Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Complement C1 Inhibitor Protein”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,423 records · Page 79Linked to original sources
PubMed2004

The powerful neuroprotective action of C1-inhibitor on brain ischemia-reperfusion injury does not require C1q.

C1-inhibitor (C1-INH) is a major regulator of the complement classical pathway. Besides this action, it may also inhibit other related inflammatory systems. We have studied the effect of C1-INH in C57BL/6 mice with focal transient brain ischemia induced by 30 minutes of occlusion of the middle cerebral artery. C1-INH induced a dose-dependent reduction of ischemic volume that, with the dose of 15 U/mouse, reached 10.8% of the volume of saline-treated mice. Four days after ischemia the treated mice had significantly lower general and focal neurological deficit scores. Fluoro-Jade staining, a marker for neuronal degeneration, showed that C1-INH-treated mice had a lower number of degenerating cells. Leukocyte infiltration, as assessed by CD45 immunostaining, was also markedly decreased. We then investigated the response to ischemia in C1q(-/-) mice. There was a slight, nonsignificant decrease in infarct volume in C1q(-/-) mice (reduction to 72.3%) compared to wild types. Administration of C1-INH to these mice was still able to reduce the ischemic volume to 31.4%. The study shows that C1-INH has a strong neuroprotective effect on brain ischemia/reperfusion injury and that its action is independent from C1q-mediated activation of classical pathway.

Animals↗
PubMed2004

The critical concentration of C1-esterase inhibitor (C1-INH) in human serum preventing auto-activation of the first component of complement (C1).

C1-esterase inhibitor (C1-INH) was depleted from normal human serum (NHS) at 4 degrees C by affinity chromatography with a monoclonal anti-C1-INH antibody (mAb 13 E1) coupled to CNBr-activated Sepharose 4B. The C1-INH-depleted serum (C1-INH-depl-HS) had normal levels of C1, C4, and CH 50 and C1-INH concentration was less than 10% of normal (15 microg/ml in C1-INH-depl-HS compared to 230 microg/ml in NHS). C1-auto-activation in C1-INH-depl-HS was followed by measuring C4-consumption in a haemolytic assay and by detection of activated C1s in a C1s-ELISA. After a lag phase of 10-20 min, C1-auto-activation in C1-INH depl-HS occurred and reached its maximum after 40 min at 37 degrees C. In contrast, neutralization of C1-INH activity in NHS by addition of monoclonal antibodies directed against its C1s-binding site, resulted in an immediate, spontaneous C1-activation without a lag-phase and reached its maximum already after 20 min (mAb 140) and 25 min (mAb 88G2). Addition of highly purified C1-INH or NHS as source of C1-INH to C1-INH-depleted serum to a final concentration of 55 microg/ml (22% of normal C1-INH concentration in HS) was sufficient to control spontaneous C1-activation.

Animals↗
PubMed1996

Relevance of lymphoproliferative disorders and of anti-C1 inhibitor autoantibodies in acquired angio-oedema.

We looked for autoantibodies to C1 inhibitor (C1-INH) and evaluated the relationship of their presence to the associated lymphoproliferative diseases and to the cleaved form of C1-INH in 13 patients with acquired C1-INH deficiency (acquired angio-oedema (AAE)). At the time of manifestation of angio-oedema symptoms or within a few years the following diseases were diagnosed: liver angioma (n = 1), M-components (n = 7, one of whom also had echinococcal liver cysts), breast cancer (n = 1), chronic lymphocytic leukaemia (CLL; n = 1); three patients had no associated disease. Anti-C1-INH autoantibodies, measured both as immunoglobulin binding to C1-INH immobilized onto microtitre plates (ELISA) and as plasma inhibitory activity of C1-INH function, were found in 12 patients. Binding of C1-INH to paraproteins, transferred to Immobilon after agarose gel electrophoresis, was detectable in five of seven M-components associated with AAE. Immunoblotting analysis of SDS-PAGE-separated plasma demonstrated that C1-INH circulated in the cleaved 96-kD form in the 12 patients with autoantibodies, but not in the one without. In conclusion, the large majority of our patients have autoantibodies to C1-INH. Circulating autoantibodies are necessary for the generation of cleaved C1-INH. The paraproteins associated with AAE are frequently autoantibodies to C1-INH and thus account for its consumption.

Adult↗
PubMed1995

Changes in the contact system during orthotopic liver transplantation with and without aprotinin.

