Search PubMed⌕ Search

Biomedical subjects

B Alving

Publications and source records attributed to B Alving.

14 recordsLinked to original sources
PubMed1999

How to improve transfusion medicine. A treating physician's perspective.

As transfusion medicine becomes more complex, cooperative strategies are gaining increasing importance in relaying information to the treating physician and in incorporating the treating physician into the education and quality control processes. The broad domain of transfusion medicine is illustrated by the variety of disciplines involved in defining the use of products such as fresh frozen plasma and the newly released solvent-detergent-treated plasma, fibrin glue and highly purified fibrin sealant, and leukoreduced and irradiated blood products. Cooperative efforts among physicians and other personnel of multiple disciplines are essential to ensure appropriate use and continuous evaluation of blood products.

Blood Transfusion↗
PubMed1998

Women with thrombophilia: assessing the risks for thrombosis with oral contraceptives or hormone replacement therapy.

Women with inherited or acquired thrombophilia are at increased risk for venous thromboembolism (VTE) when they use oral contraceptives (OCs) of either the second or third generation. For women who are heterozygous for Factor V Leiden, the risk is probably 28 to 50 of 10,000 women-years compared to 2 to 5 of 10,000 years for those not known to have thrombophilia. The thrombotic risk is highest during the first year that OCs are used. Whether women with thrombophilia are at increased risk for VTE when they use hormone replacement therapy (HRT) has not been assessed in any study. For women without thrombophilia, the risk for VTE associated with HRT is probably 2 to 3 of 10,000 years. The benefits of HRT include reduced risk for myocardial infarction and Alzheimer's disease, and increased bone density. The physiological changes induced by HRT are not the same as those induced by OCs. Small studies have suggested that for women who have additional risks of thrombosis (i.e., perioperative setting, underlying systemic lupus erythematosus), HRT does not confer the same increased risk of thrombosis, as does the use of OCs. Until data are available to address the magnitude of any increase in thrombotic risk induced by HRT for women with thrombophilia, physicians probably serve their patients best by providing information about the benefits of HRT, emphasizing that the risk of VTE is unknown, and encouraging patients to take an active role in decisions about their healthcare.

Contraceptives, Oral↗
PubMed1996

Profound normovolemic hemodilution: hemostatic effects in patients and in a porcine model.

Previous systematic investigations of the hemostatic effects of normovolemic hemodilution (NHD) have not explored the influence of hematocrits less than 20% in humans or animals. However, clinical interest in maximizing the perioperative conservation of erythrocytes may involve profound NHD beyond traditionally accepted empiric end points. We report here on coagulation data in eight healthy adolescent patients undergoing profound NHD in concert with surgical correction of idiopathic scoliosis, and in 29 swine undergoing experimental stepwise NHD until death. Blood was replaced with 5% albumin in 0.9% saline in our patients, and with 5% albumin in lactated Ringer's solution in our pigs. A 75% blood volume exchange in our patients yielded a platelet count (PLT) of 158 +/- 26 x 10(3)/microL, fibrinogen concentration (FIB), 50 +/- 7 mg/dL, prothrombin time (PT), 25.4 +/- 2.6 s, activated partial thromboplastin time (aPTT), 87 +/- 15s, and a nadir hemoglobin of 2.8 +/- 0.2 g/dL; however, global oxygen delivery as assessed by body oxygen consumption remained adequate. Coagulation during the experimental porcine hemodilution was assessed by measuring PLT, FIB, PT, and aPTT, as well as by measurement of coagulation factor activities. In neither species did clinically significant thrombocytopenia (PLT < 100 x 10(3)/ microL) become manifest prior to clinical or other laboratory evidence of coagulopathy. Rather, a combined deficiency of coagulation factors explains the coagulopathy developing during NHD in both patients and swine. Abnormal hemostasis develops prior to compromise of global tissue oxygenation, assessed by mixed venous oxygen saturation and total body oxygen consumption, during NHD in healthy patients anesthetized as described. Therefore, NHD may be more limited by preservation of normal coagulation than of global oxygen delivery and consumption.

Adolescent↗
PubMed1996

Laboratory testing for hypercoagulable disorders.

Evaluation of inherited hypercoagulability in patients with venous thromboembolism includes testing for the functional activity of protein S, protein C, antithrombin III, and for resistance to activated protein C. Resistance to activated protein C can be assessed with plasma as well as with DNA-based assays that are commercially available. Acquired disorders include the development of antibodies against phospholipid-protein complexes (as would occur in patients with the antiphospholipid syndrome). The inherited and acquired abnormalities are most commonly apparent as superficial or deep venous thromboembolism in younger patients, most of whom have additional risk factors for thrombosis, such as use of oral contraceptives or recent trauma. These tests are cost effective if the results will influence patient management or will have potential value in the care of family members in situations of increased thrombotic risk.

