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Biomedical subjects

B J Bain

Publications and source records attributed to B J Bain.

At least 55 records · Page 3Linked to original sources
PubMed1999

Pathogenesis and pathophysiology of anemia in HIV infection.

Anemia is common in human immunodeficiency virus infection, particularly in patients with acquired immunodeficiency syndrome. Anemia is multifactorial. HIV infection itself causes anemia, probably as a consequence of HIV infection of stromal cells rather than HIV infection of hematopoietic stem cells. Other common causes of anemia in AIDS are anemia of chronic disease consequent on opportunistic infections, bone marrow suppression by antiretroviral therapy, and hemolytic anemia induced by oxidant drugs. Thrombotic microangiopathy is a significant complication of HIV infection and may respond to plasmapheresis.

AIDS-Related Opportunistic Infections↗
PubMed1999

An analysis of relative costs and potential benefits of different policies for antenatal screening for beta thalassaemia trait and variant haemoglobins.

AIMS: To investigate the costs and potential benefits of different policies for antenatal screening for haemoglobinopathies in two multiethnic London communities. METHODS: 1000 consecutive antenatal patient samples referred to each of two London teaching hospital laboratories for haemoglobinopathy testing were investigated using the standard procedures of the laboratory in question. When the standard procedures did not include high performance liquid chromatography (HPLC), this technique was added, in order to assess its diagnostic value and cost-effectiveness. A comparison was made between the costs and potential benefits of universal testing for variant haemoglobins and beta thalassaemia trait using HPLC and the costs and potential benefits of universal testing for variant haemoglobins and selective testing for beta thalassaemia trait using the mean cell haemoglobin (MCH) as a screening test and less automated techniques than HPLC for definitive diagnosis. RESULTS: The costs of the two policies were found to be comparable, as the higher reagent/instrument costs of HPLC were offset by the lower labour costs. Universal testing of 2000 consecutive samples did not disclose any extra cases of beta thalassaemia trait which would not have been detected by universal screening and selective testing. However, six patients were found to have a haemoglobin A2 variant which can interfere with the diagnosis of beta thalassaemia trait. CONCLUSIONS: The introduction of universal testing by HPLC into British laboratories could be cost neutral and has potential benefits. If a higher cost is accepted then the greater degree of automation could be used to release skilled staff for other tasks within the laboratory.

Chromatography, High Pressure Liquid↗
PubMed1999

The relationship between the myelodysplastic syndromes and the myeloproliferative disorders.

As a result of clonal evolution typical cases of one of the myelodysplastic syndromes may develop myeloproliferative features. Similarly, typical cases of one of the myeloproliferative disorders may develop dysplastic features, either as part of the natural history of the disease or as a result of exposure to mutagenic drugs or isotopes. There is also an important group of "overlap syndromes" in which cases, at presentation, have both dysplastic and proliferative features. Chronic myelomonocytic leukaemia and many cases of atypical chronic myeloid leukaemia, juvenile chronic myeloid leukaemia and the childhood monosomy 7 syndrome are "overlap syndromes". In addition, a significant minority of cases which fit the generally agreed criteria for a diagnosis of one of the myelodysplastic syndromes (refractory anaemia, refractory anaemia with ring sideroblasts or refractory anaemia with excess of blasts) also have thrombocytosis, neutrophilia, monocytosis, eosinophilia or basophilia.

Chromosomes, Human, Pair 7↗
PubMed1999

Thrombocytosis with sideroblastic erythropoiesis: a mixed myeloproliferative myelodysplastic syndrome.

Some patients with haematological neoplasms have features which overlap between a myelodysplastic syndrome and a myeloproliferative disorder. Two such patients are reported, both having sideroblastic erythropoiesis and thrombocytosis and one sequentially developing features of atypical chronic myeloid leukaemia, idiopathic myelofibrosis and acute megakaryoblastic leukaemia. The prevalence of thrombocytosis among cases of refractory anaemia with ring sideroblasts may be as high as 15-20% and has implications for choice of therapy.

Anemia, Sideroblastic↗
PubMed1998

Lymphomas and reactive lymphoid lesions in HIV infection.