The main cause of nonsurgical bleeding during orthotopic liver transplantation has been attributed to be hyperfibrinolysis due to high plasma levels of tissue plasminogen activator. The aim of this study was to investigate contact activation and its possible contribution to fibrinolysis during OLT with and without aprotinin. Aprotinin or placebo was given to 20 patients undergoing OLT as part of a randomized double-blind trial. Plasma samples were collected before, during, and after OLT. There were decreased preoperative levels of prekallikrein and factor XIIa (P < 0.05), with a trend for kallikrein and factor XIIa activity to increase during OLT peaking on reperfusion (P < 0.05). Kallikrein inhibition, C1 esterase inhibitor, and alpha-2-macroglobulin levels were normal before surgery, with low normal levels of antithrombin III and alpha-2-antiplasmin; these levels decreased during OLT with no specific change on reperfusion. In the aprotinin-treated group, kallikrein inhibition levels increased (P < 0.05) from preoperative mean (+/- SD) values of 101 +/- 47% to 154 +/- 42% and antiplasmin levels increased (P < 0.05) from 72 +/- 28% to 243 +/- 53% during the anhepatic phase, reflecting the effect of aprotinin. The antifibrinolytic effect of aprotinin was demonstrated by decreased levels of D-dimer on reperfusion (P < 0.05) and at the end of OLT (P < 0.001) in the aprotinin-treated group. We have shown that contact activation during OLT is minimal and that aprotinin does not alter the pattern of contact activation, but provides an antikallikrein effect.

Adult↗
PubMed1995

Cardioprotective effects of a C1 esterase inhibitor in myocardial ischemia and reperfusion.

BACKGROUND: Myocardial injury after ischemia and reperfusion can be attributed largely to the effects of polymorphonuclear leukocytes (PMN). The complement system plays an important role as a chemotactic agent, affecting adhesion molecule expression and neutrophil accumulation. METHODS AND RESULTS: In the present study, the cardioprotective effects of C1 esterase inhibitor (C1 INH) were examined in a feline model of myocardial ischemia and reperfusion (90 minutes of ischemia followed by 270 minutes of reperfusion). C1 INH (15 mg/kg) administered 10 minutes before reperfusion significantly attenuated myocardial necrosis compared with vehicle (10 +/- 2% and 29 +/- 2% necrosis as a proportion of area at risk, respectively; P < .01). Myocardial preservation was also related to reduced plasma accumulation of creatine kinase activity. C1 INH treatment resulted in improved recovery of cardiac contractility and preservation of coronary vascular endothelial function, as assessed by relaxation in response to acetylcholine, compared with contractility and preservation of endothelial function in vehicle-treated animals (69 +/- 6% and 20 +/- 4% relaxation, respectively; P < .01). In addition, cardiac myeloperoxidase activity (an index of PMN accumulation) in the ischemic area was significantly reduced after C1 INH treatment. Furthermore, immunohistochemical analysis of ischemic-reperfused myocardial tissue demonstrated deposition of the first component of the classic complement pathway, C1q, on cardiac myocytes and coronary vessels. CONCLUSIONS: Blocking of the classic complement pathway by C1 INH appears to be an effective means of preserving ischemic myocardium from reperfusion injury. The mechanism of this cardioprotective effect appears to be inhibition of PMN-endothelium interaction; this inhibition leads to preservation of normal endothelial function, which results in reduced cardiac necrosis.

Animals↗
PubMed2003

Effects of C1 esterase inhibitor administration on intestinal functional capillary density, leukocyte adherence and mesenteric plasma extravasation during experimental endotoxemia.

OBJECTIVE: To determine the effects of C1 esterase inhibitor (C1-INH) administration on intestinal functional capillary density, leukocyte adherence, and mesenteric plasma extravasation during experimental endotoxemia. DESIGN AND SETTING: Prospective, randomized, controlled animal study in the experimental laboratory of a university. SUBJECTS: 42 male Wistar rats. INTERVENTIONS: The animals were divided into three groups. One half of the animals of each group underwent studies of intestinal functional capillary density and leukocyte adherence on venular endothelium by intravital fluorescence microscopy. In the other half of the animals mesenteric plasma extravasation (FITC albumin) was determined by intravital fluorescence microscopy. Treatment groups received endotoxin infusion of 2.5 mg/kg per hour (group 2 and 3) and 100 U/kg b.w. C1-INH (group 3) during the 2 h of endotoxemia. MEASUREMENTS AND RESULTS: Endotoxemia resulted in a significant decrease in mucosal functional capillary density (18.5% vs. controls), which was reduced by C1-INH administration (9.5%). Treatment with C1-INH also significantly attenuated intestinal leukocyte adherence in submucosal venules (35% vs. endotoxin group) and mesenteric plasma extravasation (44% vs. endotoxin group). CONCLUSIONS: C1-INH administration diminishes endotoxin-induced changes in the intestinal microcirculation during experimental endotoxemia.

