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PubMed1996

Circulating complement proteins in patients with sepsis or systemic inflammatory response syndrome.

The systemic inflammatory response of the body to invading microorganisms, termed sepsis, leads to profound activation of the complement system. Pathophysiological concepts suggest that complement activation occurs very early in this syndrome. Thus, we discuss whether the determination of concentrations of the complement components C3a, C5a, and C3 in plasma as well as of the C3a/C3 ratio might be helpful to diagnose sepsis early. For this purpose, 33 patients from an intensive care unit were monitored for 10 days. In comparison with healthy donors, C3a levels and the C3a/C3 ratio of intensive-care-unit patients were significantly elevated (P < 0.0001) on admission. In contrast, C3 levels were significantly reduced (P < 0.0001) but increased during the study. C5a levels in the plasma of healthy donors and patients were identical. Twenty-two of 33 patients fulfilled microbiological and clinical criteria of sepsis. Eleven patients had signs of systemic inflammatory response syndrome but no microbiological evidence of sepsis. The groups could be differentiated from each other by their C3a levels or their C3a/C3 ratios during the first 24 h after the clinical onset of sepsis (P < 0.05). Septic patients in shock had higher C3a levels than normotensive septic patients, although the differences were not significant. Nonsurvivors had significantly higher C3a levels on admission than survivors (P = 0.0185). No differences were found between septic patients who developed adult respiratory distress syndrome and those who did not. Thus, determination of C3a concentrations in plasma may prove useful (i) to diagnose sepsis early, (ii) to differentiate between patients with sepsis and those with systemic inflammatory response syndrome, and (iii) to assess prognosis.

Adolescent↗
PubMed1996

Association of complement alleles C4AQ0 and C4B5 with rheumatoid arthritis in Koreans.

OBJECTIVE: To investigate the association of complement C4 allotypes with rheumatoid arthritis in Koreans. METHODS: 65 rheumatoid arthritis patients and 255 controls were typed for C4 allotypes and HLA-A, B, C, DR, and DQ antigens. RESULTS: The frequencies of C4AQ0 (32.3% v 14.9%, P < 0.005) and C4B5 (29.2% v 12.2%, P < 0.005) were significantly increased in rheumatoid arthritis patients compared with healthy control subjects. Among rheumatoid patients, the frequency of C4AQ0 was significantly increased in both the rheumatoid factor (RF) positive (27.3%) and the RF negative (66.7%) subgroups. The frequencies of C4B5 and HLA-DR4 were significantly increased only in RF positive subgroup. C4B5 was strongly associated with HLA-DR4, whereas C4AQ0 did not show association with DR4. CONCLUSIONS: In Koreans, C4AQ0 and C4B5 are associated with susceptibility to rheumatoid arthritis, as in the Japanese. C4B5 is strongly associated with HLA-DR4. C4AQ0 is considered to be a DR4 independent risk factor, and a disease susceptibility allele in linkage disequilibrium with C4AQ0 is suggested in Korean patients with rheumatoid arthritis.

Adult↗
PubMed1995

DR-positive T cells in autism: association with decreased plasma levels of the complement C4B protein.

Autism is a developmental disorder characterized by severe communication, social and behavioral abnormalities. Over the past several years a fair amount of evidence has accumulated suggesting that some cases of autism may be associated with immune abnormalities and with products of the HLA complex including the C4B gene located in the class III region of HLA. This study sought additional evidence for an association of autoimmune processes with autism by investigating the presence of activated T cells in 26 autistic subjects. Fourteen of the autistic subjects had DR+ T cells, an indicator of activated T cells, but none of the autistic subjects had T cells expressing the interleukin-2 receptor, another indicator of T cell activation. Similar findings of incomplete or partial T cell activation have been reported in autoimmune disorders and in a recent study of autism. In the current investigation, the DR+ T cells were not found to be associated with age of the autistic patients but were inversely correlated with a decreased plasma level of the C4B protein. In conclusion, this study provides additional evidence for the involvement of an autoimmune mechanism in autism.

Adolescent↗
PubMedDate not supplied

Serum complement (C3, BF, C4) types in Swedish Saamis.

Serum complement (C3, BF, C4) types were examined in Swedish Saamis (Lapps). In agreement with previous studies, a very low frequency of the C3*F allele (0.033) was found. Compared to Swedes and other Caucasian populations, Swedish Saamis showed a significantly increased frequency of the BFS, C4A4 and C4B2 variants, and a lower frequency of C4 deficiency. BFS, C4A4 and C4B2 show haplotype associations and thus the frequency of the S-A4-B2 complotype is significantly increased among the Saamis. Although the serum complement constitution of the Saamis shows some similarity with that of Asiatic Mongoloid populations it is unlikely to be due to Asiatic ethnic influence. The marked genetic deviations of the Saamis from all other populations has often been interpreted as a result of the founder effect and genetic drift. In this particular case, however, immunogenetic adaptation appears to be a plausible alternative explanation for the deviations in genetic complement factors.

