ANTI-THROMBINneo IgG IN AN ASYMPTOMATIC PATIENT WITH A BENIGN MONOCLONAL GAMMOPATHY

1987 ◽  
Author(s):  
B S Coller ◽  
J Jesty
Keyword(s):  
Monoclonal Gammopathy ◽  
Asymptomatic Patient ◽  
Protein A ◽  
Thrombin Time ◽  
X Rays ◽  
Excessive Bleeding ◽  
Bone Marrow Histology ◽  
Benign Monoclonal Gammopathy ◽  
History Of ◽  
And Control

A 68 year old male hospitalized for cardiac disease was found to have an elevated prothrombin time (18.5/12.4 s) and aPTT (59.6/25.9s). He had no history of excessive bleeding or bruising. Subsequent evaluation revealed: thrombin time >500/34.1 s; fibrinogen 260 mg/dl functional and 522 mg/dl immunologic; reptilase 25.6/18.1 s; thrombin-induced platelet release of ATP (patient=0 and control=14.6 nmoles/109 platelets at 0.5 U/ml); AT-III 89% functional and 36.5 mg/dl immunologic; and prothrombin 167%. Mixing experiments showed the presence of an inhibitor of the thrombin time, and purification of IgG by protein A affinity chromatography showed the inhibitor of fibrin formation to reside in the IgG fraction. When coupled to Affi-gel 10, patient IgG (but not control IgG) removed purified thrombin from solution; the same gel did not remove prothrombin. The patient's IgG did not inhibit thrombin’s cleavage of a chromogenic substrate (Chromozym TH). Studies on the patient's serum revealed: IgG 2,360 mg/dl, IgA 371 mg/dl, and IgM 107 mg/dl. Serum protein electrophoresis and immunoelectrophoresis showed a monoclonal IgG lambda protein with probably normal amounts of normal IgG. Other parameters (hematocrit, albumin, calcium, bone marrow histology, bone X-rays) indicated that the patient has a benign monoclonal gammopathy, not multiple myeloma. We conclude that our patient is producing an IgG inhibitor that reacts with a neo-antigen produced by the cleavage of prothrombin to thrombin; the IgG can prevent the interaction of thrombin with fibrinogen and the thrombin receptor on platelets, but not small synthetic substrates. We suspect that his monoclonal IgG is the inhibitor and find it remarkable that he has no increase in bleeding.

Fibrinogen New Orleans: An Inherited Variant with Abnormal Peptide Release

1979 ◽  
Author(s):  
S.I. Chavin ◽  
W.A. Andes ◽  
W.G. Beltran ◽  
W.J. Stuckey
Keyword(s):  
Laboratory Finding ◽  
Polyacrylamide Gel Electrophoresis ◽  
Complete Fusion ◽  
Thrombin Time ◽  
Clotting Time ◽  
Excessive Bleeding ◽  
Normal Limits ◽  
Peptide Release ◽  
Mother And Daughter ◽  
History Of

An inherited fibrinogen abnormality is described in a 30-year old woman with a history of several episodes of excessive bleeding. The initial laboratory finding was a prolonged thrombin time, and a comparable prolongation was present in the plasmas of her mother and daughter, but not of her father. The abnormal fibrinogen gave a reaction of complete fusion with normal fibrinogen in an Ouchterlony plate, and by immunoelectrophoresis, it had a slightly faster than normal anodal migration. The patient’s plasma and purified fibrinogen were able to prolong the clotting time of normal plasma. Using SDS-polyacrylamide gel electrophoresis, we have detected a marked delay in release of a major proportion of the A peptide and a lesser delay in release of the B peptide, after thrombin treatment. B peptide release appeared to be completed before that of A peptide release, in contrast to the situation with normal fibrinogen. Cross-linking of the resulting fibrin was delayed but eventually complete. The rate and extent of monomer aggregation, measured by spectrophotometry, were within normal limits.

scholarly journals Prolonged Thrombin Time in Asymptomatic Patient with Hypo Dysfibrogememia Tucson

2021 ◽  
Vol 4 (2) ◽  
pp. 7-8
Author(s):  
Suresh B Katakkar
Keyword(s):  
Breast Cancer ◽  
Fibrinogen Level ◽  
Asymptomatic Patient ◽  
Normal Serum ◽  
Protein Electrophoresis ◽  
Thrombotic Complication ◽  
Thrombin Time ◽  
History Of ◽  
Thrombotic Complications ◽  
Work Up

A 61 years female patient with known diagnosis of the breast cancer in remission for more than 10 years has Renaud’s disease. During her work up for lupus and lupus anticoagulant which both were negative a prolonged thrombin time was noted which was done by mistake. She has no history of bleeding or thrombosis and last recent surgery was 5 years ago for spinal stenosis and was uncomplicated. Her clinical examination is normal without evidence of any spontaneous bruises but colder hands. The thrombin time was greater than 125 seconds on two different occasions and correction of it by addition of normal plasma was down to 56 seconds and was thus incomplete. Her prothrombin time and PTT were normal and there was no evidence of FDP or D-Dimers. There was no evidence of circulating heparins. The fibrinogen level was normal. The para proteinmia was excluded by normal serum protein electrophoresis and by immunofixation . Thus it is felt that this patient has dysfibrinogenemia or hypo dysfibrinogenemia without bleeding or thrombotic complication. The literature review shows approximately 55% of dysfibrinogenemia patients do not have bleeding or thrombotic complications.