Infection by the human immunodeficiency virus (HIV) causes depletion of CD4-positive lymphocytes with consequent immunodeficiency. HIV infection also causes, by direct or indirect mechanisms, both reactive and neoplastic changes in lymphoid tissues. In primary infection reactive changes are a direct response to HIV. Later in the course of the disease there are reactive changes in lymph nodes and extranodal lymphoid tissues which are likely to be largely an indirect effect of HIV infection, being a response to opportunistic infection by other organisms. There is also an increased incidence of autoimmune phenomena in HIV-infected subjects which is likely to be consequent, at least in part, on impaired control of the proliferation of self-reactive B-cell clones. A second mechanism of immune damage of blood cells, probably operating in the case of HIV-related immune thrombocytopenic purpura, is that of cellular damage by immune complexes containing antiviral antibodies. Lymphoid neoplasms associated with HIV infection include non-Hodgkin's lymphoma, Hodgkin's disease and, uncommonly, plasma cell dyscrasias. HIV-associated lymphomas have distinct clinicopathological features and generally a poor prognosis. As for reactive lymphoid lesions, induction of neoplasia is likely, in the majority of cases, to be an indirect rather than a direct effect of the virus. The combination of chronic B-cell stimulation and impaired T-cell function is important, and interaction of lymphoid cells with virus-infected stromal cells may also play a role. Infection by oncogenic viruses such as the Epstein-Barr virus and human herpes virus 8 is also aetiologically important. In rare cases of T-cell lymphoma, HIV may be directly oncogenic.

HIV Infections↗
PubMed1998

Hematological malignancies with t(9;11)(p21-22;q23)--a laboratory and clinical study of 125 cases. European 11q23 Workshop participants.

This paper reports clinical and cytogenetic data from 125 cases with t(9;11)(p21-22;q32) which were accepted for a European Union Concerted Action Workshop on 11q23. This chromosome abnormality is known to occur predominantly in acute myeloid leukemia (AML) FAB type M5a and less often in AML M4; in this series it was also found to occur, uncommonly, in other AML FAB types, in childhood acute lymphoblastic leukemia (ALL) (nine cases), in relatively young patients with myelodysplastic syndrome (MDS) (five cases), acute biphenotypic leukemia (two cases), and acute undifferentiated leukemia (one case). All age groups were represented but 50% of the patients were aged less than 15 years. The t(9;11) was the sole abnormality in 57 cases with AML; trisomy 8 was the most common additional abnormality (23 cases, including seven with further abnormalities), and 28 cases had other additional abnormalities. Among the t(9;11)+ve patients with AML, the white cell count (WBC) and age group were significant predictors of event-free survival; central nervous system (CNS) involvement or karyotype class (sole, with trisomy 8, or with other), also contributed to prognosis although our data could not show these to be independent factors. The best outcome was for patients aged 1-9 years, with low WBC, and with absence of CNS disease or presence of trisomy 8. For patients aged less than 15 years, the event-free survival for ALL patients was not significantly worse than that of AML patients.

Acute Disease↗
PubMed1998

Myelodysplastic syndromes associated with 11q23 abnormalities. European 11q23 Workshop participants.

Most hematological neoplasms associated with 11q23 chromosomal rearrangement have been cases of acute lymphoblastic or acute myeloid leukemia. Although cases of myelodysplastic syndrome (MDS) are a minority, these syndromes should also be recognized as part of the spectrum of hematological disorders associated with 11q23 rearrangement. In this series of 550 patients with such rearrangement there were 28 (5.1%) who presented with MDS. A further five patients had a history of MDS but had evolved to AML by the time cytogenetic analysis was first undertaken. There were thus a total of 33 patients (6.0%) with an 11q23 abnormality whose initial presentation was as MDS. Of these 33 patients, a quarter (seven patients) were cases of secondary (therapy-related) MDS. Complex karyotypes and other poor prognosis chromosomal abnormalities such as -7 and 7q- were common and were not confined to secondary cases. The likelihood of presentation as MDS differed between different cytogenetic categories. The 28 patients in whom cytogenetic analysis was performed at presentation as MDS showed a wide age distribution, from 1 to 82 years; there were four children, two of 1 year of age. All FAB types of MDS were represented. Median survival was only 19.1 months. Leukemic transformation occurred in five patients including one case of transformation to a biphenotypic M5a/T-lineage acute leukemia.

Adolescent↗
PubMed1998

Secondary acute leukemia and myelodysplastic syndrome with 11q23 abnormalities. EU Concerted Action 11q23 Workshop.