Animals↗
PubMed1985

Acquired deficiency of the inhibitor of the first component of complement: report of five additional cases with commentary on the syndrome.

The association of late onset recurrent angioedema with a deficiency of the inhibitor of the first component of complement (C1INH) and of the binding subunit of the first component, Clq, defines the syndrome of acquired C1INH deficiency. The description of five new cases, along with the original two and the 18 others in the literature, brings the total reported cases to 25 and highlights the associated B cell abnormalities that are present in 23 and are of a malignant nature in 19 cases. In three of the five newly reported cases, the occurrence of angioedema, which prompted recognition of the acquired deficiency of C1INH, C1q, and C4, preceded the delineation of the underlying B cell malignancy by 2 to 3 yr despite efforts to recognize neoplastic disease in two of these patients throughout the interval. Because the acquired C1INH deficiency reflects increased catabolism rather than impaired biosynthesis, only high-dose attenuated androgens elicit a measurable increment in serum C1INH. The occurrence of the syndrome with multiple myeloma is noted for the first time.

Aged↗
PubMed1986

Behaviour of the contact phase of blood coagulation in the adult respiratory distress syndrome (ARDS).

In order to assess the role of the kallikrein-kinin (K-K) system in the pathogenesis of the adult respiratory distress syndrome (ARDS) we have prospectively determined coagulation contact phase, blood gas and hemodynamic parameters in patients with ARDS at 0, 36 and 72 h from diagnosis. Compared to normal values, significantly lower mean levels of factor XII (71.4 +/- 9.8%, p less than 0.0005), prekallikrein (PPK) (52 +/- 5.7%, p less than 0.0005), high molecular weight kininogen (HMWK) (73 +/- 2%, p less than 0.0005) and alpha 2-macroglobulin (alpha 2-M) (51 +/- 7.1%, p less than 0.0005) were found in ARDS patients. The functional kallikrein inhibitory activity (KKI) and C1-esterase inhibitor antigenic (CIINH) were significantly higher in these patients (113.2 +/- 5, p less than 0.005 and 124.7 +/- 7.6, p less than 0.0005 respectively) compared with normal values during the entire study period. The KKI/CIINH ratio decreased significantly in our ARDS patients at 0, 36 and 72 h (p less than 0.025; p less than 0.05 and p less than 0.005 respectively). We found a significant correlation between PPK levels and oxygenation index (r = 0.69, p less than 0.001), PPK and the static thoracic compliance values (r = 0.64, p less than 0.001). There was also a significant correlation between PPK levels and Qs/Qt (r = -0.89, p less than 0.001). ARDS patients that survived presented a stability in the PPK values in successive tests. Nevertheless non-survivors showed a progressive decrease in PPK levels during the follow-up period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

C1 inactivator-C1s complexes in inflammatory joint disease.

A newly developed enzyme linked immunosorbent assay for the quantitation of C1 inhibitor (C1In)-C1s complexes was used to study activation of the classical pathway of complement in inflammatory joint diseases. Synovial fluid (SF) specimens were obtained from patients with rheumatoid arthritis (RA), other arthritides and non-inflammatory joint effusions. Paired serum (S) samples were obtained in 17 cases. Immune complexes (IC) were measured by the staphylococcal binding assay. C1In-C1s were higher in RA SF samples than in paired RAS samples (P less than 0.01). IC were higher in RA SF than non-RA SF. There was a significant inverse correlation between SF C1In-C1s complexes and SF total haemolytic complement. For all SF samples there was a correlation between IC and C1In-C1s complexes, but for RA SF alone there was no significant correlation between these parameters. There was no correlation between titre of rheumatoid factor and C1In-C1s complexes. These results demonstrate that activation of the classical pathway of complement is the hallmark of rheumatoid synovitis, yet also suggest functional heterogeneity of both circulating and intra-articular IC.

Antigen-Antibody Complex↗
PubMed1996

Activation of factor XII and cleavage of high molecular weight kininogen during acute attacks in hereditary and acquired C1-inhibitor deficiencies.

