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C Kaplan

Publications and source records attributed to C Kaplan.

At least 19 recordsLinked to original sources
PubMed1992

[Fetal and neonatal immune thrombocytopenias. Study group "Mother-child immune thrombopenias"].

Neonatal thrombocytopenia has benefited from the advances achieved during the last few years in platelet immunology and foetal therapy. The major risk of the disease is cerebral haemorrhage resulting in death or neurological sequelae. Establishing the aetiological diagnosis of immune thrombocytopenia makes it possible nowadays to apply the appropriate treatment and eventually to take care of future pregnancies. Treatments in utero of foeto-maternal alloimmunization have radically altered the natural course of foetal thrombocytopenia, thereby permitting the management of pregnancies at risk. On the other hand, so far no prenatal treatment has proved to be effective against thrombocytopenia due to maternal autoimmunity.

Adrenal Cortex Hormones↗
PubMed1992

Relationship of HLA to schizophrenia not supported in multiplex families.

The role of the human histocompatibility complex (HLA) in the pathogenesis of schizophrenia has been suggested in previous reports. We conducted a genetic study in 33 new families. Our linkage analysis, which used the affected sib-pair method, did not provide evidence for nonrandom assortment. Moreover, the results of an association study using the "haplotype relative risk" method failed to confirm the positive association between HLA A9 and schizophrenia. Taken together, our data did not support any relationship of HLA type to schizophrenia.

Genetic Linkage↗
PubMed1992

[Platelet group polymorphism in Provence. Comparison with the frequencies of platelet-specific allo-antigens observed in other populations].

Systems HPA-1 (Pla); HPA-3 (Bak) HPA-5 (Br) are involved in neonatal alloimmune thrombocytopenia and post-transfusion purpura. The frequencies of platelet-specific antigens in these three systems have been studied among one hundred one unrelated blood donors from Provence (South of France) for three generations. Typing was performed by the MAIPA test (monoclonal antibody-specific immobilization platelet antigen). The phenotypes frequencies found were: HPA-1a (PlA1): 97%; HPA-3a (Baka): 88.1%. These frequencies are quite similar to those reported in Europe and North America, but are different compared to Oriental and South American populations. Our Provence population has the highest frequency of HPA-5b (Bra) yet reported: 23.8%. These results define the polymorphism of platelet-specific antigens in the Provence population. Similar studies, among other populations, would provide new data for geographical haematology, which has so far been based on erythrocyte, leucocyte and serum polymorphisms. The variations between populations in these platelet-specific polymorphisms would be so many useful descriptive elements for the epidemiological study of associated diseases.

Blood Donors↗
PubMed1992

Fetal and neonatal alloimmune thrombocytopenia: current trends in diagnosis and therapy.

Neonatal thrombocytopenia affects 20-40% of the infants in intensive care units. The frequency of neonatal alloimmune thrombocytopenia (NAIT) is estimated at 1/1500 to 1/5000 live births. The risk of morbidity is significant with 20% neurological sequelae and the death rate is estimated at 10% of affected infants. During recent years considerable efforts have been made to prevent fetal bleeding and to avoid birth trauma, which have significantly changed the natural history of NAIT.

Antigens, Human Platelet↗
PubMed1992

Anti-HPA-4b (anti-Yuk(a)) neonatal alloimmune thrombocytopenia: first report in a Caucasian family.

Neonatal alloimmune thrombocytopenia (NAIT) is caused by platelet antigen incompatibility between the mother and fetus. NAIT is mainly due to alloimmunization; the frequency varying among ethnic groups. In Caucasians HPA-1a is the antigen most frequently implicated. In Japan, NAIT due to anti-HPA-4b antibody has already been described, but this is the first case to be reported in Caucasians.

Adult↗
PubMed1992

Human platelet aggregation by Yersinia pseudotuberculosis is mediated by invasin.

