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C Breederveld

Publications and source records attributed to C Breederveld.

At least 19 recordsLinked to original sources
PubMed1990

Protein C activity and antigen levels in childhood.

Hereditary protein C deficiency is an important risk factor for thrombosis. To enable its diagnosis shortly after birth, we determined reference values of protein C antigen and activity levels for the first 3 months of life. To establish an age-related range of protein C levels we also determined median values for individuals up to 18 years of age. A good correlation between the two levels was seen from the 3rd/4th month of life onwards, whereas in the first 2 months the activity levels were significantly lower than the antigen levels. This was not due to interference by the increased plasma citrate concentration at high haematocrit values, and may suggest a dysfunctional protein C molecule in the neonatal period. We found a rapid rise in protein C activity and antigen levels until the age of 7-9 months, followed by a slower progression toward adolescence. In contrast to previous reports, our results indicate that adult values are probably not achieved until sometime during the 2nd decade of life.

Adolescent↗
PubMed1989

[Is circumoral cyanosis a sign of peripheral or of central cyanosis?].

Two hundred Dutch paediatricians were invited to give their description and interpretation of the concept of 'circumoral cyanosis'. Analysis of the results shows great inter-doctor variability: 63% considered the circumoral cyanosis as a pathologic sign and 70% as an expression of central cyanosis, although in textbooks and publications this sign is defined as an expression of peripheral cyanosis and is not considered to be pathological.

Cyanosis↗
PubMed1989

Low antithrombin III: accurate predictor of idiopathic respiratory distress syndrome in premature neonates.

A prospective study was performed in premature neonates to determine the predictive values of antithrombin III (AT III) deficiency immediately after birth, for the subsequent development of idiopathic respiratory distress syndrome (IRDS), intraventricular haemorrhage (IVH) and death. Of the 81 premature infants studied, 24 developed IRDS (30%). Of these 24 premature infants, 8 also developed IVH and 9 infants died within the follow-up period of 7 days. The mean plasma AT III level was significantly lower in the infants developing IRDS (0.23 U/ml vs 0.35 U/ml, P less than 0.0005). Within this study group 33 neonates of less than 30 weeks' gestation showed a prevalence for IRDS of 48%. In this group, AT III activity levels below 0.30 U/ml were 8.5 times as likely to result from infants with IRDS than from infants without IRDS. The diagnostic accuracy indices of criteria for the development of IRDS were: a sensitivity of 100%, a specificity of 88%, a positive predictive value of 89% and a negative predictive value of 100%. The predictive values for the development of IVH and occurrence of death were insignificant. Therefore, in premature neonates the combination of less than 30 weeks' gestation and an AT III below 0.30 U/ml is highly suggestive of IRDS and may facilitate the evaluation of early treatment.

Antithrombin III↗
PubMed1989

Low AIDS attack rate among Dutch haemophiliacs compared to homosexual men: a correlate of HIV antigenaemia frequencies.

A cohort of 180 haemophiliacs followed between 1983 and 1986 and a cohort of 961 homosexual men followed between 1984 and 1986 were compared for the prevalence and incidence of HIV-1 antibody (HIV-1-Ab) seropositivity, the incidence of AIDS-related complex (ARC) and AIDS and the prevalence and incidence of serological and immunological markers for HIV-related disease progression. Among the haemophiliacs 23 (12.8%) patients were HIV-1-Ab seropositive at entry and 20 (12.7%) of the remaining 157 seroconverted for HIV-1-Ab during follow-up. Of the homosexual men 238 (24.8%) were HIV-1-Ab seropositive at entry and 68 (9.4%) of the 723 at entry seronegatives seroconverted during follow-up. Clinical follow-up of the HIV-1-Ab seropositive and seroconverted men was 59 months in the haemophiliac cohort and 60 months in the homosexual cohort. Among the HIV-1-Ab seropositive and seroconverted haemophiliacs and homosexual men the cumulative ARC/AIDS incidence was 2 and 18%, respectively. Occurrence of HIV-1-antigenaemia was more frequent among seropositive and seroconverted homosexual men (28%) than among haemophiliacs (7%) (p = 0.001). The groups did not differ significantly for the absence or loss of anti-HIV core antibodies or the occurrence of low CD4+ cell numbers. These data indicate a slower progression of HIV-related disease in seropositive haemophiliacs compared to seropositive homosexual men.

AIDS-Related Complex↗
PubMed1988

HIV-antibody seroconversions in Dutch haemophiliacs using heat-treated and non heat-treated coagulation factor concentrates.

