The fibrinolytic enzyme system in prostatic cancer

Phillips, Louise Lang; Skrodelis, Valija; Furey, Clement A.

doi:10.1002/1097-0142(195907/08)12:4<721::aid-cncr2820120415>3.0.co;2-g

Cited by 27 publications

(11 citation statements)

References 24 publications

(1 reference statement)

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“…17 Also, increased titers of fibrin(ogen) degradation products (FDP), D-dimer, fibrinopeptide A and B, cryofibrinogens, fibrin monomer, B-ß 15-42 and related peptides, platelet factor 4, ß-thromboglobulin, and altered fibronectin and antithrombin levels are seen in many individuals with disseminated malignancy. 7,[17][18][19][20][21][22][23][24][25][26][27] These laboratory findings vividly imply that many patients with cancer have a low-grade disseminated intravascular clotting process. 28,29 The shortened survival of fibrinogen, platelets, and other coagulation proteins is often followed by an overcompensatory increase in coagulation factors and fibrinolytic enzymes, although these latter proteins may be decreased in some myeloproliferative disorders.…”

Section: Hypercoagulability and Thrombosis Pathophysiologymentioning

confidence: 96%

“…This is noted particularly with administration of estrogens, whereas testosterone has been noted to enhance coagulation abnormalities in many patients. 19,41,42 Hypercoagulability in cancer patients may also arise from platelet abnormalities. The role of platelets in contributing to thrombosis in malignancy was suspected many years ago, and the first large study of this phenomenon was initiated by Moolten et al in 1949, 43 which showed abnormal increases in platelet numbers and abnormal morphology, platelet lysis, and defective adhesion to glass wool.…”

Section: Hypercoagulability and Thrombosis Pathophysiologymentioning

confidence: 99%

“…This form of DIC has been noted in association with almost all types of solid tumors and is most commonly seen in carcinoma of the lung, gallbladder, stomach, colon, breast, ovary, malignant melanoma, 5,12,16,37,[113][114][115][116] and is especially common in carcinoma of the prostate. 19,39,40,117 Table 7 depicts malignancies most commonly associated with DIC. In these latter disorders, initiation of chemotherapy has occasionally been associated with triggering or acceleration of DIC.…”

Section: Hemorrhage and Solid Tumorsmentioning

confidence: 99%

See 2 more Smart Citations

Coagulation Abnormalities in Malignancy: A Review

Bick¹

1992

Semin Thromb Hemost

215

150

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As outlined in this review, patients with cancer may harbor many alterations of hemostasis. These are multifaceted and must be taken into account when trying to control hemorrhage or thrombosis in cancer patients. Often, hemorrhage or thrombosis is the final fatal event in many patients with metastatic solid tumor or hematologic malignancies. Patients with malignancy present a major clinical challenge in this new era of oncologic awareness and more aggressive care, which has led to prolonged survival for patients and a longer time frame during which these complications may develop. Therefore, these complications are occurring more commonly. It is important to realize that these alterations of hemostasis exist and must be approached in a sequential and logical manner with respect to diagnosis; only in this way can responsible, efficacious, and rational therapy be delivered to patients. By far the most common alteration of hemostasis in malignancy is that of hemorrhage associated with thrombocytopenia, either drug-induced, radiation-induced, or from bone marrow invasion. However, hemorrhage resulting from DIC is also quite common and may present as hemorrhage, thrombosis, thromboembolus, or any combination thereof. Many antineoplastic drugs and radiation therapy may lead to or significantly enhance hemorrhage in patients with malignancy. Thrombosis, also commonly seen in patients with malignancy, is often a manifestation of low-grade DIC, conspicuous as an intravascular thrombotic or thromboembolic event instead of an intravascular proteolytic (hemorrhagic) event. When suspecting this, confirmatory laboratory evidence must be sought and the patient treated appropriately. When approaching the patient with malignancy and either hemorrhage or thrombosis, all the potential defects in hemostasis must be taken into account, defined from the laboratory standpoint, and treated in as precise and logical manner as possible.

