EFFECTS OF VITAMIN K ON VITAMIN K DEPENDENT PROTEINS IN NEWBORN INFANTS

1987 ◽  
Author(s):  
K YAMADA ◽  
T MEGURO ◽  
A SHIRAHATA ◽  
T NAKAMURA ◽  
A ASAKURA
Keyword(s):  
High Risk ◽  
Vitamin K ◽  
Protein C ◽  
High Performance ◽  
Newborn Infants ◽  
Total Activity ◽  
Functional Assay ◽  
Factor X ◽  
Before And After ◽  
High Risk Infants

Plasma levels of vitamin K (VK) and VK dependent proteins ( factor E, factor VH, factor X, protein C and osteocalcin)were determined before and after VK administration to 22 newborn infants. Vitamin K2 syrup ( 2 mg/kg of body weight ) was orally administered to 9 healthy premature, 11 high risk and 2 VK deficient infants under 3 days of age. VK families extracted from plasma were separated by high performance liquid chromatography using a Cosmosil 5 Ci8 column, and separated VK families were detected by a fluorometry after their reaction with ethanolic sodium borohydride in a reaction coil connected by one-line to a chromatographic column. Total activity of factor E, factor VE and factor X was assayed by a Normotest ( Nyegaard ), and protein C was measured by protac/APTT and protac/chromogenic substrate ( S-2366 ) functional assay system ( American Diagnostica ). Osteocalcin levels were assayed by using of a RIA method before and after the absorption of plasma by hydroxyapatite.After VK administration, plasma VK2 ( menaquinone-4 ) content increased from levels less than 0.012yg/ml to levels between 15.9 and 70.9μg/ml, excluding one case in whom plasma VK was not detected after VK administration. Compared with Normotest values and osteocalcin levels of age-matched healthy newborn infants treated without VK, premature, high risk and VK deficient infant levels significantly increased after 24 hrs and after 7 days of VK administration. No correlation was seen between the increase of plasma VK contents and the increase of Normotest values after VK administration. On the other hand, no significant increase of protein C assayed by both methods was observed in healthy premature and high risk infants after VK administration.These results indicate that the change of protein C after VK treatment is different from that of factor II, VII, X and osteocalcin.

Dietary Changes in Fasting Levels of Factor VII Coagulant Activity (FVII: C) Are Accompanied by Changes in Factor VII Protein and other Vitamin K-dependent Proteins

1995 ◽  
Vol 73 (02) ◽  
pp. 239-242 ◽  
Author(s):  
E M Bladbjerg ◽  
T Tholstrup ◽  
P Marckmann ◽  
B Sandström ◽  
J Jespersen
Keyword(s):  
Fatty Acids ◽  
Vitamin K ◽  
Protein C ◽  
Saturated Fatty Acids ◽  
Factor Vii ◽  
Dietary Regimen ◽  
Blood Samples ◽  
Dietary Changes ◽  
Coagulant Activity ◽  
Before And After

SummaryThe mechanisms behind dietary effects on fasting coagulant activity of factor VII (FVII: C) are not clarified. In the present study of 15 young volunteers, two experimental diets differing in composition of saturated fatty acids (C18:0 [diet S] or C12:0 + C14:0 [diet ML]) were served for 3 weeks each. Fasting blood samples were collected before and after the dietary regimen and analysed for triglycerides, FVII:C, and protein concentrations of FVII, FII, FX, protein C, CRP, albumin, fibrinogen, and F1+2. FVII:C was significantly reduced on diet S compared with diet ML. This was accompanied by a decrease in FVII protein, F1+2 and the vitamin K-dependent proteins FII, FX, and protein C. In contrast, no changes were observed in triglycerides, FVII:C/FVII: Ag, albumin and CRP. Fibrinogen was increased on diet S compared with diet ML. Our findings suggest that the change in fasting FVII:C was part of a general change in concentrations of vitamin K-dependent proteins.

TWO CASES OF NEONATAL PURPURA FULMINANS HOMOZYGOUS FOR PROTEIN C DEFICIENCY IN A CHINESE FAMILY

1987 ◽  
Author(s):  
M C SHEN ◽  
S H CHEN ◽  
K S LIN
Keyword(s):  
Vitamin K ◽  
Protein C ◽  
Newborn Infants ◽  
Purpura Fulminans ◽  
Coagulation Factors ◽  
Chinese Family ◽  
Factor V ◽  
Autosomal Dominant Disorder ◽  
Protein C Deficiency ◽  
Venous Thromboembolic

