Effects of probenecid on the pharmacokinetics of mizoribine and co-administration of the two drugs in patients with nephrotic syndrome
INTERNATIONAL JOURNAL OF CLINICAL PHARMACOLOGY AND THERAPEUTICS
Authors: Utsunomiya, Y.; Hara, Y.; Ito, H.; Okonogi, H.; Miyazaki, Y.; Hashimoto, Y.; Hosoya, T.
Abstract
Probenecid (PRB) is an agent that reduces the systemic level of uric acid, and has the ability to inhibit the renal tubular secretion of agents that are co-administered with it In this study, we evaluated the effects of PRB co-administered with mizoribine (MZR) on the pharmacokinetics (PK) of MZR in 12 patients with nephrotic syndrome The elimination rate constant (k(el)) was used as an indicator of changes in the PK of MZR when the secretion of MZR was inhibited by co-administration of PRB, in order to determine the extent to which MZR was influenced by PRB In 4 of the 12 patients studied, kel decreased and the biological half-life (t(1/2)) of MZR was prolonged when co-administered with PRB, in comparison with the values when MZR was used alone, thus revealing that the PK of MZR was influenced by PRB Co-administration of PRB with MZR appears to be effective in prolonging the biological half-life of MZR and enhancing its effect in patients with nephrotic syndrome, although further studies will be required to determine the optimal dosage of PRB and renoprotective effects
Clinical Significance of an Alloantibody against the Kell Blood Group Glycoprotein
TRANSFUSION MEDICINE AND HEMOTHERAPY
Authors: Maris Mattaloni, Stella; Arnoni, Carine; Cespedes, Rosario; Nonaka, Claudia; Trucco Boggione, Carolina; Lujan Brajovich, Melina Eliana; Trejo, Andrea; Zani, Nestor; Silvia Biondi, Claudia; Castilho, Lilian; Miguel Cotorruelo, Carlos
Abstract
Background: Kell null (K-0) individuals can produce anti-Ku, an antibody against many epitopes in the Kell glycoprotein, after transfusion and/or pregnancy. Since sensitized K-0 patients are rare, little is known about anti-Ku clinical relevance and in particular about its association to hemolytic disease of the fetus and newborn. Case Report: This work describes a case of neonatal hyperbilirubinemia due to immune-mediated erythrocyte destruction by an alloantibody directed against the Kell glycoprotein. Serologic and molecular approaches identified an anti-Ku alloantibody in maternal serum. A homozygous IVS3 + 1g>a point mutation (KEL*02N.06 allele) was found to be responsible for the lack of Kell antigen expression in the mother's red blood cell and subsequent alloimmunization after a previous pregnancy. Even though in most cases Kell antibodies are clinically severe and may cause suppression of erythropoiesis, in our case the newborn had a moderate anemia and hyperbilirubinemia that was successfully treated with phototherapy without requiring exchange transfusion. Serological and molecular studies performed in the proband's family members allowed us to provide them with proper counseling regarding alloimmunization after transfusion and/or pregnancy. Conclusions: This case enlarges the understanding of the clinical significance of alloantibodies against Kell blood group antigens. (C) 2016 S. Karger GmbH, Freiburg