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L’organisation pluridisciplinaire de la medecine de premier recours, la prise en compte des performances en termes de qualite dans la remuneration des medecins, la culture de l’evaluation et de la transparence, la promotion du choix des patients, la prise en compte du calcul medico-economique dans les decisions sont autant de caracteristiques du systeme anglais qui peuvent contribuer a notre reflexion sur les evolutions du systeme francais. Il ne s’agit pas pour autant de faire du systeme de soins anglais un modele ne serait-ce que parce qu’il semble encore avoir des resultats inferieurs a ceux du systeme francais. Il sera interessant, des lors que l’on aura un peu de recul, d’examiner si, compte tenu de la forte augmentation du budget du NHS, le systeme anglais les a ameliores significativement au cours de la decennie 2000.

The present invention relates to a method and apparatus for performing selective acoustic signal filtering. The apparatus comprises two acoustic ports, an electrical output port and an acoustic signal processing device, where all three ports have an impedance characteristic. The acoustic signal processing device includes a diaphragm which will manifest vibration in response to an admitted input acoustic signal and generates an output acoustic signal. The signal processing device is characterized by a frequency response such that the spectrum level of the output acoustic signal will have predetermined differences with respect to the input acoustic signal. The frequency response characteristic of the signal processing device may be set and adjusted by the manipulation of the impedance characteristics of either the acoustic output load or the electrical output load.

In the present study, we report on alterations in plasma lipid, lipoprotein and apolipoprotein patterns in three separate populations of alcoholic patients, one without liver damage (Group I), a second presenting steatosis or mild alcoholic hepatitis or both (Group II) and a third with alcoholic cirrhosis (Group III), using a healthy, normolipidemic, nonalcoholic group as controls (Group C). Total plasma cholesterol levels were elevated in Groups II and III when compared with Groups I and C, while the ratio of esterified to free cholesterol was considerably lower in Group III than in the other groups. Plasma apo-AI levels were higher in Groups I and II than in Group C, but varied over a wide range in Group III. Apo-AII was present at higher concentrations in Groups I and II than in both Groups III and C. In contrast, no significant differences were detected in total apo-B levels, irrespective of the group. Modifications in the chemical composition of plasma lipoproteins primarily concerned a reduction in the cholesteryl ester content of low-density lipoproteins (LDL) and high-density lipoprotein (HDL) in Group III, this being compensated by a reciprocal increase in triglyceride. In addition, Group III lipoproteins, with the exception of HDL3 (density 1.100 to 1.140 gm per ml), exhibited a greater content of phospholipids than those of corresponding density from patients in Groups I and II. No significant differences were found in very low-density lipoprotein concentrations, while LDL levels increased in parallel with the severity of liver injury. In Groups I and II, HDL2 concentrations were elevated relative to Group C, while HDL3 decreased in parallel with the degree of impairment of liver function and thus from Group C to Group III. Such opposing tendencies led to an HDL2:HDL3 ratio which was more than 5-fold higher than normal in Group III. The distribution of apoprotein B in the ultracentrifugal subfractions revealed no significant modification between the different groups. By contrast, in Groups I and II, apo-AI and apo-AII levels increased consequent to higher concentrations of HDL2. Our data suggest that abnormal HDL particles preferentially enriched in apo-AII and possibly apo-AI were present in Group I, while the lowest levels of both apo-AI and apo-AII were seen in Group III. No simple association is evident between a well-defined plasma lipid, lipoprotein and/or apolipoprotein profile and chronic alcoholism in the presence or absence of liver injury. Nonetheless, our findings suggest that measurement of the absolute concentrations and ratio of HDL2 and HDL3, as well as of the levels and ratio of apo-AI and apo-AII in these subclasses, may permit differentiation of certain of the subpopulations of chronic alcoholics described herein.

We compared the presence of serologic markers of hepatitis B virus (HBV) infection with the presence of the viral DNA in the livers of patients with alcoholic liver disease with or without hepatocellular carcinoma. Among 51 patients with various kinds of alcoholic liver disease but without hepatocellular cancer, 19 had one or more serologic markers of HBV, but only three had viral surface antigen in their serum. These three patients, as well as three others who had HBV antibodies but no viral antigen in their serum and two others who had no serologic markers of any kind, had HBV DNA in their liver cells. In at least five of the eight patients with viral DNA in the liver, the DNA was integrated into the genome. Among 20 patients with alcoholic cirrhosis and hepatocellular carcinoma, nine of the 16 tested had serologic markers of HBV infection, but all 20 had HBV DNA integrated into the genome of the neoplastic liver cells. These data suggest that HBV plays a part in the pathogenesis of primary liver-cell cancer in alcoholics.

Summary We present the case of a 25-year-old man with Crigler-Najjar disease who had since birth a marked unconjugated hyperbilirubinemia without bilirubin overproduction, without any neurological involvement and in whom phenobarbital administration failed to produce any effect. Analysis of his biliary bile pigments on two occasions showed (i) a decreased excretion of bilirubin, as indirectly suggested by a high ratio of biliary bile acids over total bilirubin; (ii) an increase in unconjugated bilirubin IX α quantitated by thin-layer chromatography (TLC) following alkaline methanolysis and by direct extraction and TLC of the tetrapyrroles; (iii) a high proportion of bilirubin monoconjugates whereas the excretion of diconjugates was very low. Classification of the present patient into Crigler-Najjar disease type I or II was not possible. The most striking and practical difference among the various cases of Crigler-Najjar disease remains the response to phenobarbital. Among cases of Crigler-Najjar disease which respond to enzyme induction and Gilbert's syndrome, the continuous spectrum suggests a common defect.

Summary We report the cases of 3 patients in whom ajmaline-induced acute hepatitis was followed by anicteric cholestasis persisting for more than 1 year after cessation of administration of the drug. Ajmaline was given for 8–16 days before the onset of acute hepatitis. Jaundice was preceded by fever, chills and abdominal pain, and was associated with hypereosinophilia. The initial lesions included centrilobular cholestasis and portal inflammatory infiltration. Jaundice lasted for 3 weeks to 11 months. In these 3 patients, (1) liver tests were still abnormal 17–26 months after ajmaline withdrawal; (2) histological examination, performed 9–26 months after the onset of jaundice, showed a decreased number of interlobular bile ducts, ductular proliferation, and mild portal fibrosis; (3) circulating immune complexes were demonstrated. These observations demonstrate that prolonged cholestasis can follow ajmaline-induced acute hepatitis. Persistence of cholestasis long after the withdrawal of ajmaline suggests some form of autoimmunity.