Search PubMed⌕ Search

Biomedical subjects

P Tani

Publications and source records attributed to P Tani.

At least 37 records · Page 2Linked to original sources
PubMed1987

A specific assay for anti-HLA antibodies: application to platelet donor selection.

Alloimmunization to donor class I HLA antigens represents a major obstacle to successful platelet transfusion therapy. It is desirable to distinguish alloimmunization from nonimmunologic causes of poor platelet survival to assess the need for HLA-matched, single-donor platelets. We describe a new in vitro assay for anti-HLA antibodies and report its application to the problem of platelet crossmatching. In contrast to previously described crossmatch techniques, the immunobead assay is specific for anti-HLA antibodies. The assay was used to evaluate 51 single-donor platelet transfusions given to seven patients from 35 different donors. Recipient plasma was assayed for antibodies directed against HLA antigens present on donor platelets. A one-hour posttransfusion corrected count increment of greater than or equal to 7,500 was considered a successful outcome. Twenty-nine of 33 (87.9%) transfusion episodes associated with a negative immunobead assay had successful outcomes. The four unsuccessful transfusions were associated with potential nonimmunologic causes of poor platelet survival. Only two of 18 (11.1%) episodes associated with a positive assay had successful outcomes. Only one unsuccessful transfusion episode was associated with a negative immunobead assay and a positive radiolabeled antiglobulin test result, which suggested that isolated alloantibodies to antigens other than class I HLA antigens are not a common cause of platelet refractoriness. Platelets stored in suspension at 4 degrees C or frozen in liquid nitrogen were found suitable for crossmatch testing.

Adult↗
PubMed1987

Platelet-associated and plasma anti-glycoprotein autoantibodies in chronic ITP.

Chronic immune thrombocytopenic purpura (ITP) is due to platelet destruction by circulating antiplatelet antibody. Although autoantibodies against the platelet glycoprotein IIb/IIIa (GPIIb/IIIa) complex and GPIb have been demonstrated using various methods, practical assays for detection of platelet-associated or plasma autoantibodies have not been available. We studied 59 patients with chronic immune thrombocytopenic purpura in whom platelet-associated and plasma autoantibodies against the GPIIb/IIIa complex and GPIb were measured using a newly developed immunobead assay and a previously reported microtiter-well assay. Platelet-associated autoantibody was detected using the immunobead assay in 21 of 28 patients (75.0%; 13 with anti-GPIIb/IIIa, 8 with anti-GPIb). Plasma autoantibodies were noted in 34 of 59 patients (57.6%; 21 with anti-GPIIb/IIIa, 11 with anti-GPIb, and 2 with both). Positive results were noted in 30 of 59 patients using the immunobead assay and in only 14 of 59 using the microtiter-well assay, suggesting that solubilization of the platelets prior to antibody addition, as in the microtiter-well assay, alters epitope stability. Of the 31 thrombocytopenic control patients studied, all gave negative results using both assays. We conclude that these clinically adaptable assays allow detection of autoantibodies in most patients with chronic ITP, confirming the presence of an autoimmune process.

Autoantibodies↗
PubMed1986

Complement activation in vitro by antiplatelet antibodies in chronic immune thrombocytopenic purpura.

Many chronic ITP patients have increased amounts of platelet-associated IgG, C3, C4 and C9, suggesting in vivo complement activation. In this study, we assessed the ability of various antiplatelet antibodies (APA) to activate and deposit complement proteins and to cause platelet lysis in vitro. Platelet sensitization with rabbit APA, anti-P1A1 antibody (one patient), anti-HLA antibody (two patients) and ITP autoantibodies (four patients) resulted in the deposition of C4 and C3 onto platelets in an amount proportional to the quantity of antibody-containing sera used to sensitize the platelets. Although C9 deposition onto platelets could not be quantitatively demonstrated on platelets sensitized with ITP serum, platelet lysis (51Cr release) was noted after incubation with each of three ITP sera and complement. When compared, ITP autoantibodies, anti-HLA and anti-P1A1 antibodies activated complement to a similar degree. We conclude that some autoantibodies in chronic ITP activate the classical complement pathway. The demonstration of in vitro platelet lysis by autoantibodies and complement suggests that in vivo platelet lysis may occur in some chronic ITP patients.

Autoantibodies↗
PubMed1984

Maternal isoimmunisation resulting in combined immunodeficiency and fatal graft-versus-host disease in an infant.

