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Biomedical subjects

E F Mammen

Publications and source records attributed to E F Mammen.

At least 73 records · Page 4Linked to original sources
PubMed1988

"Sticky platelet syndrome": a congenital platelet abnormality predisposing to thrombosis?

We have identified a number of patients with coronary artery disease, TIAs and/or strokes and idiopathic ischemic optic neuropathy who have a platelet population which is in vitro hyperaggregable with epinephrine and ADP and hyperresponsive to surface contact. These patients have no identifiable risk factors. Several families have been identified in which multiple members had these findings. Many, but not all have had clinical symptoms. An autosomal (dominant) pattern of heredity seems to evolve. We refer to this as "sticky platelet syndrome" and hypothesize that it may represent a congenital platelet abnormality which potentially predisposes to thromboembolisms. The precise nature of the defect is not known at this time.

Adolescent↗
PubMed1988

Oral contraceptives and the hemostatic system.

We studied 30 control women and 131 pill users to evaluate effects of birth control pills and clinical factors on hemostasis. When control patients were matched with an equal number of pill users, none of the direct markers of activated hemostasis (fibrinopeptide A, platelet factor 4, and beta thromboglobulin) were increased. Plasminogen, prekallikrein, and protein C (protective against clotting) were significantly higher in pill users. Fibrinogen, antithrombin, alpha-2 antiplasmin, and fibronectin were comparable. Among the 131 pill users, antithrombin levels decreased with a family history of thromboembolism. Fibrinogen and fibronectin were increased with obesity, but there was no evidence of activated hemostasis. Overall, pill use did not appear to result in hypercoagulability. Considering family history of thromboembolism might further improve the safety of oral contraceptive use.

Adult↗
PubMed1987

Concomitant occurrence of disseminated intravascular coagulation and factor VIII inhibitor in a patient with prostatic cancer.

An 86-year-old man, diagnosed as having carcinoma of the prostate, stage D, was admitted to the hospital. Soon after admission, he developed bleeding from various sites, including intravenous puncture sites and gastrointestinal and urinary tracts. A clinical diagnosis of disseminated intravascular coagulation (DIC) was made, which was corroborated by laboratory data. A factor VIII inhibitor of 12.5 Bethesda units was also identified in the patient's plasma. Concomitant occurrence of disseminated intravascular coagulation and an acquired factor VIII inhibitor has not been reported previously.

Aged↗
PubMed1987

Preeclampsia, delivery, and the hemostatic system.

To determine the effects of preeclampsia and delivery, the hemostatic system was evaluated before and 24 to 48 hours after delivery in 59 nulliparous patients without clinical signs of disseminated intravascular coagulation. Fifteen patients with mild preeclampsia and 18 with severe preeclampsia were compared with 26 pregnant control patients. Preeclampsia was associated with high fibronectin (p less than 0.001), low antithrombin III (p less than 0.001), and low alpha 2-antiplasmin (p less than 0.005), suggesting endothelial injury, clotting, and fibrinolysis, respectively. After delivery, fibronectin decreased only in preeclamptic patients (p less than 0.005); alpha 2-antiplasmin increased in all groups (p less than 0.001). Endothelial injury in preeclampsia appeared to resolve soon after delivery, which could contribute to the rapid clinical improvement noted in the early puerperium.

Adult↗
PubMed1987

Mechanisms for reduced colloid osmotic pressure in preeclampsia.

The determinants of plasma colloid osmotic pressure were studied in 32 patients with preeclampsia and their matched control subjects. Although plasma colloid osmotic pressure was significantly related to preeclampsia, its severity, and proteinuria, it was most highly correlated with an elevated fibronectin level, suggesting that endothelial injury, rather than proteinuria, is the major mechanism of reduced colloid osmotic pressure in preeclampsia.

Adult↗
PubMed1986

A fully automated immuno-turbidimetric determination of fibrin(ogen) degradation products.

A fully automated procedure for the determination of fibrin(ogen) degradation products was developed using the I. L. Multistat Centrifugal Analyzer (MCA). The assay is based on the turbidometric measurement of the interaction between antibodies to human fibrinogen and defibrinogenated specimens. The method allows, with high reproducibility, for the accurate quantitation of degradation products between 10 and 160 micrograms/ml. A comparative study of 100 normal and abnormal patient samples revealed an excellent correlation with the semi-quantitative manual procedure. The method can be adapted to existing automated coagulation procedures and can become part of coagulation panels.

Antibodies↗
PubMed1986

Platelet hyperaggregability in patients with chest pain and angiographically normal coronary arteries.

