Emetic effects of morphine and piritramide.

BACKGROUND: Successful management of postoperative pain requires that adequate analgesia is achieved without excessive adverse effects. Opioid-induced nausea and vomiting is known to impair patients' satisfaction, but there are no studies providing sufficient power to test the hypothesis that the incidence of opioid-induced nausea and vomiting differs between micro -opioid receptor agonists. Thus, we tested the hypothesis that the incidence of vomiting and nausea differs between morphine and piritramide. METHODS: In a prospective, randomized, double-blind fashion, we administered either morphine (n=250) or piritramide (n=250) by patient-controlled analgesia (PCA) for postoperative pain relief. We used a bolus dose of 1.5 mg with a lockout time of 10 min. Incidence and intensity (numerical rating scale) of postoperative nausea, vomiting, pain, patient satisfaction (score 0-10), side-effects (score 0-3) and drug consumption were measured. RESULTS: Mean drug consumption did not differ between the piritramide and morphine groups (30.8 (SD 22.4) mg day(-1) vs 28.4 (21.8) mg day(-1)) during the first postoperative day and there were no significant differences in the overall incidence of nausea (30% vs 27%) and vomiting (19% vs 15%). Intensity of nausea correlated inversely (P=0.01) with morphine consumption but not with piritramide consumption. Pain scores both at rest (2.2 (1.9) vs 2.6 (2)) and during movement (4.4 (2.2) vs 4.9 (2.3)) were slightly but significantly less with morphine. CONCLUSIONS: Opioid-induced emesis was observed in about one-third of the patients using morphine and piritramide for PCA and the incidence of vomiting was one-half of that. Potential differences in the incidence of vomiting during PCA therapy between these micro-opioid receptor agonists can be excluded.

Alloimmunization against Iy, a low-frequency antigen on platelet glycoprotein Ib/IX as a cause of severe neonatal alloimmune thrombocytopenic purpura.

Neonatal alloimmune thrombocytopenia (NAIT) is usually induced by platelet-specific antibodies against HPA-1a (Zwa) or HPA-5b (Bra). Recently, low-frequency alloantigens on the platelet glycoprotein (GP) IIb/IIIa complex have been discovered as a cause for NAIT. In this report, a new low-frequency platelet-specific alloantigen, Iy, is described which induced severe NAIT. The corresponding antigen was detected in 1/249 unrelated German blood donors. Antibody binding assays with trypsin-digested platelets (ELISA, immunoprecipitation with biotin-labelled platelets) indicate that the antigen is not localized on the glycocalicin moiety of GP Ib alpha, but may be situated on the remnant moiety of GP Ib alpha, GP IX or GPIb beta. Apparently, Iy is not related to the HPA-2 (Ko) antigen system.

New polymorphism on platelet glycoprotein IIIa gene recognized by endonuclease Msp I: implications for PlA typing by allele-specific restriction analysis.

BACKGROUND: Five human platelet alloantigen systems have been shown to result from single base pair substitutions in encoding regions of platelet glycoprotein genes IIIa, Ib, IIb, and Ia. For each of the diallelic systems, at least one restriction enzyme is known to cut only one of the two haplotypes. In the PlA system, restriction endonucleases Nci I and Msp I both recognize the PlA2 allele. STUDY DESIGN AND METHODS: A causal observation of an unexpected Msp I restriction pattern of a PlA2/PlA2 individual was made. Samples from 261 blood donors were then typed for antigens of the PlA system by restriction fragment length polymorphism analysis using the Nci I and Msp I restriction enzymes. RESULTS: Applying both enzymes, concordant restriction patterns were found in 258 of 261 blood donors. Three donors had a base pair mutation on the PlA2 allele, which creates an additional restriction site for Msp I 20 base pairs downstream from the PlA polymorphic site. Nucleotide sequence analysis revealed a CT217-->CG217G base exchange resulting in a Leu40-->Arg40 polymorphism of glycoprotein IIIa. CONCLUSION: Presuming that the mutation is not a singular phenomenon and also occurs with the PlA1 haplotype, it could lead to false interpretations of restriction analysis with Msp I. To exclude that possibility, Nci I is preferred for restriction fragment length polymorphism typing in the PlA system.

[Immunization against a new, infrequent alloantigen (Iy) on the platelet glycoprotein Ib/IX as a cause of a serious case of neonatal alloimmune thrombocytopenia]. / Immunisierung gegen ein neues, niedrigfrequentes Alloantigen (Iy) auf dem thrombozytären Glykoprotein Ib/IX als Ursache für einen schweren Fall von neonataler Alloimmunthrombozytopenie.

Neonatal alloimmune thrombocytopenia is the consequence of maternal alloimmunization against platelet-specific alloantigens, usually PIA1 or Br(a). The clinical picture is characterized by signs of haemorrhagic diathesis as a result of marked thrombocytopenia. In the last years, rare cases of immunization against 'low-frequency' or 'private' platelet alloantigens on the platelet glycoprotein (GP) complex IIb/IIIa have been found. This is the first report on NAIT due to maternal immunization against a low-frequency platelet alloantigen ('Iy') localized on platelet GP Ib/IX.