Kidney failure is a contraindication to interferon therapy, and active chronic hepatitis is incompatible with kidney transplantation. Our study was aimed at investigating the activity and tolerability of leukocyte interferon-alpha in patients undergoing pre-transplant dialysis and suffering from chronic active hepatitis due to Hepatitis C virus infection. Ten patients, with persistently high ALT levels, were treated with leukocyte interferon-alpha, at a dose of 1 MU three times weekly for one year. Viraemia, ALT levels and other blood and urine tests, hepatitis stage and drug tolerance were all monitored throughout the study and the six-month follow-up period. After six months of treatment, two patients had continuing normalisation of ALT, negative HCV-RNA tests and normalisation of histological features ('long-term responders'). Four patients relapsed; three did not respond to treatment; and one patient discontinued it because of intolerance. The four relapsing patients received a second cycle with the same interferon, at a dose of 3 MU three times weekly, with attainment, in one patient, of complete remittance after six months of follow-up. Leukocyte interferon-alpha yielded an overall 30% therapeutic response in dialysed patients with chronic hepatitis C. Its use is helpful in enabling dialysed patients to undergo transplantation.
The natural history of cystic hydatid disease (CHD) can be divided into two stages. The first is characterized by the proliferation of the parasite: the second is marked by involution, ie, when the hydatid undergoes spontaneous distress or is subjected to pharmacological treatment Echography makes it possible to study this evolution and to evaluate the stages of this parasitic pathology.This study of the evolution of abdominal CHD in 81 patients suffering from 127 cysts, with or without Albendazole treatment suggests a new sonographic classification: type I: simple CHD; type 11: multiple CHD, type 111: with detachment of membrane CHD; type IV: mixed CHD; type V: heterogeneous CHD; type VI: hyperechogenic CHD; type VII calcified CHD.Forty-seven patients suffering from 90 cysts of types I, 11,111, IV, and V were treated with Albendazole; 31, suffering from 34 CHD of types VI and VII, were not treated, as they were considered involutional; 3 patients with 3 cysts refused therapy. Albendazole treatment resulted in the disappearance of 9 and in the solidification of 62 cysts. Of the remaining cases of CHD, 10 cysts showed sonographic alterations and 5 showed no modifications. Surgery was necessary for 2 patients (4 cysts).This new classification seems to be an aid in the recognition of the natural and therapy-induced involution of CHD and seems to improve the evaluation of the efficaciousness of the therapy. 0 1996 John Wiley & Sons, Inc.
The natural history of cystic hydatid disease (CHD) can be divided into two stages. The first is characterized by the proliferation of the parasite; the second is marked by involution, ie, when the hydatid undergoes spontaneous distress or is subjected to pharmacological treatment. Echography makes it possible to study this evolution and to evaluate the stages of this parasitic pathology. This study of the evolution of abdominal CHD in 81 patients suffering from 127 cysts, with or without Albendazole treatment suggests a new sonographic classification: type I: simple CHD; type II: multiple CHD, type III: with detachment of membrane CHD; type IV: mixed CHD; type V: heterogeneous CHD; type VI: hyperechogenic CHD; type VII calcified CHD. Forty‐seven patients suffering from 90 cysts of types I, II, III, IV, and V were treated with Albendazole; 31, suffering from 34 CHD of types VI and VII, were not treated, as they were considered involutional; 3 patients with 3 cysts refused therapy. Albendazole treatment resulted in the disappearance of 9 and in the solidification of 62 cysts. Of the remaining cases of CHD, 10 cysts showed sonographic alterations and 5 showed no modifications. Surgery was necessary for 2 patients (4 cysts). This new classification seems to be an aid in the recognition of the natural and therapy‐induced involution of CHD and seems to improve the evaluation of the efficaciousness of the therapy. © 1996 John Wiley & Sons, Inc.
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