Fibrinolytic Response to Oral Glucose

Tanser, A. R.

doi:10.1016/s0140-6736(66)92427-5

“…This confirms earlier reports of decreased fibrinolysls In hypertension. 27 ' a The causal relationship between diabetes itself and increased PA-inhibitor activity cannot be derived from our cross-sectional study, and multiple correlation analysis can only suggest possible etiologic factors. Nevertheless, since diabetics, and especially noninsulin-dependent patients, present several factors (like obesity, hypertension, hyperinsulinism, and old age) which are associated with a decreased fibrinolytic capacity, probably mediated by an The independent variables induded in the regression model were: age, BMI, SBP, DBP, duration of diabetes, insulin dose, HbA,, PAP, fibrinogen, and fibrin plate assay.…”

Section: Discussionmentioning

confidence: 93%

Tissue-type plasminogen activator antigen and plasminogen activator inhibitor in diabetes mellitus.

Auwerx

¹

,

Bouillon

²

,

Collen

³

et al. 1988

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Parameters of flbrlnolysls, Including euglobulln fibrlnolytlc activity, tissue-type plasminogen activator (t-PA) antigen, plasminogen activator Inhibitor (PA-lnhlbltor) activity, and plasmln-aj-antlplasmln complex (PAP) were studied In 62 patients (35 women and 27 men; ages 53 ± 16 years) with either Insulin-dependent (IDDM) or nonlnsulln-dependent (NIDDM) diabetes mellKus. Compared to a control group of similar age (n = 57), the diabetic patients had a significantly lower mean euglobulln fibrlnolytlc activity (1.2 ±0.7 vs. 1.7 ±1.1 ng/ml, p<0.01) but significantly higher mean t-PA antigen (15.7 ± 8.4 vs. 6.6 ± 2.9 ng/ml, p < 0.001) and PA-lnhlbltor activity (2.6 ± 1.3 vs. 1.5 ± 0.7 lU/ml, p<0.001) levels. Significant unlvarlate correlations were observed between PA-lnhlbttor activity and age (r=0.32, p<0.05), dlastollc blood pressure (r = 0.42, p < 0.01) and euglobulin fibrlnolytlc activity (r = -0.40, p < 0.01). In multlvariate analysis, only body mass Index (positively) and euglobulin fibrlnolytlc activity (negatively) remained significantly related to PA-lnhlbltor activity In the total diabetic population as well as In the NIDDM group. The only parameter In the IDDM group significantly related to PA-lnhlbltor activity was dlastollc blood pressure. These results suggest that PA-lnhibltor plays a role In the regulation of flbrlnolysls In diabetes patients and that factors like obesity and hypertension may be related to reduced flbrlnolysls via PA-lnhlbltor levels. (Arteriosclerosis 8:68-72, January/February 1988) D iabetes patients are predisposed to cardiovascular complications, which occur earlier and more frequently than in comparable nondiabetic patients. Abnormalities in both lipid metabolism and hemostasis contribute to the development of vascular damage.1 In diabetes patients, spontaneous fibrinolytic activity is reported to be normal or low, 2 -6 while release of plasminogen activator from the vascular endothelium is abnormal in some cases. 59 recently demonstrated that elevated tissue-type plasminogen activator (t-PA) antigen levels in poorly controlled diabetics could be decreased by insulin administration. These authors argued that a decrease of t-PA antigen in hyperinsulinemic, insulin-treated diabetics could hamper the fibrinolytic capacity and thereby favor the development of atherosclerosis.In the present study we have evaluated t-PA antigen and plasminogen activator inhibitor (PA-inhibitor) activity by both univariate and multtvariate analysis in a well-defined group of moderately controlled diabetic patients, including both insulin-dependent and noninsulin-dependent subjects. MethodsSixty-two diabetic patients (35 women and 27 men) ages 16 to 79 years (53 ± 16 years, mean ± SD) were

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“…Furthermore, three patients had diabetes mellitus. Glucose increases blood fibrinolytic activity34 35 and antidiabetic drugs influence the fibrinolytic activity of blood.36-38 One Fodstad of van Rossum's patients had nephritis, and AMCA should not be given to patients with impaired renal function.39 Finally, four of his patients were receiving anticoagulants, which could also have influenced the rebleeding rate. In Kaste and Ramsay's series nine patients did not have their rebleedings confirmed by lumbar puncture or neuroradiology.…”

