Kawasaki Syndrome, Reye Syndrome, and Aspirin

PEDIATRICS ◽  
1986 ◽  
Vol 77 (4) ◽  
pp. 617-617
Author(s):  
MARTHA BUSHORE

In Reply.— Because the incidence of each of these serious pediatric diseases is low, but the need for prompt recognition and skillful management is essential to optimal outcome, Drs Takahashi and Mason's excellent review and knowledgeable guidance are invaluable to the practicing pediatrician who rarely manages either of these disorders. Our concern that aspirin may interfere with platelet adhesion (when not therapeutically desirable), may increase airway resistance, and may be associated with Reye syndrome should not lead us to discontinue recommending appropriate use of this excellent drug when therapeutic benefit outweighs risk.

PEDIATRICS ◽  
1986 ◽  
Vol 77 (4) ◽  
pp. 616-617
Author(s):  
MASATO TAKAHASHI ◽  
WILBERT MASON

To the Editor.— Aspirin is the mainstay of therapy for Kawasaki syndrome. Its early initiation and continued low-dose therapy have been effective in reducing morbidity and mortality.1 However, a dark cloud of fear has arisen for those physicians and parents involved with Kawasaki syndrome. A number of reports, including a pilot study by the Public Health Service Task Force, cite association between use of aspirin and Reye syndrome.2 Let us examine epidemiologic features of both syndromes.


Author(s):  
W. H. Zucker ◽  
R. G. Mason

Platelet adhesion initiates platelet aggregation and is an important component of the hemostatic process. Since the development of a new form of collagen as a topical hemostatic agent is of both basic and clinical interest, an ultrastructural and hematologic study of the interaction of platelets with the microcrystalline collagen preparation was undertaken.In this study, whole blood anticoagulated with EDTA was used in order to inhibit aggregation and permit study of platelet adhesion to collagen as an isolated event. The microcrystalline collagen was prepared from bovine dermal corium; milling was with sharp blades. The preparation consists of partial hydrochloric acid amine collagen salts and retains much of the fibrillar morphology of native collagen.


1982 ◽  
Vol 47 (2) ◽  
pp. 194-199 ◽  
Author(s):  
Bernd Weinberg ◽  
Yoshiyuki Horii ◽  
Eric Blom ◽  
Mark Singer

Prosthesis airway resistance calculations were completed for five Blom-Singer prostheses and esophageal source airway resistance estimated were made of five laryngectomized patients using the Singer-Blom voice restoration method. Airway resistance of the Blom-Singer prostheses ranged from 46 to 121 cmH 2 O/LPS, while source airways resistance in these subjects ranged from about 155 to 270 cmH 2 O/LPS. These results revealed that the opposition of the voicing sources used in esophageal speech production to airflow through them is substantial and larger than that established for the normal, laryngeal source. Findings are interpreted to highlight major advantages the Singer-Blom (1980) method of speech/voice restoration has over esophageal speech/voice produced on a conventional basis and to reveal specific reasons for the failure of may laryngectomized patients to develop consistent voice and functionally serviceable speech.


2000 ◽  
Vol 5 (6) ◽  
pp. 1-7
Author(s):  
Christopher R. Brigham ◽  
James B. Talmage ◽  
Leon H. Ensalada

Abstract The AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), Fifth Edition, is available and includes numerous changes that will affect both evaluators who and systems that use the AMA Guides. The Fifth Edition is nearly twice the size of its predecessor (613 pages vs 339 pages) and contains three additional chapters (the musculoskeletal system now is split into three chapters and the cardiovascular system into two). Table 1 shows how chapters in the Fifth Edition were reorganized from the Fourth Edition. In addition, each of the chapters is presented in a consistent format, as shown in Table 2. This article and subsequent issues of The Guides Newsletter will examine these changes, and the present discussion focuses on major revisions, particularly those in the first two chapters. (See Table 3 for a summary of the revisions to the musculoskeletal and pain chapters.) Chapter 1, Philosophy, Purpose, and Appropriate Use of the AMA Guides, emphasizes objective assessment necessitating a medical evaluation. Most impairment percentages in the Fifth Edition are unchanged from the Fourth because the majority of ratings currently are accepted, there is limited scientific data to support changes, and ratings should not be changed arbitrarily. Chapter 2, Practical Application of the AMA Guides, describes how to use the AMA Guides for consistent and reliable acquisition, analysis, communication, and utilization of medical information through a single set of standards.


2010 ◽  
Vol 30 (03) ◽  
pp. 150-155 ◽  
Author(s):  
J. W. Wang ◽  
J. Eikenboom

SummaryVon Willebrand factor (VWF) is a pivotal haemostatic protein mediating platelet adhesion to injured endothelium and carrying coagulation factor VIII (FVIII) in the circulation to protect it from premature clearance. Apart from the roles in haemostasis, VWF drives the formation of the endothelial cell specific Weibel-Palade bodies (WPBs), which serve as a regulated storage of VWF and other thrombotic and inflammatory factors. Defects in VWF could lead to the bleeding disorder von Willebrand disease (VWD).Extensive studies have shown that several mutations identified in VWD patients cause an intracellular retention of VWF. However, the effects of such mutations on the formation and function of its storage organelle are largely unknown. This review gives an overview on the role of VWF in WPB biogenesis and summarizes the limited data on the WPBs formed by VWD-causing mutant VWF.


1992 ◽  
Vol 68 (06) ◽  
pp. 694-700 ◽  
Author(s):  
Roy R Hantgan ◽  
Silvia C Endenburg ◽  
I Cavero ◽  
Gérard Marguerie ◽  
André Uzan ◽  
...  

SummaryWe have employed synthetic peptides with sequences corresponding to the integrin receptor-recognition regions of fibrinogen as inhibitors of platelet aggregation and adhesion to fibrinogen-and fibrin-coated surfaces in flowing whole blood, using a rectangular perfusion chamber at wall shear rates of 300 s–1 and 1,300 s–1. D-RGDW caused substantial inhibition of platelet aggregation and adhesion to fibrinogen and fibrin at both shear rates, although it was least effective at blocking platelet adhesion to fibrin at 300 s–1. RGDS was a weaker inhibitor, and produced a biphasic dose-response curve; SDRG was inactive. HHLGGAK-QAGDV partially inhibited platelet aggregation and adhesion to fibrin(ogen) at both shear rates. These results support the identification of an RGD-specific receptor, most likely the platelet integrin glycoprotein IIb: III a, as the primary receptor responsible for platelet: fibrin(ogen) adhesive interactions under flow conditions, and indicate that platelet adhesion to surface bound fibrin(ogen) is stabilized by multivalent receptor-ligand contacts.


1987 ◽  
Vol 58 (02) ◽  
pp. 786-789 ◽  
Author(s):  
O Behnke

SummaryAdhesion of rat blood platelets to native rat tail collagen fibrils was studied in the electron microscope under conditions that preserved collagen-associated proteoglycans (CAPG). The CAPG molecules were aligned in chain-like configurations that encircled the fibrils with a 65 nm period; they appeared to coat the fibrils completely and extended 60-100 nm away from the fibril. The initial platelet-fibril contact occurred between the platelet glycocalyx and the CAPG of the fibrils i.e. between two surfaces with net-negative charges. When close contact was established between the fibril surface proper and the platelet membrane, CAPG were not identified in the area of contact, and the collagen-platelet distance was reduced to a ~10-12 nm wide gap traversed by delicate links in register with fibril periodicities.


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