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Biomedical subjects

K Tanikawa

Publications and source records attributed to K Tanikawa.

At least 397 records · Page 22Linked to original sources
PubMed1978

[Hepatitis A].

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Animals↗
PubMed1977

Clinical studies on dissolution of gallstones using ursodeoxycholic acid.

Ursodeoxycholic acid (UDCA), 7beta hydroxy epimer of chenodeoxycholic acid (CDCA), has been used as a choleretica for 20 years in Japan. Recent report showing increased excretion of UDCA in bile after CDCA administration may suggest the possibility that UDCA has similar effects to CDCA on bile cholesterol unsaturation and on gallstone dissolution. The present paper describes the clinical usefulness of UDCA for gallstone patients during the past two years. Seventy-four gallstone patients with functioning gall-bladders, 19 men and 55 women with a mean age of 48 years, have been treated for 6 months or more. UDCA, supplied in tablets (Ursosan), was given 450 mg per day. The disappearance or the reduction of stone size or number, or both (dissolution effect) was recognized in 32 out of 74 patients (43%). In case of radiolucent stones, the overall effective rate was estimated for 24 of 46 patients (52%). There may be no significant difference in dissolution effect between CDCA and UDCA treatment, however, the merit of UDCA treatment seems to have its few side effects.

Adult↗
PubMed1976

Marked delay in indocyanine green plasma clearance with a near-normal bromosulphophthalein retention test: a constitutional abnormality?

Five patients showing a normal to near-normal BSP test and a marked delay in ICG plasma clearance, and two families with clustering of the same abnormality, are described. Two had Gilbert's syndrome, one was convalescing from acute hepatitis, and the other two had no detectable liver abnormality. Measured indices of ICG metabolism indicated a marked reduction in the hepatic uptake, storage capacity, biliary transport maximum, and an increased reflux into plasma. Biochemical studies on the binding of ICG by plasma proteins failed to demonstrate any difference from normal controls. Thus, the primary defect seems to be in the transport of ICG by the hepatocyte. Although the relationship of the defect in ICG metabolism to other constitutional hyperbilirubinaemias is not clear, it is possible that the defect in these patients is a constitutional one involving some steps in the hepatic disposal of organic anions.

Adult↗