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Biomedical subjects

C R Spillert

Publications and source records attributed to C R Spillert.

At least 37 records · Page 2Linked to original sources
PubMed1995

Modified recalcification time (MRT): a sensitive cancer test? Review of the evidence.

In the past, hypercoagulability causing cancer-related thrombosis (Trousseau phenomenon) remained unproven for lack of an appropriate coagulation test. This review proves that a modified recalcification time (MRT) test can detect cancer-related hypercoagulability. The hallmark of this test involves incorporating tissue factor (TF) in accurately assessing coagulability. Blood from controls and cancer patients was incubated with saline and endotoxin (to enhance clotting ability by monocyte-generated TF). The MRT with saline incubation (MRTS) and the MRT with endotoxin incubation (MRTE) were determined instrumentally. The MRTE is a more inclusive measure of total TF activity than the MRTS in nonadvanced cancer. The MRTE values (minutes +/- standard deviation) were: controls-5.69 +/- 0.8; miscellaneous cancers-3.17 +/- 1.1; head, neck, and colon cancers-3.9 +/- 0.6; breast cancers-3.6 +/- 0.6; gynecological cancers-4.1 +/- 0.9; and prostate cancers-3.4 +/- 1.1. The MRTE, by demonstrating hypercoagulability in nonadvanced (including occult) cancer, qualifies as a more sensitive marker for cancer than the Trousseau phenomenon. The data suggest that this test may be the most sensitive blood test to detect early cancer.

Arterial Occlusive Diseases↗
PubMed1994

In vitro effect of hirudin on recalcification time.

Hirudin, in its recombinant form (r-hirudin), is emerging as an ideal anticoagulant. As with any anticoagulant, the true anticoagulant property of hirudin should be contingent not on clinical criteria nor on anticoagulant levels, but on a functional assay that monitors changes in the rate at which blood clots. The purpose of this study was to determine the recalcification time (RT) of whole blood and of plasma on incubation with hirudin in vitro. Citrated human venous blood (n = 6) and plasma (n = 9) were incubated at 37 degrees C with either saline or 0.2 U/mL final concentration hirudin. The RT was measured instrumentally after neutralization of the citrate with CaCl2. Compared with saline, mean RT +/- SD values (minutes) with hirudin in blood increased from 6.9 +/- 0.8 to 7.6 +/- 0.6 minutes (P = .04) and in plasma from 9.0 +/- 1.4 to 11.2 +/- 1.4 (P = .001). We conclude that hirudin increases the RT values in both blood and plasma. The increased RT value in plasma is greater compared with that in blood. Whether this method can be used to titrate the dosage of hirudin warrants in vivo assessment.

Blood Coagulation Tests↗
PubMed1994

Hypertension-related coronary thrombosis: prothrombic role of angiotensin II.

Although hypertension is a major risk factor in acute myocardial infarction, concomitant hypercoagulability causing thrombosis leading to myocardial infarction remains unproven for lack of an appropriate coagulation test. This study was devised to determine whether a modified recalcification time (MRT) test can demonstrate that angiotensin II, a potent vasoconstrictor, also accelerates coagulation to promote thrombosis. The MRT incorporates blood cells and chemical coagulants for maximizing sensitivity. Four groups (A, B, C, and D) of aliquots of citrated human blood were incubated for 2 hours at 37 degrees C after adding to A--20 microL saline, to B--10 micrograms Escherichia coli endotoxin, to C--20 micrograms angiotensin II, and to D--a combination of E coli endotoxin and angiotensin II. The experiment was repeated with nonincubated aliquots. Modified recalcification time values +/- standard deviation in minutes were: A--5.5 +/- 1.5, B--4.6 +/- 1.1, C--4.9 +/- 1.0, and D--3.9 +/- 1.0. Significance (Student's t test) was as follows: B versus A P < .001; C versus A, P < .05; C versus D, P < .001; B versus C, P < .05; and B versus D, P < .001. No significant changes occurred in nonincubated blood. We conclude that angiotensin II has a hypercoagulable effect, as does endotoxin. The hypercoagulability in concert with vasospasm can explain the role of hypertension in acute myocardial infarction. This in vitro study excludes the role of other in vivo mechanisms in the development of angiotensin II-induced hypercoagulability.

