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Biomedical subjects

T Ruutu

Publications and source records attributed to T Ruutu.

At least 109 records · Page 6Linked to original sources
PubMed1989

Monitoring of bone marrow transplant recipient liver by fine-needle aspiration biopsy.

Acute graft-versus-host disease (aGVHD) of the liver was studied with fine-needle aspiration biopsies of thirty-four bone marrow transplant recipients. White cell differentials of liver FNABs and simultaneously taken blood samples were performed, and the increment and corrected increment methods were used to quantitate the inflammatory reaction in the liver. Biopsies taken before transplantation were used as the baseline. During aGVHD, the percentage of lymphoid cells and monocytes increased in the liver. The appearance of immunological blasts, together with a high proportion of activated lymphocytes in the FNABs, were typical findings during aGVHD. In patients with apparent prolonged liver graft-versus-host disease small lymphocytes were the predominating cell type. After initiating corticosteroid treatment, the number of blasts and the proportion of activated lymphocytes decreased. There was no significant difference in the proportions of CD4- and CD8-positive lymphoid cells in FNABs during or after aGVHD.

Acute Disease↗
PubMed1989

Characterization of neoplastic and reactive cells in T-cell lymphomas with cytogenetic, surface marker, and DNA methods.

Three patients with T-cell lymphoma were studied with a combined cytogenetic-immunological analysis (MAC) as well as by Southern blotting analysis. The MAC method, which allows simultaneous study of both chromosomes and immunophenotype of a mitotic cell, revealed that in each case the karyotypically abnormal and, therefore, neoplastic cells originated from different stages of T-cell maturation. In one case the abnormality was seen in cells expressing CD3 and CD10, in the second in cells expressing CD3 and CD8, and in the third case in cells expressing CD4 but not CD3. Mitoses were frequent also in non-neoplastic cells, but these mitoses were normal. Southern blotting analysis revealed TCR beta rearrangements in all patients. In addition, one patient displayed TCR gamma rearrangement, and one patient a rearrangement in the IgH joining region.

Aged↗
PubMed1989

Spontaneous erythroid colony formation in the differential diagnosis of erythrocytosis.

Erythroid colony formation in vitro was studied in 80 patients with erythrocytosis. 43 of the patients had polycythaemia vera (PV), 18 patients had secondary erythrocytosis, 6 had normal red cell mass, and 13 patients were regarded as unclassified. Spontaneous erythroid colony formation, in the absence of exogenous erythropoietin in the cultures, was discovered in all patients with PV, whereas no patient with secondary erythrocytosis or with normal red cell mass showed this phenomenon. 8 of the 13 patients with unclassified erythrocytosis spontaneously formed erythroid colonies. 7 patient with unclassified erythrocytosis have been followed for 5 yr. 3 of the 4 patients with spontaneous colony growth but none of the 3 without it can now be classified as PV. Thus, spontaneous erythroid colony formation indicates PV even in early and atypical cases. Therefore, the culture of erythroid progenitors is very useful in the differential diagnosis of problematic cases with erythrocytosis.

Adult↗
PubMed1989

Colony formation by megakaryocyte progenitors in myelodysplatic syndromes.

In vitro megakaryocytic colony formation by progenitors from the bone marrow was studied in 40 myelodysplastic syndrome patients. Megakaryocytic colonies were decreased in number or absent in 30 patients; only 10 showed normal colony growth. The growth correlated to some extent with the FAB-class. Patients with normal colony formation had either RA or RARS, but also in these two FAB-types half of the patients showed reduced megakaryocytic colony formation. Only 1 out of 15 patients with RAEB or RAEBt had normal megakaryocyte growth. The patients with CMML did not show any megakaryocytic colonies. The growth of erythroid colonies was normal in 3 patients and reduced or absent in the others. All 3 with normal erythroid colony formation also showed normal megakaryocyte growth, and all patients with normal megakaryocyte colony formation also had normal granulocyte-macrophage colony growth. Granulocyte-macrophage colony and cluster formation was normal in 17 patients. Defective formation of megakaryocytic, erythroid, and granulocyte-macrophage colonies was seen in 22 patients, compatible with a defect in a pluripotent stem cell. Megakaryocytic colony formation had no obvious correlation with any specific chromosome abnormality, and the distribution of the growth patterns was almost similar in patients with a normal and those with an abnormal karyotype.

Adult↗
PubMed1989

Chromosome 7 long-arm deletions in myeloid disorders: terminal DNA sequences are commonly conserved and breakpoints vary.

Deletions in the long arm of chromosome 7 are common recurrent abnormalities in secondary leukemias and myelodysplastic syndromes. To learn more about the basic mechanisms involved, we used Southern blot analysis to study four patients with different 7q--deletions to determine the exact break-points and to define the extent of the deletions. Several genes and DNA sequences from 16 different loci were found to be deleted, as judged by the absence or considerable weakening of an allelic band in granulocytic DNA in patients with constitutional heterozygosity. A terminal segment was present in each of the partially deleted chromosomes, as shown by heterozygosity for probes from the region 7q35----qter in granulocyte DNA. This indicated that the chromosome 7q deletions were interstitial, rather than terminal, in each of these patients. The length of the preserved terminal segment varied among the patients. Our results support gene loss as a mechanism contributing to leukemogenesis. Since the deletions are interstitial, hybrid genes may be formed at the junction, but the variation in breakpoints argues against the existence of a common hybrid gene of importance to the malignant process.

