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PubMed1976

Changes in plasma renin activity and plasma aldosterone in the induced paralytic attack of thyrotroxic periodic paralysis.

Changes in serum electrolytes, haematocrit, plasma renin activity and plasma aldosterone induced by glucose and insulin (GI) infusion were serially investigated in seven patients with periodic thyrotoxic paralysis. An attack which developed into complete quadriplegia was induced within 90 min after the beginning of the GI infusion in four out of seven patients. Only a slight paralysis of the legs was produced in another two patients and induction of an attack did not materialize in one. In four patients with complete quadriplegia, the mean values of serum sodium and potassium concentrations, haematocrit, plasma renin activity and plasma aldosterone slightly decreased immediately after the beginning of the GI infusion. Induction of a paralytic attack was not accompanied by any significant changes in serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone either 15 min before or after the onset of attack, while the serum potassium concentration progressively decreased, and an increase in plasma aldosterone associated with an increase of haematocrit and plasma renin activity reached a peak level at the stage of complete quadriplegia. On the other hand, in the three patients in whom an infusion produced slight or no paralysis of the legs, changes in the serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone were insignificant and the serum potassium concentration was slightly but insignificantly decreased. These results suggest that hyperaldosteronism may not be a trigger for the induced paralytic attack but a phenomenon secondary to volume depletion and a change in potassium homoeostasis induced by GI infusion.

Adult↗
PubMed1979

Plasma clearance of cortisol as a function of plasma cortisol levels in normal and obese persons and in patients with uraemia or cirrhosis of the liver.

Plasma cortisol levels in 2 normal persons, 2 obese persons, 2 uraemic patients, and 2 patients with cirrhosis of the liver were raised in 4 steps by a combination of iv priming doses and continuous infusions of cortisol. Plasma cortisol levels and transcortin binding were measured as well as plasma clearance rates of labelled and unlabelled cortisol during each of the 5 experimental periods. Plasma cortisol levels increased less and plasma clearance rates of labelled and unlabelled cortisol increased more in obese persons than in normal persons; in patients with disturbed metabolism of cortisol (uraemia, cirrhosis of the liver) the reverse is true. Plasma clearance rates of free cortisol were calculated and differed from an estimated hepatic plasma flow of 0.7 1/min under certain conditions. Since free cortisol is metabolized faster than transcortin-bound cortisol, increasing plasma clearance rates of cortisol are probably due to increasing ratios free/bound cortisol when total plasma cortisol levels are raised. Low plasma clearance rates of cortisol in uraemia and cirrhosis of the liver are thought to be due to endproduct inhibition, respectively reduced liver cell mass.

Adult↗
PubMed2002

Diurnal rhythm of plasma 1,25-dihydroxyvitamin D and vitamin D-binding protein in postmenopausal women: relationship to plasma parathyroid hormone and calcium and phosphate metabolism.

OBJECTIVE: Diurnal variations in plasma levels of 1,25-dihydroxyvitamin D (1,25(OH)(2)D) have previously only been investigated in young individuals, and these studies have failed to demonstrate a diurnal rhythm. We have studied whether plasma levels of 1,25(OH)(2)D and vitamin D-binding protein (DBP) vary in a diurnal rhythm in postmenopausal women. METHODS: Blood and urine were sampled with 2- and 4-h intervals in order to assess diurnal variations in plasma levels of 1,25(OH)(2)D, DBP and parathyroid hormone (PTH), as well as in plasma levels and urinary excretion rates of calcium and phosphate. Additionally, the free 1,25(OH)(2)D index was calculated (the molar ratio of 1,25(OH)(2)D to DBP). RESULTS: Plasma 1,25(OH)(2)D exhibited a diurnal rhythm (P<0.01) with a nadir in the morning (99+/-12 pmol/l), followed by a rapid increase to a plateau during the day (113+/-13 pmol/l, i.e. 14% above nadir level; P=0.005). A similar pattern of variation was found in plasma levels of DBP with peak levels 15% above nadir levels (P<0.01). The free 1,25(OH)(2)D index did not vary in a diurnal rhythm. PTH and plasma levels and urinary excretions of calcium and phosphate exhibited a diurnal pattern of variation. The diurnal rhythm of DBP was correlated with the rhythm of 1,25(OH)(2)D (r=0.47, P<0.01) and plasma albumin (r=0.76, P<0.01). Moreover, the rhythm of plasma calcium and PTH varied inversely (r=-0.36, P=0.02). CONCLUSIONS: With the disclosure of a diurnal rhythm of total plasma 1,25(OH)(2)D, all major hormones and minerals related to calcium homeostasis have now been shown to exhibit diurnal variations. In clinical studies, the diurnal variations of 1,25(OH)(2)D and DBP must be considered, i.e. blood sampling must be standardised according to the time of day.

