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Biomedical subjects

M Tulliez

Publications and source records attributed to M Tulliez.

At least 19 recordsLinked to original sources
PubMed1992

Role of human immunodeficiency virus replication in defective in vitro growth of hematopoietic progenitors.

A number of hematologic abnormalities, including cytopenias, have been observed in patients with human immunodeficiency virus (HIV) infection. To elucidate their mechanisms, a group of 27 patients with HIV-1 infection was studied. In all patients, a marked reduction of in vitro colony formation by erythroid, granulomacrophagic, and megakaryocytic bone marrow progenitors was observed in comparison to normal donors. HIV-1 infection of marrow progenitors was investigated in studying individual colonies with the polymerase chain reaction (PCR) technique. No HIV-1 DNA could be detected in these colonies, suggesting either that marrow progenitors were not infected or that infected progenitors were not able to generate colonies in vitro. The addition of antisense oligonucleotides directed against HIV tat or nef sequences in the culture medium led to a significant increase in colony formation, suggesting that HIV replication in hematopoietic progenitors could be responsible for their defective growth. However, no HIV-1-infected colonies could be detected by PCR after the antisense treatment, indicating that the increase in colony number was not due to the proliferation and differentiation of infected progenitors but to an inhibition of HIV replication in an accessory cell. This last hypothesis was further confirmed by the absence of effects of antisense oligomers on the plating efficiency of hematopoietic progenitors grown from CD34+ cells. These data indicate that hematologic abnormalities of HIV-infected patients cannot be explained by a direct infection of hematopoietic progenitor cells and suggest that a defective modulation of progenitor cell growth by HIV replication outside these cells might play a role in these abnormalities.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Pulmonary Hodgkin's disease in HIV-infected patient. Diagnosis by bronchoalveolar lavage.

We report herein the pulmonary recurrence of Hodgkin's disease coincidental with a marked decrease in the peripheral blood CD4 lymphocyte count in an HIV-seropositive patient with alveolar consolidation on chest roentgenogram. The diagnosis of lung parenchyma involvement was made by bronchoalveolar lavage cell analysis and illustrates the reliability of Reed-Sternberg cell identification in bronchoalveolar lavage for the diagnosis of pulmonary localization of Hodgkin's disease.

Adult↗
PubMed1992

[Large cell lymphomas: effect of histologic groups on the prognosis. Study of 210 cases treated with the same therapeutic protocols].

As part of a study of two therapeutic protocols initiated in 1982 and 1985, respectively, for localized (n = 134) and disseminated (n = 76) large cell lymphomas, histologic type was determined for each patient by several pathologists using the Kiel classification for morphologic features and the international working formulation for protocol assignment and multifactorial statistical analysis. Therapeutic results in the two hundred and ten cases were correlated with a number of prognostic factors including age, stage, tumor size, extranodal disease, and clinical or biological markers for disease activity such as the LDH level. The previously reported influence of histologic subgroup on prognosis was not found with these highly effective protocols, whether histologic type was considered alone or in combination with other prognostic factors. The only consistent finding was that anaplastic large cell lymphomas, despite their aggressive features, were most likely to have a favorable outcome.

Adolescent↗
PubMed1992

Diet-dependent carcinogenesis of pancreatic islets and liver in transgenic mice expressing oncogenes under the control of the L-type pyruvate kinase gene promoter.

The liver-type pyruvate kinase (L-PK) gene is controlled positively by insulin and carbohydrates, negatively by glucagon and fasting. Diet-inducible models of carcinogenesis were obtained using the L-PK gene promoter and regulatory sequences to control the expression of c-myc and SV40 T oncogenes in transgenic mice. L-PK/c-myc and L-PK/Tag animals fed a carbohydrate-rich diet developed hepatocarcinomas. In addition, L-PK/Tag animals developed diet-dependent, aggressive endocrine pancreatic tumors, preceded by islet hyperplasia involving the different analysed cell populations (alpha, beta and delta). Expression of the L-PK gene was demonstrated in pancreatic tumors, in rat isolated islets and in rat insulinoma-derived cells (RIN line), revealing a new tissue specificity of the L-PK gene. Our results suggest that this gene may be expressed in islet progenitor cells from which the different mature endocrine cells derive.

Animals↗
PubMed1991

[Role of giardiasis in non-ulcer dyspepsia].

In 1987 and 1988, 340 consecutive patients attended the endoscopy centre of Cochin hospital, Paris, and underwent oesophago-gastroduodenal endoscopy in a search for Giardia lamblia parasitology and histology. Two-hundred and eight of these patients presented with non-ulcer dyspepsia and entered a prospective study aimed at determining the advisability of a systematic search for Giardia lamblia in this population. Six biopsies were positive for giardiasis, including 3 in patients with acquired immunodeficiency, 1 in a case of chronic diarrhoea with atrophic villi and 2 in dyspeptic patients. Giardiasis, therefore, cannot be regarded as a cause of non-ulcer dyspepsia, and a systematic search for the parasite is of little interest in such cases. However, giardiasis remains a cosmopolitan parasitic disease with a non-negligible prevalence in France among subjects at risk, such as communities, children, travellers, homosexuals and immunodeficient patients.

