Results 151 to 160 of about 749,451 (200)
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Pregnancy and protein C deficiency
European Journal of Obstetrics & Gynecology and Reproductive Biology, 1992This report examines a patient with recurrent attacks of thrombo-embolism due to a protein C deficiency. Alterations in the coagulation during pregnancy and the possible consequences of an altered coagulation during pregnancy will be discussed.
A M, van Heusden +2 more
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Isolated Protein C Deficiency in a Newborn
Clinical Laboratory, 2023Congenital protein C deficiency is a rare hereditary thrombophilia, neonatal purpura fulminans is the most serious form of this deficit. The purpose of this observation is two-fold. The first is the need to make an early diagnosis in order to improve the prognosis. The second, is to discuss the need.
H, Bencharef +8 more
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SUCCESSFUL TREATMENT OF HOMOZYGOUS PROTEIN C DEFICIENCY BY HEPATIC TRANSPLANTATION [PDF]
Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/85510/1/Successful treatment of homozygous protein c deficiency by hepatic transplantation ...
Howard Markel +2 more
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Severe antigenic deficiency of protein C associated with moderate deficiency of protein C activity
Thrombosis Research, 1985The available literature shows that activated protein C is a potent anticoagulant enzyme in vitro (1,2). Moderate deficiency of protein C (30-60X of normal levels) of an hereditary type has been shown recently to be associated with recurrent thrombotic disease (3,4).
E, Melissari +3 more
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Homozygous protein C deficiency—management with protein C concentrate
European Journal of Pediatrics, 1995Two unrelated female infants with homozygous protein C (Pr C) deficiency are reported. Both are of U.K. Pakistani origin and in each case the parents are consanguinous. A previous sibling had died in each family. Both sets of parents were shown to be carriers. The concentration of Pr C in both infants was low at birth.
V, Baliga +5 more
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Hereditary Protein C Deficiency
Haemostasis, 2009Hereditary protein C deficiency, which is inherited as an autosomal-dominant trait, predisposes to venous thrombotic disease. Heterozygotes are at risk for superficial thrombophlebitis, deep venous thrombosis and/or pulmonary embolism, which may occur without apparent cause at a young age.
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Priapism in a patient with protein C deficiency
Clinical and Laboratory Haematology, 1997We present the case of a patient with classical protein C deficiency presenting with acute priapism during warfarinization for thrombophlebitis. Priapism is a well-recognized complication of a number of conditions including sickle cell disease and haematological malignancies, but to our knowledge it has not previously been reported in association with ...
S, Daryanani, J T, Wilde
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Archives of Surgery, 1988
Familial hypercoagulable states are a collection of syndromes characterized by an inherited deficiency of various proteins involved in the control of coagulation and include antithrombin III, plasminogen, protein C, and protein S. Affected patients usually develop venous thrombosis as adults. During a 15-month interval, we identified five patients with
D F, Tollefson +4 more
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Familial hypercoagulable states are a collection of syndromes characterized by an inherited deficiency of various proteins involved in the control of coagulation and include antithrombin III, plasminogen, protein C, and protein S. Affected patients usually develop venous thrombosis as adults. During a 15-month interval, we identified five patients with
D F, Tollefson +4 more
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The mutational demography of protein C deficiency
Human Genetics, 1995The geographical distribution and prevalence of 256 single base-pair substitutions (105 of them being different) within the coding region of the human protein C (PROC) gene were correlated with their initial likelihoods of generation. A significant positive correlation was observed between these "mutational likelihoods" and the geographical dispersal ...
M, Krawczak, P H, Reitsma, D N, Cooper
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Severe Protein C Deficiency in a Newborn
Journal of Pediatric Hematology/Oncology, 1988An infant presented at birth with a cutaneous lesion that developed the characteristics of purpura fulminans. He sustained a cerebral infarction during the first 4 days of life, which was initially misinterpreted to be cerebral hemorrhage resulting from thrombocytopenia and hypofibrinogenemia.
C H, Pegelow, R, Curless, B, Bradford
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