Aged↗
PubMed2004

Alterations in plasma vitamin E distribution in type 2 diabetic patients with elevated plasma phospholipid transfer protein activity.

Mouse studies indicated that plasma phospholipid transfer protein (PLTP) determines the plasma distribution of vitamin E, a potent lipophilic antioxidant. Vitamin E distribution, antioxidant status, and titer of anti-oxidized LDLs (oxLDL) autoantibodies were evaluated in plasma from control subjects (n = 31) and type 2 diabetic patients (n = 31) with elevated plasma PLTP concentration. Unlike diabetic and control HDLs, which displayed similar vitamin E contents, diabetic VLDLs and diabetic LDLs contained fewer vitamin E molecules than normal counterparts. Plasma PLTP concentration in diabetic plasmas correlated negatively with vitamin E in VLDL+LDL, but positively with vitamin E in HDL, with an even stronger correlation with the VLDL+LDL-to-HDL vitamin E ratio. Circulating levels of oxLDL were significantly higher in diabetic plasmas than in control plasmas. Whereas the titer of IgG autoantibodies to modified LDL did not differ significantly between diabetic patients and control subjects, diabetic plasmas showed significantly lower levels of potentially protective IgM autoantibodies. The present observations support a pathophysiological role of PLTP in decreasing the vitamin E content of apolipoprotein B-containing lipoproteins, but not of HDL in plasma of type 2 diabetic patients, contributing to a greater potential for LDL oxidation.

Antioxidants↗
PubMed1981

Responses of plasma adenosine 3',5'-monophosphate, blood glucose and plasma insulin to glucagon in humans.

The effect of glucagon on plasma cyclic AMP (cAMP), insulin and blood glucose was examined in normal adult subjects. After an i.v. injection of glucagon there was a rapid, dose-dependent increase of plasma cAMP as well as insulin and blood glucose. Multiple injection of glucagon to the same subject with 60 min intervals gave almost identical responses of plasma cAMP and blood glucose, whereas the insulin response tended to decrease with time. Dose-dependent increases of plasma cAMP, insulin and blood glucose were also seen during a continuous i.v. infusion of glucagon. With the lowest doses of glucagon the blood glucose and plasma insulin concentrations were increased without any change of plasma cAMP. Plasma cAMP, insulin and blood glucose declined prior to the termination of glucagon infusion. During an endogenous hyperglucagonaemia, induced by alanine injection, there was no discernible change of plasma cAMP. We conclude that the early events of glucagon action may be studied in vivo by monitoring plasma cAMP. However, variations of plasma glucagon within the physiological range are not accompanied by measurable changes of cAMP in the peripheral circulation.

Adult↗
PubMed1982

The reversible activation of inactive renin in human plasma: role of acid and of plasma kallikrein and plasmin.

Inactive renin in normal plasma, Factor XII-deficient plasma and prekallikrein-deficient plasma was fully activated by dialysis to pH 3.0 for 24 hours at 4 degrees C. This activation was reversed after neutralization and incubation of the plasma at 37 degrees C. The reversible activation-inactivation was not affected by the presence of soya bean trypsin inhibitor. If acidified normal plasma was neutralized and stood at 4 degrees C, plasma kallikrein, but not plasmin, was generated. This rendered the initial acid-activation irreversible. Since no kallikrein was generated in the deficient plasmas, the acid-activation was reversible in these plasmas even after neutralization and standing at 4 degrees C. Thus the apparent activation of inactive renin by kallikrein in acidified, neutralized plasma is not a direct action by the serine protease on inactive renin but a two-stage process in which the inactive renin is first fully activated by acid treatment and the reverse reaction is prevented by plasma kallikrein.

Cold Temperature↗
PubMed2000

Measurement of plasma and intracellular S-adenosylmethionine and S-adenosylhomocysteine utilizing coulometric electrochemical detection: alterations with plasma homocysteine and pyridoxal 5'-phosphate concentrations.

