Fasting Plasma Caffeine Level in Cirrhotic Patients: Relation to Plasma Levels of Catecholamines and Renin Activity

Abstract

Fasting plasma caffeine concentrations, plasma levels of catecholamines and plasma renin activity were measured in patients with cirrhosis and control patients without hepatic dysfunction. A careful dietary history showed no significant difference in caffeine consumption (mean +/- S.E.) among 46 cirrhotics (86 +/- 7 mg per day) vs. 34 control patients (91 +/- 8 mg per day). Fasting plasma caffeine concentrations, however, were significantly higher (7.68 +/- 1.42 micrograms per ml) in cirrhotics than in controls (1.01 +/- 0.20 micrograms per ml) (p less than 0.01). Fasting plasma caffeine concentrations in cirrhotics varied significantly with Child's criteria, namely Child's A patients (2.06 +/- 0.38 micrograms per ml); Child's B patients (6.92 +/- 1.86 micrograms per ml), and Child's C patients (17.70 +/- 3.65 micrograms per ml) (p less than 0.001). In 44 cirrhotics, fasting plasma caffeine concentrations were compared with plasma levels of catecholamines and plasma renin activity. Plasma epinephrine concentrations were normal; however, plasma norepinephrine concentrations were increased in six cirrhotics, and plasma renin activities were increased in 28 cirrhotics. After a 3-day caffeine abstinence, plasma caffeine concentration and renin activity were significantly decreased (p less than 0.01), and high plasma norepinephrine levels were also decreased in 12 cirrhotics. Plasma caffeine concentration, renin activity and norepinephrine level did not change in a control group of cirrhotics who continued to receive caffeine for 3 days (n = 6). After abstinence from caffeine, the decrease of fasting plasma caffeine concentration correlated well with the decrease of plasma renin activity (r = +0.746, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Caffeine Suppresses the Activation of Hepatic Stellate Cells cAMP-Independently by Antagonizing Adenosine Receptors

“…Moreover, the plasma caffeine concentration in liver disease patients has been shown to be 7 times higher than that in healthy subjects. 33) This also supports the clinical use of caffeine.…”

“…33) It is important to point out that caffeine contacts to HSCs before metabolizing by hepatocytes, and the plasma caffeine level in the portal vein should be higher than that in whole body. It is, therefore, possible to say that caffeine acts on HSCs at mM range.…”

Liver cancer risk, coffee, and hepatitis C virus infection: a nested case–control study in Japan

“…Our results from this prospective cohort study support the findings in some (Gelatti et al, 2005;Ohfuji et al, 2006), although not all (Montella et al, 2007), case-control studies that suggested a protective effect of coffee among HCV-positive individuals. Some patients with hepatitis or liver cirrhosis, however, may have decreased coffee consumption at their physician's advice or due to impaired caffeine metabolism in the liver (Hasegawa et al, 1989). Observational studies among subjects without active hepatitis or intervention studies will further clarify the role of coffee in the possible prevention of HCV-related HCC.…”

Coffee and risk of death from hepatocellular carcinoma in a large cohort study in Japan

“…The effect of coffee drinking on hepatocellular cartinogenesis may be associated with inhibiting the progression from hepatitis to cirrhosis or from cirrhosis to HCC. Another possible explanation is that persons might reduce coffee intake because of symptoms related to impaired caffeine clearance (Hasegawa et al, 1989) of poor liver function or nonspecific medical advice. Coffee consumption, however, was not significantly associated with history of liver diseases at baseline survey.…”