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PubMed1997

[Syndrome of abnormal chromatin clumping in leucocytes with a high fraction of bone marrow cells in S-phase and in vitro autonomous growth].

Syndrome of abnormal chromatin clumping in leucocytes syndrome (ACCLS) is an uncommon entity which shares clinical and biological features with the myelodysplastic (MDS) and chronic myeloproliferative syndrome. In fact, as some authors consider ACCLS a new type of MDS, others maintain that it is in Ph'negative/bcr-abl negative chronic myeloid leukaemia. A new case of ACCLS appeared in a 68 year old woman, who presented with anaemic symptoms, bleeding and recurrent infections, and a haematological picture including progressive macrocytic anemia, thrombocytopenia and leuco-erythroblastosis. Marrow hypercellularity with granulocytic hyperplasia, and mature granulocytes presenting nuclear hyposegmentation and large peripheral blocks of chromatin separated by clear zones were the characteristic features of this case. No cytogenetic abnormalities were found and DNA flow-cytometry content was normal (euploid), supporting the thought that a disequilibrium exists in the hetero-chromatin/eucromatin ration in AACLS. Reverse PCR for bcr-abl transcripts was negative. The cell-cycle-phase analysis showed a high fraction of S-cells in the bone marrow (27%) in contrast to a very low S-phase (0.2%) in the peripheral blood, pattern that is different from both CMML and CML. In vitro clonogenic assays showed a high colony forming capacity and a certain grade of autonomous proliferation of the bone marrow cells, which is reminiscent of the CMML growth behaviour in culture. The patient was treated with vitamin D3, low dose Ara-C, prednisone and hydroxyurea until her demise, fifteen months after diagnosis. In total, the patient received 47 units of packed cells and 114 of platelet concentrates, and was transfused only when she presented anaemic or hemorrhagic symptoms. These clinical and haematological features suggest that ACCLS is a distinct entity that should be considered a sixth type of MDS, beside CMML, with which it has much in common.

Aged↗

PubMed1996

Hematological modifications induced by estrogens in cirrhotic animals.

Estrogens are known to have mitogenic activities and to influence hematic crasis. A wide literature on this subject allows us to re-evaluate the results of research performed in 1950. Estrogens injected into the peritoneum (estradiol propionate 2.5-5 mg, twice weekly) or into tibial bone marrow (estradiol propionate 1.5 mg weekly) of guinea pigs, after carbon tetrachloride induced cirrhosis (CCI4 inhalation for 7-15 min twice weekly), caused hyperchromic anemia, with erythroblastosis and leucocytosis; hyperplasia of reticulo-hystiocitary cells of bone marrow and lymphoid organs; splenic hemosiderosis; hyperplasia of immature bone marrow cells, with maturative inhibition; and terminal bone marrow hypoplasia. Our results agree with recent literature data concerning the role played by natural estrogens and environmental xenoestrogens that are capable of stimulating bone marrow progenitor cell proliferation and delaying their maturation, by the secretion of growth factors, especially from hyperplastic stromal cells, in solid and hematological tumors.

Animals↗

PubMed1976

Strain-, age-, and tumor-dependent distribution of terminal deoxynucleotidyl transferase in thymocytes of mice.

The distribution of terminal deoxynucleotidyl transferase (TdT) peak I and peak II in thymuses and peripheral lymphoid tissues was examined in a variety of mouse strains in relation to tumor burden and age. TdT peak I was found to be present in all strains at comparable levels, which did not change with age. TdT peak II levels were also comparable for the strains examined at 1 week of age. In contrast to peak I, however, in NIH Swiss and AKR mice, peak II activity decreased rapidly at 2 weeks of age and by 6 weeks of age less than 2% of the initial activity remained. In C57BL/6 mice there was a similar loss of peak II activity with age although this change started at about 4 months of age and by 8 months of age approximately 15% of the initial activity remained. These changes did not appear to be due to the presence of an inhibitor. Leukemic C57BL/6 and AKR mice were also examined for TdT. Both strains characteristically had TdT peak I in peripheral lymphoid tissues infiltrated with transformed thymocytes. AKR mice had only TdT peak I in the thymus, whereas C57BL/6 thymuses had both peak I and II at levels comparable to age-matched controls. No aberrant distribution of TdT was observed in a spontaneous reticulum cell sarcoma or Rauscher MuLV-induced erythroblastosis.

