Thrombocytopenia is resulted from many causes, and it could be decreased in quantity or quality of thrombocyte. Causes are: increased destruction due to immune causes and non-immune causes such as increased consumption or destruction of thrombocyte), decreased production of thrombocyte (due to decreased production or blocking of platelet, and infiltration of bone marrow), and disturbance of distribution of platelet. It isn’t difficult to diagnose thrombocytopenia but it’s complicated to find out the cause, so it must be cautions
Thrombocytopenia ; Blood Platelets ; Antigen-Antibody Complex

OBJECTIVE: The purpose of this study was to evaluate whether serum C1q-circulating immune complexes (C1q-CIC) serve as a predictive marker for renal flares in patients with lupus nephritis. METHODS: Twenty-five patients with lupus nephritis and 24 healthy controls were enrolled. Patients with lupus nephritis had their serum C1q-CIC titers and other serologic parameters such as serum C3, C4, anti-dsDNA antibody, and erythrocyte sedimentation rate measured simultaneously. The systemic lupus erythematosus disease activity index (SLEDAI) was also checked. RESULTS: Serum C1q-CIC titers were higher in patients with lupus nephritis than in healthy controls (109.33+/-53.79 microg/mL vs. 75.28+/-22.91 microg/mL, p=0.008). A statistically significant association was found between serum C1q-CIC titers and C3 (p=0.011), C4 (p=0.027), and anti-dsDNA antibody (p=0.014). SLEDAI was also correlated with serum C1q-CIC titers (p=0.022). CONCLUSION: Serum C1q-CIC appears to be related to renal disease activity in patients with lupus nephritis. These results suggest that serum C1q-CIC is a predictive marker for renal flares in patients with lupus nephritis.
Antigen-Antibody Complex ; Blood Sedimentation ; Humans ; Lupus Erythematosus, Systemic ; Lupus Nephritis

complex on platelet surfaces. This complex activates platelets, which leads to multiple coagulation in venous and arterial blood. We report here on a rare occurrence of HIT type II following fibula free flap surgery.]]>
Antigen-Antibody Complex ; Blood Platelets ; Fibula ; Free Tissue Flaps ; Heparin ; Platelet Factor 4 ; Thrombocytopenia ; Venous Thrombosis

OBJECTIVETo explore the characteristics of Helicobacter pylori (H. pylori) antigen in serum and to evaluate its clinical diagnostic value.

METHODSEnzyme-linked immunosorbant assay (ELISA) was developed to detect the soluble H. pylori antigen (S-Hp) and circulatory specific H. pylori antigen immunocomplexes (Hp-IC) in serum.

RESULTSThe positive rate of S-Hp was 90.91% from 66 patients with H. pylori infection, which was much greater than 0% found in 28 controls (P < 0.001). Moreover, its concentration closely reflected the number of H. pylori in the gastric mucosa layer. We also found that Hp-IC existed bound with IgG and/or IgA in patients with positive S-Hp. However, there is no evidence to show the concentration of S-Hp reduced significantly in followed-up subjects after effective therapy.

CONCLUSIONSThese methods as newly and noninvasive complementary tools can be used for clinical diagnosis of H. pylori infection. In addition, S-Hp and Hp-IC may be of importance in H. pylori pathogenesis.

Adult ; Antibody Specificity ; Antigen-Antibody Complex ; blood ; Antigens, Bacterial ; blood ; Female ; Helicobacter Infections ; immunology ; Helicobacter pylori ; immunology ; Humans ; Immunoglobulin A ; blood ; Immunoglobulin G ; blood ; Male

