Flow cytometry crossmatch and kidney graft outcome.
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Chi-Square Distribution↗
Biomedical subjects
F Pisani
Publications and source records attributed to F Pisani.
Hepatitis C reinfection after liver transplantation in relation to virus genotype.
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Alanine Transaminase↗
Disappearance of oxidative damage to red blood cell membranes in uremic patients following renal transplant.
Hemodialysis patients display increased oxidative damage to red blood cell (RBC) membranes, characterized by elevated levels of malonyldialdehyde (MDA), a short chain aldehyde produced by the oxidation of the polyunsaturated fatty acids (PUFA) in the RBC membranes. This is the result of a metabolic blockage of the pentose-phosphate shunt in uremic patients, which causes reduced detoxification of highly oxidative free radicals. The oxidative damage induces increased RBC rigidity and decreased RBC deformability, therefore favoring hemolysis. The aim of this work was to determine if a functioning renal graft would restore normal erythrocyte metabolism, reducing the oxidative damage. To this end, we have determined RBC MDA concentrations in 20 hemodialysis (HD) patients (RBC MDA 18.22 +/- 4.36 micrograms/ml packed RBC), 20 renal transplant (T) patients with well functioning grafts (serum creatinine less than 2 mg%) (RBC MDA 1.2 +/- 0.4 micrograms/ml packed RBC) (T vs. HD P less than 0.005) and 20 healthy controls (HC) (RBC MDA 1.44 +/- 0.6 micrograms/ml packed RBC) (HC vs. HD P less than 0.005; HC vs. T NS). Our findings show that a well-functioning renal graft restores normal RBC metabolism and eliminates the oxidative damage induced by uremia.
Adolescent↗
Sodium valproate and valpromide: differential interactions with carbamazepine in epileptic patients.
To evaluate the comparative effects of valproic acid (VPA) and valpromide (VPM) on plasma levels and protein binding of carbamazepine (CBZ) and CBZ-10,11-epoxide (CBZ-E), 12 adult epileptic patients stabilized on CBZ monotherapy were divided into two groups. One group (n = 6) received sodium valproate (1,100 mg/day) for 2 weeks, while the other group (n = 6) was given, for the same period, a dosage of VPM (1,200 mg/day) expected to produce VPA levels equivalent to those achieved with valproate. Plasma CBZ levels were not affected by either treatment. In the valproate-treated group, plasma CBZ-E levels increased by 101% (range, 29-238%) within 1 week of combined therapy (p less than 0.02) and returned to baseline values after VPA treatment was stopped. In the VPM-treated patients, the elevation of plasma CBZ-E levels was much greater. In this group, plasma CBZ-E increased by 330% (range, 110-864%), and this was associated in two patients with the appearance of adverse effects which subsided after reducing the VPM dosage. The plasma protein binding of CBZ and CBZ-E was not affected significantly by VPM or valproate therapy. Plasma VPA levels were similar in the two groups. It is concluded that VPM is not simply a prodrug of VPA. Although both VPA and VPM increase CBZ-E levels--probably by inhibiting the enzyme epoxide hydrolase--the interaction caused by VPM is of much greater magnitude and potential clinical significance.
Carbamazepine↗
Interaction of carbamazepine-10,11-epoxide, an active metabolite of carbamazepine, with valproate: a pharmacokinetic study.
The mechanism responsible for the valproate (VPA)-induced elevation of serum carbamazepine-10,11-epoxide (CBZ-E) levels was investigated in 6 normal subjects who received single oral doses of CBZ-E (100 mg) in a control session and during concurrent treatment with sodium VPA [500 mg twice daily (b.i.d.)]. VPA caused a significant prolongation of CBZ-E terminal half-life (t1/2 from 6.3 +/- 1.2 to 9.0 +/- 2.0 h, mean values +/- SD) and decreased CBZ-E clearance (from 90.6 +/- 18.8 to 63.2 +/- 16.1 ml h-1 kg-1, mean values +/- SD) without affecting CBZ-E apparent volume of distribution (from 0.82 +/- 0.19 to 0.81 +/- 0.24 l kg-1, mean values +/- SD). These findings indicate that VPA impairs the elimination of CBZ-E, presumably by inhibiting its metabolism.
Absorption↗
The influence of electroencephalographic focus laterality on efficacy of carbamazepine in complex partial and secondarily generalized tonic-clonic seizures.
