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PubMed2003

Angioedema of the tongue due to acquired C1 esterase inhibitor deficiency.

We describe the management of an 83-year-old woman who presented with upper airway obstruction due to angioedema of the tongue. Following definitive airway management, investigation showed a diagnosis of acquired C1 esterase inhibitor deficiency (acquired angioedema) that was considered to be subsequent to haematological malignancy. Resolution of the macroglossia followed treatment with C1 esterase inhibitor concentrate, but the patient failed to wean from ventilatory support and died in the Intensive Care Unit. This case report highlights the potential for acquired angioedema to cause upper airway obstruction. The various treatment modalities for acquired C1 esterase inhibitor deficiency are summarized.

Aged↗
PubMed1989

Studies on contact activation: effects of surface and inhibitors.

Contact activation is initiated when the plasma proteins, Hageman factor (factor XII), prekallikrein and high molecular weight kininogen interact with negatively charged materials. The activation of the intrinsic pathway of blood coagulation and the production of bradykinin are among the sequelae of contact activation. The kinetics of the activation of the contact system are modified by plasma inhibitors, C1 inhibitor being quantitatively the most important. We propose that the activation of the system requires that the stimulus provided by the surface must be greater than a threshold value to overcome the effects of the inhibitors. We show in this paper that the amount of surface required for activation is much reduced in the absence of C1 inhibitor (Hereditary Angioedema) or in the cold where the inhibitor loses much of its effectiveness. Antithrombin III inhibition of activated Hageman factor is augmented by heparin which is also an activator of Hageman factor. The rate constants for inhibition remain much lower than for C1 inhibitor, however.

Antithrombin III↗
PubMed1980

C1 esterase inhibitor protein associated with human cancer: a tumour marker.

The concentration of a cancer-associated serum C1 esterase inhibitor protein was determined in 194 cases of human cancer, grouped according to their clinical activity. As control groups healthy blood donors and patients having non neoplastic chronic lung and liver diseases were included in the study. The results showed highly significant differences when the values obtained for "active" malignant tumors were compared with the two control groups and the quiescent tumours. The authors conclude that C1 esterase inhibitor protein measurement may be useful as a clinical tumour marker.

Complement C1 Inactivator Proteins↗
PubMed1989

Acquired C1 inhibitor (C1-INH) deficiency type II. Replacement therapy with C1-INH and analysis of patients' C1-INH and anti-C1-INH autoantibodies.

The response of two patients with autoantibody-mediated C1-inhibitor (C1-INH) deficiency to replacement therapy with C1-INH was studied over a period of 3 d. In patient 1 an acute attack of angioedema was successfully managed by infusion of 1,000 U of C1-INH concentrate. C1-INH function returned to normal levels within 30 min, while CH50 and C4 peaked after 6-7 h and C1 hemolytic activity reached 50-60% of normal after 3 d. Immediately after the injection an increase in C1-INH-anti-C1-INH complexes was observed. Based on NH2-terminal sequence analysis of the patients' Mr 96,000 C1-INH, it is concluded that this fragment is generated after cleavage of C1-INH in its active site by one of its target proteases without generating a covalent C1-INH-enzyme complex. In a second patient with a four to five times higher anti-C1-INH antibody titer, the infusion of 500 ml of plasma or of 2,000 U of C1-INH concentrate influenced neither the severity of the patient's angioedema nor the tested parameters, except for an increase in the amount of C1-INH-anti-C1-INH complexes. Analysis of patients' anti-C1-INH antibodies revealed that the antibodies recognize different epitopes within the C1-INH. This suggests that patients with acquired angioedema type II are a heterogenous group with respect to the C1-INH autoantibodies.

Amino Acid Sequence↗
PubMed1981

[Proteinase inhibitors and fibrinogen split products in patients with malignant diseases (author's transl)].

Fibrinogen degradation products could be detected frequently in patients with metastasized tumour disease. Plasminogen, antithrombin III and fibrinogen were not found to be elevated. The proteinase inhibitors alpha 2-macroglobulin, alpha 1-antitrypsin and C1-esterase inactivator were measured before and after chemotherapy. alpha 1-antitrypsin and C1-esterase inactivator were elevated in patients with pulmonary and/or retroperitoneal metastases. Regardless of the stage of the tumour disease serum level of alpha 1-antitrypsin and C1-esterase inactivator in increased under cytotoxic chemotherapy.

Antifibrinolytic Agents↗
PubMed1997

Preoperative prophylaxis for C1 esterase-inhibitor deficiency in patients undergoing oral surgery: a report of three cases.

C1-inhibitor deficiency, or hereditary angioedema, is a genetic disorder characterized by recurrent circumscribed, nonpruritic, nonpitting subepithelial edema. Minor trauma to the tissue, such as tooth extraction, can trigger life-threatening laryngeal edema. The use of fresh frozen plasma and/or danazol before treatment prevents angioedema attacks. A critical review of the treatment regimen and prophylaxis for C1-inhibitor deficiency is presented, and three new cases are described.

