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Effect of dopaminergic receptor blockade on plasma aldosterone and sodium excretion in CIR rhosis
EFFECT OF DOPAMINERGIC RECEPTOR BLOCKADE ON PLASMA ALDOSTERONE AND SODIUM EXCRETION IN CIRRHOSIS. 29 M. Bernardi, F. Trevisani, D. Zoni, C. Santini, R. Malatesta*, R. De Palma, D. Servadei, G. Gasbarrini Patologia Speciale Medica III and *Semeiotica Medica, Universit~ di Bologna; Italy.
Recent studies suggest that a reduction in dopaminergic activity could play a role in the deve lopment of secondary hyperaldosteronism, as in idiopathic edema. Changes in adrenergic activity have been reported in cirrhosis, but no data are available on the effect of dopaminergic receptor blockade on plasma aldosterone (PA) in these patients. Metoclopramide (M) -10 mg iv- was given to 8 healthy controls and 19 cirrhotics (9 without -GI- and 10 with -G2- ascites). Plasma renin activity (PRA) and PA were determined after 2h of bed rest and 15,30,60 and 120 min from M injection. During the experiment glomerular filtration rate (GFR) and renal sodium excretion (UNa V) were also evaluated. M led to significant increases of PA, peaking at 15 min, in all groups, whereas PRA was not affected. The 2h response above basal levels was not different in controls (256~51 pg/ml), GI (256~43) and G2 (343+49; ns). Similar results were obtained by evaluating 2h response as per cent change. However G2 patients with markedly increased PA (up to 2 fold the upper normal limit) had reduced 2h% response (p<0.05). GFR did not change. UNaV of G2 was inversely related to PA under basal conditions (r=-0.94; pp>0.05). No changes in controls' and G1 UNa V were found. Derangements o f d o p a minergic system may contribute to aldosterone hypersecretion only in advanced cirrhosis. TheMinduced increase of PA does not assume clinical relevance, since sodium excretion was virtual ly not affected.
FULMINANT HEPATIC FAILURE DUE TO AUTOIMMUNE HEPATITIS 30
J.Bernuau,~C.Valli, N.Boyer, C.Degott, J.C.Homberg~ B.Rueff, J.P.Benhamou, • HSpital Beaujon, Clichy, and HSpital Saint-Antoine, Paris, France
Autoimmunity is a recognized cause of chronic active hepatitis; the commonest serological marker of this autoimmune disorder is antibody to smooth muscle. The purpose of this communication is to show (a) that fulminant hepatic failure may occur early in the clinical course of autoimmune hepatitis, and (b) that anti-liver-kidney microsome antibody type I (ALKMA 1) is associated with this severe form of autoimmune hepatitis. From 1975 to 1984, 46 patients were admitted for autoimmune active hepatitis: the diagnosis was based on histologic lesions, low alcohol intake, absence of injection or ingestion of a hepatotoxic drug, absence of serological and/or circumstantial arguments for A, B, non A non B, and CMV infection. Wilson's disease was excluded in all the patients. In 42 of these patients, no encephalopathy developed within the 6 months following the onset of jaundice; all the patients were alive 1 year after admission; serum aminotransferases exceeded 500 U in only 5 (normal, 0-40); antibody to smooth muscle was present in 40 and ALKMA 1 in 2. In the 4 other patients (3 women and 1 man aged 20, 35, 42 and 24 years), asterixis and confusion developed 1 to 3 months after the onset of jaundice; in 3, encephalopathy progressed to coma and death within the 6 months after the onset of jaundice; serum aminotransferases exceeded 500 U in the 4 patients; ALKMA 1 was present and antibody to smooth muscle was absent in all the 4 patients. Hepatitis was preceded by hyperthyroidism in 1 and idiopathic thrombopenic purpura in 1. In conclusion, (a) in about 10% of patients with autoimmune hepatitis, fulminant hepatic failure develops 1 to 3 months after the onset of jaundice; (b) early mortality rate is high in this type of autoimmune hepatitis; (c) ALKMA 1 is associated with this type of liver disease.
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Recent studies suggest that a reduction in dopaminergic activity could play a role in the deve lopment of secondary hyperaldosteronism, as in idiopathic edema. Changes in adrenergic activity have been reported in cirrhosis, but no data are available on the effect of dopaminergic receptor blockade on plasma aldosterone (PA) in these patients. Metoclopramide (M) -10 mg iv- was given to 8 healthy controls and 19 cirrhotics (9 without -GI- and 10 with -G2- ascites). Plasma renin activity (PRA) and PA were determined after 2h of bed rest and 15,30,60 and 120 min from M injection. During the experiment glomerular filtration rate (GFR) and renal sodium excretion (UNa V) were also evaluated. M led to significant increases of PA, peaking at 15 min, in all groups, whereas PRA was not affected. The 2h response above basal levels was not different in controls (256~51 pg/ml), GI (256~43) and G2 (343+49; ns). Similar results were obtained by evaluating 2h response as per cent change. However G2 patients with markedly increased PA (up to 2 fold the upper normal limit) had reduced 2h% response (p<0.05). GFR did not change. UNaV of G2 was inversely related to PA under basal conditions (r=-0.94; p
FULMINANT HEPATIC FAILURE DUE TO AUTOIMMUNE HEPATITIS 30
J.Bernuau,~C.Valli, N.Boyer, C.Degott, J.C.Homberg~ B.Rueff, J.P.Benhamou, • HSpital Beaujon, Clichy, and HSpital Saint-Antoine, Paris, France
Autoimmunity is a recognized cause of chronic active hepatitis; the commonest serological marker of this autoimmune disorder is antibody to smooth muscle. The purpose of this communication is to show (a) that fulminant hepatic failure may occur early in the clinical course of autoimmune hepatitis, and (b) that anti-liver-kidney microsome antibody type I (ALKMA 1) is associated with this severe form of autoimmune hepatitis. From 1975 to 1984, 46 patients were admitted for autoimmune active hepatitis: the diagnosis was based on histologic lesions, low alcohol intake, absence of injection or ingestion of a hepatotoxic drug, absence of serological and/or circumstantial arguments for A, B, non A non B, and CMV infection. Wilson's disease was excluded in all the patients. In 42 of these patients, no encephalopathy developed within the 6 months following the onset of jaundice; all the patients were alive 1 year after admission; serum aminotransferases exceeded 500 U in only 5 (normal, 0-40); antibody to smooth muscle was present in 40 and ALKMA 1 in 2. In the 4 other patients (3 women and 1 man aged 20, 35, 42 and 24 years), asterixis and confusion developed 1 to 3 months after the onset of jaundice; in 3, encephalopathy progressed to coma and death within the 6 months after the onset of jaundice; serum aminotransferases exceeded 500 U in the 4 patients; ALKMA 1 was present and antibody to smooth muscle was absent in all the 4 patients. Hepatitis was preceded by hyperthyroidism in 1 and idiopathic thrombopenic purpura in 1. In conclusion, (a) in about 10% of patients with autoimmune hepatitis, fulminant hepatic failure develops 1 to 3 months after the onset of jaundice; (b) early mortality rate is high in this type of autoimmune hepatitis; (c) ALKMA 1 is associated with this type of liver disease.
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