Higher levels of IgE-containing immune complexes (IC) have been reported in sera from patients with allergic diseases than in sera from controls. To evaluate the possibility of an IC-mediated mechanism in the pathogenesis of bronchial asthma, we measured circulating C3-containing IgE IC (C3-IgE IC) using anti-C3 ELISA from 20 house dust mite (HDM)-sensitive asthmatics, 20 non-atopic asthmatics, and 14 non-atopic controls. C3-IgE IC levels were significantly higher in HDM-sensitive asthmatics (mean +/- S.D.: 12.2 +/- 7.8 AU/ml) than in non-atopic asthmatics (6.5 +/- 7.5 AU/ml) or controls (5.8 +/- 4.4 AU/ml). C3-IgE IC levels were significantly correlated with HDM-specific IgE levels (r = 0.50, p<0.05), but not with total IgE levels (r = 0.36, p< 0.05) in HDM-sensitive atopic asthmatics. C3-IgE IC levels in sera did not significantly change during HDM-bronchoprovocation test in six HDM-sensitive asthmatics who showed positive reaction. Part of C3-IgE IC could be precipitated by protein G coupled beads. In conclusion, C3-IgE IC levels were elevated in sera from HDM-sensitive asthmatics; moreover IgG antibodies might be a component of C3-IgE IC. Our results suggest that an IgE IC-mediated mechanism could be involved in the pathogenesis of atopic asthma.
Adult ; Animal ; Antigen-Antibody Complex/*blood ; Asthma/*immunology ; Complement 3/*analysis ; Dust ; Human ; Immunoglobulin E/*blood ; Mites/immunology

OBJECTIVES: To evaluate serum Interleukin 8 (IL-8) as a predictor of disease activity in SLE and to provide insight into the potential role of IL-8 in the pathogenesis of SLE. METHODS: Sixty-four paired sera from the 32 SLE patients and 10 healthy control sera were obtained. Serum IL-8 levels were determined by ELISA technique. Tests for other laboratory parameters, such as circulating immune complex (CIC), C3, C4, ANA, anti-dsDNA, Hb, Hct, leukocyte, lymphocyte, platelet and ESR, were performed for every sample coincidently with assessment of clinical disease activity by the Lahita scales. RESULTS: We found that serum IL-8 levels in SLE patients were significantly higher than those of healthy controls. Serum IL-8 levels significantly correlated with clinical disease activity. Serum IL-8 levels correlated with CIC, but it had no correlation with other laboratory parameters. CONCLUSON: These findings suggest that serum IL-8 can be used as a marker of disease activity in patients with SLE. These results may have implication in the pathogenesis of SLE.
Antigen-Antibody Complex ; Blood Platelets ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-8* ; Interleukins* ; Leukocytes ; Lupus Erythematosus, Systemic* ; Lymphocytes ; Weights and Measures

Skin lesions of erythema nodosum leprosum(ENL) occurs as crops of erythematous papules with microscopical features of vasculitis, and these are considered to he immune complex mediated. Recent studies by several investigators detected high levels of circulating immune complexes in over fifty percent of patients with ENL, using well known Clq binding assay or monoclonal rheumatoid factor assay. Moreover they found immuoglobulins (Ig) and complement components in the blood vessels of these patients. These immunopathologic data presented more support to the immune complex mediated pathogenesis of the skin lesions in ENL spectrum. In connection with these findings, examinations of the skin lesions of Korean patient with ENL by immunofluorescent techniques were done. Among seven biopsy specimens from each seven patients, four revealed deposits of Igs (G and M) along with CR in dermal blood vesseIs. Alpha-1 antitrypsin and fibrin were also found in some patients.
Antigen-Antibody Complex ; Biopsy ; Blood Vessels ; Complement System Proteins ; Erythema Nodosum* ; Erythema* ; Fibrin ; Humans ; Research Personnel ; Rheumatoid Factor ; Skin ; Vasculitis

BACKGROUNDSkin lesions are common manifestations in systemic lupus erythematosus (SLE). It is still unknown what the definite pathogenesis of skin involvement was and whether DNA participated in it. Our study was designed to explore the pathogenetic role and nature of nuclear antigen (DNA) deposited in the skin lesions of patients with SLE.

METHODSThirty skin samples from patients with SLE and 2 normal skin samples were studied. Extracellular DNA was evaluated by indirect immunofluorescence methods. The deposited immune complexes were extracted by cryoprecipitation, and DNA was then isolated with phenol and chloroform. DNA fragment sizes were detected by agarose gel electrophoresis. Finally, 8 different probes were used to analyze the origin of these DNA molecules using Dot hybridization.

RESULTSExtracellular DNA staining was found only in skin lesions, mainly those located in the basement membrane zone, vascular wall, and hair follicle wall. Normal skin and non-lesion SLE skin showed no fluorescence at locations outside the nuclei. There were no differences in the rate and intensity of extracellular DNA staining when comparing active phase to remission phase patients. No relationship was found between extracellular DNA and circulating anti-dsDNA antibodies. Deposited DNA fragments clustered into four bands of somewhat discrete sizes: 20 000 bp, 1300 bp, 800-900 bp, 100-200 bp. Small sized fragments (100-200 bp) were positively correlated with disease activity (P < 0.05, r = 0.407). Dot hybridization showed significant homology of the various extracellular DNA fragments examined with human genomic DNA, but not with DNA from the microorganisms and viruses we examined. There were also homologies between DNA samples from different individuals.

