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All patients were treated with combined chemo- and radiotherapy; three were autotransplanted. Four patients attained clinical remission absence of symptoms, normal marrow, no further lesions by CIP ; , lasting a mean of 23 mos. r. 6-31 ; . During remission, Tc99m-sestaMIBI showed only variable degree of diffuse uptake in absence of focality, which reappeared in relapse. Five patients never attained a complete disease control: in four of them CIP and Tc99m-sestaMIBI were concordant, but in one patient, who previously had showed focal tracer uptake, a bulky symptomatic tumor adjacent to L2 developed after chemotherapy was not detected by the tracer. In conclusion, Tc99m-sestaMIBI seems an excellent tracer in nsMM, both at diagnosis and during the follow up. If confirmed, these data could prompt to reconsider the exclusion of this subset of patients from controlled multicentric studies and requip.

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George sgouros 1 , susan knox 2 , michael joiner 3 , william morgan 4 and amin kassis 5 1 school of medicine, johns hopkins university, baltimore, maryland; 2 school of medicine, stanford university, stanford, california; 3 wayne state university and karmanos cancer institute, detroit, michigan; 4 school of medicine, university of maryland, baltimore, maryland; and 5 harvard medical school, boston, massachusetts correspondence: for correspondence or reprints contact: george sgouros, phd, crb ii, 4m61, 1550 orleans st. 1690-2 ; , british physicians endorse the first-line use of steroids in children with more severe cases, but they maintain that the jury remains out for children with milder cases and methotrexate.

Walter Martz * , Niels Tobias and Bernd Mhlbauer Institute of Clinical Pharmacology, Klinikum Bremen-Mitte, St.-Jrgen-Strasse 1, D-28177 Bremen A toddler who had lived with drug addict parents, was found dead. The autopsy could not confirm any unequivocal cause of death. Therefore, a toxicological screening was ordered by the prosecutor. The goal of our examination was to identify or exclude drugs potentially contributing to the death of the child. This screening involved Cloned-Enzyme-Donor-Immunoassay CEDIA ; and FPIA ; , a Systematic Toxicological Analysis STA ; using GC MS and a LC MS search for amphetamines. All analyses turned out to be blank. In one of the loose tablets seized in the apartment we found methylphenidate and identified it as the branded drug RitalinTM. A hair analysis showed a positive result for methylphenidate. In order to illuminate the ante-mortem application, we re-examined the autopsy material for the major metabolite ritalinic acid, which was not included in the STA. We synthesized ritalinic acid by hydrolysis of methylphenidate in methanolic potassium hydroxide solution. Employing HPLC DAD the yield was near 100 % based on their peak areas at 222 nm ; . The sample preparation is crucial. Due to the amphoteric character of the substance liquid-liquid-extraction fails. The best results were obtained with an optimized SPE procedure. LC MS MS with electrospray ionization appeared to be the most suitable method for the quantification of both methylphenidate and ritalinic acid. Using the procedure described here, neither methylphenidate nor ritalinic acid were detectable in kidney, liver, muscle tissue or in putrescence liquid. Thus, an administration of methylphenidate to the child ante-mortem could not be proven in the autopsy material available.

Escola Paulista de Medicina, UNIFESP, Sao Paulo, Brazil; 2 University of Montreal, Montreal, QC, Canada; and 3BioMep Inc., Montreal, QC, Canada The PHEX gene phosphate-regulating gene with homologies to endopeptidases on the X chromosome ; encodes a protein with structural homologies to members of the M13 family of metallopeptidases. Mutations in the PHEX gene are responsible for X-linked hypophosphatemia XLH ; , the most prevalent form of inherited rickets in humans, characterized by growth retardation, osteomalacia, hypophosphatemia, and renal defects in phosphate reabsortion and vitamin D metabolism. However the mechanism by which loss of PHEX function results in the disease phenotype and the endogenous PHEX substrate s ; remain unknown. In order to study PHEX substrate specificity, combinatorial fluorescent peptide libraries were synthesized and tested as PHEX substrates. In contrast with other members of M13 family, PHEX showed a strict requirement for acidic amino acid residues Asp or Glu ; in S1 subsite with a strong preference for Asp. Subsites S2 , S1 and S2 exhibited less defined specificity requirements, but the presence of Leu, Pro or Gly in P2 , or Val, Ile or His in P1 precluded hydrolysis of the substrate by the enzyme. In addition, using fluorescent peptides derived from FGF-23 or MEPE sequences flanked by Abz and EDDnp , we show that these physiologically relevant proteins are potential PHEX substrates. Finally, our results clearly indicate that PHEX does not have a Neprilysin-like substrate specificity. Supported by FAPESP, CNPq and Canadian Institutes for Health Research.
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