Forty-one patients with chest pain and angiographically normal coronary arteries were studied for platelet abnormalities. Patients with conditions known or suspected to be associated with chest pain or platelet dysfunction were excluded. After coronary angiography and 2-week withdrawal from all medications, platelet aggregometry was performed using peripheral venous plasma samples and 3 concentrations of adenosine diphosphate, 2.34, 1.17 and 0.58 microM, and epinephrine, 11, 1.1 and 0.55 microM, as stimuli. Platelet morphology in response to surface contact (adhesion) was evaluated by transmission electron microscopy to determine the percentage of platelets in the round/abortive (inactive), dendritic (intermediate) and spread (activated) forms. Plasma specimens obtained from healthy volunteers of similar age and sex were analyzed in parallel and served as control subjects. Compared with control subjects, patients had increased aggregation at all concentrations of both adenosine diphosphate and epinephrine (p less than 0.001). Patients also had fewer platelets in the dendritic form and more in the round/abortive and spread forms. Thus, patients with chest pain and normal coronary arteries have platelet hyperaggregability in vitro, although the clinical relevance of this finding is unclear.

Adenosine Diphosphate↗
PubMed1986

Antithrombin, prekallikrein, and fibronectin levels in surgical patients.

Antithrombin (AT), prekallikrein (PK), and fibronectin (FN) levels were measured in the plasma of 290 patients. The mean (+/- SD) lowest AT level measured in 287 patients was 70% +/- 18% (normal, 75% to 120% of control). The mean lowest AT level in 81 septic patients (49% +/- 17%) was significantly lower than in the 206 patients without sepsis (78% +/- 22%). The mean AT level in 60 patients who died (42% +/- 22%) was significantly lower than in 227 patients who lived (78% +/- 19%). The mean lowest PK level measured in 71 patients was 42% +/- 17% (normal, 80% to 120%). The mean PK level in 32 septic patients (26% +/- 12%) was significantly lower than in 39 patients who were not septic (54% +/- 19%). The mean lowest FN level measured in 45 patients was 193 +/- 86 micrograms/mL (normal, 160 to 240 micrograms/mL). The mean FN level in 15 septic patients (128 +/- 72 micrograms/mL) was significantly lower than in the 30 nonseptic patients (266 +/- 84 micrograms/mL). Following AT, PK, and FN levels in critically ill surgical patients may allow earlier diagnosis and more effective treatment of sepsis.

Antithrombins↗
PubMed1986

Hemorrhage vs rethrombosis after thrombolysis for acute myocardial infarction.

To determine whether or not the timing of heparin infusion affects either bleeding or reocclusion following intracoronary streptokinase for acute myocardial infarction, heparin was infused immediately after streptokinase in 89 patients and was delayed for 12 hours in the subsequent 93. Bleeding occurred in 22 immediate-heparin patients and was major in five (one fatal); there were 14 hemorrhages in the delayed-heparin group, all minor. At discharge, reocclusions were observed in 18% (12/68) of immediate-heparin patients, and 11% (3/27) of the latter. Bioassayed fibrinogen levels displayed sustained depression regardless of bleeding for 20 hours after streptokinase; however, defibrinogenation measured by immunoassay was much less striking. This suggests that high levels of fibrinogen degradation products spuriously affect the bioassay of fibrinogen. We conclude that bleeding is related to the anticoagulant effects of fibrinogen degradation products interacting with heparin, and may be largely independent of hypofibrinogenemia. Delaying heparin for 12 hours may decrease the risk of bleeding while little affecting the risk of reocclusion.

Coronary Disease↗
PubMed1985

A fully automated method for clot based coagulation panels using an MCA Multistat Centrifugal Analyzer.

Small modifications of the commercially available software of the I.L. Multistat Centrifugal Analyzer (MCA) enabled us to evaluate clot based prothrombin times (PT), activated partial thromboplastin times (APTT) and thrombin times (TT) simultaneously within one run. This imparted a great deal of flexibility to this procedure in that batches and/or panels of clot based and other types of turbidimetric tests can be performed concurrently in any combination. The PT and TT by this turbidimetric procedure correlated very well with those of the Fibrometer in normal specimens as well as in a wide variety of coagulation defects. The turbidimetric APTT procedure, however, often produced clotting times longer than those achieved with the Fibrometer. The discrepancy between the Fibrometer and turbidimetric APTT procedures was shown to be the consequence of greater sensitivity of the latter to detect low concentrations of heparin, elevated fibrinogen split products and mild factor deficiencies. The available clot based procedures are suitable for use in detecting specific factor deficiencies and the presence of coagulation inhibitors.

Autoanalysis↗
PubMed1985

Combined factor V/VIII deficiency: a case report including levels of factor V and factor VIII coagulant and antigen as well as protein C inhibitor.