Section: Discussionmentioning

confidence: 99%

Tranexamic acid (AMCA) in aneurysmal subarachnoid haemorrhage

Fodstad¹

1980

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Subarachnoid haemorrhage due to a ruptured cerebral aneurysm is a dramatic event in neurosurgery and one of the most destructive. Its management is complicated by the risks of rebleeding and cerebral vasospasm and their sequelae. Rebleeding and vasospasm rarely occur before three days after the primary bleed.'2 Angiographic vasospasm is seen most often 10 to 17 days after bleeding.3 Because of the brain's vulnerability during spasm many surgeons prefer to wait until two weeks after the primary bleed to obliterate the aneurysm.4 Sano and Saito5 reported fatal postoperative vasospasm in patients operated upon on days 4 and 7 after a haemorrhage. However, the 'spasm period' coincides with the time when rebleeding is most likely. The incidence of rebleeding is highest at the end of the first week and at the beginning of the second after the primary bleed, and the mortality after the first recurrence is reported to be between 43 % and 64 %. 6 Thus most surgeons accept spontaneous mortality due to either progressive deterioration or to rebleeding during the first and second week. The surgical mortality when the patient has recovered from this deterioration can be low. It is therefore necessary to look for ways of lessening the risk of rebleeding during the first critical two weeks.The aim in treating patients with a ruptured aneurysm with antifibrinolytic agents is to prolong the duration of the formed blood clot within and about the wall of the aneurysm and thus prepare the way for mechanical repair of the rupture. Promising results with aminocaproic acid (EACA)7-11 and AMCA12-19 have been reported. Others, however, found that these drugs had no effect on rebleedings.20-24 In this paper I report the results of two controlled clinical trials of the effect of AMCA on aneurysmal rebleeding, vasospasm, hydrocephalus, and circulatory disturbances. Patients and methodsThe trials were conducted over the years 1972 to 1978. The sealed-envelope technique was used instead of the double-blind method, since it was considered unethical to give placebo injections for a prolonged period. Only patients admitted to the hospital within three days after a subarachnoid haemorrhage due to a ruptured aneurysm and in whom treatment was started within 72 hours were included in the trials. The diagnosis was verified by spinal fluid (CSF) examination and cerebral angiography. In the second series all patients were also examined with CT-scan.The patients were randomly assigned to conservative treatment (bedrest and sedation) or conservative treatment together with the administration of AMCA. In a first series of 46 patients 23 were given AMCA by slow intravenous injection in a dosage of 1 g 4-hourly during the first week, 1 g 6-hourly during the second to fifth weeks inclusive, and 1 g 8-hourly during the sixth week. In a second series of 59 patients 30 received AMCA in hourly intravenous infusions 6 g daily during the first week, 4 g daily during the second week, and 1 5 g by mouth four times a day during the third to sixth weeks. The patient...

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“…Furthermore, three patients had diabetes mellitus. Glucose increases blood fibrinolytic activity34 35 and antidiabetic drugs influence the fibrinolytic activity of blood. [36][37][38] Fodstad of van Rossum's patients had nephritis, and AMCA should not be given to patients with impaired renal function.39 Finally, four of his patients were receiving anticoagulants, which could also have influenced the rebleeding rate.…”

Section: Discussionmentioning

confidence: 99%

Tranexamic acid (AMCA) in aneurysmal subarachnoid haemorrhage

Fodstad¹

1980

Journal of Clinical Pathology

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Subarachnoid haemorrhage due to a ruptured cerebral aneurysm is a dramatic event in neurosurgery and one of the most destructive. Its management is complicated by the risks of rebleeding and cerebral vasospasm and their sequelae. Rebleeding and vasospasm rarely occur before three days after the primary bleed.'2 Angiographic vasospasm is seen most often 10 to 17 days after bleeding.3 Because of the brain's vulnerability during spasm many surgeons prefer to wait until two weeks after the primary bleed to obliterate the aneurysm.4 Sano and Saito5 reported fatal postoperative vasospasm in patients operated upon on days 4 and 7 after a haemorrhage. However, the 'spasm period' coincides with the time when rebleeding is most likely. The incidence of rebleeding is highest at the end of the first week and at the beginning of the second after the primary bleed, and the mortality after the first recurrence is reported to be between 43 % and 64 %. 6 Thus most surgeons accept spontaneous mortality due to either progressive deterioration or to rebleeding during the first and second week. The surgical mortality when the patient has recovered from this deterioration can be low. It is therefore necessary to look for ways of lessening the risk of rebleeding during the first critical two weeks.The aim in treating patients with a ruptured aneurysm with antifibrinolytic agents is to prolong the duration of the formed blood clot within and about the wall of the aneurysm and thus prepare the way for mechanical repair of the rupture. Promising results with aminocaproic acid (EACA)7-11 and AMCA12-19 have been reported. Others, however, found that these drugs had no effect on rebleedings.20-24 In this paper I report the results of two controlled clinical trials of the effect of AMCA on aneurysmal rebleeding, vasospasm, hydrocephalus, and circulatory disturbances. Patients and methodsThe trials were conducted over the years 1972 to 1978. The sealed-envelope technique was used instead of the double-blind method, since it was considered unethical to give placebo injections for a prolonged period. Only patients admitted to the hospital within three days after a subarachnoid haemorrhage due to a ruptured aneurysm and in whom treatment was started within 72 hours were included in the trials. The diagnosis was verified by spinal fluid (CSF) examination and cerebral angiography. In the second series all patients were also examined with CT-scan.The patients were randomly assigned to conservative treatment (bedrest and sedation) or conservative treatment together with the administration of AMCA. In a first series of 46 patients 23 were given AMCA by slow intravenous injection in a dosage of 1 g 4-hourly during the first week, 1 g 6-hourly during the second to fifth weeks inclusive, and 1 g 8-hourly during the sixth week. In a second series of 59 patients 30 received AMCA in hourly intravenous infusions 6 g daily during the first week, 4 g daily during the second week, and 1 5 g by mouth four times a day during the third to sixth weeks. The patient...

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Fibrinolytic Response to Oral Glucose

Cited by 8 publications

References 6 publications

Tissue-type plasminogen activator antigen and plasminogen activator inhibitor in diabetes mellitus.

Tissue-type plasminogen activator antigen and plasminogen activator inhibitor in diabetes mellitus.

Tranexamic acid (AMCA) in aneurysmal subarachnoid haemorrhage

Tranexamic acid (AMCA) in aneurysmal subarachnoid haemorrhage

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