Forty-five outpatients with chronic epilepsy with complex partial seizures (CPS) alone or associated with secondarily generalized tonic-clonic seizures (SGTCS) were treated with carbamazepine (CBZ) monotherapy. All patients had only a unilateral scalp electroencephalographic (EEG) focus. Left- (n = 29) and right- (n = 16) sided foci patients were comparable for age, sex, duration, and etiology of epilepsy as well as total and free CBZ serum levels. CBZ significantly improved CPS irrespective of the side of the EEG focus, whereas SGTCS were controlled for greater than 1 year in 15 of 19 patients with left focus and in three of 11 patients with right focus. When patients with poorly controlled seizures discontinued CBZ and changed to other therapies, they achieved a significant reduction in number of SGTCS, whereas the number of CPS was unchanged. The side of EEG focus seemed to be relevant to the control of SGTCS by CBZ. Interhemispheric neurotransmitter asymmetries may be involved in the EEG focus side-dependent CBZ response.
Adult↗
Carbamazepine-valnoctamide interaction in epileptic patients: in vitro/in vivo correlation.
Six patients stabilized with carbamazepine (CBZ) therapy received an 8-day "add-on" supplement of valnoctamide (VCD), a tranquilizer available over the counter (OTC) in several European countries that exhibits promising anticonvulsant activity in animal models. During VCD intake, serum levels of the active CBZ metabolite, carbamazepine-10,11-epoxide (CBZ-E), increased fivefold from 1.5 +/- 0.7 micrograms/ml at baseline to 7.4 +/- 4.4 micrograms/ml after 4 days of VCD therapy and 7.7 +/- 3.1 micrograms/ml after 7 days of VCD therapy (means +/- SD, p < 0.01). In 4 patients, the increase in serum CBZ-E levels was associated with clinical signs of CBZ intoxication. CBZ-E levels returned to baseline after VCD therapy was discontinued. Serum CBZ levels remained stable throughout the study. The interaction observed in this study is similar to that described in patients treated with CBZ and valpromide (VPD, an isomer of VCD). In a mechanistic study, therapeutic concentrations of VCD inhibited hydrolysis of styrene oxide in human liver microsome preparations. Thus, VCD is a potent inhibitor of microsomal epoxide hydrolase (IC50 15 microM). There was a striking similarity between in vitro and in vivo inhibition potencies. In this study, VCD clearance was higher in epileptic patients (treated with CBZ) than in healthy subjects.
Adult↗
Allopurinol as add-on therapy in refractory epilepsy: a double-blind placebo-controlled randomized study.
The antiepileptic effect of allopurinol was assessed in a double-blind, randomized, placebo-controlled, cross-over trial in 84 patients with epileptic seizures refractory to standard antiepileptic drugs (AEDs). During a retrospective baseline period, patients experienced at least four seizures of any type per month. The effects of allopurinol and matching placebo were examined for 4-month periods. Allopurinol dosage was 150 mg daily for children weighing < 20 kg and 300 mg daily for other patients. Efficacy analysis based on the Wilcoxon rank-sum test was conducted for the 80 patients who completed the study. No significant period effect or treatment-period interaction was noted. Allopurinol significantly reduced total seizures (p = 0.005), and secondarily generalized seizures (p = 0.0015). Median seizure reduction for total seizures was 10.5 and 27.9% for secondarily generalized seizures. Subjective preferences by clinicians evaluated blindly significantly favored allopurinol. No significant change occurred in the plasma concentration of concomitant AEDs between treatment periods, but serum urate decreased by 32% during allopurinol treatment. No clinically relevant side effects or changes in routine laboratory clinical chemistry or hematology were ascribed to allopurinol.
Adolescent↗
Clinically relevant anti-epileptic drug interactions.
Anti-epileptic drugs frequently interact due to pharmacokinetic features (induction or inhibition of metabolism, production of active metabolites, low therapeutic indices) and the need for prolonged treatment with possible addition of other drugs to treat concomitant diseases. The most important pharmacokinetic interactions are those that inhibit phenytoin, carbamazepine and phenobarbitone metabolism and thus increase their toxicity. Drugs inhibiting metabolism include antibiotic macrolides, chloramphenicol, isoniazide, some sulphonamides, propoxyphene, cimetidine, valproic acid and sulthiame. Anti-epileptic drugs can induce hepatic microsomal enzymes and, therefore, may increase metabolism of corticosteroids, oral contraceptives, oral anticoagulants, cardiovascular agents, antibiotics, chemotherapeutic agents, psychotropic drugs and non-opiate analgesics, thereby reducing their efficacy. Advantageous pharmacodynamic interactions include synergism of ethosuximide plus valproic acid and of carbamazepine plus valproic acid. A pharmacodynamic mechanism may be responsible for the reduced sensitivity of chronically treated epileptics to some neuromuscular blockers.