CONCLUSIONSDNA and its immune complexes may contribute to the pathogenesis of skin lesions in SLE. These DNA molecules range in size from 100 bp to 20 kb and may be endogenous in origin.

Antibodies, Antinuclear ; blood ; Antigen-Antibody Complex ; analysis ; DNA ; analysis ; immunology ; Humans ; Lupus Erythematosus, Systemic ; immunology ; Skin ; immunology ; Staining and Labeling

Recent reports have indicated that a significant number of immune complex glomerulonephritis (GN) cases are associated with antineutrophilic cytoplasmic antibody (ANCA). However, most of the reported cases were associated with underlying primary glomerular diseases. When primary glomerular diseases were not found, immune deposits tended to be non-specific and the level of ANCA is usually borderline. We report here upon a case of life-threatening pulmonary-renal syndrome manifested simultaneously with immune complex GN and myeloperoxidase (MPO)-ANCA seropositivity. A 29- year-old man was admitted with pulmonary hemorrhage and rapidly progressing renal dysfunction. On admission, ANCA revealed perinuclear staining with a titer of 1:160. The MPO-ANCA level was 59 IU by ELISA. Other serologic markers including ANA, anti-DS-DNA and anti-GBM Ab were negative. Renal biopsy showed cellular crescents in eight of 18 glomeruli. Immunofluorescence staining showed strong granular deposits of C3, C1q, IgG and IgM in the capillary loop and the mesangium. Electron microscopy showed multifocal electron dense deposits scattered in the mesangium, paramesangium, and the subendothelial and subepithelial areas. The patient initially responded to steroid and cyclophosphamide. MPO-ANCA decreased to less than 10 IU. Twenty three days after hospital discharge, the patient was re-admitted urgently with fever, generalized papulonodular skin lesions, and a recurrence of massive pulmonary hemorrhage and renal dysfunction. He died from uncontrolled pulmonary hemorrhage and respiratory insufficiency. P-ANCA titer and MPO-ANCA level at the second admission were 1:320 and 82 U/ml respectively. Interestingly, relapse was shown to be triggered by varicella zoster infection.
Adult ; Antibodies, Antineutrophil Cytoplasmic/*blood ; Antigen-Antibody Complex/*metabolism ; Glomerulonephritis/*etiology ; Hemorrhage/complications ; Human ; Lung Diseases/blood/*complications ; Male ; Peroxidase/*blood

BACKGROUND & OBJECTIVES: The pathogenic mechanism of aspirin-sensitive asthma (ASA-BA) remains to be further defined. To evaluate the role of circulating immune complex (CIC) in ASA-BA. SUBJECTS & METHODS: We measured IgG- and IgA-IC level by ELISA using anti-C3 antibody in 33 ASA-BA patients whose sensitivity was confirmed by lysine-aspirin bronchoprovocation test, and compared with those of 14 allergic, 14 intrinsic asthma patients and 7 healthy controls. RESULTS: There was no significant difference in IgG-IC level among the four groups (p > 0.05), while IgA-IC levels of aspirin-sensitive asthma were higher than those of other groups (p = 0.0035). Patients with nasal polyp had significantly higher IgG-IC than those without it (p = 0.02). No differences were found according to medication and symptom scores, and presence of atopy, rhino-sinusitis, urticaria or concurrent sensitivity to sulfite (p > 0.05). Insignificant correlation was found between IgG-IC level and asthma duration, total IgE level, or circulating eosinophil count. CONCLUSION: These findings suggest a possible contribution of IgG-IC to the development of nasal polyp in ASA-BA. Further study will be needed to clarify the role of IgA-IC in the pathogenesis of ASA-BA.
Adult ; Aged ; Antigen-Antibody Complex/blood* ; Aspirin/adverse effects* ; Asthma/immunology* ; Asthma/etiology* ; Asthma/complications ; Case-Control Studies ; Human ; IgA/blood ; IgG/blood ; Middle Age ; Nasal Polyps/etiology