Aging↗

PubMedDate not supplied

[Congenital toxoplasmosis].

INTRODUCTION: Toxoplasma gondii is a ubiquitous parasite of all species of mammals and birds (1). Most often the infection in the immunocompetent persons is asymptomatic. Symptoms (if present) are usually mild and self-limited. Infection in the fetus and immunodeficient patients may lead up to clinically severe and often fatal toxoplasmosis (2). ETIOLOGY: Toxoplasma exists in three forms: oocysts, tissue cysts and tachyzoites. The definitive hosts of Toxoplasma are members of the cat family. They shed unsporulated oocysts in the feces. After sporulation oocysts become infectious. Tachyzoites are crescent-shaped forms responsible for manifestations of acute Toxoplasma infection in the intermediate hosts (6,7). Cysts are formed, particularly in brain, heart muscle and skeletal muscles. The cyst forms of the parasite are seen in the latent stage of the infection. Postnatally acquired toxoplasmosis is a consequence of infection from cysts (by ingestion of undercooked meat of infected animals), oocysts (by ingestion of soil, fruits, vegetables contaminated by cat feces) and tachyzoites (by blood transfusion). Congenital Toxoplasma infection causes congenital toxoplasmosis. PATHOGENESIS: Some authors represented the concept that latent (chronic) infection with Toxoplasma during pregnancy can result in congenital infection in the offspring (8-11). Now it is generally agreed that congenital transmission of Toxoplasma occurs only when the infection is acquired during gestation (6,7, 12-16). More than half of the fetuses escape infection, one-third are definitely infected, and the infection is more often subclinical than clinically obvious (15). The fetus is infected hematogenously from inflammatory foci in the placenta formed during parasitemia in the mother. CLINICAL MANIFESTATIONS: Approximately 75% of congenitally infected newborns are asymptomatic. Wilson's study indicates that nearly all such children will develop adverse sequelae (neurologic, intellectual, audiologic and ophthalmologic) 21). Severe forms of congenital toxoplasmosis occur only in 10% of infected offsprings. Clinical manifestations of congenital toxoplasmosis are different. Clinical findings in patients with congenital toxoplasmosis may include: chorioretinitis and other ocular findings, central nervous system abnormalities (such as microcephaly, hydrocephalus, encephalomyelitis, seizures and mental retardation), icterus, hepatosplenomegaly, rash, anemia, erythroblastosis, thrombopenia. INCIDENCE: Incidence of human congenital toxoplasmosis is different in different countries. The incidence in Britain is 0.6 subclinical infection and 0.09 severe illnesses per 1000 births (22). The incidence in USA is between 1/1000 and 1/8000 live births (23). In France the incidence is 1/2000. In Slovenia the incidence is 2.3 cases per 1000 births (25). DIAGNOSIS: Diagnostic methods are: 1. Isolation of the parasite from the placenta, blood, body fluids (by inoculation of specimens into mice or tissue cultures). 2. Histologically by demonstration of tachyzoites in tissue sections or smears of body fluids. 3. Serologic diagnosis. The most important diagnostic methods are serologic tests. For diagnosis of congenital toxoplasmosis determination of IgM antibody (in the serum of newborn infant) has the greatest importance. The fetus is able to produce IgM specific antibody. The presence of IgM antibodies in serum obtained from the neonate is an evidence of fetus infection in utero. Maternal IgM antibodies do not pass the placenta. IgM antibodies may be demonstrable by indirect fluorescent antibody test (IgM-IFA), enzyme linked immunosorbent assay (IgM-ELISA), double sendwich IgM enzyme-linked immunosorbent assay (DS-IgM-ELISA), IgM immunosorbent agglutination assay (IgM-ISAGA) and reversed enzyme immunoassay (REI). For diagnosis of congenital toxoplasmosis the next tests are also applied: Sabin-Feldman Dye test, indirect fluorescent antibody test for IgG antibodies (IgG-IFA) and enzyme

Female↗

PubMed1998

Clinical Usefulness of Flow Cytometry in Detection and Quantification of Fetomaternal Hemorrhage.