Protein C (PC) deficiency associated with hereditary venous thromboembolic disease was first reported in 1981 and is inherited as an autosomal dominant disorder. The prevalence of heterozygous PC deficiency is estimated to be 1 to 4% in venous thrombotic diseases. The homozygous PC deficiency is even rare, and has been reported in only about 10 families througout the world. It usually presents in newborn infants as purpura fulminans or severe thrombotic disease. We herein report two newborn brothers in a Chinese family, who manifested with purpura fulminans soon after birth and died at age of 21 days and 27 days respectively. Vitamin K was administered to the second baby after birth. Both parents are not consanguineous and there were no family histories of thromboembolism on paternal and maternal sides. Blood sample was not available for specific studies in the first baby. PC antigen level by electroimmunoassay was <6% in the second baby and 49% and 60% respectively in their mother and father. Antithrombin III activity by amidolytic method was 49% in the second baby, and 90% and 97% respectively in their mother and father. Vitamin K-dependent coagulation factors and factor V were within the expected range for a newborn. Factor VIII and fibrinogen level were notably decreased. Autopsy findings of the two newborns demonstrated the similar pictures characterized by fibrin thrombi in blood vessels causing extensive hemorrhagic infarts of skin, lung, liver, kidneys, testis, urinary bladder, esophagus and brain. Our Data indicate that neonatal purpura fulminans can be familial and caused by severe homozygous PC deficiency.

Coagulation Activation in Extracorporeal Hemodialysis

1997 ◽  
Vol 20 (3) ◽  
pp. 163-165 ◽  
Author(s):  
M. Camici ◽  
L. Evangelisti ◽  
P. Balestri ◽  
L. Cioni ◽  
P. Fundi ◽  
...  
Keyword(s):  
Protein C ◽  
Serum Lipoprotein ◽  
Factor Vii ◽  
Maintenance Hemodialysis ◽  
Factor X ◽  
Lipoprotein A ◽  
Activity Factor ◽  
Before And After ◽  
Protein C Activity

The Authors evaluated the behavior of protein C activity, factor X and factor VII coagulant activity and serum lipoprotein(a) before and after dialytic treatment in patients on maintenance hemodialysis. They observed depressed protein C activity that significantly (p<0.005) increased and became normal immediately after hemodialysis while factor X and factor VII increased (p<0.01; p<0.05) despite heparinization together with amount of serum lipoprotein(a). In vitro incubation (30 'at 37°C) of uremic and healthy blood showed a decrease in serum lipoprotein(a) concentration. After heparin addition (final concentration 0.5 U/ml) lipoprotein(a) increased in the uremic blood only. The clinical and physiopathological implications of these results are discussed.

scholarly journals Autonomic Nervous System Function in Infants With Transposition of the Great Arteries

2011 ◽  
Vol 14 (3) ◽  
pp. 257-268 ◽  
Author(s):  
Tondi M. Harrison ◽  
Roger L. Brown
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
High Frequency ◽  
Heart Defects ◽  
Newborn Infants ◽  
Low Frequency ◽  
Autonomic Nervous ◽  
Healthy Infants ◽  
Before And After ◽  
High Risk Infants

The ability to maintain and respond to challenges to homeostasis is primarily a function of the autonomic nervous system (ANS). In infants with complex congenital heart defects this ability may be impaired. This study described change in ANS function before and after surgical correction in infants with transposition of the great arteries (TGA) and in healthy infants. A total of 15 newborn infants with TGA were matched with 16 healthy infants on age, gender, and feeding type. The ANS function was measured using heart rate variability (HRV). Data were collected preoperatively in the 1st week of life and postoperatively before, during, and after feeding at 2 weeks and 2 months of age. Infants with TGA demonstrated significantly lower high-frequency and low-frequency HRV preoperatively ( p < .001) when compared with healthy infants. At 2 weeks, infants with TGA were less likely than healthy infants to demonstrate adaptive changes in high-frequency HRV during feeding (Wald Z = 2.002, p = .045), and at 2 months, 40% of TGA infants exhibited delayed postfeeding recovery. Further research is needed to more thoroughly describe mechanisms of a physiologically adaptive response to feeding and to develop nursing interventions supportive of these high-risk infants.