A national multicentre study was performed to investigate the effects of donorselection and the use of heat-treated plasma products on seroconversion to HIV in 157 Dutch haemophiliacs. All patients included in the study were seronegative for HIV antibodies in 1983. Thirteen percent (20/157) seroconverted between 1983 and 1986. Nineteen of 20 seroconversions could be related to the use of non heat-treated products in the year preceding HIV antibody seroconversion. One seroconversion occurred in a person using heat-treated non donor screened product. Seroconversion rate decreased as a result of the policy to discourage high risk blood donors and no seroconversions were observed following the introduction of donor screening in 1985.

Blood Coagulation Factors↗
PubMed1987

Pathogenesis of HIV and its implications for serodiagnosis and monitoring of antiviral therapy.

Human immunodeficiency virus (HIV) is lymphotropic and neurotropic. In vivo clinical and immunological abnormalities develop in a large proportion of long-term HIV antibody seropositive persons. Different stages of HIV infection are marked by expression of HIV genes, production of HIV antibodies, formation of antigen/antibody complexes and clearance of such complexes. Transient HIV antigenemia appearing generally 6-8 wk prior to HIV antibody (HIV-Ab) seroconversion and lasting 3-4 mth is generally seen in acute infection. IgM antibodies predominantly to core proteins may occasionally be detectable when, or just before, IgG antibodies appear. If IgG antibodies to both envelope and core proteins persist in the absence of HIV-Ag the short-term prognosis is relatively good. However, HIV-Ag seroconversion may appear at any time after HIV-Ab seroconversion. Progression to AIDS is strongly associated with declining or absent levels of IgG antibodies to p24. IgG2 and IgG4 antibodies to HIV, which are mainly directed to p24, disappear most dramatically. Titers of antibodies to HIV p24 below 64 are strongly associated with the presence of HIV antigen and a poor clinical outcome. HIV antigen was detected frequently in sera from children in all stages of infection in contrast to adults whose sera were generally HIV-Ag negative when asymptomatic and positive when AIDS was apparent. HIV antigen may be less efficiently detected with the present assays in sera from regions where the prototype strains of HIV (HTLV-III and LAV) are less prevalent, like Central Africa. Persistence of HIV-Ag in cerebrospinal fluid (CSF) appears to be pathognomonic for progressive encephalopathy, particularly in children. Levels of HIV-Ag in serum, and possibly in CSF, can be decreased by nucleoside analogues, such as AZT. This indicates HIV-Ag and possibly antibody to HIV core protein p24 as suitable markers for selecting individuals for antiviral therapy as well as monitoring the efficacy of such therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Cerebral thromboembolism due to antithrombin III deficiency in two children.

Despite numerous well-described causes of stroke in infancy and childhood, a significant proportion remains unexplained. Venous thromboembolism is a common complication in adult patients undergoing surgery, and after severe trauma, but not in otherwise healthy children less than 10 years old. However, it may also occur spontaneously without recognizable cause. It has been known for a long time that some patients are particularly prone to venous thrombosis and in recent years great efforts have been made to identify the risk factors. The attention of haematologists has been focused on the possibility that certain abnormalities of coagulation may be associated with a tendency to thrombosis, but only in a few instances a clear causal relationship has been established. One such example is a deficiency of antithrombine III, but such a deficiency has hitherto been recognized as a cause for thrombosis in children only in very particular circumstances. We present two young children with stroke of which one was purely ischemic and the other ischemic with secondary hemorrhage. Both our patients showed an AT III deficiency. Patient one also had a cyanotic congenital heart disease with right to left shunting which made cerebral embolism originating from a thrombus in the iliac vein possible to occur. We consider her hematocrit values too low to be a predisposing factor for this thrombosis. AT III deficiency may be caused by several different mechanisms. Either it exists as a congenital (hereditary) or as an acquired disorder. In patient two the family history was positive for hereditary AT III deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Antithrombin III Deficiency↗
PubMed1987

Normal synthesis and expression of endothelial IIb/IIIa in Glanzmann's thrombasthenia.

Glanzmann's thrombasthenia is a bleeding disorder, inherited in an autosomal recessive way and characterized by an absence or deficiency of the platelet glycoprotein (GP) IIb/IIIa complex. Recently, we and others demonstrated that cultured human umbilical vein endothelial cells synthesized a membrane protein complex similar to the platelet GP IIb/IIIa complex. In this article, we demonstrate that endothelial cells isolated from the umbilical vein of a newborn with Glanzmann's thrombasthenia, as compared with normal endothelial cells, show no difference in their ability to synthesize and express this GP IIb/IIIa complex. Our results indicate that Glanzmann's thrombasthenia is not accompanied by an "endotheliopathy."

Blood Platelet Disorders↗
PubMed1986

Antibodies to the human T-cell lymphoma/leukemia virus type I in Dutch haemophiliacs.