Angiotensin II↗
PubMed1994

Hydrocele of the canal of Nuck.

The authors discuss hydrocele in the female processus vaginalis (hydrocele in the canal of Nuck) and present new case reports. The treatment of choice is surgical excision. The hydrocele is excised through a groin incision. The authors present four new cases.

Adolescent↗
PubMed1993

Coagulation effects of cyclosporine in liver transplantation.

Thromboembolic complications have been described in graft recipients receiving cyclosporine (CS). Whether these individuals have a hypercoagulable state when compared to healthy controls was evaluated. Recalcification times (RT) of saline-incubated citrated whole blood and endotoxin-incubated whole blood of both control and transplant patients were determined. There was no difference between the RT saline or RT endotoxin groups in both patient groups. These data suggest that CS alone has no procoagulant effects, but that additional factors such as endotoxin and/or graft-induced antigen production may provoke the thrombotic complications.

Blood Coagulation↗
PubMed1993

Prothrombotic effects of endothelin-2 (ET-2).

In this report we demonstrate that ET-2, in addition to its powerful vasoconstrictor properties and its role in hypertension, is capable of creating a hypercoagulable (prothrombotic) state. This study was facilitated by the utilization of a sensitive modified recalcification time (MRT) test that can measure coagulation at all points in the coagulation spectrum. The MRT was determined on aliquots (1 ml) of citrated blood which were added to saline (MRTS), to 10 micrograms of endotoxin (MRTE), and to 10 pg of ET-2 (MRT ET-2). The mean values of MRTS, MRTE, and MRT ET-2 were 4.3 +/- 0.8, 3.7 +/- 1.0, and 3.9 +/- 0.8 min, respectively. There was a statistically significant difference between MRTE vs. MRTS and MRT ET-2 vs. MRTS using the two-tailed t-test (p < 0.02 and p < 0.005, respectively).

Blood Coagulation↗
PubMed1993

Procoagulant property of platelet activating factor (PAF).

Platelet-activating factor (PAF) is known to activate platelets and thus promote clot formation in most mammalian species including humans. In this communication, the ability of PAF to hasten the overall coagulation process by measuring the recalcification time (RT) is described. Assessment of the RT in vitro indicated that the RT was significantly reduced by PAF (p < 0.001). This information adds a new dimension to the role of PAF in coagulation and also provides an exciting lead to the development of drugs for controlling the state of accelerated coagulation by pharmacologic means.

Blood Coagulation↗
PubMed1993

Modified recalcification time: a global coagulation screening test.

Hypercoagulability with resultant thrombosis as a leading cause of death remains unproven due to the lack of a global screening coagulation test documenting antecedent hypercoagulability. To fill this need a modified recalcification time (MRT) test that incorporates the contribution of all the circulating cellular and chemical mediators, including the important but neglected tissue factor, to coagulation is described. Aliquots of blood are incubated with saline and with endotoxin, and the MRT is instrumentally determined. Values outside the normal ranges of 5.3 to 8.5 minutes (saline) and 4.5 to 7.5 minutes (endotoxin) in the coagulation spectrum of 0 to 10 minutes to infinity are abnormal. Shorter values are inversely related to the degree of hypercoagulability. To assess MRT in detecting hypercoagulability, MRT values in conditions with known thrombotic risk that were reported individually are presented by indicating the percentages of each in the abnormal ranges. The conditions, all with statistically significant hypercoagulability, included early breast cancer, diabetes, head, neck, and colon cancer, peripheral vascular disease, and pregnancy. Modified recalcification time meets the criteria of a global coagulation screening test because of: 1) age-related prevalence of asymptomatic cancer and thrombotic cardiovascular disease, 2) specificity and sensitivity, and 3) expected lower morbidity and mortality with early intervention.

