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S Urcan

Publications and source records attributed to S Urcan.

At least 19 recordsLinked to original sources
PubMedDate not supplied

[Serum acetylcholinesterase changes after pancuronium administration].

The acetylcholinesterase activity was followed, as a variant of true cholinesterase, in three groups on non-selected patients: 10 of these were under local anesthesia with lidocaine, 12 were under general anesthesia with thiopenthal and halotane and 43 were under the same type of general anesthesia, that had also been given Pancuronium as a muscle relaxant. A slight inhibition was noted of the enzyme activities in the course of local anesthesia and a more significant one in the course of general anesthesia. The enzyme concentrations were lower in those patients that had also received Pancuronium, suggesting a cummulative inhibitory effect on serum acetylcholinesterase. The changes were not significant from the statistical viewpoint.

Acetylcholinesterase↗
PubMedDate not supplied

A prospective study of postacute viral hepatitis: the role of HBsAg.

Twenty-two patients with HBsAg positive acute viral hepatitis have been followed-up for two years after the acute episode. Besides the usual clinical, pathological and biological examinations, the following tests were carried out: serum HBsAg: circulating T and B lymphocytes: serum IgG, IgA, IgM: leukocyte migration test to HBsAg; serum complement: autoantibodies, rheumatoid factors, cryoglobulins, alpha-fetoprotein. Serum HBsAg persistence was correlated with some features of the acute episode: protracted clinical form: recurrences or relapses; splenomegaly; decrease of circulating T-lymphocytes; presence of lymphocyte sensibilization to HBsAg. Among the seven serum HBsAg carriers, three developed a chronic hepatitis. The state of healthy chronic HBsAg carrier was associated with high levels of serum IgA (over 300 IU/ml). A chronic hepatitis has been also diagnosed in four out of the 15 patients who cleared their serum HBsAg. The presence, on the one hand, of a chronic hepatitis among the patients who cleared their HBsAg and, on the other hand, its absence in some of the HBsAg carriers suggest that HBsAg persistence is not a sine qua non condition for the development of the chronic liver disease. The onset of autoimmune phenomena due to the disturbance of immunologic homeostasis and perhaps other genetic or environmental factors seemingly allow the perpetuation of a hepatic damage.

Acute Disease↗