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Biomedical subjects

K Gohchi

Publications and source records attributed to K Gohchi.

53 records · Page 3Linked to original sources
PubMed1993

beta 2-Glycoprotein I-dependent and-independent anticardiolipin antibody in patients with end-stage renal disease.

We investigated whether anticardiolipin antibody (aCL), which is common in patients with end-stage renal disease (ESRD), was dependent on beta 2-glycoprotein I (GPI), a cofactor of aCL. Lupus anticoagulant (LA) was identified in 13/39 hemodialysis (HD) patients. GPI-independent aCL was positive in 12/39 of this group, five of whom had both GPI-independent aCL and LA. Three of the 20 patients on symptomatic and supportive treatment other than HD had LA, but none of them were aCL positive. When GPI was added to the assay system to allow for GPI-dependent aCL measurement, the optical density (OD) readings of 10/12 HD patients decreased, thus proving that they were negative for aCL. In contrast, the OD readings of 6 control patients with systemic lupus erythematosus (SLE) increased markedly (3/6) or decreased slightly to moderately (3/6), however, within the limits of positive range, indicating GPI-dependent cCL positivity. These results suggested that LA and GPI-independent aCL were produced in ESRD patients, especially those on HD, possibly through mechanisms related to the hemodialysis membrane. However, the significance of GPI-independent aCL in this clinical setting, which may differ from the GPI-dependent aCL detected in SLE patients, as well as the possible participation of serum GPI in the production of aCL remain to be clarified.

Adult↗
PubMed1993

Measurement of beta 2-glycoprotein I (apolipoprotein H)-independent anticardiolipin antibody in human immunodeficiency virus-1-positive and -negative hemophiliacs.

The authors studied whether or not anticardiolipin antibody (aCL), which is frequently detected in hemophiliacs with human immunodeficiency virus-1 (HIV-1) infection, is dependent on beta 2-glycoprotein I (GPI), a cofactor of cardiolipin (CL). GPI-independent aCL was positive in 27 of 36 hemophiliacs with HIV-1 antibody (75%) and in 23 of 29 patients without HIV-1 antibody (79%). However, only six HIV-1-positive and four HIV-1-negative patients were positive for GPI-dependent aCL. Thus the aCL in these hemophiliacs was GPI independent and therefore different from the aCL found in autoimmune diseases, such as systemic lupus erythematosus.

Antibodies, Anticardiolipin↗
PubMed1993

Anticoagulant activity of an anti-beta 2-glycoprotein I antibody is dependent on the presence of beta 2-glycoprotein I.

We studied whether or not an anti-beta 2-glycoprotein I antibody (aGPI) had lupus anticoagulant-like activity, employing the diluted Russel viper venom time (dRVVT) and kaolin clotting time (KCT) as indices. aGPI prolonged the dRVVT and KCT of beta 2-glycoprotein I (GPI)-depleted normal plasma in the presence of extrinsic GPI. This prolongation of the dRVVT and KCT occurred immediately after the addition of aGPI and GPI, and was subsequently enhanced further in a time-dependent manner. The GPI/aGPI combination was judged to have lupus anticoagulant-like activity by the dRVVT-platelet neutralization test, but this was not confirmed by a lupus anticoagulant-specific test, i.e., the activated partial prothrombin time (APTT) using hexagonal phospholipid. From these findings, it can be concluded that aGPI has lupus anticoagulant-like activity in the presence of GPI, but may be a partially or considerably different antiphospholipid antibody from lupus anticoagulant. Further investigations may be needed to clarify this point.

Antibodies↗
PubMed1993

Serum adenosine deaminase 2 and neopterin levels are increased in a majority of hemophiliacs irrespective of infection with human immunodeficiency virus type 1.