Arterial Occlusive Diseases↗
PubMed1993

Altered coagulability: an aid to selective breast biopsy.

Difficulty in discriminating nonadvanced breast cancer from benign breast disease results in many cancer negative biopsies. Development of a test to better differentiate between these two entities to reduce the number of cancer negative biopsies was the purpose of this blind study. The clue that prompted the development of this test resides in the state of hypercoagulability in cancer. Hypercoagulability can be measured by assessing tissue factor-mediated altered coagulability. The amount of tissue factor release is contingent on prior activation of the monocyte (the only blood cell that generates tissue factor) in vivo.

Adolescent↗
PubMed1992

Monocyte activation in acquired immunodeficiency syndrome.

The monocyte plays a key role in the pathophysiology of AIDS and ARC. This preliminary report adds insight into monocyte activation associated with HIV seroconversion, by comparing recalcification times in healthy controls and HIV-positive patients.

AIDS-Related Complex↗
PubMed1992

Cold-induced hypercoagulability in vitro: a trauma connection?

Injury severity score and hypothermia can lead to a high level of mortality when combined clinically. In acute trauma, the presence of a coagulopathy is difficult to treat and the aim is prevention. Aliquots of whole blood from healthy human volunteers (n = 9) were added to saline (control) and saline plus endotoxin (activated). The control and activated groups were divided and subjected to 60 minutes of normothermia (24 degrees C) or hypothermia (0 degrees C). The samples were returned to 37 degrees C; then the recalcification times were determined using fibrin formation and the viscous drag as the determining factors. The activated hypothermic group showed a decreased recalcification time of 345 (+/- 48.9) seconds compared to 405 (+/- 60.8) for the activated normothermic group (P less than 0.001). When the normothermic and hypothermic groups were compared without endotoxin added, the differences were not significant. The authors conclude that the effects of endotoxin on clotting time are worsened by hypothermia in vitro and act synergistically to possibly cause the coagulopathy seen in trauma patients.

Bacteremia↗
PubMed1991

Contribution of the monocyte to thrombotic potential.

The circulating monocyte exhibits the capacity to initiate and accelerate the coagulation cascade. We have devised a simple whole blood clotting assay which quantitates the monocyte's contribution of procoagulant (a marker of monocyte activation) to the clotting process and in addition, measures the in vivo activation of the cell. Citrated whole blood is added to saline and the recalcification time (RT) determined without incubation (RT control), with two hours incubation (RT saline), or added to endotoxin with incubation (RT endotoxin). The reduction in value between RT control and RT saline is a measure of monocyte activation in vivo. The reduction in time between RT saline and RT endotoxin is a marker of monocyte activation in vitro. This simple test enables the measurement of monocyte activation and this cells contribution to the hypercoagulability described in many disease states.

Blood Coagulation↗
PubMed1990

Dermatobia hominis myiasis masquerading as an infected sebaceous cyst.

In an apparently routine case, what appeared to be infected sebaceous cysts of the scalp turned out to harbour botfly larvae imported from a tropical country. Although the parasite Dermatobia hominis is not indigenous to the United States, cutaneous myiasis caused by the fly is fairly common in Central and South America, and several cases have been reported in people returning or emigrating from these regions. The authors therefore suggest that infection resulting from D. hominis invasion be considered in persons who present with furuncular lesions and give a history of travel to endemic areas.

Adult↗
PubMed1990

Direct correlation between injury severity and two markers of the functional status of the immune system.

