preoperative blood flow volumes of the splenic and portal veins were especially high, but were markedly lower--even than normal--after the operation. However, the results of pre- and postoperative peripheral platelet counts and coagulation function tests did not differ remarkably. The dramatic change in portal hemodynamics caused by the splenectomy was thought to be the main factor in the formation of the portal thrombi.
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