Giuseppe Bombardieri

Comparative effects of experimental lead poisoning on enzymatic activities of kidney and liver in rat.

Abstract Rats were fed for 6 months with 0.1% lead acetate diet. At the end of the intoxication period urinary levels of ALA and lead were comparable with the usual urinary levels of chronically lead exposed humans. In kidney homogenates of poisoned rats succinate dehydrogenase, cytochrome oxidase and lactate dehydrogenase were unmodified, malate dehydrogenase and glutamate dehydrogenase were decreased, while Dt diaphorase and glucose-6-phosphate dehydrogenase were greatly increased compared with controls. In liver homogenates of the same poisoned animals no alteration of the enzymatic activities was observed.

Correlation of MRI liver volume and doppler sonographic portal hemodynamics with histologic findings in patients with chronic hepatitis C.

The purpose of this study was to correlate portal hemodynamics on sonography and liver volume on MRI with histologic findings in asymptomatic patients with chronic hepatitis C.

EFFECTS OF A SINGLE, SHORT INTRAVENOUS DOSE OF ACETYL-l-CARNITINE ON PATTERN-REVERSAL VISUAL-EVOKED POTENTIALS IN CIRRHOTIC PATIENTS WITH HEPATIC ENCEPHALOPATHY

1 In animals and in cultured neurons, l‐carnitine and acetyl‐l‐carnitine (ALCAR) have been shown to counteract some of the toxic effects of ammonia. In order to detect similar properties in humans, we studied neuronal function after ALCAR administration in cirrhotics with hepatic encephalopathy (HE). 2 Eighteen cirrhotic patients with persistent HE and hyperammonaemia were investigated in the present study and six subjects with a prior transient ischaemic attack were used as controls. 3 The prominent positive component that occurs approximately 100 msec after the pattern reversal (P100) latencies of visual‐evoked potentials were used to evaluate neuronal function. At first, the P100 latency was measured in six cirrhotic patients with HE and in the six controls before the administration of 0.5 g ALCAR in 50 mL isotonic saline (infusion rate 10 mL/min) and 15, 30, 60 and 90 min later. 4 A significant reduction in P100 latencies was identified 30 min after ALCAR infusion in HE patients, whereas no differences were observed in controls. 5 Thereafter, the P100 latency was evaluated in the 12 other cirrhotic patients with HE only before and 30 min after ALCAR infusion. The mean of the P100 latencies measured in these subjects was significantly shorter after ALCAR infusion compared with values obtained before ALCAR administration (mean (SD) 130.78 5.50 vs 136.08 6.45 msec, respectively; P = 0.0013). 6 The present study suggests that a single intravenous dose of ALCAR may transiently improve neuronal function in cirrhotic patients with persistent HE and hyperammonaemia.

Proximal splenic artery embolization allows pegylated interferon and ribavirin combination therapy in chronic hepatitis C virus-infected patients with severe cytopenia.

In particular, we appreciated the results obtained when the authors utilized splenic artery embolization to increase the platelet and neutrophil counts before antiviral therapy in hepatitis C virus (HCV)-infected subjects with severe thrombocytopenia and/or neutropenia. They could bring an end to a complete course of standard interferon and ribavirin therapy in all patients previously treated with splenic artery embolization.

Somatostatin and Peripheral Blood Flow in Man

Somatostatin (SS), a physiological substance which inhibits secretion of GH, TSH, glucagon and insulin, was evaluated as a vasoactive agent. In normal and arteriopatic subjects SS was administered intravenously by bolus for 3 minutes and by infusion for 30 minutes. Rheography and plethysmography of lower limbs were performed before, during and after somatostatin administration. A marked improvement of blood flow, provoked by somatostatin, was ob served. A reduction of heart rate was also observed. Some hypotheses about the mechanism with which SS acts upon peripheral circulation are discussed.

Plasma amine oxidases in Wilson's disease

Abstract Plasma Mono- and Diamine-Oxidase activities (MAO and DAO), two copper containing enzymes, were estimated in 5 patients with Wilsons disease, without treatment and during D-Penicillamine treatment. Ceruloplasmin and “free” copper plasma levels were simultaneously measured. MAO was elevated in all cases, while DAO was within normal limits. D-Penicillamine administration did not result in significant reductions of these enzyme activities. It is likely that alterations of copper metabolism induced by Wilsons disease and by D-Penicillamine administration do not affect the activity of MAO or DAO. The increase in MAO activity in Wilsons disease probably results from the hepatic fibrosis.