BACKGROUND: The relative changes in plasma and intracellular concentrations of S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) may be important predictors of cellular methylation potential and metabolic alterations associated with specific genetic polymorphisms and/or nutritional deficiencies. Because these metabolites are present in nanomolar concentrations in plasma, methods of detection generally require time-consuming precolumn processing or metabolite derivatization. METHODS: We used HPLC with coulometric electrochemical detection for the simultaneous measurement of SAM and SAH in 200 microL of plasma, 10(6) lymphocytes, or 10 mg of tissue. Filtered trichloroacetic acid extracts were injected directly into the HPLC system without additional processing and were eluted isocratically. RESULTS: The limits of detection were 200 fmol/L for SAM and 40 fmol/L SAH. In plasma extracts, the interassay CV was 3.4-5.5% and the intraassay CV was 2.8-5.6%. The analytical recoveries were 96.8% and 97.3% for SAM and SAH, respectively. In a cohort of healthy adult women with mean total homocysteine concentrations of 7.3 micromol/L, the mean plasma value was 156 nmol/L for SAM and 20 nmol/L for SAH. In women with increased homocysteine concentrations (mean, 12.1 micromol/L), plasma SAH, but not SAM, was increased (P <0.001), and plasma pyridoxal 5'-phosphate concentrations were reduced (P <0.001). Plasma SAM/SAH ratios were inversely correlated with homocysteine concentrations (r = 0.73; P <0.01), and the SAM/SAH ratio in plasma was directly correlated with the intracellular SAM/SAH ratio in lymphocytes (r = 0.70; P <0.01). CONCLUSIONS: Increased homocysteine in serum is associated with an increase in SAH and a decrease in the SAM/SAH ratio that could negatively affect cellular methylation potential. Accurate and sensitive detection of these essential metabolites in plasma and in specific tissues should provide new insights into the regulation of one-carbon metabolism under different nutritional and pathologic conditions.

Adult↗
PubMed1979

Biologically active luteinizing hormone (LH) in plasma. III. Validation of the in vitro bioassay when applied to male plasma and the possible role of steroidal precursors.

An in vitro bioassay method for measuring LH activity was applied to male plasma. This method is based on the specific testosterone response to LH activity by interstitial cells from mouse testes. In contrast to assays conducted on female plasma, non-parallel response lines were obtained between serial dilutions of untreated male plasma and the International Reference Preparation for Human Pituitary Gonadotrophins FSH and LH/ICSH) for bioassay (code no. 69/104). In an attempt to eliminate this source of error, which would invalidate the assays, plasma was subjected to either ether extraction or charcoal adsorption prior to assay. While ether extraction was ineffective, charcoal treatment eliminated the source of non-parallelism. Evidence is presented indicating that the inclusion of a charcoal pre-treatment step provides an assay method for LH which fulfils the recognized criteria of reliability when applied to male plasma. An investigation of the likely causes of non-parallelism was undertaken by incubating mouse interstitial cells with various steroids and steroid sulphates at concentrations likely to be present in plasma. While most of the presumed precursors of testosterone were converted to testosterone, steroid sulphates (dehydroepiandrosterone sulphate and pregnenolone sulphate) at high concentrations as present in male plasma were the most active compounds in forming testosterone. However, the amount of testosterone produced from these precursors under controlled conditions was insufficient to account entirely for the deviation from parallelism observed with male plasma. Hence, the non-parallelism observed with untreated plasma samples cannot be entirely explained by the presence of steroidal testosterone precursors in male plasma.

Adsorption↗
PubMed1989

[Plasma homocysteine, a risk factor for premature vascular disease. Plasma levels in healthy persons; during pathologic conditions and drug therapy].

