Setting new standards for social work case management.
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Humans↗
Biomedical subjects
C Kaplan
Publications and source records attributed to C Kaplan.
The placenta and viral infections.
Many viruses can infect the fetus in utero, by either ascending or hematogenous routes. Much is known about the maternal-fetal passage of virus from clinical, virologic, and serologic studies. Although transplacental passage is a key aspect of these infections, there is much more limited information about changes in the placenta. For a few infections, placental characteristics have been well described, and there is now increasing information on many others. Newer techniques for in situ demonstration of viruses will hopefully yield much information about diagnosis and the mechanisms of transplacental passage.
Erythema Infectiosum↗
Childhood-onset systemic lupus erythematosus: antiphospholipid antibodies in 37 patients and their first-degree relatives.
OBJECTIVE: Antiphospholipid antibodies (aPL) are noted with increased frequency in patients with systemic lupus erythematosus (SLE). The main manifestations found to be associated with aPL are arterial and venous thrombotic events, thrombocytopenia, and recurrent pregnancy loss. This study is an attempt to define the incidence of aPL in patients with childhood-onset SLE and in their relatives and to correlate their presence with clinical manifestations, and especially, to evaluate the risk of thrombosis in aPL-positive subjects. METHODOLOGY: We studied 37 unrelated patients and 107 of their first-degree relatives. VDRL, IgG and IgM anticardiolipin, and IgG antiphosphatidylethanolamine antibodies were studied in all probands during periods of clinical remission and in first-degree relatives at the time of interview. Lupus anticoagulant had only been studied in probands during an SLE flare-up. RESULTS: Thirty-eight percent of probands and 19% of relatives were positive for at least one aPL, with little overlap between the different aPL studied. -No aPL-negative proband developed thrombosis. Two of the aPL-positive probands had thrombotic events before testing, and a third one showed thrombosis after testing. Only two probands had high levels of IgG aCL and showed thrombosis. The occurrence of aPL positivity in relatives was not always related to its presence in probands. None of the aPL-positive relatives had had thrombosis, but recurrent fetal loss was noted in one aPL-positive mother with SLE. Although there was a high frequency of SLE, SLE-like disease, auto-immune disorders or positive serological findings for lupus in first-degree relatives, many of these relatives did not test positive for aPL. CONCLUSION: The high levels of IgG aCL may be considered a risk factor for thrombosis. Findings in relatives suggest a multifactorial origin for autoimmune disease and antibody production.
Abortion, Habitual↗
Enhancing the consumer-family-staff relationship in adult services.
The present paper was written in an effort to improve mutual understanding among staff members of adult service agencies, their clients, and their clients' families and to encourage the implementation of procedures and practices that facilitate this goal. My aim was to foster strong, positive relationships among these groups by viewing the individual perspective of each and studying their interactions.
Activities of Daily Living↗
Diagnosis and management of foetal thrombocytopenia.
Platelet counts remain stable during intrauterine life (245 +/- 65 x 10(9)/litre, mean +/- SD). Before diagnosing thrombocytopenia (< 150 x 10(9)/litre), a foetal blood sample must be checked for contamination with amniotic fluid, since even slight contamination can activate coagulation and lead to a false positive result. In this paper, we review the major causes of thrombocytopenia and discuss their pathogenesis and management. Foetal thrombocytopenia can be caused by maternal complications (immune thrombocytopenic purpura, neonatal alloimmune thrombocytopenia, gestational thrombocytopenia, preeclampsia, alloimmune haemolytic disease) or infectious diseases (toxoplasmosis, cytomegalovirus, rubella) or be of true foetal origin (chromosomal abnormalities, malformations, congenital thrombocytopenia, intrauterine growth retardation.
Female↗
Placental pathology for the nineties.
Examination of the placenta in a problem pregnancy is potentially very valuable, yielding information about the nature and duration of processes occurring in gestation. Such evaluation requires thoughtful gross examination, careful sectioning, and an understanding of the basic microscopic changes in a variety of pathologic processes. As there are very few absolute associations in placental pathology, it is most important to appreciate the range of normal in assessing the potential importance of lesions. This chapter has tried to provide the essential relevant material, with emphasis on commonly encountered problem areas, and a variety of topics potentially related to maternal and fetal morbidity and mortality.
Extraembryonic Membranes↗
[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↗
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↗
[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↗
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↗
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↗
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↗
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↗
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↗
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↗
Idiopathic thrombocytopenic purpura, autoantibodies, autoantigens. An overview.
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Autoantibodies↗
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↗
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↗