Vox Sanguinis 

About: Vox Sanguinis is an academic journal published by Wiley-Blackwell. The journal publishes majorly in the area(s): Antigen & Antibody. It has an ISSN identifier of 0042-9007. Over the lifetime, 9291 publications have been published receiving 176916 citations.

A retrospective study on transmission of adult T cell leukemia virus by blood transfusion: seroconversion in recipients.

Abstract: Possible transmission of adult T cell leukemia virus (ATLV) by blood transfusion was studied retrospectively. Of 41 recipients of whole blood or blood components containing cells from donors having antibodies to antigen that is associated with ATLV (anti-ATLA), 26 (63.4%) produced anti-ATLA. However, no anti-ATLA was detected in all 14 recipients of fresh-frozen plasma prepared from anti-ATLA-positive donors. None of 252 recipients of blood with cell components from anti-ATLA-negative donors produced anti-ATLA. The development of anti-ATLA in the recipients may correspond to antibody production after establishment of primary infection with ATLV that is associated with cells in blood from anti-ATLA-positive donors who are ATLV carriers.

ABH and related histo-blood group antigens; immunochemical differences in carrier isotypes and their distribution.

Abstract: This review summarizes present knowledge of the chemistry of histo-blood group ABH and related antigens. Recent advances in analytical carbohydrate chemistry (particularly mass spectrometry and NMR spectroscopy) and the introduction of monoclonal antibodies (MoAbs) have made it possible to distinguish structural variants of histo-blood group ABH antigens. Polymorphism of ABH antigens is induced by: (i) variations in peripheral core structure, of which four (type 1, 2, 3 and 4) are known in man; (ii) variation in inner core by branching process (blood group iI), leading to variation of unbranched vs. branched ABH determinants; (iii) biosynthetic interaction with other glycosyltransferases (Lewis, P. T/Tn blood systems) capable of acting on the same substrate as the ABH-defined transferases, and finally (iv) the nature of the glycoconjugate (glycolipid, glycoprotein of N- or O-linked type). ABH variants induced by item (i) above have been clearly distinguished qualitatively by MoAbs; e.g., at least six types of A determinants can be distinguished by qualitatively different classes of antibody. The variants induced by item (ii) create mono- vs. bivalent antigens which may be responsible for observed differences in antibody-binding affinity. Detailed studies of the chemistry of these antigens have increased our insight into blood groups, providing the basis for blood group iI and A subgrouping, as well as a relation between the ABH and Lewis, P, and T/Tn systems. A survey of the literature on distribution patterns of ABH variants is presented. It has been assumed that expression of histo-blood group antigens is developmentally regulated. Relationships between histo-blood group expression, development, differentiation and maturation, as well as malignant transformation, are discussed.

Clinical expertise in the era of evidence-based medicine and patient choice.

Abstract: You are caring for a 68 year old man who has hypertension (intermittently controlled) with a remote gastrointestinal bleed and non-valvular atrial fibrillation (NVAF) for 3 months, and an enlarged left atrium (so cardioversion is unlikely). The patient has no history of stroke or transient ischaemic attack. His father experienced a debilitating stroke several years ago and when he learns that his atrial fibrillation places him at higher risk for a stroke, he is visibly distressed. The concepts of evidence-based medicine are evolving as limitations of early models are addressed. In this editorial, we present a new model for evidence-based clinical decision making based on patients' circumstances, patients' preferences and actions, and best research evidence, with a central role for clinical expertise to integrate these components. Traditionally, clinicians have been credited with clinical acumen according to their skills in making a diagnosis and prescribing or administering a treatment. The advent of major investments in biomedical research, leading to new and better tests and treatments, has spurred the development of critical appraisal of the medical literature and evidence-based medicine,1 and application of current best evidence from healthcare research is now an expected adjunct to clinical acumen. Initially, evidence-based medicine focused mainly on determining the best research evidence relevant to a clinical problem or decision and applying that evidence to resolve the issue. This early formulation de-emphasised traditional determinants of clinical decisions, including physiological rationale and individual clinical experience. Subsequent versions of evidence-based decision making have emphasised that research evidence alone is not an adequate guide to action. Rather, clinicians must apply their expertise to assess the patient's problem and must also incorporate the research evidence and the patient's preferences or values before making a management recommendation (figure 1).2 Figure 1 Early model of the key elements for evidence-based clinical decisions Figure …