Homocysteine is a branch-point metabolite, the biological fate of which is linked to vitamin B12, reduced folates and vitamin B6. Various inborn defects in homocysteine metabolism, among which cystathionine beta-synthase deficiency is most common, lead to the clinical condition homocystinuria. A central feature of this clinical state is premature arteriosclerosis. These patients benefit from agents serving as cofactors in homocysteine metabolism which both reduce the homocysteine levels in plasma and the incidence of vascular episodes. Experimental data point to homocysteine as an arteriosclerotic agent. Homocysteine in human plasma exists mainly as mixed disulfides with albumin (70 per cent) and cysteine. New methods determine total plasma homocysteine which includes all these species. Normal values for plasma homocysteine are lower in premenopausal women than in men and postmenopausal women. Impaired homocysteine metabolism seems to exist in 15-30 per cent of patients with premature cardiovascular disease. Moderate homocysteinemia is as a risk factor for cardiovascular disease, independent of conventional risk factors. Apart from homocystinuria, vitamin B12 deficiency causes the most extreme elevations of plasma homocysteine, and it has been established that plasma homocysteine is a more responsive parameter to impaired vitamin B12 function than serum cobalamin. Massive increase in plasma homocysteine level is also observed in folate deficiency, whereas renal failure, some malignant states and psoriasis cause a moderate homocysteinemia. High doses of folic acid reduce plasma homocysteine, and this innocuous mean should be considered as an intervention in patients with increased plasma level. Drugs like methotrexate, some anticonvulsants and 6-azauridine triacetate induce moderate elevation of plasma homocysteine, whereas a reduction is observed after penicillamine administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗
PubMed1987

In vivo effects of camostat mesilate on plasma kallikrein, plasma kininase II and renal kallikrein of man.

N,N-Dimethylcarbamoylmethyl-4-(4-guanidino-benzoyloxy)phenylacetat e methanesulfonate (camostat mesilate) is reported to be an effective inhibitor of plasma kallikrein. It was shown in vitro to inhibit not only plasma kallikrein, but also renal kallikrein and plasma kininase II. These inhibitory activities, however, were very weak. The inhibition of plasma kallikrein in human plasma was limited in time, since a rapid reactivation of plasma kallikrein was noticed when samples were incubated at room temperature. In order to establish whether camostat mesilate was able to inhibit plasma kallikrein, kininase II and renal kallikrein also in vivo the inhibitory activity of camostat mesilate on these enzymes was studied in 5 healthy volunteers. After an oral intake of a single dose of 600 mg of camostat mesilate, plasma kallikrein was inhibited significantly, while kininase II in plasma was unaffected. Renal kallikrein activity determined by urinary excretion of active kallikrein remained unchanged after camostat mesilate intake. Thus, the results demonstrate that camostat mesilate in vivo inhibits only plasma kallikrein and has no effect on the activity of kininase II or renal kallikrein.

Adult↗
PubMed1985

Plasma therapy of primary rat mammary carcinoma: dependence of consumption of C3 during absorption of plasma with sepharose derivatives on the anticoagulant.

A previous study demonstrated inhibition of growth of primary rat mammary carcinomas after infusion of tumor-bearer plasma absorbed against Sepharose derivatives. In this report we have quantitated changes in individual complement components that occur during absorption of rat plasma with Sepharose derivatives and defined optimal conditions for consumption of the third component of complement (C3) (other complement components defined similarly). The concentration of functionally active C1 to C9 was measured before and after absorption in plasmas from both normal rats and rats with mammary tumors. C3 activity in plasmas from normal and tumor-bearing rats was reduced (consumed) during absorption under appropriate conditions with Sepharose 4B, inactivated CNBr Sepharose, or Protein A-Sepharose. The concentration of functionally active C1 and C4 did not decrease significantly during absorption with Sepharose derivatives. Consumption of C3 in rat plasma was influenced by the anticoagulant and by the time and temperature of incubation with Sepharose derivative. C3 consumption in rat plasma anticoagulated with acid citrate dextrose solution was variable; addition of Mg2+ (5 mM) to plasma anticoagulated with acid citrate dextrose solution augmented C3 consumption. There was no C3 consumption in plasma anticoagulated with ethylenedinitrilotetraacetic acid (a chelator of calcium and magnesium). In contrast, this reduction was observed in plasma anticoagulated with [(ethylenebis(oxyethylenenitrilo)]tetraacetic acid (a chelator of calcium). The results demonstrate optimal conditions for activation of the alternative pathway of complement during absorption of rat plasma with Sepharose derivatives and suggest in vivo experiments to define the role of this pathway in inhibition of growth of mammary tumors.

Absorption↗
PubMed1979

The relationship of the lithium erythrocyte: plasma ratio to plasma lithium level.