Adaptation, Biological↗
PubMed1992

Anticoagulation-dependent inhibition of in vitro complement activation by anti-apo-B sepharose 4B CL.

During LDL apheresis, various combinations of heparin and citrate are used for anticoagulation. With an in vitro batch system we examined whether heparin/citrate combinations can be optimized in terms of complement activation inhibition without the loss of anticoagulant potency. Plasma anticoagulated by using six clinically applicable regimens was incubated with anti-apo-B antibody-coupled Sepharose 4B CL, and the anaphylatoxin content of the supernatant was investigated. A significant dose-dependent reduction of complement activation was achieved by anticoagulating whole blood with 10 U/ml heparin (p < 0.05) if compared with serum whereas citrate inhibited more effectively the generation of C5a (desarg) even at a low concentration (ACD-B 1:20) (p < 0.01). The lowest anaphylatoxin level was generated when heparin (10 U/ml) plus citrate (ACD-B 1:10) were applied, although such an approach may be of limited clinical interest. The empirically chosen heparin plus citrate ratio (2 U/ml, 1:20, respectively) provides for an optimal and almost ideal inhibition of complement activation and contributes considerably to the good tolerability of the immunoadsorbent.

Apolipoproteins B↗
PubMed1993

HLA class I, II, and III polymorphism in Italian patients with sarcoidosis. The Pavia-Padova Sarcoidosis Study Group.

We studied the HLA polymorphisms (class I, II, and III) in 107 Italian patients with biopsy specimen-proven sarcoidosis in order to investigate the immunogenetic background of this disease. The mean age of onset of the disease was 36.08 +/- 12.4 years. Four patients (3.73 percent) were in radiologic stage 0, 38 patients (35.51 percent) were in radiologic stage I, 40 patients (37.38 percent) were in stage II, and 25 (23.36 percent) were in stage III. Thirty-eight patients (35.51 percent) had one or more extrapulmonary localization(s) of the disease. Positive association between sarcoidosis and HLA-B8 (chi 2 = 6.07, p = 0.0127, RR = 1.91) was confirmed. Regarding the age of onset of the disease, HLA-B35 was more frequent (chi 2 = 7.34, p = 0.0056, pc < 0.05, RR = 4.62) in patients with early onset of symptoms and/or signs, before the mean age of 36 years. With reference to the radiologic stage of the disease, HLA class II marker DR3 was more frequent in patients with stage I (chi 2 = 7.22, p = 0.0061, pc < 0.05, RR = 7.08). No significant relationship was found between sarcoidosis and HLA class III markers. These results seem to confirm an association of sarcoidosis with HLA classic genes and can sustain the hypothesis of a genetic heterogeneity of this disease.

Adult↗
PubMed1999

Complement activation in coronary artery bypass grafting patients without cardiopulmonary bypass: the role of tissue injury by surgical incision.

STUDY OBJECTIVES: Complement activation is a trigger in inducing inflammation in patients who undergo coronary artery bypass grafting (CABG) and is usually thought to be induced by the use of cardiopulmonary bypass (CPB). In this study, we examined whether tissue injury caused by chest surgical incision per se contributes to complement activation in CABG patients. DESIGN: Prospective study. SETTING: Thorax center in university hospital. PATIENTS: Twenty-two patients undergoing CABG without CPB were prospectively divided into two groups: a small chest incision via an anterolateral thoracotomy representing a minimized tissue injury (lateral group, n = 8), and a conventional median sternotomy representing a large tissue injury (median group, n = 14). Biochemical markers indicating complement activation as well as systemic inflammatory response were determined before, during, and after the operation. MEASUREMENTS AND RESULTS: Plasma concentrations of complement 3a increased in both the lateral and median groups right after chest incision (p < 0.01 and p < 0.05, respectively) and by the end of operation increased only in the median group (p < 0.01). The terminal complement complex 5b-9 did not increase in the lateral group, but it did increase in the median group both after incision and by the end of the operation (p < 0.05 and p < 0.05, respectively). During surgery, complement 4a did not increase, suggesting that it is the alternative rather than the classic pathway that is involved in complement activation by tissue injury. Postoperatively, interleukin-6 production was greater in the median group (p < 0.01) than the lateral group (p < 0.05), suggesting a more pronounced inflammatory response to a larger chest incision. CONCLUSIONS: Tissue injury caused by surgical incision contributes to complement activation in CABG patients who are operated on without CPB. A small anterolateral thoracotomy is associated with reduced complement activation in comparison with a median sternotomy.

