Mycophenolate mofetil therapy for children with intractable nephrotic syndrome

BACKGROUND: Cyclosporin A (CyA) can suppress relapses and reduce proteinuria in frequent-relapse nephrotic syndrome (FRNS) and steroid-resistant nephrotic syndrome (SRNS). However, some patients remain resistant to CyA therapy. The purpose of the present paper was to evaluate mycophenolate mofetil (MMF) treatment in pediatric patients with CyA-resistant intractable nephrotic syndrome. METHODS: MMF therapy was given to 11 patients with FRNS who had relapse despite CyA therapy, and one patient with SRNS who had been receiving combined therapy using steroid and CyA until immediately before the start of MMF. MMF was administered at a daily dose of 750-1000 mg/m(2) in two divided doses. RESULTS: Ten of the 11 patients with FRNS were able to maintain remission. Among them, seven patients remained relapse free for 1 year, and two patients had a decrease in the frequency of relapse after initiation of MMF therapy. One patient, however, had repeated cycles of remission and relapse, and was considered resistant to MMF therapy. The total prednisolone dose during the period from month 6 to month 12 after the start of MMF therapy was significantly lower than that during the 6 month period before the start of MMF therapy. The patient with SRNS, who had not achieved remission despite CyA administration, had complete remission on MMF. No serious adverse effects were seen in any of the present patients. CONCLUSION: MMF could be useful in CyA-treatment-refractory FRNS and CyA-resistant SRNS.     

Experimental study on cross‐reactivity of α‐arbutin toward p‐phenylenediamine and hydroquinone in guinea pigs

Hydroquinone (HQ) has been used as a skin‐lightening cosmetic ingredient, while it has been known that HQ shows sensitizing potential and cross‐reactivity toward a strong sensitizer, p‐phenylenediamine (PPD). α‐Arbutin, a glycoside of HQ (4‐hydroxyphenyl α‐D‐glucopyranoside), is used worldwide as a skin‐lightening agent. The aim of this study was to evaluate the cross‐reactivity of α‐arbutin toward PPD and HQ. All tests were performed using the guinea pig maximization test. In experiments on the cross‐reactivity of α‐arbutin or HQ to PPD, six animals in each group were induced with PPD at 0.1% by i.d. injection and at 1.0% by topical application. The animals were challenged with α‐arbutin, HQ or PPD (as a positive control) at concentrations of 0.01%, 0.05% and 0.1%. In experiments on the cross‐reactivity of α‐arbutin to HQ, four animals in each group were induced with HQ at 2% by i.d. injection and at 1% by topical application. The animals were challenged with α‐arbutin or HQ (as a positive control) at concentrations of 0.2%, 2% and 20%. The cross‐reactivity toward PPD was observed with HQ (4/6) only at 0.1% challenge. However, α‐arbutin showed no apparent cross‐reactivity to either PPD or HQ even at their highest challenge concentrations. Potent sensitization was observed with PPD (6/6) even at 0.01% challenge and with HQ (3/4) at 0.2%. In conclusion, glycosylation of HQ remarkably reduced the sensitization potency of HQ and the cross‐reactivity of HQ to PPD.