Plasmid-free strains of Yersinia pseudotuberculosis induce aggregation of human platelets in vitro. It appears that this phenomenon is mediated by invasin (Inv), a 103-kDa outer membrane protein that permits bacteria to penetrate mammalian cells, since (i) an isogenic inv-deficient mutant failed to aggregate platelets compared with the parental strain; (ii) a monoclonal antibody directed against invasin inhibited platelet aggregation; (iii) Inv+ Escherichia coli HB101 promoted platelet aggregation. Platelet receptors for invasin were identified by using a panel of anti-platelet glycoprotein monoclonal antibodies in a bacterial adhesion assay. We found that bacteria bind to platelet membrane glycoproteins Ic and IIa. Electron microscopic study of bacterium-platelet interactions also revealed that bacteria expressing invasin attach to and are phagocytized by thrombocytes, in contrast to inv-deficient bacteria, indicating that these anucleated cells are able to internalize bacteria in vitro after specific interaction with invasin.

Adhesins, Bacterial↗
PubMed1992

Alloimmune thrombocytopenia: in utero treatment by high doses of intravenous gamma globulins.

The authors report successful in utero treatment by high doses of intravenous gamma globulins in a case of neonatal alloimmune thrombocytopenia. Early diagnosis allows an appropriate management: fetal blood sampling as early as 20 weeks of gestation; in case of fetal thrombocytopenia, treatment by intravenous gamma globulin (1.0 g/kg/b.w.) each week during 8 weeks or more; ultrasound screening of in utero hemorrhage, particularly intracranial hemorrhage; fetal blood sampling before delivery at term and in utero transfusion of platelet antigen negative in case of persistence of fetal thrombocytopenia.

Adult↗
PubMed1992

In vitro effect of plasmin on human platelet function in plasma. Inhibition of aggregation caused by fibrinogenolysis.

BACKGROUND: Plasmin has been reported both to activate platelets and to inhibit platelet functions. The latter effect was thought to be caused by proteolysis of the main membrane glycoproteins. METHODS AND RESULTS: We found that incubation of citrated human platelet-rich plasma with streptokinase (SK) (300 IU/ml) does not produce any detectable activation but leads to a time-dependent inhibition of ADP-induced aggregation accompanied by substantial fibrinogenolysis. These effects were abrogated by previous addition of a plasmin inhibitor, aprotinin. Crossover experiments (SK-treated or control platelets mixed with SK-treated or control plasma) demonstrated that the platelets remained functional and that the aggregation defect was caused by fibrinogenolysis. Further experiments (addition of purified fibrinogen to fibrinogen-depleted plasma with either SK or thrombin) suggested that in addition to the low residual level of fibrinogen, fibrinogen degradation products had an inhibitory effect. Under the same conditions, tissue-type plasminogen activator (t-PA) (3,000 ng/ml) had no effect on platelet aggregation, and plasma fibrinogen was not significantly lowered. The effects on glycoproteins IIb-IIIa of incubation with SK, t-PA, or plasmin were assessed with immunoblots with murine monoclonal antibodies directed against either part of the complex, which is the receptor for fibrinogen. Proteolysis was detected only in the presence of EDTA, a potent chelator of divalent cations. CONCLUSIONS: The incubation of human platelets in citrated plasma with SK concentrations obtained during therapy leads to an aggregation defect that is related to the decrease in fibrinogen, the adhesive protein involved in this function, and to the impeding effect of fibrinogen degradation products on its binding onto platelets but not to an alteration of the corresponding platelet receptor, the heterodimer glycoproteins IIb-IIIa.

Blood Platelets↗
PubMed1992

Psychological profile of somatizing patients attending the integrative clinic.

OBJECTIVE: A clinic to evaluate and treat referred somatizing patients was established in the medicine clinic of a university medical center. METHOD: Fifty-four patients were evaluated and compared to an age- and sex-matched non-somatizing patient group. RESULTS: Somatizing patients had increased rates of psychiatric and alcohol and substance abuse histories. Somatizing patients scored high on all subscales of the SCL-90 and were most frequently found in the Anxious/Moody Cluster of the MBHI. These patients also endorsed highly beliefs in medical problems as a focus of their lives. CONCLUSIONS: These patients' psychological beliefs set the stage for conflict in the medical setting. The implications of these results are discussed in relation to liaison clinics, early identification, and treatment approaches.