We investigated serum levels of adenosine deaminase 2 (ADA2) and neopterin (NP) in hemophiliacs with or without infection with human immunodeficiency virus type 1 (HIV-1). The mean (+/- SD) serum ADA2 level in hemophiliacs positive for HIV-1 (45.2 +/- 17.6 U/L) and negative for HIV-1 (34.9 +/- 15.8 U/L) was significantly higher than that in healthy controls (12.0 +/- 7.0 U/L) (P < .01). The mean serum NP level was also higher in HIV-1-positive hemophiliacs (10.2 +/- 6.1 nmol/L) and HIV-1-negative hemophiliacs (7.0 +/- 2.9 nmol/L) than in the healthy controls (4.3 +/- 1.3 nmol/L). Although the HIV-1-positive hemophiliacs had higher mean ADA2 and NP levels than did hemophiliacs in the HIV-1-negative group (P < .01), the levels of most of the patients in both groups were similar. ADA2 and NP levels in serial samples from asymptomatic carriers and patients with stable AIDS showed no marked changes over a period of up to 6 years. These findings indicate that ADA2 and NP are not specific markers of HIV-1 infection in hemophiliacs. Nonspecific immunologic activation due to the repeated infusion of antihemophilic factor concentrate could be one cause for the increased serum levels of ADA2 and NP in hemophiliacs.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Distinguishing beta 2-glycoprotein I dependent (systemic lupus erythematosus type) and independent (syphilis type) anticardiolipin antibody with Tween 20.

We investigated whether or not the use of Tween 20 could help to distinguish beta 2-glycoprotein I (GPI) independent anticardiolipin antibody (aCL) (syphilis-type aCL) from GPI-dependent aCL (SLE-type aCL) in a GPI-dependent/independent aCL ELISA. aCL was positive in all 16 SLE patients and all 15 syphilis patients, who were positive for aCL in the standard ELISA, in the GPI-independent ELISA with Tween 20. GPI-dependent aCL was detected in 12/16 SLE patients by the GPI-dependent ELISA with Tween 20. aCL was not detected in any of the syphilis patients by GPI-dependent ELISAs. On the basis of these results, we recommend that Tween 20 should be used in ELISAs to distinguish GPI-dependent aCL from GPI-independent aCL.

Adult↗
PubMed1993

Polymorphonuclear leucocyte function tests: a comparison of cytochrome C reduction and flow cytometric analysis.

Assay results were compared between the cytochrome C reduction test and flow cytometry using fluorescent beads or DCFH-DA (2', 7'-dichlorofluorescein diacetate) granules, in examining the phagocytosing and killing properties of polymorphonuclear leucocytes (PMN). When PMN samples from 20 healthy persons were assayed, no correlation was found between the cytochrome test and the phagocytosis (fluorescent beads) test or phagocytosing-killing (DCFH-DA) test by flow cytometry techniques. It is suggested that this might be caused by the fact that for technical reasons the two tests employed different stimulants and different substances to be phagocytosed. The simple flow cytometry procedure is now in widespread use as a PMN function test rather than the cytochrome C or nitroblue tetrazolium (NBT) dye reduction tests, and caution should be exercised in comparing and interpreting test results reported from separate laboratories. Because results using these two tests do not necessarily agree with each other, it seems preferable for PMN function testing to employ a combination of two or more approaches relying on different assay principles.

Adult↗
PubMed1993

High prevalence of anti-cardiolipin antibody, C1q-, C3d-, and mRF-IgG immune complexes, and anti-nuclear antibody in hemophiliacs irrespective of infection with human immunodeficiency virus type 1.

We investigated the prevalence of various autoantibodies [anti-cardiolipin antibody (aCL), lupus anticoagulant (LA), immune complexes (ICs), anti-nuclear antibody (ANA), and anti-deoxyribonucleic acid antibody (aDNA)] in hemophiliac individuals with (n = 50) and without (n = 42) infection by human immunodeficiency virus type 1 (HIV-1). The positivity rate for ANA was similar in both groups, and none of the patients was positive for LA and aDNA. aCL was positive in 35 of 50 (70%) HIV-1-positive hemophiliac individuals and 33 of 42 (79%) HIV-1-negative hemophiliac individuals. However, the majority of the aCL was revealed to be beta 2-glycoprotein I independent, thus corresponding to a syphilis type aCL that does not cause the so-called antiphospholipid syndrome. A total of 39 of the 45 HIV-1 positive hemophiliac individuals (87%) and 34 of 41 HIV-1-negative hemophiliac individuals (83%) had at least one type of IC [C1q-, C3d-, and/or murine monoclonal rheumatoid factor (mRF)- IgG]. The mechanism producing various autoantibodies in hemophiliac persons irrespective of their HIV-1 status is still unclear, but pathogens (e.g., HIV-1, hepatitis B, and hepatitis C) and alloantigens in the blood products that these patients require may be possible candidates. The clinical significance of the presence of these autoantibodies and the underlying mechanisms involved both need to be clarified further.