The relationship of the lithium erythrocyte:plasma ratio to plasma lithium concentration was reviewed in inpatients and outpatients with affective disorders. For some patients, there was a linear correlation between the erythrocyte lithium:plasma lithium ratio and the plasma lithium concentration. For these patients a graph of the slopes and intercepts of the lithium erythrocyte:plasma ratio vs. plasma lithium data formed a line that was not significantly different from the data of Lee et al. (1975). Significant correlations were found between the slopes and intercepts of the lithium erythrocyte:plasma ratio vs. plasma lithium data and the magnitude of active lithium efflux (Ko) from the erythrocyte. Our data confirm the finding of Lee et al. (1975) that the lithium erythrocyte:plasma ratio is dependent on the plasma lithium concentration. We relate this finding to lithium efflux from the erythrocyte.

Adult↗
PubMed1983

The effects of converting enzyme inhibitors on plasma angiotensinogen and plasma aldosterone in sodium-depleted rats.

Plasma angiotensinogen was measured by two different methods in three groups of sodium-depleted rats: control rats, captopril-treated rats and enalapril-treated rats. The enzymatic method of measurement is an exhaustion technique which measures the amount of angiotensin I liberated from plasma by an excess of renin. Direct radioimmunoassay measures both angiotensinogen and its inactive residue, des-angio I-angiotensinogen, and the difference between the results of both methods can be used as an indirect measurement of plasma des-angio I-angiotensinogen. Both converting enzyme inhibitors decreased blood pressure, stimulated renin secretion, decreased plasma angiotensinogen and increased des-angio I-angiotensinogen. Plasma des-angio I-angiotensinogen levels were positively correlated with plasma renin levels. In converting enzyme inhibitor-treated rats, plasma aldosterone was slightly, but not significantly, lower than in control rats. Although plasma aldosterone was significantly correlated with plasma renin both in control rats and converting enzyme inhibitor-treated rats, plasma renin was elevated 10-fold in treated rats.

Aldosterone↗
PubMed1983

Studies of C1 inactivator-plasma kallikrein complexes in purified systems and in plasma.

An enzyme-linked immunosorbent assay (ELISA) has been developed for the quantification of C1 inactivator-kallikrein (C1In-K) complexes. The formation of complexes assayed by this method parallelled the inhibition of plasma kallikrein esterase activity by C1 inactivator in purified systems. C1In-K complexes were detected when a final concentration of 5.7 nM plasma kallikrein was added to plasma, equivalent to the activation of 1% of the plasma prekallikrein. Exogenous Hageman factor fragment added to plasma induced the rapid formation of C1In-K complexes, whereas there was an appreciable delay when the plasma contact system was activated by the addition of kaolin. In both systems, the rate of formation and final amount of complex generated were directly related to the concentration of Hageman factor fragment or of kaolin added, indicating that this proteolytic pathway is tightly regulated. C1In-K complexes were not generated by kaolin in plasma congenitally deficient in Hageman factor or prekallikrein or by kallikrein in hereditary angioedema plasma deficient in C1 inactivator, thus confirming the specificity of the assay. Sucrose gradient ultracentrifugation studies showed plasma C1In-K complexes to have a molecular weight consistent with a 1:1 molar complex. In contrast, the complex displayed an anomalously high molecular weight on gel filtration chromatography. These data demonstrate that a sensitive and specific probe has been developed for documenting plasma kallikrein activation.

Angioedema↗
PubMed1997

Determinants of plasma platelet-activating factor acetylhydrolase: heritability and relationship to plasma lipoproteins.

Plasma platelet-activating factor acetylhydrolase (PAF-AH) is the enzyme that inactivates PAF (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine). We determined the relative contributions of genetic and environmental factors to variation in plasma PAF-AH activity in 240 individuals from 60 nuclear families. Regression of mean-offspring PAF-AH activity on the mid-parent value indicated that 62% of the variation in plasma PAF-AH activity was heritable. Spousal values were weakly negatively correlated, indicating that familial aggregation of PAF-AH activity is due to genetic rather than to environmental factors. Among normolipidemic individuals, plasma PAF-AH activity was strongly correlated with the plasma concentration of low density lipoprotein cholesterol (LDL-C), and treatment with lovastatin resulted in proportional decreases in plasma PAF-AH activity and LDL-C concentrations. To further elucidate the relationship between PAF-AH and plasma concentrations of LDL, plasma PAF-AH activity was measured in families with well-defined, monogenic disorders of LDL metabolism. Plasma PAF-AH activity cosegregated with plasma LDL-C concentrations in familial hypercholesterolemia, but not in familial hypobetalipoproteinemia. We speculate that the rate of removal of LDL from the circulation may determine the clearance rate of PAF-AH, thereby modulating the activity of PAF-AH in blood.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1998

Influence of plasma expansion on plasma protein binding of ketorolac.