Forty of the 550 patients (7%) entered to the 11q23 Workshop had secondary (s) acute lymphoblastic leukemia (nine cases), s-acute myeloid leukemia (25 cases, predominantly of FAB type M5), s-acute leukemia unspecified (one case) or s-myelodysplastic syndrome (five cases) following treatment for a primary malignancy. Breast cancer (12 cases) and non-Hodgkin's lymphoma (eight cases) were the most frequent primaries. Twenty-three patients had been treated with either an epipodophyllotoxin (seven patients) or an anthracycline (10 cases) or both (four cases) frequently combined with alkylating agents (12 cases) and with radiotherapy (six cases). Two further patients had alkylating agents and two had radiotherapy alone. Time between diagnosis of the primary and secondary malignancy was between 10 months and 22 years (median 24 months). The incidence of secondary malignancies in 11q23 subgroups was: t(11;19)(q23;p13.1) (33%), t(9;11) (8%), t(4;11) (5.5%), t(10;11)(5%), t (6;11) (3%), del11q23(2%) and 10 patients had a rare 'other' abnormality. No associations were seen between type of prior malignancy and 11q23 subgroup, or between prior malignancy and leukemia subtype. Remission, when achieved (32 patients), was short (median 5 months). Two patients survived following a bone marrow transplant for s-leukemia and s-myelodysplastic syndrome.

Acute Disease↗
PubMed1998

Trisomy 13 and myeloid malignancy--characteristic blast cell morphology: a United Kingdom Cancer Cytogenetics Group survey.

We retrospectively report data on 28 patients with haematological malignancy and trisomy 13 (25 cases) or tetrasomy 13 (three cases) as the primary acquired cytogenetic change. Peripheral blood and/or bone marrow morphology was reviewed in 25/28 cases and the final diagnosis was as follows: AML M0 (11), AML M1 (6), AML M2 (2), AML M4 (2), AML M5b (1), AML M6 (1), RAEB-t (3), RAEB (1), RA (1). All three cases with tetrasomy 13 had AML M0. Characteristic small hand-mirror blasts with cytoplasmic blebs and tails and scanty small granules were seen in 13/25 cases and 18/25 cases had small blasts which could easily be mistaken for lymphoblasts. Trilineage dysplasia was present in 8/28 cases. Median patient survival was 3 months. We conclude that trisomy 13 is particularly associated with acute myeloid leukaemia with minimal differentiation (AML MO), often has distinctive morphological features, and has a poor prognosis.

Acute Disease↗
PubMed1998

Loss of singing ability caused by vincristine.

Two patients who received vincristine therapy for lymphoma suffered marked impairment of ability to sing as a consequence of neurotoxicity. Slow recovery occurred on drug withdrawal.

Aged↗
PubMed1998

A survey of current United Kingdom practice for antenatal screening for inherited disorders of globin chain synthesis. UK Forum for Haemoglobin Disorders.

AIMS: To document current United Kingdom practice for antenatal screening for inherited disorders of globin chain synthesis and to compare such practice with guidelines published by the British Committee for Standards in Haematology and the Standing Committee on Sickle Cell, Thalassaemia and other Haemoglobinopathies (SMAC). METHODS: The members of the UK Forum on Haemoglobin Disorders were surveyed about their current practice for antenatal haemoglobinopathy screening. The UK Forum is a national group of haematologists, paediatricians, laboratory scientists, and counsellors working in the field of diagnosis and management of disorders of haemoglobin synthesis; such disorders including the alpha and beta thalassaemias, sickle cell disease, and other haemoglobinopathies. RESULTS: Completed questionnaires from 38 hospitals (or cooperating groups of hospitals) were analysed. The great majority of hospitals were applying appropriate laboratory methods, but problems were commonly encountered in ensuring that appropriate testing of antenatal patients and, when necessary, of their partners, was carried out early in pregnancy. When screening was selective there was quite often a failure to identify all women in whom testing was indicated, and cut off points used as an indication for further testing were sometimes inappropriate. CONCLUSIONS: Many practical problems are still encountered in following guidelines for the antenatal diagnosis of haemoglobinopathies. A need for improved administrative procedures and increased funding was identified. In addition there is a need for agreed guidelines giving more specific advice on technical aspects of laboratory practice.

Female↗