Comprehensive coagulation studies were performed on members of a family with combined factor V/VIII deficiency. The purpose of these studies was to investigate the hypothesis that combined factor V/VIII deficiency is due to a lack of the inhibitor to activated protein C. The analyses performed included routine APTT and PT, factor V and VIII coagulant activity and antigen levels, von Willebrand factor levels, protein C antigen assay, and both protein C inhibitor activity and antigen levels. Three of the 19 family members studied were found to have a deficiency of both factors V and VIII. These three individuals showed prolonged APTTs and PTs and decreased levels of factor V and factor VIII coagulant activity and antigen. Factor VIII related antigen and ristocetin cofactor (von Willebrand factor) levels were normal. Protein C and both protein C inhibitor activity and antigen levels were also found to be normal. These findings confirm the results of other recent investigators and indicate that the autosomal, inherited combined factor V/VIII deficiency is not due to a protein C inhibitor deficiency. The real defect in this combined deficiency remains to be determined.

Adult↗
PubMed1985

Hemostasis changes during cardiopulmonary bypass surgery.

A number of hemostasis parameters were studied in a total of 63 patients undergoing cardiopulmonary bypass (CPB) for open heart surgery. In 33 patients fibrinogen, Factors II, V, VIII:C, X, XI, antithrombin, plasminogen, alpha 2-antiplasmin, and platelet counts were assayed before surgery, during maximal hypothermia, at the end of the bypass procedure, before and after protamine sulfate infusion, in the intensive care unit, and 48 hours postoperatively. All factors assayed decreased markedly when the patients were placed on the bypass machine, the drop fairly well paralleling the decrease in hematocrit. During bypass the factors remained low, although a slight tendency toward an increase was noted. Only platelet counts remained low with a decreasing trend until the end of bypass. In the intensive care unit a second decrease in fibrinogen, Factors II and V and antithrombin was noted. This drop was unrelated to four patients who experienced a greater blood loss during this time than the others. Forty-eight hours postoperatively, a marked increase could be found in all clotting factors and near normal levels were measured. Platelet counts remained low, however. The decrease in factors rarely dropped into a range where one would expect a compromised hemostasis (less than 30%). Although antithrombin levels decreased below 60%, no difficulties with heparinization were encountered. Several factors were assayed manually and by automated analyzer (Multistat III), and excellent correlations were found between both procedures. Also a good correlation was found between the activated whole blood clotting times and quantitative heparin assays. In 30 additional patients platelet function was studied before surgery, after thoracotomy, after heparin administration, after initiation of bypass, at maximal hypothermia, before and after protamine sulfate infusion, and 24 hours postoperatively. Platelet counts once again decreased as patients were placed on the CPB machine and remained low throughout the procedure. Mean platelet volumes were unchanged until protamine was given. At that time, a significant drop in mean platelet volume was recorded. Twenty-four hours postoperatively the volumes were normal again. Platelet aggregation studies were performed on a whole blood aggregometer using two concentrations of ADP, collagen, and ristocetin as aggregation inducers. A significant decrease in aggregability was seen when the patients were connected to the CPB apparatus.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1985

Human antithrombin concentrates and experimental disseminated intravascular coagulation.

The effect of human antithrombin III concentrates was studied in a dog model in which DIC was produced by the infusion of 0.66 M lactic acid. In 35 animals infused with lactic acid only, platelet counts, fibrinogen levels, alpha 2-antiplasmin levels, and antithrombin levels decreased significantly over a 4-hour observation period. At the same time, the levels of fibrin(ogen) split products increased. At the end of the experimental period, the glomeruli of the dogs' kidneys contained significant quantities of fibrin. Hemodynamically, the dogs experienced a significant decrease in cardiac output, whereas the mean arterial blood pressures remained unchanged. Urine output seemed to decline during the time of study. Appreciable quantities of heparin could be measured in the dogs' plasmas. In 13 dogs that were treated in the same manner as the just described 35 animals, 1 U of human antithrombin concentrate per ml of calculated dog plasma was infused over a 90-minute time span, beginning after 1 hour of acidosis. Although no differences were noted in the decrease in platelet counts between the two groups, fibrinogen levels and alpha 2-antiplasmin levels declined less drastically in the antithrombin-treated group. Also the levels of fibrin(ogen) split products increased less in the treated group. The antithrombin activity levels increased markedly and remained at their high levels even after the infusion of antithrombin had ceased. The amount of human antithrombin circulating was followed by immunologic assays using a human antibody to antithrombin. Also, with this technique, the levels of infused antithrombin did not decrease. The amount of fibrin found in the glomeruli of this group of animals was significantly lower than in the nontreated group (p less than 0.001). Even cardiac output was higher in the treated group and urine production seemed to increase. Also, these dogs had appreciable quantities of heparin in their plasmas. In a control group of six animals who were infused with saline instead of lactic acid, no major changes were observed in the coagulation and cardiovascular parameters. These data seem to suggest that antithrombin concentrates exert a certain protective effect in this particular DIC animal model.