Isoimmunisation to platelet and lymphocyte antigens occurred during a woman's seven pregnancies and resulted in congenital thrombocytopenia and lymphocytopenia in the last two offspring. The youngest baby died aged 16 days of severe combined immunodeficiency (SCID) with maternal graft-versus-host disease. The other affected child, however, recovered fully from thrombocytopenia and lymphocytopenia after exchange transfusion for presumed sepsis. The clinical courses indicated that an isoimmune process had caused both the thrombocytopenia and the lymphocytopenia. In accord with this conclusion, maternal titres of IgG antibodies against paternal platelets fell continuously in serial blood samples taken after the last pregnancy. Cytotoxicity studies of the maternal serum towards lymphocytes from the other siblings and from unrelated donors showed that the paternal antigen involved was a non-HLA determinant. It is postulated that isoimmune lymphocytopenia with subsequent immunological suppression is a potential mechanism for SCID and intrauterine engraftment of maternal lymphocytes.

Adult↗
PubMed1984

Autoantibodies to platelet glycoprotein IIb/IIIa and to the acetylcholine receptor in a patient with chronic idiopathic thrombocytopenic purpura and myasthenia gravis.

The coexistence of chronic idiopathic thrombocytopenic purpura and myasthenia gravis has been infrequently reported. We report another case and show the coexistence of autoantibodies to the platelet glycoprotein IIb and IIIa complex and the acetylcholine receptor. Autoantibody levels were followed during 8 weeks of treatment with cyclophosphamide, vincristine, and prednisone; the concentration of both autoantibodies fell during treatment but without measureable clinical improvement.

Adult↗
PubMed1984

Autoantibodies against platelet glycoprotein Ib in patients with chronic immune thrombocytopenic purpura.

The present studies provide direct evidence that some patients with chronic immune thrombocytopenic purpura (ITP) have autoantibodies reactive with platelet glycoprotein Ib ( GPIb ). Microtiter wells coated with a monoclonal antibody that recognized GPIb were reacted with either platelet extract or a control cell extract. After washing and incubating with test plasma, well-bound IgG was quantitated using radioactive anti-IgG. When compared to plasma from normal subjects, plasma from 3 of 106 patients with chronic ITP had significantly increased quantities of IgG bound to microtiter wells reacted with platelet extracts. Negative results were obtained with the remaining 103 patients with chronic ITP and 59 patients with a variety of other platelet disorders. Plasma from two of the three positive patients precipitated a protein from 125I-surface-labeled platelet extract with a molecular weight similar to GPlb . One of the three patients with anti- GPlb antibody also had demonstrable autoantibodies to the platelet glycoprotein llb / llla complex.

Acute Disease↗
PubMed1983

An enzyme-linked immunosorbent assay for platelet compatibility testing.

The selection of platelet donors for patients who are refractory to random donor platelets often presents a difficult clinical problem. We describe an enzyme-linked immunosorbent assay (ELISA) for evaluating alloantibodies in refractory patients. Platelets from prospective donors are immobilized on microtiter plates and, after incubation with test serum and washing, platelet-bound IgG is detected with enzyme-linked anti-human IgG. Platelets from 46 prospective donors were tested. Twenty-two were judged compatible (reciprocal of the antibody titer less than 16) and, of these, 15 were used as platelet donors; each gave a measurable platelet increment after transfusion. The magnitude of the response was roughly proportional to the assay results. Platelets from donors giving antibody titers less than 4 resulted in platelet increments at 1 hr ranging from 4,890 to 22,200 (median 12,600), while platelets from donors giving titers of 8 or 16 resulted in lesser increments (550-4548). Conversely, 5 of the 24 patients found incompatible by the assay (titer greater than 16) gave no platelet increment, and in 3 instances, the recipient developed fever and chills after the transfusion. The assay is sensitive, simple, and adaptable to the clinical laboratory. Platelets from volunteer donor panels can be plated and stored for up to 6 mo.

Blood Platelets↗
PubMed1982

Evaluation of platelet surface antigens: localization of the PlA1 alloantigen.

An approach is described for localizing antigenic determinants to specific platelet proteins. Platelets are solubilized, electrophoresed and transferred to nitrocellulose paper where they are immobilized. After incubation with radiolabelled specific antibody, the antigenic determinants are localized by radioautography. Purified proteins ranging in size from 50000 to 540000 could be studied in this manner and still retain their antigenicity. Solubilized immobilized platelet proteins were reacted with serum IgG from two patients with post-transfusion purpura known to have anti-PlA1 antibodies. The radioactivity was associated with a major protein band with an apparent molecular weight of 100000 daltons. However, when purified anti-PlA1 antibody eluted from PlA1 (+) platelets was used, at least six additional minor bands were noted with molecular weights ranging from about 86000 to 175000. No radioactive bands were noted using PlA1 negative platelets or reduced PlA1 (+) platelet proteins. Reaction of the antibody from one patient wih proteins from thrombasthenic platelets resulted in a marked reduction in the intensity of all radioactive bands. In addition, a new high molecular weight band was noted which was not present in reactions containing PlA1 (+) platelets. These data suggest that the PlA1 antigen is primarily but not entirely localized to glycoprotein IIIa. This approach is relatively simple, requires only minimal amounts of antibody and should be generally useful in the study of cellular antigens and other complex mixtures of proteins.