Hereditary and acquired C1-inhibitor (C1-INH) deficiencies (hereditary angioedema, HAE and acquired angioedema, AAE) are characterized by episodic increases in vasopermeability due to kinin release. Despite continuously defective C1-INH levels, symptoms only recur occasionally suggesting an episodic generation of pathogenetic factors induced by activation of the protease systems regulated by C1-INH. We evaluated activation of factor XII by measuring plasma levels of FXIIa with a commercial ELISA and cleavage of high molecular weight kininogen by performing SDS PAGE and immunoblotting analysis during 5 attacks in 5 different patients with HAE and during 7 attacks in 3 patients with AAE. The patients were also studied during remission. We confirmed our previous data indicating that during attacks both HAE and AAE patients had very high levels of cleaved HK (p < 0.0001) whereas during remission cleaved HK levels were normal in HAE and significantly increased in AAE (p < 0.0001). Both in HAE and in AAE, plasma levels of FXIIa were normal during remission and significantly increased during acute attacks (p = 0.0126; p = 0.0003). Our data suggest that the activation of a contact system is required to produce clinical symptoms.

Acute Disease↗
PubMed1983

Autoactivation of human complement subcomponent C1r involves structural changes reflected in modifications of intrinsic fluorescence, circular dichroism and reactivity with monoclonal antibodies.

Autoactivation of C1r is closely correlated with an irreversible increase of its intrinsic fluorescence. The activation and the fluorescence increase of C1r are accelerated on addition of activated C1r. Ca2+, di-isopropyl phosphorofluoridate and C1 inhibitor, which all inhibit, although to different extents, C1r activation, inhibit in parallel the fluorescence increase. C1r activation is blocked at pH 4.0-5.0, whereas it is accelerated at pH 10.5; under the same conditions the fluorescence increase shows parallel effects. No such fluorescence increase is observed during C1s activation by trace amounts of C1r. Far-u.v. circular-dichroism spectra of C1r indicate 73 and 78% of unordered form in both the proenzyme and the activated species respectively. The slight changes observed on activation are not restricted to C1r, as comparable results are obtained for proenzyme and activated C1s. C1r activation appears thus to involve structural changes leading to an 'activated state' distinct from the 'proenzyme state'. Monoclonal antibody to activated C1r is poorly reactive with proenzyme C1r, a finding that also supports this hypothesis.

Antibodies, Monoclonal↗
PubMed1987

Factor XII, plasma prekallikrein, alpha 2-macroglobulin and C1-inhibitor levels in renal allograft recipients during immunosuppression with cyclosporin A--sequential measurements over four months in 17 patients.

Factor XII clotting activity (F XII), plasma prekallikrein amidolytic activity (PK), alpha 2-Macroglobulin (alpha 2-M) and C1-Inhibitor (C1-Inh) antigens have been measured in 17 patients immediately before and sequentially for up to four months after kidney transplantation. Before transplantation mean F XII and PK levels were normal (99 +/- 27% and 102 +/- 21%, respectively, mean +/- S.D.) and alpha 2-M and C1-Inh levels were slightly elevated (115 +/- 55% and 129 +/- 32%, respectively, mean +/- S.D.). In the first two weeks after transplantation a significant decrease of F XII to 65 +/- 27%, of PK to 67 +/- 20% and of alpha 2-M to 88 +/- 42%, and a rise of C1-Inh to 201 +/- 44% (mean +/- S.D.) were observed (2 p less than 0.005). F XII levels four month after operation remained significantly (2 p less than 0.05) lower than preoperatively. PK and alpha 2-M values, however, were significantly higher (2 p less than 0.05) at four months as compared to the pretransplant period. Mean F XII levels in the 17 patients at various time points after transplantation correlated positively with PK, alpha 2-M and serum albumin and negatively with CyA level and dose and serum bilirubin. PK and alpha 2-M correlated positively with each other and albumin and negatively with creatinine, bilirubin and CyA (2 p less than 0.01). Whether CyA has a direct influence on production or consumption of F XII, PK, alpha 2-M and C1-Inh, or whether the changes merely reflect altered protein metabolism awaits further study.

Adult↗
PubMed1987

Antibody-independent activation of C1. I. Differences in the mechanism of C1 activation by nonimmune activators and by immune complexes: C1r-independent activation of C1s by cardiolipin vesicles.