Academic Medical Centers↗
PubMed1992

Phenotype of villous stromal cells in placentas with cytomegalovirus, syphilis, and nonspecific villitis.

Villous stromal cells (VSC) play an important role in fetomaternal placental immune function. We studied the phenotype of VSC in infection by cytomegalovirus (CMV) and syphilis as well as nonspecific villitis and compared the findings with gestational age-matched controls. Monoclonal antibodies directed against total leukocytes, T cells, B cells, macrophages, dendritic cells, granulocytes and HLA-DR as well as polyclonal antibodies against S-100, alpha-1 antichymotrypsin, and lysozyme were used. In controls, the immunocytochemical response for each marker was either negative or weakly positive. In contrast, the VSC in CMV-infected and nonspecific villitis showed intense reactivity to various macrophage markers. In syphilis, reactivity with macrophage markers such as lysozyme and MAC387 were weaker, and reactivity to HLA-DR and S-100 was much stronger. Endothelial cells strongly expressed the monocyte/granulocyte marker CD15 in the diseased states, especially in syphilis, relative to controls. We conclude that the phenotype of VSC is altered in disease states and that the changes are dependent to some degree on the specific subset of chronic villitis.

Antibodies, Monoclonal↗
PubMed1992

Intrapulmonary neuroglial heterotopia.

Nonteratomatous intrapulmonary neuroglial heterotopia not associated with birth trauma or frank vascular embolization has been described rarely. This article briefly reviews the literature, and presents two additional cases of intrapulmonary neuroglial heterotopia. We found 14 cases in the literature. Twelve of these cases had central nervous system disruption, where neuroglial elements were in direct contact with amniotic fluid. Several hypotheses have been proposed, including fetal aspiration of detached neural fragments within amniotic fluid, neural crest migration defects, and vascular embolization with implantation. Of our two cases, one represents the first occurrence where central nervous system abnormalities were secondary to mechanical disruption, rather than to a primary neural tube defect. Our second case represents the youngest documented occurrence (17 weeks gestation) of intrapulmonary neuroglial heterotopia. Additionally, immunohistochemical studies were performed on these lesions, the results of which favor their neural origin. We present these findings and suggest they support the aspiration mechanism for neuroglial heterotopia in lung tissue.

Abnormalities, Multiple↗
PubMed1991

Recommendations for the evaluation and treatment of neonatal autoimmune and alloimmune thrombocytopenia. The Working Party on Neonatal Immune Thrombocytopenia of the Neonatal Hemostasis Subcommittee of the Scientific and Standardization Committee of the ISTH.

The following recommendations of the Neonatal Hemostasis Subcommittee of the Scientific and Standardization Committee of the ISTH for the management of neonatal immune thrombocytopenia were prepared by the working party on neonatal immune thrombocytopenia. Evaluation, diagnosis, and treatment of the mother and neonate with alloimmune and autoimmune thrombocytopenia are discussed and current recommendations provided. This document is likely to require frequent future revision(s).

Autoimmune Diseases↗
PubMed1991

Osteonectin is an alpha-granule component involved with thrombospondin in platelet aggregation.