Prediction of Vitamin K Response Using the Echis Time and Echis-Prothrombin Time Ratio

1990 ◽  
Vol 64 (03) ◽  
pp. 353-357 ◽  
Author(s):  
C Solano ◽  
R G Cobcroft ◽  
D C Scott
Keyword(s):  
Prothrombin Time ◽  
Vitamin K ◽  
Factor X ◽  
Time Ratio ◽  
Factor Ii ◽  
Before And After ◽  
K Deficiency ◽  
Echis Carinatus ◽  
Factor X Activation ◽  
K Response

Summary Echis carinatus venom contains proteases capable of activating both normal and descarboxy prothrombin. We showed this venom (Sigma) principally activates prothrombin with almost no factor X activation. Echis time in combination with prothrombin time can predict vitamin K responsiveness since the Echis time is usually normal in the presence of descarboxy prothrombin associated with vitamin K deficiency.38 patients with abnormal routine prothrombin times (PT) had both coagulant and immunogenic factor II assays along with Echis times done before and after vitamin K. Of 22 patients responding to vitamin K, based on correction of PT, 21 had normal initial Echis times and of 16 not responding, 11 had abnormal Echis times, giving a sensitivity of 95.4% and specificity of 68.8% for vitamin K responsiveness. 90% of patients with a PT/Echis time ratio <1.3 and a prolonged Echis time did not correct their PTs with vitamin K therapy.The 5 non-responders with normal Echis times all showed normal initial coagulant and antigenic prothrombin, but 3 had low F V and/or F VII.

ACUTE INTERRUPTION OF ORAL ANTICOAGULANT THERAPY: A THROMBOTIC RISK?

1987 ◽  
Author(s):  
J Rouvier ◽  
H Vidal ◽  
J Gallino ◽  
M Boccia ◽  
A Scazziota ◽  
...  
Keyword(s):  
Anticoagulant Therapy ◽  
Vitamin K ◽  
Oral Anticoagulant ◽  
Protein C ◽  
Oral Anticoagulant Therapy ◽  
Factor Vii ◽  
Factor X ◽  
Functional Protein ◽  
Thrombotic Risk ◽  
Factor Ii

It is still on discussion how oral anticoagulant therapy must be interrupted. A progressive diminution of drug intake have been proposed in order to avoid a MreboundM of vitamin K-dependent procoagulant factors. At the present, it is well known that coumarin drugs affect not only the biologic activity of factors II, VII, IX and X but also Protein C (PC), an inhibitor of coagulation kinetics, and their cofactor Protein S. With the aim to determine the recovery level of PC in relation with the others vitamin K-dependent factors, the effect of suppression of anticoagulant therapy in patients under chronic treatment with acenocoumarin was studied.Quick time, functional factors II, VII, X (one stage methods), functional PC (Francis method) and immunological Factor II and Protein C (Laurell) were determined before and 36 hours after suspension of acenocoumarin administration.Results showed that: 1) Recovery levels of functional Protein C (increased from 28.55% ±2.57 to 72.64% ±5.9) were significantly higer than functional Factor II (22.09% ±2.34 to 30.73% ±8.64), Factor VII (22.55% ±2.01 to 40.73% ±4.85) and Factor X (23.27% ±2.66 to 39.18% ±3.19). Statistical analysis (Newmann-Keuls test) showed at least a p<0.01 between PC increase and factors II, VII or X increment.2) No significant differences were seen between immunological levels of Factor II before and after suspension of acenocoumarin.3) Levels of immunological PC in patients under anticoagulant therapy were higer than functional PC. After acenocoumarin suppression, not correlation was seen between immunological and functional Protein C recovery.It is concluded that acute suppression of acenocoumarin does not induce a thrombotic tendency because the recuperation of functional Protein C is more important than factors II, VII and X recovery.

Comparison of infant heart rate assessment by auscultation, ECG and oximetry in the delivery room

2018 ◽  
Vol 103 (5) ◽  
pp. F490-F492 ◽  
Author(s):  
Madeleine C Murphy ◽  
Laura De Angelis ◽  
Lisa K McCarthy ◽  
Colm Patrick Finbarr O’Donnell
Keyword(s):  
Heart Rate ◽  
High Risk ◽  
Pulse Oximetry ◽  
Clinical Assessment ◽  
Newborn Infants ◽  
Mean Difference ◽  
Low Risk ◽  
Delivery Room ◽  
Reasonable Accuracy ◽  
High Risk Infants

Clinical assessment of an infant’s heart rate (HR) in the delivery room (DR) has been reported to be inaccurate. We compared auscultation of the HR using a stethoscope with electrocardiography (ECG) and pulse oximetry (PO) for determining the HR in 92 low-risk newborn infants in the DR. Caregivers auscultated the HR while masked to the HR on the monitor. Auscultation underestimated ECG HR (mean difference (95% CI) by −9 (−15 to –2) beats per minute (bpm)) and PO HR (mean difference (95% CI) by −5 (−12 to 2) bpm). The median (IQR) time to HR by auscultation was 14 (10–18) s. As HR was determined quickly and with reasonable accuracy by auscultation in low-risk newborns, study in high-risk infants is warranted.

