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At least 667 records · Page 37Linked to original sources
PubMed1992

[Growth retardation in children with frequent relapsing nephrotic syndrome on steroid--improvement of height velocity after administration of immunosuppressive agent].

In a study involving 22 cases of nephrotic syndrome in children, investigations were made of growth disturbance caused by corticosteroid in relation to dose of the steroid and age levels at steroid treatment and also of the effects of concomitantly used immunosuppressive drugs. The final height of frequent relapsing nephrotic syndrome was below M-2SD in approximately 30% of cases. Final heights of boys receiving the steroid from 12 to 16 years of age and of girls treated with the steroid from 10 to 14 years of age were below M-2SD and 10 cm lower than the target height. Final heights of boys and girls who could be withdrawn from steroid therapy by the age of 14 and 12, respectively, were invariably within or above the normal range. The addition of azathioprine therapy resulted in no appreciable reduction of steroid dosage nor improvement of yearly growth rate, although the frequency of relapse for that year was diminished. Under a regimen of concomitant cyclophosphamide the frequency of relapse and steroid dosage was also reduced but the growth rate was accelerated, no significant reduction of steroid consumption was achieved. The administration of cyclosporin A in doses of 1.5-5.0 mg/kg was marked by a reduction in steroid dosage as well as in the frequency of relapse and allowed for near normal growth rate, with no significant differences being observed between the high dose group (3-5 mg/kg/day) and the low dose group (1.5-2.5 mg/kg/day). Prolonged steroid therapy in frequent relapsing nephrotic syndrome may produce dwarfism and other distressing side effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Treatment of multiple sclerosis with cladribine (2-CDA), a new immunosuppressant agent. Theoretical basis and preliminary results].

The rationale for immunosuppressive treatment of multiple sclerosis comes from current concepts of pathogenesis of this disease. However, clinical effects of immunosuppression have been largely disappointing. Cladribine (chloro-2'-deoxyadenosine, 2CdA) is a new antileukaemic drug which also shows a strong immunosuppressive activity in vitro and in vivo. Being successfully used to treat lymphoproliferative diseases during last few years, cladribine is currently tested in multiple sclerosis. Preliminary results of two independent randomized, placebo-controlled trials are very promising. The indicate that treatment with cladribine may halt the progression of chronic progressive MS, and decrease the frequency of relapses and improve neurological status in remitting-relapsing stage of the disease.

Blood-Brain Barrier↗
PubMed2001

Transport activity and surface expression of the Na+-Ca2+ exchanger NCX1 are inhibited by the immunosuppressive agent cyclosporin A and by the nonimmunosuppressive agent PSC833.

Cyclosporin A (CsA) treatment of HEK 293 cells expressing the rat heart RHE-1 (NCX1.1, EMBL accession number ) or the rat brain RBE-2 (NCX1.5, GenBank(TM) accession number ) Na(+)-Ca(2+) exchanger inhibited their transport activity in a concentration-dependent manner. The inhibition was detectable at 2 microm CsA, and exposure of the cells to 20 microm CsA resulted in a decrease of the Na(+)-dependent Ca(2+) uptake to about 20% relative to that of untreated cells. Determination of the surface expression of the exchanger protein revealed a parallel concentration-dependent reduction in the amount of the immunoreactive protein. No reduction was detected in the amount of total immunoreactive exchanger protein in CsA-treated cells relative to untreated ones. Among the different drugs tested, only PSC833, an analog of cyclosporin D, mimicked the effects of CsA. Exposure of the transfected cells to the chemically related cyclosporin D and macrolide drugs (FK506 or rapamycin) had no effect on the transport activity or the surface expression of the Na(+)-Ca(2+) exchanger. Co-expression of the human multidrug transporter P-glycoprotein (of which both drugs are modulators) with the cloned Na(+)-Ca(2+) exchanger revealed that transport activity and surface expression of each transporter in the co-transfected system were similar to those of each transporter alone in both the presence and absence of CsA or PSC833. CsA and PSC833 inhibited the surface expression of the NCX1 protein but did not alter the surface expression of P-glycoprotein. Unlike some P-glycoprotein endoplasmic reticulum-retained mutants (Loo, T. W., and Clarke, D. M. (1997) J. Biol. Chem. 272, 709-712), CsA did not rescue RBE-2/F913-->Stop, an endoplasmic reticulum-retained function-competent mutant of the Na(+)-Ca(2+) exchanger (Kasir, J., Ren, X., Furman, I., and Rahamimoff, H. (1999) J. Biol. Chem. 274, 24873-24880) and did not induce its kinesis to the surface membrane, further demonstrating molecular differences between P-glycoprotein and NCX1 mutants for interaction with CsA.

ATP Binding Cassette Transporter, Subfamily B, Mem↗