Adult↗
PubMed1989

Chromosome 7 long arm deletion in myeloid disorders: a narrow breakpoint region in 7q22 defined by molecular mapping.

The involvement of the erythropoietin (EPO), plasminogen activator inhibitor type I (PAI1), and multi-drug resistance (MDR2) genes located in chromosomal region 7q21-22 was studied in patients with myeloid disorders and with or without a chromosome 7 abnormality. Separated blood mononuclear cells and granulocytes from 21 patients were used in restriction fragment length polymorphism (RFLP) studies with gene-specific DNA probes. A marked weakness of one of the allelic bands was observed in granulocyte-derived DNA from heterozygous patients with monosomy 7. In four patients with a partial deletion of chromosome 7 long arm (7q-), marked weakness of an allelic band was observed in granulocyte-derived DNA with PAI1 probe (four heterozygous patients) and MDR2 probe (one heterozygous patient), implying deletion of these genes. In contrast, the EPO gene was not deleted in these patients, as demonstrated by the presence of two allelic bands of equal strength in granulocyte-derived DNA (two patients) or by gene dosage estimation (two patients). Two allelic bands of equal strength were also observed in three heterozygous patients with an arbitrary probe (pKV13) located in 7cen-q21.3. Unexpected hemizygosity or hybridization bands were not observed in any patient. We conclude that PAI1 and MDR2 are located distally of EPO in 7q22, and that none of these genes is commonly rearranged in myeloid disorders. The chromosome 7 long arm deletion breakpoint is located in a relatively narrow segment between the PAI1 and EPO genes in different patients. The deletion may involve a specific site in DNA, since the genetic distance between the PAI1 and EPO genes is only 3 cM.

Adult↗
PubMed1989

In situ hybridization using a Y-specific probe--a sensitive method for distinguishing residual male recipient cells from female donor cells in bone marrow transplantation.

A non-radioactive in situ hybridization method was used to detect residual host cells after bone marrow transplantation (BMT). A biotinylated Y-specific DNA probe was hybridized to bone marrow cells of three male patients who had received a bone marrow graft from their sisters for the treatment of acute leukaemia. Host cells were detected in two of the three patients, both in clinical remission, in six and seven cells out of 1000 cells analysed, respectively. Only one of a total of 3000 cells from three female controls showed a 'Y-signal'; 2580 cells out of a total of 3000 cells from three male controls showed a positive signal. These results indicate that in situ hybridization is a reliable and sensitive method for the detection of host cells after BMT.

Adolescent↗
PubMed1988

Heme arginate treatment for myelodysplastic syndromes.

Heme arginate was given to 26 patients with a myelodysplastic syndrome (MDS) as infusions of 2-3 mg/kg body weight weekly for 8-12 weeks. Most of the patients first received a loading dose on four consecutive days. Six of the patients showed improvement in cytopenias during the therapy. In three of the responders severely depressed blood cell counts recovered to normal or close to normal. So far the maximum duration of a response after the cessation of the treatment is 25 months, and the two ongoing responses have lasted for 11 and 12 months, respectively. In two responders of the eight patients with more than 15% ring sideroblasts the number of ring sideroblasts decreased during the treatment but remained unchanged in six non-responders. The responders were characterized by a low or low normal heme synthase activity which increased during the treatment, whereas the non-responders showed a higher mean heme synthase activity which decreased during the treatment. In general, the responders had significantly fewer defects in heme synthetic enzyme activities than the non-responders. FAB type, karyotype or growth pattern in in vitro cultures of hematopoietic progenitors did not predict the response. Apart from one case of mild venous irritation, no other adverse effects were seen. The present study shows that heme arginate induces beneficial effects on cytopenia in some MDS patients and has very few side-effects.

Adult↗
PubMed1988

Megakaryocytic colony formation in polycythaemia vera and secondary erythrocytosis.

Megakaryocytic colony formation by progenitor cells of 18 patients with polycythaemia vera, seven with secondary erythrocytosis and four with erythrocytosis of unexplained origin was studied in vitro by the methyl cellulose culture assay. Fourteen of the 18 patients with polycythaemia vera showed spontaneous megakaryocytic colony formation, i.e. colony growth with normal human plasma as the only source of colony stimulation. None of the patients with secondary erythrocytosis or erythrocytosis of unknown origin or of the normal controls grew colonies in the presence of normal human plasma only. When the plasma of a patient with aplastic anaemia was used instead of normal human plasma and phytohaemagglutinin stimulated leucocyte conditioned medium (PHA-LCM) was added to the culture medium, two of the patients with polycythaemia vera and one with secondary erythrocytosis formed slightly increased numbers of megakaryocytic colonies, while the rest of the patients showed normal colony formation. All of the patients with polycythaemia vera but none of those with secondary erythrocytosis or erythrocytosis of unknown origin showed spontaneous erythroid colony growth. The present study shows that most patients with polycythaemia vera form spontaneous megakaryocytic colonies in vitro. This phenomenon has recently also been demonstrated in essential thrombocythaemia and it is apparently analogous to spontaneous erythroid colony growth seen in all myeloproliferative disorders.