STUDY OBJECTIVE: To determine the effect of dilution with intravascular volume expanders commonly used by anesthesiologists on clinically relevant levels of free serum ketorolac. DESIGN: In vitro study. SETTING: Pharmaceutics laboratory of a medical college. INTERVENTIONS: The effect of 6% hydroxyethylstarch, 5% albumin, 6% dextran 60, and lactated Ringer's solution on in vitro plasma protein binding of ketorolac was investigated by ultrafiltration. The binding was studied at three different drug concentrations: low therapeutic (0.3 microgram/ml), high therapeutic (3 micrograms/ml), and toxic (10 micrograms/ml), and at two or more volume expander dilutions. MEASUREMENTS AND MAIN RESULTS: The effect of plasma dilution on free ketorolac was consistent across all volume expanders tested and for each ketorolac concentration studied. As the plasma dilution with albumin, hydroxyethylstarch, dextran 60, or lactated Ringer's solution increased, the unbound ketorolac also increased from 3.2% to 3.3% in undiluted plasma to 5.0% to 8.7% in 50% dilution of the plasma with the investigated expanders. Dilution of plasma by only 10% resulted in a significant, but relatively minor, increase of unbound ketorolac to 3.2% to 3.8%. CONCLUSION: Because of the pharmacokinetic properties of ketorolac, this pharmacokinetic interaction can be expected to have only minor effects on unbound ketorolac concentrations when ketorolac is administered after the plasma expander. When ketorolac administration is followed by rapid plasma expander infusion, a transient increase of unbound ketorolac in plasma can be expected.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

Volume expansion and plasma protein clearance during intravenous infusion of 5% albumin and autologous plasma.

Autologous plasma may be used to replace plasma volume and plasma proteins during surgery, but its effectiveness is largely unknown. In the present study, the characteristics of predonated frozen and thawed autologous plasma were compared with those of 5% albumin in 15 male volunteers who received 10 ml/kg of body weight of these colloids as intravenous infusions over 30 min. Venous blood was sampled and urine was collected over 8 h to outline the volume expansion and blood-interstitial fluid space transport of three plasma proteins (albumin, fibrinogen and antithrombin) by means of mass balance analysis. The maximum plasma dilution of 5% albumin and autologous plasma averaged 17 and 21% respectively, and their half-lives were 2.5 and 2.9 h respectively (P<0.03). The between-subject variability in dilution was most pronounced for autologous plasma. Transport of protein from blood to the interstitial space occurred faster when the infused fluid contained the protein in question. The rate was highest at 60 min, and the process was still in progress at 8 h when approx. 60% of the infused albumin, 45% of the fibrinogen and 75% of the infused antithrombin had been translocated to the interstitial fluid space. In contrast with the proteins, excess plasma water was removed by urinary excretion. It is concluded that the volume expansion is equivalent for the two colloid fluids, although it is more predictable for 5% albumin. The transport of protein outlasted the volume expansion.

Adult↗
PubMed2003

Quality assessment of seven types of fresh-frozen plasma leucoreduced by specific plasma filtration.

BACKGROUND AND OBJECTIVES: A study was undertaken to determine plasma quality after specific filtration. MATERIALS AND METHODS: Seven types of plasma were tested, after filtration of plasma from filtered or non-filtered whole blood. Leucocyte counting was carried out after a 30-fold concentration of the sample. Twenty-nine parameters (including coagulation testing, proteins, coagulation factors and activation markers) were measured before and after filtration, and after 6 months of storage. RESULTS: After specific plasma filtration, the average residual leucocyte counts were less than 2250/l. In spite of small statistically significant changes in proteins, coagulation factors and complement activation, this study showed that plasma filtration did not alter plasma quality. After 6 months of storage at -30 degrees C, factor VIII recovery varied between 91 and 109%. Haemostasis parameters and activation markers remained within the normal range. CONCLUSIONS: Specific plasma filtration reduced the leucocyte number to < 104 leucocytes/l. The quality of plasma was not altered by the additional step of specific plasma filtration.

Biomarkers↗