Liver Disease Function Research Articles

Lecithin:cholesterol acyltransferase deficiency and cell membrane lipids and function in human liver disease.

There are several lipoprotein abnormalities in human liver disease, many of which can be related to a reduced LC AT activity. Exchange is known to occur between the lipids of the plasma lipoproteins and their counterparts in the membranes of erythrocytes and other cells. There have been few studies on the effect of this exchange on cell lipid composition and function in liver disease. In agreement with other workers we found erythrocyte lipid composition to be altered in both parenchymal liver disease and obstructive jaundice with increases in cholesterol and lecithin concentrations and raised cholesterol: phospholipid molar ratio (C/P). Plasma LCAT activity showed significant inverse correlations with these erythrocyte lipid changes in parenchymal liver disease but not in obstructive jaundice. Increase in membrane C/P ratio is associated with decreased membrane fluidity, and in erythrocytes from patients we have demonstrated the C/P ratio to be related to an abnormal permeability to sodium and to an enha...

Adrenocortical function in liver diseases

主要代謝臓器である肝に強い障害がある場合, 副腎皮質機能はステロイド代謝異常により二次的に障害されると推論されている.しかしながら肝疾患時の副腎皮質機能を直接的に研究した報告は少い.著者は肝疾患々者にACTH-Z試験を施行し, 副腎皮質機能の検討を試みたが, 急性肝炎恢腹期, 慢性肝炎, 肝硬変のいずれにおいても, ステロイド代謝異常の存在と共に副腎皮質機能の低下をうかがわしめる成績をえた.

Liver function in disease and in preoperative evaluation.

With proper utilization of the tests discussed there is no question that the management of patients with hepatic disease can be improved. However, of much greater importance than the specific tests is their consistent reproducibility, and the physician's recognition of the potentialities and limitations of these tests under the various conditions of use.

Renal function in liver disease and malnutrition.

Renal function in liver disease and malnutrition.

STUDIES ON THE HYALURONIDASE INHIBITOR IN SERUM

Serum hyaluronidase inhibitor activity (HDI) was determined by turbidimetric method in this experiment.1) The existence of HDI in normal human subjects was recognized, and there is no difference in HDI value between man and woman.2) HDI increased in both liver and kidney disease. HDI value has a certain interdependence with liver function in liver disease, and with proteinuria, urine volume, hematuria, blood pressure, plasma protein electrophoretic pattern, and edema etc. in kidney disease. That is, HDI value has a relationship with the severity of disease clearly.3) In the rabbits with experimentally injured kidney HDI increased day after day, and the increase of HDI kept pace with the severity of the disease.4) HDI increased by the administration of both cortisone and ACTH, but do not increase or decrease by DOCA, increased by adrenalin. Moreover, in nephrotic syndrome accompanied with the clear increase of HDI, effective cases in ACTH, Prednisolone treatment had the normalization of HDI value. Therefore, it is supposed that HDI value is regulated by pituitary-adrenocortical system.5) In whole body X-ray irradiated rats, HDI value increased at 48 hrs after irradiation.6) Sulfhydryl reagents (ferricyan, PCMB, IAc) inhibited the hyaluronidase activity in vitro, recovered by addition of L-cysteine into the system. Moreover, normal serum and nephrotic serum inhibited the hyaluronidase activity, recovered by addition of L-cysteine, According to this fact, a close relationship between HD, HDI and SH-radical was suggested.

Liver-function tests.

NUMEROUS attempts have been made for over half a century to measure the function of the liver by one or another test; these procedures have been proposed for several purposes. First, in cases in which the diagnosis is entirely obscure, it has been hoped that the presence of liver disease might be ruled in or out. Second, in the presence of known liver disease function studies have been used to define, if possible, the degree of damage and the type of lesion. Finally, these procedures seem to have a valuable place in appraising the course of hepatic disturbances— whether downhill or toward recovery. The discovery of the glycogenic activity of the liver, in 1857, by Claude Bernard, stimulated extensive studies of carbohydrate metabolism, and by the late decades of the century alert clinicians were attempting to develop carbohydrate tests for liver function. The general idea was that, if one fed