Antibodies, Anticardiolipin↗
PubMed1992

Clinical significance of the venous occlusion test on systemic lupus erythematosus patients with a focus on changes in blood levels of tissue plasminogen activator, von Willebrand factor antigen, and thrombomodulin.

We investigated the clinical significance of the venous occlusion (VO) test on patients with systemic lupus erythematosus (SLE) with or without circulating lupus anticoagulant (LA) concerning whether changes in the blood coagulation and fibrinolysis system in vivo subsequent to VO reflect mechanical stimulation of the endothelium or presence/development of endothelial damage. The tissue plasminogen activator antigen (tPA:Ag) before VO was much lower in the LA-positive patients than in the LA-negative ones (p < 0.01) and the von Willebrand factor antigen (VWF:Ag) pre-VO was significantly higher in the patient group, regardless of LA status, than in the control group (p < 0.01). But the mean increment in tPA:Ag and VWF:Ag post-VO, when expressed as the percentage of the baseline level, showed no appreciable difference between LA-positive and -negative groups. Thrombomodulin (TM) basically, on the other hand, was higher in the patients of either LA status than in the controls (p < 0.01) with a significant post-VO increase in the SLE group, which was more marked in the LA-positive patients, against no substantial change in the controls (p < 0.01). It is known that tPA and VWF:Ag are released simply as a result of endothelial stimulation and that the release of TM is preceded by endothelial damage. Based on the present results, we may well conclude that (1) the endothelium is functionally intact in SLE patients, (2) an injury of the endothelium, possibly as a consequence of vasculitis, preexists in LA-positive patients, and thus to measure the TM response to VO would offer a helpful tool in diagnosing the preexisting endothelial damage in these clinical settings.

Adult↗
PubMed1992

Effect of total-body cold exposure on plasma concentrations of von Willebrand factor, endothelin-1 and thrombomodulin in systemic lupus erythematosus patients with or without Raynaud's phenomenon.

The effect of total-body cold exposure on plasma concentrations of von Willebrand factor (vWF), endothelin-1 (ET) and thrombomodulin (TM), all of which are considered to be generated from the endothelium, was studied in systemic lupus erythematosus (SLE) patients with and without Raynaud's phenomenon. The plasma levels of vWF, ET and TM in SLE patients, irrespective of the presence of Raynaud's phenomenon, were significantly higher than in normal controls even before the cold provocation test. After the cold provocation test, plasma levels of vWF and ET were significantly higher in SLE patients with Raynaud's phenomenon than in those without and in normal controls. No significant increase in TM was observed in either the SLE patients or the controls. These results suggest that SLE patients, regardless of the presence of Raynaud's phenomenon, are in a hypercoagulable state and that this state may be further intensified by cold exposure. Hence, it is concluded that we should consider antithrombotic therapy for SLE patients, especially those with Raynaud's phenomenon, to prevent unwanted activation of the coagulation system and possible endothelial damage.

Adult↗
PubMed1992

[Overview of our patients with chronic fatigue syndrome (CFS) from the pathoetiological aspects].

We interviewed 285 patients who visited our department claiming with a complaint of chronic fatigue syndrome (CFS) and subsequently diagnosed 55 as having CFS, according to the criteria for CFS of the centers for disease control (CDC). We measured various virus antibody titers, 2-5, adenylate synthetase levels in the serum lymphocyte subset in blood, employing a double staining technique with monoclonal antibodies. In this paper, we pathoetiology of CFS, based on our findings and other researchers' is discussed.

2',5'-Oligoadenylate Synthetase↗