Acidosis↗
PubMed1985

Changes in antithrombin, antiplasmin, and plasminogen during and after cardiopulmonary bypass.

Platelet counts and several clotting parameters, especially antithrombin, alpha 2-antiplasmin, and plasminogen, were determined in 33 patients undergoing cardiopulmonary bypass surgery. Except for Factors VIII and XI, all activities measured fell significantly as the patients were placed on the pump. This initial drop paralleled the drop in hematocrit, i.e., the drop was most likely due to hemodilution. During the entire procedure the activities remained decreased, again paralleling the hematocrit. Only the drop in platelet counts was greater than the hematocrit, suggesting additional consumption during bypass. In the ICU a second significant drop in antithrombin, prothrombin, and Factor V was noted that was not reflected by a drop in hematocrit. The cause for this is not known at this time. Although the patients with the lowest antithrombin levels, compared to the highest levels in the ICU seemed to have a greater need for protamine and blood and had greater chest tube drainage, none of these changes were significantly different. Comparisons between activated clotting times (ACTs) and actual heparin levels revealed a good correlation (0.886). Good correlations were also noted when manual factor assays were compared with automated assays using an automated analyzer suggesting the potential use of automation and profiling for these patients. Possible reasons for some of the most commonly encountered postoperative bleeding problems are discussed.

Adult↗
PubMed1985

Serial changes in primary hemostasis after massive transfusion.

Primary hemostasis was studied in 22 injured patients in the operating room (OR) after a minimum of 10 transfusions, 6 and 15 hours after surgery, on postoperative days 2 and 4 and during convalescence (mean 25 days after surgery). The platelet count was low in the OR and continued to fall after surgery through the second postoperative day; it began to rise by day 4 and was above normal at convalescence. Most patients had prolonged bleeding time through day 4. Platelet aggregation with adenosine diphosphate and collagen was depressed in the OR and platelet aggregation remained depressed. The platelet-specific proteins, beta-thromboglobulin and platelet factor 4, were elevated in the OR and fell throughout the first 4 postoperative days. A secondary rise in these proteins occurred at convalescence. Despite severe alterations in both the number and function of platelets after massive transfusion for injury, no patient had clinical oozing. Therefore the routine administration of platelets in comparable patients without "medical bleeding" is unwarranted.

Accidents, Traffic↗
PubMed1983

Effect of albumin resuscitation on canine coagulation activity and content.

Prior work showed that albumin resuscitation in man leads to decreased coagulation activity and coagulation protein content. These observations were tested in 20 splenectomized dogs shocked by control hemorrhage and resuscitated with the sequential infusion of: (1) 20 ml/kg balanced electrolyte solution (BES) or 5% albumin/BES; (2) shed blood; (3) 30 ml/kg BES or 5% albumin/BES; (4) 250 ml blood stored from the time of splenectomy. Either BES or 5% albumin/BES was given for the next 3 days. Coagulation activity (fibrinogen, plasminogen, factor VIII, and prothrombin) and coagulation protein content (factor VIII by specific canine antigen) were measured preshock, post resuscitation, and daily for 3 days. Albumin resuscitation significantly (p = greater than 0.05) reduced coagulation activity of fibrinogen (423 +/- 145 vs. 274 +/- 80 mg/dl SD), factor VIII:C (64 +/- 24 vs 42 +/- 16% SD), prothrombin (195 +/- 44 vs. 141 +/- 22% SD) but did not alter CPC of factor VIII:RAg (142 +/- 83 vs. 156 +/- 141% SD). Lower coagulation activity after 5% albumin/BES resuscitation in conjunction with no change in factor VIII:RAg content which is produced by the vascular endothelium suggest that impaired hepatic synthesis may lead to the reduced coagulation activity after albumin resuscitation.

Albumins↗
PubMed1982

Oral contraceptives and blood coagulation: a critical review.

Based on epidemiologic data, women who take oral contraceptives seem to have an increased risk of developing thromboembolic disease. In order to explain this association, some studies have been undertaken to find abnormalities in the hemostasis system. Many conflicting test results have been reported, probably reflecting in part the technical difficulties in use of reliable, reproducible, and specific assay systems. None of the data obtained seems to be specific for users of oral contraceptive drugs, and none was found uniformly in all takers of the drugs. Many findings are probably unimportant from the overall point of view of the physiology of hemostasis. Unfortunately, there seems to be no test procedure or even combination of tests that will reliably predict which patient might develop a thromboembolic episode in association with oral contraceptives or in association with any other condition recognized as being a risk factor. Even in most patients who do have a thrombosis, the test procedures fail to signal this event with reliability and predictability. At this time, it is not known whether oral contraceptives do or do not trigger the hemostasis system to develop a thrombosis or by which mechanism they could trigger the event. Fortunately, only a very small number of women develop thrombosis in association with oral contraceptives.

Adult↗