Liver diseases and cancer associated with lack of lymphocytic cortisol metabolism enhancing factor

A. Klein*, E. Barkan, A. Barkan, H. Hoogervorst-Spalter, R. Arie, H. Kaufmann

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


A study was carried out to determine the effect on lymphocytic cortisol metabolism of plasma from patients with liver dysfunction as compared to that of plasma from healthy donors, cancer-bearing patients with and without liver dysfunction, carriers of Australian antigen, and patients with cholelithiasis but normal liver function. Known concentrations of human lymphocytes were incubated with cortisol in media containing 50% phosphate-buffered saline (PBS) and 50% plasma from one of the following categories of subjects: cancer-bearing patients suffering from extrahepatic carcinoma with liver metastasis, cancer-bearing patients with no signs of liver involvement, patients with cholelithiasis with jaundice and impaired liver function, patients with cholelithiasis and normal liver function, patients with acute hepatitis, patients with chronic active hepatitis, patients with cirrhosis, patients with a positive test for Australian antigen but normal liver function, posthepatitis patients with normal liver functions, and healthy controls. When the cortisol metabolism obtained by lymphocytes immersed in plasma from healthy controls was considered to be 100%, 17 of the 18 plasmas from patients with liver dysfunction were seen to have a significantly lesser effect, similar to that obtained with plasma of cancer-bearing patients with no liver involvement. Five out of six of the plasmas of cancer-bearing patients with liver metastasis showed a complete lack of enhancement of the rate of metabolism. All of the plasmas from patients with normal liver function, aside from the cancer patients, showed an effect similar to that of normal plasma. These findings suggest that there may be two separate factors involved in the phenomenon of enhancement of lymphocytic cortisol metabolism, one of them originating in the liver and the other possibly elsewhere. The possibility that there may be a toxic effect involved in liver dysfunction cannot be excluded.

Original languageEnglish
Pages (from-to)780-786
Number of pages7
JournalMetabolism: Clinical and Experimental
Issue number8
StatePublished - 1980
Externally publishedYes


FundersFunder number
Israel Cancer Research Fund


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