Hereditary Hypodysfibrinogenemia with Defective Release of Fibrinogenopeptide A (Fibrinogen Freiburg)

1979 ◽  
Author(s):  
D. Böttcher ◽  
K. Hasler ◽  
E. Köttgen ◽  
J. Maurath
Keyword(s):  
Bleeding Episode ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Thromboembolic Disease ◽  
Thrombin Time ◽  
Excessive Bleeding ◽  
Major Bleeding Episode ◽  
History Of ◽  
Fibrin Monomers ◽  
Major Defect

A new autoaomally inherited hypodysfibrinogenemia was recognized in four members in three different generations of a family. Only one patient had a major bleeding episode after trauma, the other affected members had no history of excessive bleeding or thromboembolic disease.The thrombin time and Reptilase time of plasma were greatly prolonged and partially corrected by the addition of calcium. Patient plasma prolonged the thrombin time of normal plasma. Fibrinogen levels ranged between 10 to 20 mg/100ml when measured as thrombin-clottable protein, whereas immunologically the fibrinogen levels were only slightly reduced.Functionally the major defect was impaired release of fibrinogenopeptide A upon incubation of the purified abnormal fibrinogen (94% clottable protein) with thrombin and Reptilase. The abnormal fibrinogen showed a delayed polymerisation of its purified fibrin monomers. The described abnormal fibrinogen was indistinguishable from normal fibrinogen by polyacrylamide gel electrophoresis with and without sodium dodecyl sulfate.

An Inhibitor Selectively Directed Against Factor VIII-AHF In A Patient With Von Willebrand’S Disease (vWD)

1981 ◽  
Author(s):  
A Castella ◽  
J L Miller ◽  
R W Neuberg ◽  
H S Friedman
Keyword(s):  
Platelet Aggregation ◽  
Factor Viii ◽  
Replacement Therapy ◽  
Thrombin Time ◽  
Excessive Bleeding ◽  
Prolonged Bleeding ◽  
Prolonged Bleeding Time ◽  
History Of ◽  
Molecular Variant ◽  
Work Up

We have studied a 17 month old boy with previously diagnosed vWD who presented with intracerebral hemorrhage. There was a history of excessive bleeding from circumcision, after corrective surgery for pyloric stenosis, and from an upper lip cut. He had received multiple units of cryoprecipitate from the first month of life until the present admission. Work-up demonstrated prolonged bleeding time and prolonged PTT, normal prothrombin time, thrombin time, and platelet aggregation with ADP, epinephrine and collagen. Ten days after cessation of factor VIII replacement therapy he had undetectable F VIII-AHF, F VIII-Ag of 86% by the Laurell technique and F VIII-RCo of 18%. We could demonstrate a time- dependent inhibitor directed against F VIII-AHF measuring 92 Bethesda units. In mixing studies with normal plasma, little or nor inhibitory activity directed against F VIII-RCo could be identified. The patient’s platelets showed increased ristocetin-induced platelet aggregation (RIPA) at doses as low as 0.5 mg/ml.There was no evidence of a bleeding disorder in the maternal side of the family. All of the paternal family members studied showed prolonged bleeding times, decreased F VIII-RCo, and increased RIPA with low doses of ristocetin, findings similar to those patients recently characterized as having type IIb vWD. Although other members of the patient’s family had previously received cryoprecipitate replacement therapy, no inhibitors appear to have developed in these persons.Factor VIII inhibitors in vWD are uncommon, with those reported usually showing little or no inhibition of F VIII-AHF. These findings appear to represent a unique pattern of inhibitor development that may be related to a molecular variant of vWD in this patient.

Natural Oestrogen in the Female Climacteric - Influence on Blood Coagulation and Fibrinolysis

1978 ◽  
Vol 40 (02) ◽  
pp. 532-541 ◽  
Author(s):  
Anders Lagrelius ◽  
Nils-Olov Lunell ◽  
Margareta Blombäck
Keyword(s):  
Blood Coagulation ◽  
Antithrombin Iii ◽  
Coagulation Factors ◽  
Control Group ◽  
Blood Coagulation Factors ◽  
Excessive Bleeding ◽  
Oestrone Sulphate ◽  
Menopausal Women ◽  
History Of ◽  
Coagulation And Fibrinolysis

SummaryThe aim of the present study was to investigate the effect on blood coagulation and fibrinolysis of a natural oestrogen preparation, piperazine oestrone sulphate, prospectively in menopausal women. Scopolamine was given to the control group.The women were investigated before and during treatment with regard to factors VIII, VII, X, V, fibrinopeptide A, antithrombin III, plasminogen, rapid antiplasmin and α1-antitrypsin. There was no significant change towards hypercoagulability or decreased fibrinolysis in any group. In the oestrogen group, however, a tendency towards an increased level of plasminogen and a decreased level of antiplasmin was demonstrated. In the scopolamine group there was an unexpected fall in factors X and V and also in plasminogen and α1,-antitrypsin. A low level of some blood coagulation factors in some of the women before treatment is somewhat astonishing; none of them had any history of excessive bleeding.

