[Congenital syphilis despite prenatal screening? An evaluation of 14 cases]. / Konnatale Syphilis trotz Mutterschaftsvorsorge? Eine Evaluierung von 14 Fällen.

BACKGROUND: Congenital syphilis (CS) can be effectively avoided by adequate treatment of the mother during pregnancy. Nevertheless, in recent years, the Robert Koch Institute has reported 6-8 of CS cases per year. The aim of this study was to investigate cases of CS with regard to obstetrical history and results of maternal syphilis serology during pregnancy and postpartum. PATIENTS AND METHODS: Between 1997 and 2001, a total of 14 cases of CS were diagnosed after birth in the Stuttgart laboratory. Information on clinical and serological data obtained during prenatal care and at birth had been provided by the treating gynaecologists and paediatricians. Furthermore, serum samples from 11 of the 14 mothers were investigated at the Stuttgart laboratory after birth and also retrospectively at the Herford laboratory. RESULTS: All mothers presented without clinical signs of syphilis. Delayed prenatal care was observed in 6 out of 14 cases. Eleven of the 14 mothers had a positive treponemal screening test. Treatment was initiated only in two of them. During pregnancy treponemal IgM and cardiolipin antibodies were detected in none of 9 and in 5 of 8 sera of untreated mothers, respectively. In contrast, maternal serum samples investigated after birth were all positive for cardiolipin antibodies and 7 of 10 serum samples were positive for TP IgM antibodies. CONCLUSIONS: Delayed or absent prenatal care and misinterpretation of syphilis serology (or laboratory failures) in the presence of latent syphilis are mostly responsible for the inadequate management of syphilis during pregnancy and thus the occurrence of CS.

[Initial results of a prospective study with automated solid phase and column/agglutination techniques in screening for transfusion relevant IgG antibodies]. / Erste Ergebnisse einer prospektiven Studie mit automatisations-fähigen Festphasen- und Säulen-/Agglutinationstechniken beim Screening auf transfusions-relevante IgG-Antikörper.

We report the first results of a prospective study concerning antibody screening in transfusion recipients. We compared the standard tube test (Liss Coombs) with two commercial tests for the detection of red cell IgG antibodies: (1) a column/agglutination test and (2) a microplate/solid-phase system. The results of the study demonstrate several significant advantages of the two methods as compared with the standard tube test. The new methods, especially the microplate test, are superior in determining red cell antibodies which are relevant to transfusion. The two methods are more sensitive and, when automated, more efficient and safer as compared with the standard tube test.

Mutational analysis of extracellular cysteine residues of rat secretin receptor shows that disulfide bridges are essential for receptor function.

We attempted to express point-mutant secretin receptors where each of the 10 extracellular Cys residues was replaced by a Ser residue, in Chinese hamster ovary (CHO) cells. Six of the point-mutant receptors (C24-->S, C44-->S, C53-->S, C67-->S, C85-->S and C101-->S) could not be detected by binding or functional studies: the mutations resulted in functional inactivation of the receptor. In contrast, the four other point-mutant receptors (C11-->S, C186-->S, C193-->S and C263-->S) were able to bind poorly 125I-secretin, and to activate adenylate cyclase with high secretin EC50 values. These results suggest that cysteine residues 24, 44, 53, 67, 85 and 101 are necessary for receptor function, and that the two putative disulfide bridges formed by cysteine residues 11, 186, 193 and 263 are functionally relevant, but not essential for receptor expression. Secretin activated the adenylate cyclase through the quadruple mutant (C11,186,193,263-->S), the four triple mutants, and through double mutants C186,193-->S and C186,263-->S with a very high (microM) EC50 value, suggesting that, in the wild-type receptor, disulfide bridges are formed between C11-C186, and between C193-C263. Prior treatment with dithiothreitol resulted in a marked EC50 increase of the wild-type receptor and of those receptors with at least the two cysteine residues in positions 11 and 186, suggesting that the C11-C186 (but not the C193-C263) disulfide bridge was accessible to this reducing agent. Several results nevertheless indicated that, in mutant receptors, alternative disulfide bridges can be formed between cysteine 186 and cysteine 193 or 263, suggesting that these three residues are in close spatial proximity in the wild-type receptor.