> Objective: To compare the technique of immunofluorescence flow cytometry against traditional Kleihauer testing with respect to the sensitivity and specificity of clinical detection of fetomaternal hemorrhage. Methods: Blood samples from D-negative unsensitized postpartum women were analyzed by flow cytometry (customized, directly conjugated monoclonal anti-D) and Kleihauer testing using commercial kits as well as a manual technique. Results: Both flow cytometry and manual Kleihauer tests performed well in vitro against known standards, giving similar results with detectable fetal cells in the range of 2-10%. Correlation of in vivo results obtained by flow cytometry and either Kleihauer method was poor. The percentage of fetal red cells detected by flow cytometry was approximately twice that of the manual Kleihauer. Commercial Kleihauer testing proved unreliable in the in vivo setting. Conclusions: Flow cytometry offers a reliable alternative to traditional Kleihauer testing for detecting fetomaternal hemorrhage and may, with standardized methodology, help optimize immunoprophylaxis against erythroblastosis fetalis.

Journal Article↗

PubMed1998

[Diagnosis and therapy of erythrocyte alloimmunization in pregnancy].

INTRODUCTION: By preventive administration of anti-D globulin the number of cases of Rh isoimmunization declines steadily. Severe untreated isoimmunization may lead via foetal hydrops to intrauterine death, sometimes already during the 18th-19th week of gestation. The purpose of prenatal diagnosis in pregnant women with isoimmunization is to assess the danger or affection of the foetus, its prognosis and the mode of monitoring of the foetus. It is necessary to decide in time on intrauterine therapy by transfusion of erythrocyte mass and to assess the optimal time of delivery with regard to the risk of prematurity and foetal erythroblastosis, as well as with regard to intrauterine therapy. The objective of the present work was to test the protocol in the treatment of erythrocytic isoimmunization of the foetus. METHOD: During the period between January 1991 and October 1997 the authors investigated two groups of pregnant women: with a hydropic (n = 5) and non-hydropic (n = 20) foetus at the onset of treatment. In both groups amniocentesis and umbilical puncture were indicated. The authors investigated the number of cordocenteses and the volume of transfused blood per pregnancy, the number of complications and their type, gestation age of the foetuses on delivery, their birth weight, the condition of the neonates after delivery and on discharge to home care. RESULTS: During the mentioned period the authors administered 70 intraumbilical transfusions to 25 foetuses. The transfusion was not repeated more than eight times. The baseline haematocrit of non-hydropic foetuses was 26 (14-34), treatment was started on average during the 28th week (23rd-33rd). Pregnancy in women with a non-hydropic foetus was terminated during the 35th (27th-40th) week, with a mean weight of the foetuses of 2439 g (870-3520). Of 25 treated foetuses 6 were hydropic (24%) at the onset of treatment. The initial haematocrit of hydropic foetuses was 10.7 (4-19.8), treatment was started on average during the 28th (23rd-33rd) week. Pregnancy of women with hydropic foetuses was terminated during the 30th (25th-36th) week, the mean birth weight being 1838 g (660-3500). DISCUSSION: The very favourable therapeutic results in non-hydropic foetuses are in great contrast with the therapeutic results of moribund hydropic foetuses. CONCLUSION: The basic prerequisite of successful treatment by intraumbilical transfusion is to concentrate risk pregnancies in specialized centres with a high standard neonatological team for intensive care of pathological neonates.

Blood Transfusion, Intrauterine↗

PubMed1952