C1 activation is controlled by the regulatory protein C1-inhibitor (C1-INH). In contrast to immune-complex-induced activation, which is insensitive to C1-INH, antibody-independent activation of C1 is modulated by C1-INH. The mechanisms regulating nonimmune activation were studied with two phospholipids varying in their capacity to activate C1 in the presence of C1-INH: cardiolipin (CL) and phosphatidylglycerol (PG). Whereas C1-INH consistently suppressed activation by PG vesicles, a dose-dependent increase in C1 activation was measured with CL vesicles above 40 mole %. A similar dose-response binding of C1s requiring C1q, but not C1r, was detected only on CL vesicles, but neither on PG vesicles nor on immune complexes. This binding was Ca2+-dependent, suggesting that dimeric C1s is involved and was inhibited by spermine. The C1q-bound C1s was specifically cleaved at 37 degrees C into its active 58 kDa and 28 kDa chains, in the absence of C1r. On the addition of anti-CL antibodies, the C1q-mediated cleavage of C1s by CL vesicles was specifically inhibited. The cleavage of C1r on CL vesicles was also determined. When macromolecular C1 was offered in the presence of C1-INH, C1r cleavage was detected; however, the presence of C1s was a critical factor for C1r activation, because it was required on CL vesicles, but not on immune complexes. These results show that nonimmune activation of C1 presents specific features which distinguish it from immune complex-induced activation. These characteristics varied with the capacity of antibody-independent activators to activate C1 in the presence of C1-INH.

Antigen-Antibody Complex↗
PubMed2001

[Complement activity among individuals at a ground self-defense force base].

OBJECTIVE: This study aims to examine the distribution of hemolytic complement activity, the prevalence of hypocomplementemia and the disorders causing hypocomplementemia among individuals taking part in a mass screening program. METHODS: The subjects consisted of 1340 male Japanese participating in a mass screening program at a Ground Self-Defense Force base in Asaka. We measured the hemolytic complement activity (CH50) after overnight fasting. The CH50 levels for hypercomplementemia and hypocomplementemia were defined as those outside the range of mean +/- 2 SD, respectively. We next measured the concentration of complement components: CIq, C4, B, C3, C5, C9, and C1-inhibitor for men with hypocomplementemia. Rheumatoid factor, ANA, HBsAg, HbsAb, and HCVAb were also measured. RESULTS: The mean +/- SD of age was 43.7 +/- 5.7. The CH50 levels ranged from 7.2 to 66.4 U/ml (mean +/- SD = 37.1 +/- 4.0 U/ml). Twenty-one and 37 men were classified as having hypocomplementemia (CH50 < 29.1 U/ml) and hypercomplementemia (CH50 > 45.1 U/ml), respectively. The age of the individuals with hypocomplementemia was 43.9 +/- 5.6 (Mean +/- SD) years. Three men with C9 deficiencies, 2 men with C5 deficiencies and 7 men with cold activation were identified among the 21 hypocomplementemic men. Three hepatitis C and 2 hepatitis B patients were also found among the 21 hypocomplementemic men. Other disorders found among the hypocomplementemic men were 3 glomerulonephritides and 1 possible SLE. CONCLUSION: We examined the distribution of CH50 levels in 1340 adult male Japanese. We identified 21 men with hypocomplementemia, and also found 5 cases of complement component deficiencies among 21 hypocomplementemic men. In addition the measurement of the complement activity may have also helped detect the presence of hepatitis, hypocomplementemic glomerulonephritis and collagen disease at an early stage.

Adult↗
PubMed1989

Terminal complement complexes and C1/C1 inhibitor complexes in autoimmune thyroid disease.

The potential role of complement activation and the membrane attack complex in the pathogenesis of Graves' disease and Hashimoto's thyroiditis has been investigated by measuring serum concentrations of the C1r-C1s-C1 inhibitor complex (C1/C1-inh) and the terminal complement complex (TCC), and by studying the binding to thyroid tissue of monoclonal and polyclonal antibodies against TCC neoantigens. Serum C1/C1-inh and TCC concentrations were significantly increased in 29 patients with untreated Graves' disease compared with 47 healthy subjects (P less than 0.001 for both), and decreased significantly after carbimazole treatment in 18 of these patients for whom post-treatment samples were available (P less than 0.01 and P less than 0.02, respectively). The serum TCC concentration, but not that of C1/C1-inh, was also significantly increased in 15 patients with Hashimoto's thyroiditis compared with the 47 healthy subjects (P less than 0.001). TCCs were identified by immunohistochemical staining around the thyroid follicles in thyroidectomy specimens from patients with Graves' disease (six out of six) and Hashimoto's thyroiditis (two out of two); normal thyroid tissue from two subjects showed no staining. These results suggest a role for complement, in particular the membrane attack complex in the pathogenesis of autoimmune thyroid disease.