Anticonvulsants↗
Pharmacokinetics of phenylethylmalonamide (PEMA) after oral and intravenous administration.
The pharmacokinetics of phenylethylmalonamide (PEMA), one of the major metabolites of the antiepileptic drug primidone, have been studied in 6 healthy volunteers after administration of single 500mg intravenous and oral doses. Following intravenous administration, after a very short distributive phase (t1/2 = 0.23-0.53h), the decline of the log-PEMA concentration with respect to time appeared linear. The pharmacokinetic parameters, calculated according to a 1-compartment open model, showed the following values (mean +/- SD): terminal half-life, 15.7 +/- 3.4h; apparent volume of distribution, 0.69 +/- 0.10 L/kg; total serum clearance, 31.3 +/- 6.6 ml/h/kg. After oral administration, peak serum concentrations occurred at 0.5 to 4 hours and the oral bioavailability was 86.4 to 95.9%.
Administration, Oral↗
Effect of glipizide on insulin secretion and insulin metabolism in obese type II diabetic patients.
This study was designed to explore the short-term effect of glipizide on insulin secretion and metabolism. Plasma insulin and C-peptide levels in the fasting state and after a 100-g oral glucose load were measured in 17 obese newly diagnosed type II (non-insulin-dependent) diabetic subjects before and after 1 mo of treatment with glipizide (15 mg/day). Plasma glucose levels decreased significantly after treatment with glipizide. Plasma insulin and C-peptide concentrations in the fasting state did not change after glipizide treatment. Also, postglucose plasma insulin levels did not change after glipizide, whereas postglucose plasma C-peptide concentrations significantly increased. A significant relationship was found between the increase in C-peptide plasma levels and the decrease in glycemic profile after glucose load following glipizide treatment. The relation between plasma C-peptide and insulin incremental areas after the oral glucose load significantly increased after treatment. These results suggest that in obese type II diabetic patients, 1 mo of treatment with glipizide potentiates the beta-cell response to oral glucose load and increases insulin metabolism, probably within the liver.
Adult↗
One-year pilot study on tauroursodeoxycholic acid as an adjuvant treatment after liver transplantation.
BACKGROUND: The usefulness of ursodeoxycholic acid after liver transplantation is controversial. Tauroursodeoxycholic acid, the natural taurine-amidate, is a highly hydrophilic and cytoprotective bile salt currently under investigation. AIMS: To investigate the clinical usefulness of tauroursodeoxycholic acid after liver transplantation. PATIENTS: Thirty-three patients undergoing liver transplantation entered the study. METHODS: Sixteen patients were randomized to receive tauroursodeoxycholic acid (250 b.i.d. for 12 months) and 17 served as controls. Tauroursodeoxycholic acid was given from day 5 after transplantation for one year. RESULTS: Tauroursodeoxycholic acid treatment was safe and well tolerated. No drop outs occurred. Among the 29 patients undergoing long-term follow-up, five deaths occurred (3 of whom in the tauroursodeoxycholic acid group), none of which was related to treatment. The one-year actuarial survival was 78.6% in patients treated with tauroursodeoxycholic acid and 86.7% in controls (n.s.). No differences were observed with respect to early or late graft function and survival, nor to acute cellular rejection. Tauroursodeoxycholic acid therapy was associated with lower serum cholesterol levels (p < 0.02) during the early postoperative months; with milder cholestasis; with a drop in biliary cholates but no changes in endogenous hydrophobic bile salts. CONCLUSIONS: Long-term treatment with low dose tauroursodeoxycholic acid after liver transplantation is safe but does not affect graft function and survival.
Adult↗
[Multicentre observational study on peristomal skin disorders. A proposal classification].
Disorders regarding peristomal skin have been more and more investigated in order to establish the impact on quality of life of ostomy patients. The aim of this classification is to provide an objective, standardized tool for the assessment of peristomal skin complication specifically designed on the description and localization of the lesion.