We previously showed that thrombospondin, a major alpha-granule glycoprotein of human platelets, forms a specific complex with osteonectin, a phosphoglycoprotein originally described in bone that is also present in human platelets. The storage organelles and the function of osteonectin in platelets are still unknown. In this study, using electron microscopy in combination with immunogold staining, the major storage organelle for platelet-secreted proteins, the alpha-granules. Furthermore, osteonectin was qualitatively and quantitatively assessed by studying normal platelets and the platelets from a patient with gray platelet syndrome. Gray platelet syndrome is a rare congenital bleeding disorder characterized by a selective deficiency in morphologically recognizable platelet alpha-granules and in the alpha-granule secretory proteins. Binding of an iodinated antiosteonectin monoclonal antibody to gray platelet proteins transferred to nitrocellulose from SDS-polyacrylamide gels showed no band corresponding to osteonectin compared to control platelets. Using a polyclonal antiosteonectin antibody-based radioimmunoassay, gray platelets contained 0.2 +/- 0.03 ng osteonectin per 10(6) platelets, which is only 20% of the normal platelet content of osteonectin (0.93 +/- 0.16 ng per 10(6) platelets). Study of the localization of osteonectin to the surface of human platelets demonstrated that a radioiodinated antiosteonectin polyclonal antibody bound specifically to thrombin-stimulated platelets but not to resting platelets. Binding was concentration-dependent, saturable (1710 +/- 453 binding sites per platelet, Kd = 1 microM), and inhibited by an excess of cold antiosteonectin polyclonal antibody. No binding was observed on the surface of thrombin-stimulated gray platelets. To gain further insights into the role of osteonectin released from activated platelets, the effect of an antiosteonectin polyclonal antibody was tested on the aggregation of washed platelets. F(ab')2 fragments from the antiosteonectin polyclonal antibody inhibited in a dose-dependent manner the aggregation of collagen-stimulated, washed human platelets without affecting collagen-induced platelet serotonin release. To characterize the mechanism through which antiosteonectin F(ab')2 fragments inhibit platelet aggregation, the expression of endogenous thrombospondin (TSP) on the surface of thrombin-activated platelets was studied using 125I-labeled anti-TSP monoclonal antibody P10. The endogenous surface expression of TSP to thrombin-stimulated platelets was significantly inhibited in the presence of antiosteonectin F(ab')2 fragments (6286 +/- 2065 molecules of P10 per platelet) compared to 11,230 +/- 766 molecules of P10 per platelet in the presence of nonimmune F(ab')2 fragments.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1991

X-linked thrombocytopenia and Wiskott-Aldrich syndrome: similar regional assignment but distinct X-inactivation pattern in carriers.

While inherited X-linked (XL) isolated thrombocytopenia is a mild condition, the Wiskott-Aldrich syndrome (WAS) associates severe thrombocytopenia with an immunodeficiency component and has a poor prognosis. Whether these conditions correspond to separate genetic entities or to different mutations of the same gene(s) remains unresolved. The Wiskott-Aldrich syndrome locus has been assigned to Xp 11.2 by means of RFLP studies. The X-inactivation pattern in female carriers has been found to follow a skewed pattern in the hematopoietic cells, thus allowing carrier detection. We studied a family with four members affected by XL thrombocytopenia and report the results of genetic segregation analysis, together with the X-inactivation pattern of hematopoietic cells from an obligate female carrier. Although the affected locus mapped to the same region as that of WAS, lymphocytes presented a skewed pattern of X-inactivation, whereas polymorphonuclear lymphocytes (PMN) did not. These results provide further evidence that the Wiskott-Aldrich syndrome and XL thrombocytopenia are different expressions of mutations within a single locus and that the severity of the disease corresponds to distinct hematopoietic cell selections in obligate carriers.

Adult↗
PubMed1991

HPA-5b (Br(a)) neonatal alloimmune thrombocytopenia: clinical and immunological analysis of 39 cases.

Maternal alloimmunization against fetal platelets can cause fetal and neonatal thrombocytopenia (NAIT). The HPA-1a (PIA1, Zwa) antigen is by far the most common antigen implicated in NAIT. However, today another antigen often linked with that affection is HPA-5b (Br(a)). This is a report of 39 cases of NAIT involving the HPA-5b antigen. Thrombocytopenia may be of grave consequence. Three infants developed intracerebral haemorrhages (ICH). Of these, one died presumably as a consequence of ICH. Central nervous system (CNS) sequelae in the neonatal period was observed in two children. The potential hazards of death or disabling neurologic sequelae following intracerebral haemorrhage call for rapid and reliable diagnosis and effective therapy. Because there is high risk that subsequent pregnancies might be also affected by NAIT, the mothers of a previously affected child should be managed similarly to the HPA-1b mothers (PIA2, Zwb). The antenatal diagnosis of thrombocytopenia should be made and if necessary the in utero therapy instituted.

Antigens, Human Platelet↗