Adolescent↗
PubMed2001

Capillary leak syndrome in children who undergo cardiopulmonary bypass: clinical outcome in comparison with complement activation and C1 inhibitor.

OBJECTIVES: Capillary leak syndrome (CLS) is associated with significantly increased morbidity and occurs after cardiopulmonary bypass in children with congenital heart disease. We investigated the early clinical parameters that predict the development of CLS and examined the relationship between the presence of CLS and complement and contact activation and C1 esterase inhibitor (C1-INH) during and after bypass. DESIGN: In this prospective study we took serial serological measurements of the complement and contact system and C1-INH in a cohort of 27 infants before, during, and up to 96 h after open-heart surgery. RESULTS: Complement and contact activation and a decrease in C1-INH were measured in all infants during and after CPB. Ten infants developed CLS postoperatively. Younger age and longer bypass time were strongly correlated to the development of CLS. No relationship was found between the degree of hypothermia, weight, gender, or cross-clamp time. C1-INH concentration and activity were lower peri- and postoperatively in the CLS group. Infants with CLS had a more pronounced postoperative increase in the C5a and C3a levels, higher postoperative level of factor XIIa, and lower prekallikrein activity than those without CLS. CONCLUSION: Contact and complement activation occurs during cardiopulmonary bypass and contributes to CLS more frequently in infants of a younger age and with a prolonged bypass time. This activation and decrease in C1-INH was strongly expressed in the CLS group, and therefore early substitution of C1-INH may prevent CLS after open-heart surgery in high-risk infants.

Capillary Leak Syndrome↗
PubMed1996

[The use of a C1-inhibior concentrate for short-term preoperative prophylaxis in two patients with hereditary angioedema].

A commercially available C1 inhibitor (C1-INH) concentrate was used for short-term prophylaxis before surgery in two patients with hereditary angioneurotic oedema. The patients suffered from recurrent subcutaneous and submucosal oedema of the face, extremities, and gastrointestinal tract as the result of a hereditary C1-INH deficiency. Both patients were receiving tranexamic acid or danazol therapy as oral long-term prophylaxis. Over the years the patients underwent several operations in regional and general anaesthesia, with mask ventilation or intubation. The C1-INH plasma concentrations measured preoperatively were always very low (0.02-0.06 g/l, normal range 0.15-0.35 g/l), despite the oral long-term prophylaxis. Substitution treatment with 500-1000 U C1-INH was performed 1 h before surgery. No side effects were seen following the concentrate infusions. With this substitution treatment no specific symptoms of hereditary angioneurotic oedema were recognized in either case. The measurement of C1-INH plasma concentration 2 h or 4 h after C1-INH substitution showed a marked rise in both patients, though normal values were not reached in either. We suggest that infusion of C1 concentrate is an appropriate form of preoperative substitution treatment in patients with hereditary angioneurotic oedema, in view of the lower risk of infection than with infusion of fresh-frozen plasma and the observed effectiveness.

Adult↗
PubMed1989

Serum C1-esterase inhibitor, an essential and independent prognosticator of gastric carcinoma.

The preoperative concentrations of IgG were lower (P less than 0.002) and the concentrations of C4 and C1-INH higher (P less than 0.01 and P less than 0.001) in 29 patients with recurrence after potentially curative resection of gastric carcinoma, than in 31 patients alive and disease-free 5 years after surgery. These differences between the two groups of patients were consistent within each of six groups of disease extent. In each of the two groups of patients, the preoperative concentrations of IgG, C4 and C1-INH had no significant variation with the extent of disease (P greater than 0.05 or greater). Of our variables, C1-INH was the most potent prognosticator and discriminated between patients with and without recurrence with 80% accuracy. Furthermore, the predictive prognostic value of C1-INH at the time of surgery was superior to the prognostic value of the extent of disease (F values 27.00 and 12.69). Apparently, the preoperative C1-INH concentration is an essential and independent prognostic parameter of gastric carcinoma. We assume that C1-INH reflects an additional prognostic feature appropriate to the tumour or the host. Our finding that the interval between surgery and death from recurrence had an inverse relation to the preoperative C1-INH concentration also supports this assumption.

Adenocarcinoma↗