Colostomy↗
Mitoxantrone in combination with etoposide and cytarabine for treatment of poor prognosis acute non lymphoid leukemia patients.
BACKGROUND: The proved effectiveness and relatively low extrahematological toxicity of Mitoxantrone, Ara-C and Etoposide as single agents and in combination in the treatment of acute non lymphoid leukemia (ANLL) are well established. In a phase II study the efficacy and toxicity of an induction combination regimen with Mitoxantrone, Ara-C and Etoposide were evaluated for treatment of poor risk ANLL patients. METHODS: Twenty-seven poor prognosis ANLL patients were treated with Mitoxantrone, 7 mg/sm days 1-3; VP16, 150 mg/sm days 1-3; Ara-C, 200 mg/sm continuous infusion days 1-5. Median age of treated patients was 63 (17-78): 10 de novo leukemias (4 greater than 65 yrs 3 with cardiomyopathy); 12 secondary leukemias (5 secondary to a myelodysplastic syndrome, 5 to myeloproliferative syndrome, 2 to other neoplasias); 3 relapses; 2 refractory. RESULTS: Fifteen patients (55.5%) achieved CR (8 de novo leukemias, 3 relapses, 4 secondary leukemias); 7 died in induction, 5 progressed. Median remission duration was 27 weeks (range 5-70 wks) and overall median survival 13 weeks (range 4-80). Extraematological toxicity was low, but five patients died from infections and two from hemorrhages. CONCLUSIONS: The combination tested in this trial proved effective in the treatment of "poor risk" ANLL, but the results need to be confirmed on greater numbers of patients, mainly in the group of de novo leukemias that can't be treated with more aggressive regimens.
Antineoplastic Combined Chemotherapy Protocols↗
Acute nonlymphocytic leukemia in the elderly: results of a retrospective study.
Seventy-four patients over 60 years of age with new cases of ANLL diagnosed between January, 1980 and December, 1986 were retrospectively evaluated. Twenty-nine (median age 63, range 60-70) received aggressive induction polychemotherapy: 15 achieved CR (52%), 10 were resistant (34.5%) and 4 died during induction (13.5%). Overall median survival was 6 1/2 months, median CR duration and median survival of responders were 9 and 13 months, respectively. Eight patients (median age 70.4, range 64-74) received low doses of Ara-C: 2 achieved CR, 5 were resistant and 1 died during induction, with an overall median survival of 6 1/2 months; 37 patients (median age 72, range 60-86) received only supportive care and cytostatic therapy for disease control with Hydroxyurea and 6-Mercaptopurine if WBC greater than 20 x 10(9)/l: overall median survival was 6 months and 2 patients are still alive after 18 and 26 months. Aggressive chemotherapy seems to be the treatment of choice in patients less than or equal to 70 years, while for those over 70 current supportive care may offer good survival and a good quality of life.
Aged↗
[Lennox-Gestaut syndrome: therapeutic aspects].
The Lennox-Gastaut Syndrome is one of the most refractory form of epilepsy and a variety of compounds, such as traditional antiepileptics, "new anticonvulsants" and non-anticonvulsant drugs has been tested. ACTH and, among the traditional antiepileptics. Clonazepam and Sodium Valproate showed the most favorable effects. The immediate (within 6 months) therapeutic response to ACTH and Clonazepam is satisfactory, with a more than 50% reduction of seizures in about one half of patients; after one year, however, only a small percentage of cases (7-10%), rather close to that with spontaneous remission, shows some therapeutic benefit. Valproate, when used as a single drug, produces a decrease in seizures (greater than 50%) in 25-30% of pts. A list of compounds, such as amphetamine, taurine, amantadine, allopurinol and, among the new putative antiepileptics, cinromide and gamma-vinyl-GABA, has been tested with some occasionally observed improvement in seizure control. None of these compounds, however, is of really proven efficacy. An acquired general rule of treatment is to avoid complex polypharmacy and overdose; there is in fact good evidence that making the child drowsy will greatly increase the number of fits.
Anticonvulsants↗
[Adverse effects of the use of cyclosporin A in patients having undergone a kidney transplant].
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Adolescent↗
[Effects of some phenothiazine drugs on experimental hemislabyrinthation].
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Animals↗