95 Dutch haemophiliacs were tested for antibodies to membrane antigens on cells infected with human T-cell leukemia virus type I (HTLV-I-MA) by indirect immunofluorescence and to purified HTLV-I by enzyme-linked immunosorbent assay. Antibodies to HTLV-I-MA were present in 8 of 95 (8%) haemophiliacs, but only 3 (3%) had antibodies to purified HTLV-I. No clinical disease was related to HTLV-I seropositivity. The importance of iatrogenic HTLV-I transmission to haemophiliacs is discussed.

Antibodies, Viral↗
PubMed1985

Coagulation and fibrinolytic factors in the first week of life in healthy infants.

Coagulation and fibrinolytic factors were determined daily in 74 healthy term and preterm infants to obtain a reference standard. A gestational age dependency was determined for antithrombin III, factor II, and plasminogen. The mean concentrations of antithrombin III and factor II in preterm infants increased to term values within the first week of life. Factor X levels declined independent of vitamin K administration. The values for the fibrinolytic system (alpha 2-antiplasmin and plasminogen) remained stable.

Antithrombin III↗
PubMed1984

Persistent antithrombin III deficiency: risk factor for thromboembolic complications in neonates small for gestational age.

Coagulation and fibrinolytic factors were investigated daily in 24 SGA and 26 AGA neonates. The results were correlated with placental form and structure and with hematologic values. In the SGA infants, a higher incidence of placental infarction (P less than 0.01), polycythemia (P less than 0.005), and thrombocytopenia (P less than 0.001) was present. During the first 9 days, the mean antithrombin III level in the AGA group increased from 0.36 to 0.53 U/ml, whereas in SGA neonates this value was initially significantly lower (0.27 U/ml) and remained at that level for the entire observation period. The same pattern was found for alpha 2-antiplasmin. The persistent AT-III deficiency and reduced blood flow associated with polycythemia may explain the increased risk of thromboembolic complications in SGA infants described by others.

Antithrombin III Deficiency↗
PubMed1984

Neonatal antithrombin III.

Antithrombin III (AT-III) heparin cofactor activity and its antigen levels have been determined in 106 plasma samples from 42 term and preterm neonates. In contrast to healthy adult controls, a reduced activity/antigen (act/ag) ratio (ranging from 0.26 to 0.86) was observed in 90% of the samples and was independent of the state of health of the infant. By modifying the routine assay techniques, laboratory artefacts were excluded as the cause of the observed discrepancy. The relative increase in antigenic AT-III could not be accounted for by circulating AT-III-thrombin complexes, or by increased heparin cofactor II plasma levels in neonates.

Adult↗
PubMed1984

Low antithrombin III levels in neonates with idiopathic respiratory distress syndrome: poor prognosis.

Automated microanalytic chromogenic coagulation assays allow serial monitoring of critically ill newborn infants. In this study 84 premature infants [26 healthy prematures and 58 neonates with idiopathic respiratory distress syndrome (IRDS)] were studied daily during the first week of life, to investigate the possible significance of hemostatic abnormalities in IRDS. In neonates with IRDS, coagulation factors II and X, antithrombin III (AT-III), plasminogen, and alpha 2-antiplasmin were significantly lower than control values. Recovery of the initially low AT-III levels was delayed relative to the other coagulation parameters measured. An AT-III less than or equal to 0.15 U/ml was present within the first 6 h of life in eight patients who developed IRDS, seven of whom died within 48 h. Autopsy of these neonates showed widespread fibrin deposition and hemorrhage in vital organs consistent with intravascular coagulation. These findings indicate that very low levels of AT-III are associated with disseminated intravascular coagulation in neonates with IRDS and suggest that a deficiency of AT-III is predictive of a poor outcome.

Antithrombin III Deficiency↗
PubMed1983

Identification of a contaminant protein in the purification of human factor V. Comparison of two purification methods.

Coagulation factor V has been isolated from human plasma by the methods of Bolhuis and of Kane to investigate reported differences in purity and specific activity. The specific activities of the preparations are 10 and 40 units/mg, respectively. The Kane preparation shows a single band (Mr 330 000) in polyacrylamide gel electrophoresis in the presence and absence of dithiothreitol, but the Bolhuis preparation shows an additional band at Mr 190 000 upon reduction with dithiothreitol. This suggests the presence of a contaminant which could account for the lower specific activity. Modification of the Bolhuis technique to include ion-exchange chromatography on DEAE-Sepharose resulted in separation of the two isolated proteins. The proteins were identified as factor V, with characteristics indistinguishable from Kane factor V, and a dimeric subunit of alpha 2-macroglobulin (Mr 350 000). Contamination by alpha 2-macroglobulin may explain the I2-component described in some preparations of bovine factor V, which is the basis of speculation that bovine factor V has a second polypeptide chain modulating stability and activity.

Blood Proteins↗