Adult↗
PubMed1991

Phase I-II study of two consecutive courses of high-dose epipodophyllotoxin, ifosfamide, and carboplatin with autologous bone marrow transplantation for treatment of adult patients with solid tumors.

We describe a phase I-II study of two consecutive 5-day courses of a three-drug regimen of ifosfamide (IFM), carboplatin (CBDCA), and either etoposide (VP-16) (regimen 1) or teniposide (VM-26) (regimen 2) in high doses together with autologous bone marrow transplantation (ABMT), for previously treated patients with ovarian carcinoma (OC), germ cell tumors (GCT), gestational trophoblastic disease (GTD), or oat cell carcinoma (OCC). Forty-four patients entered the study. Two patients with OC received regimen 1, and 22 were given regimen 2. Sixteen patients with GCT, two with GTD, and two with OCC were treated with regimen 1. Six patients (13%) died of toxicity. Nephropathy and esophagitis were the dose-limiting toxic effects. The maximum-tolerated doses (MTDs) were 1,500 and 200 mg/m2/d for 5 days for IFM and CBDCA, respectively, in combination with VP-16 250 mg/m2/d for 5 days (regimen 1), and 150, 1,500, and 200 mg/m2/d for 5 days for VM-26, IFM, and CBDCA, respectively (regimen 2). The response rate of patients with OC was 78% (complete response [CR], 14%). For patients previously resistant to chemotherapy, the response rate was 70%. There were no long-term disease-free survivors among patients with OC. The response rate of patients with GCT was 60% (CR, 33%). All responders with GCT were resistant to previous chemotherapy. Unmaintained CRs lasted 2, 6, 8+, 27+, and 37+ months. Of the two patients with GTD, one with previous resistance to chemotherapy attained a CR of 18+ months. One patient with OCC attained a CR lasting 6 months. The regimen possesses great antitumor activity. It produced CRs of long duration in a number of patients with GCT and GTD who were previously resistant to chemotherapy.

Adult↗
PubMed1991

[Helicobacter pylori infection and the surgically treated stomach].

In 38 patients who had been operated for peptic ulcer (32) or gastric cancer (6), we performed upper GI endoscopy with biopsies. HP was found in the mucosa in 8 out of 10 patients with highly selective vagotomy, 5 out of 11 patients with gastrectomy for ulcer, 6 out of 11 patients with vagotomy-pyloroplasty and in only 1 case out of 6 with gastrectomy for cancer. These results are in agreement with other publications. Bilio-pancreatic reflux into the stump probably explains why HP was found in only 50% of cases with suppression of pyloric function, compared with 80% after highly selective vagotomy. Interstitial gastritis was present in every case infected with HP, but the same gastritis was present in one half of mucosas, without infection by HP. This particular gastritis in probably caused by reflux. The role of HP in the relapse of ulcers therefore remains to be demonstrated.

Adult↗
PubMed1991

Histopathologic features of high-grade non-Hodgkin's lymphomas in acquired immunodeficiency syndrome. The French Study Group of Pathology for Human Immunodeficiency Virus-Associated Tumors.

High-grade B-cell non-Hodgkin's lymphomas are observed in 5% to 10% of patients with acquired immunodeficiency syndrome. To describe their histologic subtypes, a group of pathologists was formed. One hundred thirteen cases were reviewed and classified according to the Working Formulation, the updated Kiel classification, and a recent description of morphologic variants of high-grade B-cell non-Hodgkin's lymphoma. Three major types of intermediate- or high-grade lymphomas were observed: (1) large-cell or centroblastic mainly polymorphic lymphomas with a component of immunoblasts (35 cases); (2) immunoblastic lymphomas with plasmablastic and plasmacytic features in most cases (33 cases); and (3) small non-cleaved cell Burkitt's or non-Burkitt's lymphoma (41 cases), with 15 cases fitting typical criteria of Burkitt's lymphoma and 26 heterogeneous cases in which the size and shape of the cells and the presence of plasmablastic features varied. The most frequent pathologic sites of involvement at presentation were the lymph nodes, gastrointestinal tract, bone marrow, brain, oral cavity, and muscles. A comparison between the histologic type and the site of involvement showed that most cases involving lymph nodes, bone marrow, or muscles were small noncleaved cell Burkitt's or non-Burkitt's lymphomas, while those that affected the gastrointestinal tract, brain, and oral cavity were centroblastic or immunoblastic lymphomas with consistent plasmacytic differentiation. In 10 cases, previous persistent generalized lymphadenopathy syndrome was present. In 13 cases, the lymphomatous proliferation was associated with follicular or diffuse hyperplasia seen on the same lymph node biopsy specimen or in another lymph node.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Acute T-cell leukemia/lymphoma mimicking Hodgkin's disease with secondary HTLV I seroconversion.