Adult↗
PubMed1980

The Clq receptor site on immunoglobulin G.

We propose that, the binding site for the complement subcomponent Clq on immunoglobulin G involves the last two (C-terminal) beta-strands of the C gamma 2 domain. This region contains a large number of accessible and highly conserved charged residues and charge is postulated as an important component of the Clq-IgG interaction. The conclusions are reached on the basis of accessibility and sequence conservation analyses of C gamma 2 amino acid residues, the use of specific inhibitors and chemical modification studies.

Amino Acid Sequence↗
PubMed1992

Manufacture and in vitro characterization of a solvent/detergent-treated human plasma.

We have developed a modified solvent/detergent (S/D) treatment to inactivate viruses in human plasma using 1% w/w final concentration of tri(n-butyl) phosphate (TNBP) and Triton X-100 and an incubation period of 4 h at 30 degrees C. The procedure inactivates > or = 10(6) chimpanzee-infectious doses (CID50) of HBV, > or = 10(5) CID50 of HCV, and > or = 10(6.2) tissue culture infectious doses (TCID50) of HIV. After virus inactivation, eleven plasma batches were lyophilized and 12 batches were deep-frozen until further use. The batches were characterized by extensive laboratory tests including measurement of clotting factors I-XIII, von Willebrand factor, plasminogen, inhibitors of blood coagulation and fibrinolysis, and other clinically important plasma proteins. All parameters were determined before and after S/D treatment. Twelve conventional single donor plasma units served as control. There were no marked losses of activities of clotting factors, antithrombin III, protein C, plasminogen, and C1-esterase inhibitor due to treatment. After the S/D step, the levels of these parameters were within the normal range in all batches. The same holds true for total protein, immunoglobulins, albumin, complement factors C3 and C4, haptoglobin, hemopexin, caeruloplasmin, alpha 1-antitrypsin, and pH. Protein S and alpha 2-antiplasmin activities decreased by about 50% and were frequently found to be slightly below the lower limit of the respective normal range after treatment. The interindividual variations of all proteins analysed were significantly lower than in the single donor plasma units. The S/D procedure did not lead to increases of markers indicating activation of hemostasis.(ABSTRACT TRUNCATED AT 250 WORDS)

Antiviral Agents↗
PubMed1988

Restriction of cell lysis by homologous complement: II. Protection of erythrocytes against lysis by newly activated complement.

Our previous work revealed that homologous complement (C) was ineffective in lysing antibody-sensitized erythrocytes (EA) even at high concentrations. It was also shown that activation of complement on homologous EA resulted in the binding of C9 and the formation of EA bearing complement proteins C1 through C9 (EAC1-9), yet few hemolytic sites were formed. Instead, as shown here, the formation of homologous EAC1-9 caused the cells to become resistant to lysis even by heterologous complement during a second incubation. In contrast, when homologous EAC1-8 were produced by incubating EA with C9-depleted serum, such intermediates were not protected against lysis by heterologous complement during a second incubation. Furthermore, homologous C9 on EAC1-9 was able to reduce the hemolytic efficiency of heterologous complement without blocking C activation and the formation of new C5b-9 complexes. Protection was not modified when homologous EAC1-9 were produced in one step, by incubation of EA with serum, or sequentially by adding C9 to EAC1-8. The minimum number of 9-sites required to confer a protective effect on EAC1-9 was less than 200 per cell. Thus, in addition to its known effect in heterologous cell killing, homologous C9 is capable of protecting homologous cells against inadvertent complement lysis.

Ammonia↗
PubMed1980

Studies on the biological functions of monoclonal immunoglobulins and their fragments.

Complement-binding ability of three isolated monoclonal proteins of IgG class, their Fab, and Fc fragments was analyzed (including tests for the presence of polymers, aggregated forms and immune complexes), and the influence of two monoclonal IgG lambda proteins on fibrinogen conversion to fibrin was determined. Two proteins--IgG1 lambda and IgG3K--bound small amounts of complement only when tested in native form, but failed to bind complement after thermal aggregation. Papain-digestion of these proteins revealed a significant ability of complement binding by Fc fragments. The third protein--M-IgG1 lambda--bound large amounts of complement when used in its native form, but after thermal aggregation this ability decreased. This protein differs in structure from monoclonal Ig described here. It was shown by the atypical elution pattern of papain digest of M-IgG1 lambda from CM-cellulose and by the anticoagulative activity of this protein. In control tests with polyclonal immunoglobulin complement-binding ability increased after thermal aggregation of the immunoglobulin, Fc fragments of the polyclonal immunoglobulin bound lower amounts of complement than whole molecules. As already mentioned, the activity of the factor inhibiting fibrinogen-to-fibrin conversion was observed in only one of two tested proteins M-IgG lambda. This activity was not connected selectively with Fab fragment. In identical concentrations polyclonal IgG had no effect on fibrinogen-to-fibrin conversion.

Adult↗

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