title: Platelet-activating factor type activity in plasma from patients with septicemia and other diseases.
abstract: The purpose of the present study was to determine whether increased levels of platelet-activating factor (PAF) type activity can be detected in plasma from patients with septicemia and other diseases. A level of PAF below 0.5 ng/mL of plasma was considered normal. We found that plasma from a patient with adverse anaphylactoidic reaction to intravenous analgetics contained 2.1 ng PAF/mL. In seven patients with septicemia, including urosepsis, endocarditis and peritonitis, and with positive blood culture, increased plasma PAF levels (1-20 ng PAF/mL) were observed. Other patients with clinical indications of septicemia had negative blood cultures and/or increased levels of C-reactive protein (CRP). Yet, in the plasma from these patients, no increased PAF levels were detected under the assay conditions used. Two patients with allergic asthma, requiring treatment with steroids, had no measurable plasma PAF. In the plasma from a patient with idiopathic thrombocytopenic purpura (ITP) only an "endogenous" inhibitor of PAF induced platelet aggregation was initially observed. In spite of this, the patient responded to treatment with the PAF antagonist WEB 2086 with a dramatic increase in platelet count (Lohmann et al., Lancet ii, 1147, 1988). Thereafter, also increased PAF levels (3.3 ng PAF/mL) were detected in plasma, although some "endogenous" inhibitor of PAF was still present. In conclusion, increased PAF levels in plasma from patients support a role of PAF in certain human disease states, such as in anaphylactoid reaction, sepsis and septic shock. The type, relevance and specificity of endogenous inhibitors of PAF deserve further study.
authors.affiliation: Department of Pharmacology, Boehringer Ingelheim, Germany.
authors.forename: H O
authors.initials: HO
authors.lastname: Heuer
authors.forename: H
authors.initials: H
authors.lastname: Darius
authors.forename: H F
authors.initials: HF
authors.lastname: Lohmann
authors.forename: J
authors.initials: J
authors.lastname: Meyer
authors.forename: M
authors.initials: M
authors.lastname: Schierenberg
authors.forename: N
authors.initials: N
authors.lastname: Treese
mesh_terms: D000328:Adult; D000818:Animals; D001381:Azepines / Q000494:pharmacology / Q000627:therapeutic use; D016470:Bacteremia / Q000097:blood*; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology; D002097:C-Reactive Protein / Q000032:analysis; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010972:Platelet Activating Factor / Q000032:analysis* / Q000037:antagonists & inhibitors / Q000494:pharmacology; D010974:Platelet Aggregation / Q000187:drug effects; D010976:Platelet Count / Q000187:drug effects; D011696:Purpura, Thrombocytopenic / Q000097:blood / Q000188:drug therapy; D011817:Rabbits; D012016:Reference Values; D014230:Triazoles / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D001381:Azepines; D010972:Platelet Activating Factor; D014230:Triazoles; C052518:WEB 2086; D002097:C-Reactive Protein