Endoscopic Sclerotherapy for Esophageal Varices After Surgical Procedures for Congenital Biliary Atresia

Abstract: The effectiveness of injection sclerotherapy for esophageal varices due to congenital biliary atresia has not yet been established. Sclerotherapy was performed to treat esophageal varices in four children with variceal bleeding who had received a hepatic portoenterostomy for congenital biliary atresia. Ethanolamine oleate was mixed with a contrast medium for the varicealography in order to determine the flow of the sclerosant by fluoroscopy. Varicealography which was conducted during the injection allowed us to stop the procedure so that mixture would fill up the varix and its feeders but would not enter the systemic circulation. Between 0.5 ml to 2.0 ml of sclerosant was injected at the variceal puncture. There was one case bleeding from the esophageal ulcer. However, it was resolved by conservative treatment. All four children experienced no rebleeding after the therapy. Therefore, injection sclerotherapy using varicealography with sclerosant–contrast medium mixture is recommended for children who develop esophageal varices after surgical procedures for congenital biliary atresia.     

Role of Hepatocyte Growth Factor in Hemopoiesis

Hepatocyte growth factor (HGF) is a polypeptide that stimulates proliferation, motility, and morphogenesis of various cells, particularly epithelial cells. There is considerable evidence that HGF is a regulator in hemopoiesis not only in mice but also in humans. In mice, HGF and c-met (its receptor) mRNA are coexpressed in the fetal liver in the middle and late stages, when hemopoiesis is most active. HGF and c-met mRNA are also expressed in the stromal cells of both fetal liver and bone marrow. Human HGF (2 to 20 ng/ml) enhances colony-forming units in culture (CFU-C) counts and cobblestone colony counts in the long-term cultures of the fetal liver and bone marrow, although HGF has no effect on freshly isolated bone marrow or fetal liver cells in the CFU-C assay. However, when the bone marrow or fetal liver cells are cocultured with HGF in the presence of IL-3, CFU-C counts increase. In humans, it has also been shown that HGF in the presence of erythropoietin induces the formation of erythroid burst-forming unit (BFU-E) colonies from CD34⁺ cells purified from the bone marrow, peripheral blood, or cord blood. This review discusses the role of HGF as a regulator in hemopoiesis.     

A Case of Stasis Papillomatosis Associated with Psoriasis Vulgaris

A markedly obese, 41-year-old Japanese man who had suffered from psoriasis vulgaris for several years visited us with elephantiasis-like swelling of his lower legs of three months' duration. His right lower leg showed marked papillomatosis with thick scales, and the left lower leg was eroded and papillomatous. Although direct lymphography of his lower extremities showed no abnormality, indirect lymphography revealed local lymphatic damage in the involved skin. Histological examination showed hyperkeratosis, marked papillomatosis, proliferation of capillaries in the upper dermis, and lymphectasia in the lower dermis. The lesions were much improved by washing and topical use of corticosteroids for two months. It was suspected that obesity and the preceding psoriatic lesions caused local lymphatic disturbances, followed by the development of stasis papillomatosis.     

Mediation of arachidonic acid metabolite(s) produced by endothelial cytochrome P-450 3A4 in monkey arterial relaxation.

We investigated mechanisms of endothelium-dependent relaxation by acetylcholine resistant to indomethacin and N(G)-nitro-L-arginine and sensitive to cytochrome P-450 (CYP) inhibitors or charybdotoxin + apamin in the monkey lingual artery. Treatment with quinacrine, an inhibitor of phospholipase A2, abolished the relaxation by acetylcholine. However, treatment with alpha-glycyrrhetinic acid, an inhibitor of gap junctions, or catalase, an enzyme which dismutates hydrogen peroxide to form water and oxygen, did not affect the relaxation by acetylcholine. Immunohistochemistry demonstrated the presence of CYP3A4 in endothelial cells of the artery. Anti-CYP3A4 antibody inhibited relaxations by products of arachidonic acid incubated with human liver microsomes rich in CYPs in the endothelium-denuded artery. Purified CYP3A4 produced epoxyeicosatrienoic acids (EETs) from arachidonic acid, and the production was abolished by a selective CYP3A inhibitor, ketoconazole. It may be concluded that endothelium-derived relaxing substance(s) other than nitric oxide and prostanoids in the monkey lingual artery opens charybdotoxin + apamin-sensitive K+ channels in smooth muscle cells, and arachidonic acid metabolite(s) produced by endothelial CYP3A4 is likely to be the major substance.     

Chronic Changes of End-Systolic Pressure-Volume Relationship After Regional Myocardial Infarction

The chronic changes of the end-systolic pressure-volume relationship (ESPVR) after regional myocardial infarction were evaluated in a sheep model. Pressure-volume area (PVA) obtained from the pressure-volume diagram and left ventricular oxygen consumption (LVO₂) were studied. The regional myocardial infarction was created by ligating distal branches of the left coronary artery. ESPVR was obtained using a conductance catheter during transient inferior vena cava occlusion. Measurements were performed at baseline (n = 13), 1 hour (n = 8), 3 months (n = 9), and 6 months (n = 4) after infarction. Ees, the slope of the ESPVR did not change at 1 hour after infarction and remained the same at 3-month and 6-month measurements (baseline 2.26 ± 1.24 mmHg/mL, 1 hour 2.71 ± 1.06, 3 months 3.46 ± 1.51, 6 months 2.45 ± 0.64, NS). Because of the ventricular dilatation, which was demonstrated as an increase in changes of end-systolic volume (Ves) correlating with the time course after infarction (y = -3.21 + 0.128±, r = 0.454, p < 0.05), V₀, the volume intercept of the ESPVR increased at 1 hour after the infarction, and showed a tendency to increase at 3 months and 6 months after the infarction (baseline -18.0 ± 22.5 mL; 1 hour -0.9 ± 11.6; 3 months 5.4 ± 10.9, 6 months 9.2 ± 23.1, baseline vs 3 months p < 0.05, baseline vs 6 months p < 0.05). PVA and LVO₂ were unchanged over time after infarction (PVA: baseline 2097 ± 1526 mmHg/mL per 100 g^-1; 1 hour 1771 ± 699; 3 months 2483 ± 1086; 6 months 1,608 ±1,010, NS), (LVO₂: baseline 40.6 ± 13.1 ± 10–³ mL/100 g^-1 per beat^-1; 1 hour 42.9 ± 9.7; 3 months 35.0 ± 8.6; 6 months 31.2 ± 18.1, NS). Chronic regional infarction in the sheep model did not affect Ees over 6 months, but significantly increased V₀ after the increase in the acute phase. PVA and LVO₂ were not affected by this regional infarction either acutely or over 6 months.