This study was conducted to identify a relationship between anatomical trauma severity and immunologic function. Four milliliters of citrated whole blood (CWB) was obtained from 14 multiply traumatized patients and their Injury Severity Score (ISS) was calculated. Each CWB sample was divided into four 1 ml aliquots with 1 microgram of E. coli endotoxin (ECE) (Difco) being added to the first, 10 micrograms of ECE to the second, 10 micrograms of pokeweed mitogen (PWM) to the third, and 20 microliters of saline to the fourth. Following a 2 hr incubation at 37 degrees C the recalcification time (RT) was determined on a Hepcon-B10. Percent shortening was calculated as the difference in the RT between the stimulated sample and the saline control. There was a significant correlation between ISS and % shortening of the ECE stimulated samples at both concentrations (for 1 microgram ECE r = 0.59, P = 0.02, and for 10 micrograms ECE r = 0.81, P = 0.00025), and also in the PWM sample (R = 0.79, P = 0.00071). This study demonstrates a significant and direct relationship between trauma severity and the patient's monocytes' ability to generate thromboplastin following ECE or PWM stimulation.

Adult↗
PubMed1990

Beneficial effect of cod liver oil in murine endotoxemia.

Cod liver oil (CLO), a marine fish oil, contains approximately 20% omega-3 fatty acids (OFA). When CLO is administered to humans, inhibition of platelet aggregation, decreased platelet arachidonic acid levels, and reduced levels of endotoxin-induced thromboplastin synthesis by monocytes are observed. Since endotoxin causes both increased platelet aggregation and monocyte generation of thromboplastin with resultant microvascular compromise, the purpose of this study was to determine whether CLO is protective in murine endotoxemia. Swiss Webster mice were given CLO (1.0mg, 10.0mg, or 100mg), or 100mg triolein (an unsaturated fat containing no OFA) or saline (control) intraperitoneally (IP) three hours prior to IP administration of 0.3mg E.coli endotoxin. Survivals at 48 hours post-endotoxin administration were as follows: (A) 1.0mg CLO (4/20, 20%); (B) 10mg CLO (5/20, 25%); (C) 100.0mg CLO (11/20, 55%); (D) 100mg triolein (1/20, 5%); (E) 0.13cc saline (1/20, 5%). The significance of groups A,B,C,D verses the control group E is as follows: A vs E, p = 0.15; B vs E, p = 0.08; C vs E, p = 0.0006; D vs E, p = 0.76. This study demonstrates the beneficial effect of 100mg parenteral CLO in murine endotoxemia. This effect is probably mediated through antiplatelet and/or antimonocyte activating mechanisms.

Animals↗
PubMed1990

Pharmacologic doses of ascorbic acid prolong the effects of pentobarbital anesthesia.

Saline or ascorbic acid (AA), 1000 mg/kg and 1400 mg/kg was administered intraperitoneally (IP) to 3 groups of female Swiss-Webster mice after they had been anesthetized with sodium pentobarbital (SP). Both doses of AA given IP after SP anesthesia significantly prolonged sleeping time. An additional 50 mice were injected IP with 0.3 ml SP containing 6 mg/ml unlabeled SP and 0.6 ng C14 labeled SP. Immediately 25 mice received 40 mg AA in 0.4 ml saline, IP, and the remainder received saline. The serum half life of the radioactively labeled SP was more than 3 times longer in AA treated mice than in the controls.

Anesthesia↗
PubMed1989

Inhibitory effect of high dose ascorbic acid on inflammatory edema.

The ability of ascorbic acid (AA) as an antioxidant to suppress the inflammatory reaction was investigated. Carrageenan-induced foot pad edema was produced in the right hind foot of anesthetized mice (n = 22). Subsequently, Group A (n = 11) received 25 mg AA in saline (IP) and Group B, an equal volume of saline. After 2 1/2 hrs the animals were sacrificed and increase in weight of the amputated right paw over the amputated left paw was expressed as percentage edema (PE). The PE in Group A was 43.8 +/- 5.9, and in Group B was 59.3 +/- 3.9 (p less than 0.05, unpaired t-test). The same experiment was repeated with the AA administered 10 minutes prior to injury. The change in edema was not statistically significant. It is concluded that high dose AA suppresses edema if given after but not before injury.

Animals↗