Adult↗
PubMed1992

Histocompatibility antigens associated with Behçet's disease in northern Han Chinese.

Among Han nationality Chinese and living in the northern area of the Yellow River, 120 patients suffering from Behçet's disease and 100 unrelated healthy individuals were typed for histocompatibility antigens (HLA)-A, -B, -C, and -DR and -DQ antigens. HLA-DR and DQ typing was performed on B-lymphocyte separated with Lympho-B-Kwik. The HLA-antisera were provided by 11th IHWC. Bf alleles and C4 allotypes were determined by immunofixation agarose-gel electrophoresis. HLA-B51 was found in 67/120 (55.83%) patients and in 12/100 (12%) controls, the Chi-square and relative risk values were 45.54 and 9.27, respectively (p < 0.0005). C4AQ0 frequency was significantly increased in the patient group. In the complete form group HLA-B51 was observed more frequently (62.79%). No significant differences of other HLA antigens, frequencies, Bf or B4 alleles were found between the groups.

Adult↗
PubMed1990

Effect of anticoagulant on biocompatibility in membrane plasmapheresis.

The effect of heparin or citrate anticoagulation on blood cellular, complement pathway and coagulation pathway was investigated in a membrane plasma exchange procedure. Two membrane plasma separators constructed of cellulose di-acetate (CA) and polyvinyl chloride (PVC) were evaluated with heparin or citrate alone for anticoagulation in a 26 year old male with myasthenia gravis. Maximum white blood cell counts decrease was 21% at 30 min for the CA with heparin while no decrease was observed for the other schemes. Platelet counts changes were comparable between heparin and citrate, while the PVC groups showed less changes than the CA groups. The CA groups, regardless of the type of anticoagulant used, indicated that complement activation occurred via the classical pathway within the module in addition to the activation via alternative pathway for the CA with heparin. In the PVC groups, complement activation was noted to occur only when heparin was used for anticoagulation. PT and PTT showed slight increases with citrate, while they were remarkably prolonged with heparin. Citrate showed less changes in cellular and humoral factors compared to heparin. CA with heparin was the most activating combination of membrane material and anticoagulant, while the PVC with citrate was the least activating combination.

Adult↗
PubMed1990

[Mutations in 21-hydroxylase gene caused by gene conversion-like events].

Two steroid 21-hydroxylase genes (CYP21A and CYP21B) alternate in tandem with two genes for the fourth component of complement (C4A and C4B) on the short arm of chromosome 6 between the loci of HLA-B and HLA-DR. The CYP21B gene encodes an adrenal microsomal cytochrome P-450, which is specific for steroid 21-hydroxylation (P450c21). A defect of this protein would cause 21-hydroxylase deficiency, which is an autosomal recessive disease and is the most common cause of congenital adrenal hyperplasia (CAH). On the other hand, the CYP21A gene, which is homologous to the CYP21B gene up to 98% in the nucleotide sequences, is a pseudogene due to several mutations in the coding region. One of the mutations is a C----T change leading a termination codon, TAG, in the 8th exon. 1) I cloned a CYP21B gene from a patient homozygous for HLA-Bw75-DRw9 by descent. I found a C----T change in the 8th exon of the CYP21B gene. This mutation would prevent a synthesis of 21-hydroxylase and was thought to be a crucial change to cause CAH in this patient. Because there was no apparent gross change in the organization of the C4-CYP21 region and this mutation is usually found in the CYP21A pseudogene, it seemed that a gene conversion-like event transferred the mutation from the CYP21A gene to the CYP21B gene. 2) A population study on the organization of C4-CYP21 region revealed that a reciprocal change, i.e. a T----C change in the 8th exon of the CYP21A gene, was observed in two HLA haplotypes, HLA-B44-DRw13 and HLA-Bw46-DRw8 haplotypes in Japanese population. The reciprocal changes also may be considered as a result of gene conversion-like events.

Gene Conversion↗
PubMed1987

Autoantibodies and immunogenetics in 30 patients with systemic sclerosis and their families.

Clinical and serological evidence of connective tissue disease was found in a high proportion of 132 family members of 30 patients with systemic sclerosis. In 20 probands with the milder CREST form of the disease, 10 had HLA-DR5 and 12 had null alleles at the C4 loci. None of 11 probands with more severe systemic sclerosis had HLA-DR5; all 11 had null alleles at the C4 loci. All but two of the probands had either HLA-DR5 or a C4 null allele, and this was also the case for the majority of the relatives with autoantibodies. Genetic markers of the major histocompatibility complex, including HLA-DR5 and C4 null alleles, appear to be closely associated with markers of disease in these probands and their families.

Antibodies, Antinuclear↗