Adult↗
PubMed1993

Rodenticide-induced coagulopathy in a young child. A case of Munchausen syndrome by proxy.

PURPOSE: To present the diagnosis and management of superwarfarin ingestion, a cause of serious and prolonged coagulopathy. METHODS: Specific identification of the anticoagulant was made by high-pressure liquid chromatography. RESULTS: A 24 month-old child developed bruises and a prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT) after receiving multiple doses of brodifacoum, a superwarfarin rodenticide. The coagulopathy was treated successfully with large doses of parenteral and oral vitamin K1; fresh frozen plasma was administered as a precautionary measure on two occasions. After the first 10 days of the child's hospitalization, the mother was identified as the source of brodifacoum, exemplifying the behavior described as Munchausen syndrome by proxy. Oral vitamin K1 was initiated and continued in an outpatient setting with tapering doses over nine months, using the PT as a guide for therapy. CONCLUSIONS: This report emphasizes the necessity of recognizing rodenticide poisoning and investigating its source. Frequent monitoring of the PT is essential to prevent hemorrhagic complications due to repeat exposure, inadequate vitamin K1 therapy, or noncompliance.

4-Hydroxycoumarins↗
PubMed1989

Coagulation factor XII (Hageman factor) Washington D.C.: inactive factor XIIa results from Cys-571----Ser substitution.

Structural studies on a congenital abnormal coagulation factor XII (Hageman factor), factor XII Washington D.C., have been performed to identify the defect responsible for its lack of procoagulant activity. Amino acid sequence analysis of a tryptic peptide isolated from the abnormal factor XII indicated that Cys-571 (equivalent to Cys-220 in the chymotrypsin numbering system) had been replaced by serine. No other substitutions in the active-site triad--namely, His-393, Asp-442, and Ser-544--were found. We propose that the Cys-571----Ser replacement found in this factor XII variant destroys the formation of the disulfide linkage between Cys-540 and Cys-571, giving rise to an altered conformation of the active-site serine residue or the secondary substrate-binding site and, thus, leads to the loss of enzyme activity.

Amino Acid Sequence↗
PubMed1989

Plasminogen activator and plasminogen activator inhibitor activities in men with coronary artery disease.

Although elevated levels of plasminogen activator inhibitor-1 (PAI-1) have been associated with the development of myocardial infarction, the correlation between the presence of coronary artery disease and increased levels of PAI-1 is controversial. The present study evaluated the association between angiographically-documented coronary artery disease and plasma levels of PAI-1 and tissue-type plasminogen activator (t-PA) in 65 men (ages 35 to 65 years) who had no previous history of myocardial infarction, angioplasty, or other medical illnesses. PAI-1 activity in these 65 patients was inversely correlated with t-PA activity, which was measured before and after venous occlusion. PAI-1 activity correlated positively with levels of triglycerides. There was a significant negative correlation between PAI-1 activity and levels of high-density lipoprotein. Each patient was placed in one of five groups according to the severity of coronary atherosclerosis, which ranged from normal vessels (group I) to greater than 50% occlusion of three vessels (group V). There were no significant differences among the five groups with respect to mean activity of PAI-1 (p = 0.98) or t-PA activity measured before venous occlusion (p = 0.22) or after occlusion (p = 0.70). T-PA and PAI-1 activities in these five groups were not different from those in 35 healthy men. These data indicate that there is no association between activities of PAI-1 or t-PA and coronary artery disease in this well-characterized male population.

Adult↗
PubMedDate not supplied

Effect of dengue virus on procoagulant and fibrinolytic activities of monocytes.

Some of the fibrinolytic and coagulation enzymes that monocytes produce are urokinase, a plasminogen activator (PA); a PA-specific inhibitor (PAI); and procoagulant activity (PCA), which has been characterized as tissue factor. Dengue infection in vivo is restricted to monocytes; however, it is unknown if dengue-infected monocytes undergo alterations in the production of PA, PAI, and PCA. This issue was addressed in studies in which monocytes were infected in vitro with dengue 2 virus in serum-free medium in the presence of enhancing antibody. No urokinase activity was detected in either control or infected cells or in their supernatants. Infection of monocytes with dengue 2 virus resulted in an almost threefold increase in PAI activity in cells and supernatants. No change in relation to the control was observed in PCA generated by the infected cells. These data indicate that dengue 2 infection enhances the production of PAI from monocytes without altering PA or PCA.

Blood Coagulation↗