Intravenous Administration of Human γ‐Globulin*

Abstract: Summary Intravenous administration of standard human γ-globulin can lead to untoward reactions. This is due to at least one endogenous and an exogenous factor. The “endogenous” factor is revealed by the finding that certain subjects only - especially patients with an antibody deficiency syndrome - react to intravenous infusions of γ-globulin administered under standard conditions. The “exogenous” factor resides in the γ-globulin preparation itself and is related to its anticomplementary activity. The “endogenous” factor can be temporarily eliminated by “desensitizing” the patient; the “exogenous” factor may be eliminated by ultracentrifugation, enzymatic breakdown of the γ-globulin, or other treatment involving exposure to low pH values. Upon clinical trial, the preparations obtained by enzymatic degradation or by exposure to pH 4 at 37 °C displayed the best tolerance after intravenous application. Enzymatically degraded γ-globulin is partially eliminated by the kidney and has no desensitizing effect. On the other hand, pH 4 exposed γ-globulin does not pass through the kidney and is still capable of desensitizing “sensitive” individuals. Resume L'administration intraveineuse de γ-globuline bumaine peut provoquer chez l'homme des reactions serieuses. Ces phenomenes d'intolerance sont dus a l'existence au moins d'un facteur endogene et d'un facteur exogene. Le facteur “endogene” se manifeste en ce sens que seul certains malades - specialement ceux souffrant d'un syndrome par carence d'anticorps - tolerent mal l'injection intraveineuse de γ-globuline. Le facteur “exogene” est associe a la γ-globuline meme et est en relation directe avec son action anticomplementaire. Le facteur “endogene” peut etre elimine temporairement par une desensibilisation du malade; le facteur “exogene” peut etre elimine par ultracentrifugation, par degradation enzymatique de la γ-globuline ou par d'autres traitements tels qu'une exposition prolongee a des acides tres dilues. Ce sont les preparation obtenues par degradation enzymatique ou par l'action d'acides dilues qui sont le mieux tolerees lors de l'injection intraveineuse. La γ-globuline digeree sous l'action d'un enzyme est eliminee partiellement par les reins et n'exerce aucune action desensibilisante. Par contre, la γ-globuline exposee a un pH de 4 ne passe pas le seuil renal, et sa capacite de desensibiliser des individus sensibles, persiste. Zusammenfassung Die intravenose Applikation von menschlichem Standard-γ-Globulin kann zu schweren Zwischenfallen Anlas geben. Diese Unvertraglichkeit beruht zumindest auf einem exogenen und einem endogenen (individuellen) Faktor. Der “endogene” (individuelle) Faktor ausert sich darin, das nur gewisse Individuen—in der Regel handelt es sich dabei um Patienten mit einem Antikorpermangelsyndrom - auf eine i.v. γ-Globulingabe mit Unvertraglichkeitserscheinungen reagieren. Der “exogene” Faktor liegt im γ-Globulinpraparat; er steht mit dessen anti-komplementarer Wirkung in direkter Beziehung. Es ist moglich, den “endogenen” Faktor vorubergehend durch “Desensibilisierung” des Patienten (rnit Standard-γ-Globulin) auszuschalten. Der “exogene” Faktor kann entweder durch Ultrazentrifugierung, durch enzymatische Verdauung, oder durch blose Ansauerung (pH 4) eliminiert werden. Bei der klinischen Prufung erwiesen sich diejenigen Praparate als gut vertraglich, die durch enzymatische Verdauung oder durch Ansauern gewonnen wurden. Enzymatisch abgebaute γ-Globuline gehen teilweise durch die Niere verloren; sie besitzen auserdem keine desensibilisierende Wirkung. Demgegenuber erscheint das durch Aneauern gewonnene Praparat nicht im Urin des Patienten. Es verhalt sich auch in bezug auf seinen desensibilisierenden Effekt wie Standard-γ-Globulin.