Antigens, Surface↗
PubMed1982

Analysis of T lymphocytes after bone marrow transplantation using monoclonal antibodies.

Using monoclonal antibodies to cell surface antigens and fluorescent cell sorter analysis, we studied peripheral blood lymphocyte subsets after bone marrow transplantation (BMT). In 13 patients studied 3 mo or more after BMT, the ratio of T-cell subsets defined by antibodies OKT4 and OKT8 was reversed (OKT4/OK%8 = 0.7 +/- 0.3) in comparison to normal volunteers or bone marrow donors (ratio OKT4/OKT8 = 1.7 +/- 0.4) (p less than 0.001). This reversed ratio persisted for up to 3 yr after BMT. In contrast to a previous report, presence of an abnormal ratio of T-cell subsets did not correlate with clinically significant graft-versus-host disease (GVHD). In agreement with a previous study, (26% +/- 8%; less than 4% in normals (p less than 0.001) and antibody OKT10 reactive cells (39% +/- 20% versus 10% +/- 4%) (p less than 0.01), suggesting in vivo activation. However, their PBL did not react with antibody B3/25 (antitransferrin receptor), a marker found on normal PBL after in vitro activation by mitogens (BMT patients less than 5%; normal PBL T cells plus PHA 45% +/- 11%). These results demonstrate that BMT patients have: (A) an abnormal ratio of T-cell subsets in the presence or absence of clinically significant GVDH disease so that these measurements were not useful in monitoring patients; (B) an increased number of T cells with cell surface phenotype (OKT8+, Ia+, OKT10+, B3/25-) that is distinct from normals but similar to patients with infectious mononucleosis or acquired hypogammaglobulinemia.

Acute Disease↗
PubMed1981

Prognosis for central vision and anatomic reattachment in rhegmatogenous retinal detachment with macula detached.

We analyzed a total of 473 eyes with rhegmatogenous retinal detachment and macular involvement for significant factors relating to anatomic success and a favorable visual outcome of 6/15 (20/50) or better. The overall success rate was 90% (427 of 473 eyes). Visual acuities of 6/15 (20/50) or better postoperatively were present in 37% (174 of 470 eyes). Important factors related to both anatomic success and favorable functional results were preoperative visual acuities of 6/15 (20/50) or better, retinal detachments that were less than total, detachments with tears located at or anterior to the equator, absence of giant retinal tears, absence of either preoperative ocular hypotony (tension less than 5 mm Hg) or ocular hypertension (intraocular pressure greater than 20 mm Hg), detachments managed by nondrainage techniques, a single operation with less than 50 cryoapplications, and noncircumferential buckling. Among the other factors related to favorable visual results were detachments lasting less than one month, a shallowly rather than highly detached macula, the absence of fixed retinal folds, a patient age of less than 60 years, and the absence of postoperative choroidal detachments sufficient to cause glaucoma. We found no statistical relationship between either anatomic success or functional result and the presence of aphakia, demarcation lines, vitreous hemorrhage, detachments of the pars plana epithelium, or predetachment glaucoma being treated.

Adolescent↗
PubMed1980

Rhegmatogenous retinal detachment without macular involvement treated with scleral buckling.

Among 173 patients who had rhegmatogenous retinal detachment with spared maculas, high percentage achieved anatomic and functional success. We reattached 171 (99%) of the retinas; 150 (76%) of the eyes had final visual acuities of 6/15 (20/50) or better. Eighteen eyes (10%) had final postoperative visual acuities reduced more than two lines from the preoperative level. This reduced visual acuity was primarily related to postoperative changes occurring in the macula. The prognosis both for anatomic reattachment and visual acuity after scleral buckling for rhegmatogenous retinal detachment is significantly better when the macula is spared than when it is not. Large numbers of cryoapplications were not associated with macular complications.

Adult↗
PubMed1980

The demonstration of antibody binding to platelet-associated antigens in patients with immune thrombocytopenic purpura.

Platelet destruction in chronic immune thrombocytopenic purpura (ITP) is due either to antibody against platelet-associated antigen(s) that attaches by the antigen-specific Fab portion of the molecule or to platelet-bound immune complexes that bind nonspecifically to a platelet Fc receptor. Since pepsin digestion destroys the Fc fragment, the effect of this agent on platelet binding should allow differentiation betwen these two mechanisms. Normal serum IgG, aggregated normal serum IgG, and IgG produced in culture by splenic cells from control subjects and ITP patients were radiolabeled and tested for platelet binding before and after pepsin digestion. The binding to target platelets of both aggregated IgG and IgG produced in culture by ITP cells was increased when compared to controls. However, F(ab)2 fragments from the ITP samples retained their binding ability while those from the aggregated IgG did not. We conclude that these ITP patients produced antibody specific for platelet-associated antigens.

Antigens↗