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Section: Hypercoagulability and Thrombosis Pathophysiologymentioning

confidence: 96%

Section: Hypercoagulability and Thrombosis Pathophysiologymentioning

confidence: 99%

Section: Hemorrhage and Solid Tumorsmentioning

confidence: 99%

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Coagulation Abnormalities in Malignancy: A Review

Bick¹

1992

Semin Thromb Hemost

215

150

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“…I t has been suggested that in this disease the proteolytic enzyme destroys antiplasmin, thereby, permitting spontaneous activation of plasminogen. 35 In another study, marked fibrinolytic activity in prostatic extracts and metastatic lesions led to the belief that there is direct activation of fibrinolysis by the tumor secretion.49 Factor VIII has been reported to be destroyed in vitro by plasmin and patients with active fibrinolysis are said to have low levels of factor VIII.5.47 This observation was not supported by the present study since five of six patients with active fibrinolysis had normal or high levels of factor VIII.…”

Section: Cancer September 1967mentioning

confidence: 60%

Coagulation disorders in cancer.I. Clinical and laboratory studies

Miller

Sánchez-Ávalos

Stefański

et al. 1967

Cancer

171

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A comprehensive study of the hemostatic and coagulation mechanisms in 50 patients with disseminated malignancy was carried out. Significant laboratory abnormalities were found in the majority of patients. The most common pattern was the “hypercoagulable state.” This included short bleeding time, decreased silicone coagulation time and partial thromboplastin time, increased tolerance to heparin, marked elevation of plasma levels of factors I, II, V, VIII, IX and XI and acceleration of thromboplastin generation. There was elevation of platelet counts, except in patients receiving chemotherapeutic drugs. Seven patients had prolonged prothrombin time due to depression of vitamin‐K‐dependent clotting factors. Fibrinolysis was detected in six patients by immunologic and other techniques. The data suggest that patients with cancer have an alteration in the hemostatic level of control with increased levels of both clotting factors and their inhibitors, resulting in a more easily disturbed balance between opposing hemostatic forces. Clinical thrombosis or bleeding may follow.

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“…They found no change in fibrinogen with treatment but did note what may be been a seasonal effect. Phillips et al 23 compared fibrinogen levels from a group of 1-5 young controls, 308 & 71 mg/100 ml, a group of 1 i benign prostatic hypertrophy patients, 381 k 99 mg/100 ml, and 35 prostatic cancer patients mostly on diethylstilbestrol treatment of unspecified dosage and duration, 415 i5 124 mg/100 ml (x & SD). This higher level of fibrinogen in the cancer patients than in the control group cannot be interpreted as a significant effect of estrogen in view of the age effects described above and the pretreatment levels and treatment effects found in this study.…”

Section: Fibrinogenmentioning

confidence: 99%

Response of plasma fibrinogen and plasminogen to hormone treatment and the relation of pretreatment values to mortality in patients with prostatic cancer

Seal

Doe

Byar

et al. 1976

Cancer

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Fibrinogen and plasminogen were measured in plasma samples from prostatic cancer patients before and after 3 months of treatment with either Premarin, Provera, Provera and diethylstilbestrol, one of three doses of diethylstilbestrol, o r placebo. Plasminogen levels generally were increased significantly with the estrogens but were unchanged following placebo o r Provera treatment. Pretreatment plasminogen levels in Study 3 were significantly lower ( p << .001) than in Study 2. Plasminogen pretreatment levels were significantly correlated with age, hemoglobin, body weight, and blood pressure. Fibrinogen pretreatment levels were significantly elevated above normal. They were not significantly correlated with age, hemoglobin, body weight, or blood pressure. Fibrinogen levels generally were significantly decreased by the estrogens. Comparisons of means of pretreatment fibrinogen and plasminogen levels from patients dying during the first year of the study with the mean pretreatment levels of the patient group alive after 1 year on study yielded no significant differences. Death rates were calculated by pretreatment plasminogen o r fibrinogen for all treatments of all Stage I11 and Stage IV patients combined for Study 2 and Study 3 separately. Such rates were calculated for all causes combined and for deaths from prostatic cancer or cardiovascular disease separately. The levels of plasminogen were significantly negatively correlated with death rate from all causes combined and with cardiovascular disease considered separately, but not with death from prostatic cancer. The levels of fibrinogen were significantly positively correlated with death rates from all causes and nearly significantly with prostatic cancer, but not cardiovascular disease. Elevated pretreatment fibrinogen levels were associated with an increased proportion of deaths at 1 year from all causes and from cancer of the prostate.

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The fibrinolytic enzyme system in prostatic cancer

Cited by 27 publications

References 24 publications

Coagulation Abnormalities in Malignancy: A Review

Coagulation Abnormalities in Malignancy: A Review

Coagulation disorders in cancer.I. Clinical and laboratory studies

Response of plasma fibrinogen and plasminogen to hormone treatment and the relation of pretreatment values to mortality in patients with prostatic cancer

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