THE RISK FACTORS OF MOLAR PREGNANCY

2017 ◽  
pp. 53-58
Author(s):  
Lam Huong Le
Keyword(s):  
High Risk ◽  
Gestational Trophoblastic Disease ◽  
Living Standard ◽  
Control Group ◽  
Uterine Perforation ◽  
Molar Pregnancy ◽  
Health It ◽  
Pregnancy Risk ◽  
History Of ◽  
And Control

Objectives: Molar pregnancy is the gestational trophoblastic disease and impact on the women’s health. It has several complications such as toxicity, infection, bleeding. Molar pregnancy also has high risk of choriocarcinoma which can be dead. Aim: To assess the risks of molar pregnancy. Materials and Methods: The case control study included 76 molar pregnancies and 228 pregnancies in control group at Hue Central Hospital. Results: The average age was 32.7 ± 6.7, the miximum age was 17 years old and the maximum was 46 years old. The history of abortion, miscarriage in molar group and control group acounted for 10.5% and 3.9% respectively, with the risk was higher 2.8 times; 95% CI = 1.1-7.7 (p<0.05). The history of molar pregnancy in molar pregnancy group was 9.2% and the molar pregnancy risk was 11.4 times higher than control group (95% CI = 2.3-56.4). The women having ≥ 4 times births accounted for 7.9% in molar group and 2.2% in control group, with the risk was higher 3.8 times, 95% CI= 1.1-12.9 (p<0.05). The molar risk of women < 20 and >40 years old in molar groups had 2.4 times higher than (95% CI = 1.1 to 5.2)h than control group. Low living standard was 7.9% in molar group and 1.3% in the control group with OR= 6.2; 95% CI= 1.5-25.6. Curettage twice accounted for 87.5%, there were 16 case need to curettage three times. There was no case of uterine perforation and infection after curettage. Conclusion: The high risk molar pregnancy women need a better management. Pregnant women should be antenatal cared regularly to dectect early molar pregnancy. It is nessecery to monitor and avoid the dangerous complications occuring during the pregnancy. Key words: Molar pregnancy, pregnancy women

Work and Technological Change

2020 ◽  
Author(s):  
Stephen R. Barley
Keyword(s):  
Artificial Intelligence ◽  
Historical Context ◽  
Energy Transformation ◽  
History Of ◽  
Work And Organizations ◽  
Role Based ◽  
Control Technologies ◽  
And Control ◽  
Work And Employment

The four chapters of this book summarize the results of thirty-five years dedicated to studying how technologies change work and organizations. The first chapter places current developments in artificial intelligence into the historical context of previous technological revolutions by drawing on William Faunce’s argument that the history of technology is one of progressive automation of the four components of any production system: energy, transformation, and transfer and control technologies. The second chapter lays out a role-based theory of how technologies occasion changes in organizations. The third chapter tackles the issue of how to conceptualize a more thorough approach to assessing how intelligent technologies, such as artificial intelligence, can shape work and employment. The fourth chapter discusses what has been learned over the years about the fears that arise when one sets out to study technical work and technical workers and methods for controlling those fears.

Galileo Unbound

2018 ◽  
Author(s):  
David D. Nolte
Keyword(s):  
Free Fall ◽  
The Sun ◽  
Quantum Field ◽  
Many Worlds ◽  
Quantum Particles ◽  
Light Rays ◽  
History Of ◽  
And Control ◽  
The Universe ◽  
Insight Into

Galileo Unbound: A Path Across Life, The Universe and Everything traces the journey that brought us from Galileo’s law of free fall to today’s geneticists measuring evolutionary drift, entangled quantum particles moving among many worlds, and our lives as trajectories traversing a health space with thousands of dimensions. Remarkably, common themes persist that predict the evolution of species as readily as the orbits of planets or the collapse of stars into black holes. This book tells the history of spaces of expanding dimension and increasing abstraction and how they continue today to give new insight into the physics of complex systems. Galileo published the first modern law of motion, the Law of Fall, that was ideal and simple, laying the foundation upon which Newton built the first theory of dynamics. Early in the twentieth century, geometry became the cause of motion rather than the result when Einstein envisioned the fabric of space-time warped by mass and energy, forcing light rays to bend past the Sun. Possibly more radical was Feynman’s dilemma of quantum particles taking all paths at once—setting the stage for the modern fields of quantum field theory and quantum computing. Yet as concepts of motion have evolved, one thing has remained constant, the need to track ever more complex changes and to capture their essence, to find patterns in the chaos as we try to predict and control our world.

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