DETECTION AND EFFECTS OF THROMBOMODULIN ACTIVITY IN CRUDE THROMBOPLASTIN PREPARATIONS FROM PLACENTA AND LUNG

1987 ◽  
Author(s):  
M L Wiesel ◽  
R Spaethe ◽  
J-M Freyssinet ◽  
T Tran ◽  
H-J Kolde ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vitamin K ◽  
Human Placenta ◽  
Protein C ◽  
Anticoagulant Activity ◽  
Protein S ◽  
Coagulation System ◽  
Factor X ◽  
Coagulant Activity ◽  
The Stability

The activation of protein C (PC) by thrombin requires the presence of an endothelial membrane cofactor, thrombomodulin (TM). Activated PC (APC) exerts its anticoagulant activity by degrading factors (F) Va and Villa in the presence of phospholipids and of a vitamin K-dependent cofactor, protein S. Tissue factor (TF) is the essential cofactor of factor Vll/VIIain the activation of factor X. TF is synthetized by several cell lines including endothelial cells. Using a specific TM assay, up to 0.85 units of TM activity could be detected in commercial thromboplastin (TP) preparations from human placenta or rabbit or porcine lung, when the amount of TP was adjusted to contain 1 unit of TF activity. Preparations from brain contained very low amounts, if any, of this activity (< 0.02 TM units). In order to evaluate the effects of the presence of TM activity in some TP preparations, the stability of F V and VIII activities was examined after activation of the coagulation system by these TP in various plasmas. PC deficient plasmas, plasmas lacking F V, VIII or IX and immunoadsorbed PC deficient plasma supplemented with purified human PC (5 Ug/ml) were used. After activation with placenta or lung TP, F V and VIII activities were markedly reduced ( ∼ 90 % reduction) in normal and hemophiliac plasmas, whereas they remained high after activation with brain TP. F V and VIII activities were preserved in protein C deficient plasma after activation by all TP preparations. The same decrease of F V and VIII activities was observed after activation of immunoadsorbed PC deficient plasma supplemented with purified PC with placenta or lung TP only. Preincubation of TP from human placenta with antibodies to human TM raised in laying hens abolished the capacity of this preparation to destroy F V activity of PC containing plasmas. These results establish the presence of TM activity in crude thromboplastin preparations from placenta or from lung. Surprisingly, this anti-coagulant activity seems to be absent from brain. TM from placenta or lung extracts is responsible for the degradation of F V and VIII.

GLA-CONTAINING PROTEINS FROM CALCIFIED HUMAN ATHEROSCLEROTIC PLAQUES

1987 ◽  
Author(s):  
L J M Van Haarlem ◽  
H C Hemker ◽  
B A M Soute ◽  
C Vermeer
Keyword(s):  
Vitamin K ◽  
Vessel Wall ◽  
High Performance ◽  
Gel Filtration ◽  
Coagulation Factors ◽  
Atherosclerotic Plaques ◽  
Factor X ◽  
Carboxylase Activity

Vitamin K-dependent carboxylase activity has been detected in human andbovine vessel wall. Studies comparingthe carboxylases from liver and vessel wall revealed that the enzyme systems may be regarded as isoenzymes withwidely different substrate specificities. The carboxylated product of vessel wall carboxylase has not yet been identified, but it seems plausible that it will be found amongst the Gla-containing proteins which are abundantly present in calcified atherosclerotic plaques (Gla= gammacarboxyglutamicacid, the abnormal amino acid formed by vitamin K-dependent carboxylase). Therefore we have started to characterize the protein constituents of hardened atherosclerotic plaques.The calcified areas from human aortae were solubilized in EDTA and the proteins extracted were partly purified by batch-wise adsorption onto QAE and elution with high salt. The crudeplaque-extract did not contain prothrombin, factor X or protein C. This excludes the possibility that Gla-containing coagulation factors are bound non-specifically from blood. Osteocalcin accounted for 20% of the total amount of protein-bound Gla-residues.Another Gla-containing protein waspurified from the crude plaque-extract by employing high performance liquid chromatography (HPLC). Gel filtration yielded a Gla-rich protein with anapparent Mr of 25 kD. In vitro boththe crude plaque-extract and the purified Gla-containing protein strongly inhibited the precipitation of calcium phosphate and calcium carbonate. A similar effect was not found with humanserum albumin nor with a thermallydecarboxylated plaque-extract. If also in vivo the Gla-containing proteinsproduced by vessel wall carboxylase prevent the precipitation of calcium salts remains to be investigated.

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