The authors observed a pleiomorphic lymphoma mimicking Hodgkin's lymphoma in a French Guyana black woman lacking antibodies for human T-cell lymphoma/leukemia virus type I (HTLV I). After two courses of chemotherapy with either mechlorethamine, vincristine, procarbazine, and prednisone (MOPP) or doxorubicin, bleomycin, vincaleukoblastine, and dacarbazine (ABVD), a typical acute T-cell leukemia/lymphoma developed with HTLV I seroconversion. Specific HTLV I DNA sequences were detected using the polymerase chain reaction (PCR) on a lymph node biopsy obtained before chemotherapy. The mechanisms of the seroconversion are discussed.

Adult↗
PubMed1988

Etiology of portal vein thrombosis in adults. A prospective evaluation of primary myeloproliferative disorders.

In a prospective study of 33 adults with portal vein thrombosis unrelated to a liver tumor, we have assessed the prevalence of primary myeloproliferative disorders using conventional criteria and cultures of bone marrow progenitor cells. A primary myeloproliferative disorder was documented in 14 patients investigated at the time of recognition of portal vein thrombosis. Among these 14 patients, the main clue to the presence of the myeloproliferative disorder was (a) the observation of suggestive abnormalities of peripheral blood cell counts in 4 patients; (b) characteristic findings at bone marrow biopsy or determination of total red cell volume in 3 patients; and (c) formation of "spontaneous" erythroid colonies in cultures of bone marrow progenitor cells in erythropoietin-poor medium in 7 patients. In 2 other patients, agnogenic myeloid metaplasia with myelosclerosis of apparently recent onset developed 5 yr after recognition of portal vein thrombosis. In conclusion, primary myeloproliferative disorders--in a full-blown or latent form, or at an early stage--are a major cause of portal vein thrombosis.

Blood Cell Count↗
PubMed1988

Hashimoto's thyroiditis with a monoclonal antithyroglobulin autoantibody: disappearance of the monoclonal antibody after thyroidectomy.

A 46-yr-old man had typical Hashimoto's thyroiditis (HT) and a serum monoclonal immunoglobulin (MIgG kappa). There was no evidence of disseminated lymphoid malignancy. Because of rapid enlargement of the goiter with pressure symptoms, a total thyroidectomy was performed. The surgery was followed by the complete disappearance of the MIgG kappa paralleled by the disappearance of serum antithyroglobulin autoantibodies. Thyroid sections demonstrated HT. Direct immunofluorescence assay showed diffuse infiltration by lymphocytes and plasma cells that were mainly IgG kappa positive. Moreover, the serum MIgG kappa had antithyroglobulin activity, as demonstrated by two different methods, namely labeling of focused serum proteins with radioiodinated human thyroglobulin and immunoadsorption of the monoclonal IgG on a human thyroglobulin affinity column. These results demonstrate that a monoclonal antithyroglobulin autoantibody was produced within the thyroid in a patient with HT. As the production of a MIg is regarded as the last stage preceding the malignant transformation of normal B lymphocytes, this report strongly suggests that a B lymphoma can directly emerge from the intrathyroidal lymphocytes involved in the pathogenesis of Hashimoto's thyroiditis.

Antibodies, Monoclonal↗
PubMed1988

Hairy cell leukemia associated with large granular lymphocyte leukemia: immunologic and genomic study, effect of interferon treatment.

The authors describe a patient who presented an association of hairy cell leukemia (HCL) and large granular lymphocyte (LGL) leukemia. An eventual relationship between these two rare entities is analyzed. Hairy cells (HCs) were present in the blood, bone marrow, and spleen. An excess of LGLs was found only in the blood and bone marrow. After splenectomy the patient received an alpha 2-interferon (alpha 2-IFN) treatment. The HCs surface phenotype was mu+delta+kappa+, CD20+, and CD25+. The LGLs consisted in CD3+, CD8+, HNK1+, WT31+ T lymphocytes. These were absent in the spleen. alpha 2-IFN treatment resulted in the disappearance of the HCs in the blood and bone marrow, whereas the LGLs remained unchanged. Before alpha 2-IFN treatment, peripheral blood cells, predominantly LGLs, exerted low cytotoxicity that increased up to a normal level after treatment. Using Southern blotting the authors studied the rearrangements of the T-cell receptor beta--chain (C beta) and gamma-chain (J gamma) genes and immunoglobulin heavy (JH)- and light (C kappa, C lambda)- chain genes. An unique JH and C kappa gene rearrangement was found in the blood and spleen, whereas C beta and J gamma gene rearrangements were present in the blood, not in the spleen. Under alpha 2-IFN treatment, the JH gene rearrangement fainted dramatically, in contrast to that of the C beta gene. The study of messenger RNA (mRNA) of the T cell receptor alpha and beta chains evidenced the 1.3-kilobase (kb) and 1.6-kb bands in the blood and their absence in the spleen. The patient was human T-cell leukemia virus (HTLV)-II negative by Southern analysis of blood and spleen cells. It is concluded that the LGL expansion was clonal and not reactive to the HCL. Although the authors cannot definitely exclude that both HC and LGL proliferations stem in a common leukemic precursor, their findings support an association of the two entities.

Antigens, Surface↗