Adult↗
PubMed1988

A new congenital dyserythropoietic anaemia.

A new dominantly inherited dyserythropoietic anaemia is described. In the bone marrow, many of the nonspecific morphological characteristics described in congenital dyserythropoietic anaemias were seen; however, dysmorphic cells were rare. The acidified serum test was positive with one out of 17 sera tested; the negative sera included two that had haemolysed HEMPAS erythrocytes in the acid Ham test. Anti-i-agglutination was negative. No aberrations of red cell membrane protein glycosylation were observed. Serum cholesterol was low. Bilirubin conjugation was deficient but icterus was resolved by treatment with phenobarbital.

Adult↗
PubMed1988

Erythroid colony formation and effect of hemin in vitro in hereditary sideroblastic anemias.

Colony formation by erythroid burst-forming units (BFU-E) and erythroid colony-forming units (CFU-E) and the effect of hemin on colony growth was studied in vitro in three Finnish families with hereditary sideroblastic anemia (HSA). Defective activity of heme synthase has been demonstrated in family A and that of delta-aminolevulinic acid synthase in family B. No biochemical defect has been recognized so far in family C. CFU-E colony growth was defective in seven of the eight persons studied. The formation of BFU-E colonies was normal in family A and increased in family C, whereas of the two members of family B one showed normal and one decreased BFU-E colony growth. Hemin in 30-120 microM concentration increased significantly both BFU-E (p less than 0.01) and CFU-E (p less than 0.005) colony formation in family C. No effect was seen in family A, and in family B the only effect was normalization of the decreased BFU-E colony growth by the highest hemin concentration in one person. This study indicates that differences exist between families with HSA in erythroid colony formation and in response to hemin in vitro, but the low number of investigated members in each family does not permit a conclusive evaluation of the impact of the carrier versus patient status or of sex on the results.

Adult↗
PubMed1988

Monocytic involvement by monosomy 7 preceded acute myelomonocytic leukemia in a patient with myelodysplastic syndrome.

Novel techniques were used to detect which cell lineages were affected by monosomy 7 in a patient who had myelodysplastic syndrome and later developed acute leukemia. The patient had had paroxysmal nocturnal hemoglobinuria for 20 years before developing refractory anemia with excess of blasts. Cytogenetic analysis at the myelodysplastic stage disclosed monosomy 7 in bone marrow mitoses. Restriction fragment length polymorphism analysis of fractionated white blood cells with the chromosome 7-specific probes MetH and MetD revealed that blood monocytes and most bone marrow erythroblasts but not blood granulocytes or lymphocytes were affected by monosomy 7. The patient later developed acute myelomonocytic leukemia with blast cells positive for markers of the myelomonocytic lineage but negative for granulocytic markers in a standard surface marker analysis. The leukemic blast cells had monosomy 7 as determined by direct cytogenetic investigation. Thus, the monocytes were found to be affected by monosomy 7 in this patient 8 months before her myelodysplastic syndrome progressed to acute myelomonocytic leukemia, and the affected cells had the same biologic markers at both stages of the disease.

Anemia, Refractory, with Excess of Blasts↗
PubMed1987

Monosomy 7 in granulocytes and monocytes in myelodysplastic syndrome.

Monosomy for all or part of chromosome 7 in bone marrow mitoses of some patients with myelodysplastic syndrome or acute nonlymphocytic leukemia has been associated with a defect in granulocyte function. To study which blood-cell lineages are affected by the monosomy, we used chromosome 7-specific DNA probes in Southern blotting experiments on DNA derived from specific cell fractions isolated from the blood of five patients. As judged by the presence or absence of two different alleles for restriction-fragment-length polymorphisms, lymphocytes of all five patients were shown to have two different chromosomes 7. Granulocytes were affected by the chromosomal abnormality in four patients (No. 1, 2, 4, and 5) and unaffected in one (No. 3). Chemotaxis was normal in Patient 3 and impaired in Patients 4 and 5. Monocytes were affected by the monosomy in two of three patients (No. 2 and 3) and mainly unaffected in one (No. 1). Thus, the granulocytes and monocytes were affected differently in different patients. We conclude that mature blood cells are derived from abnormal progenitors and that there may be heterogeneity in the involvement of different cell lineages in different patients with myelodysplastic syndrome or acute nonlymphocytic leukemia. There is an association between DNA loss and functional impairment.

Acute Disease↗