Blood transfusion in Canada: the early years.

In the early 20th Century most of the development of blood transfusion occurred in the United States. Transfusion activity in Canada dates from 1910, with evidence of its systematic use in both Toronto and Montreal prior to the First World War. Its use was quickly and widely accepted and exploited, particularly under the pressure of support for the management of war injuries. Within a decade transfusion was being used in the practice of surgery, pediatrics, internal medicine and obstetrics, both in University associated hospitals and in community and domiciliary practice, and indications for use developed.

Variation in blood collection rates in 18 countries.

BACKGROUND AND OBJECTIVES: In an attempt to determine how much scope there might be for blood conservation in Canada, the population based rate of blood collection was compared to that in other countries. MATERIALS AND METHOD: Blood collections and population size in 18 countries were obtained from national blood programs directly or by personal contact through on-line sources and national collection rates per million of population calculated. RESULTS: A greater than twofold difference in per capita collection rates was seen between the highest and lowest figure. CONCLUSION: By the wider application of evidence based best practices in blood transfusion and strategies to reduce wastage, there is likely scope for at least some jurisdictions to reduce collection rates.

Effect of a non-viral fraction of acquired immunodeficiency syndrome plasma on the vulnerability of lymphocytes to cortisol.

We have observed previously that the rate of cortisol catabolism by lymphocytes (CCL) was indicative of the vulnerability of these cells to cortisol. We attempted to ascertain whether cortisol-sensitive lymphocytes (e.g. thymocytes) metabolize cortisol at a different rate from cortisol-resistant cells and whether lymphocytes in which cortisol catabolism is inhibited become cortisol sensitive. The work was facilitated by the observation that an ethanol extract plasma from patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) had the capacity to inhibit CCL. The capacity of thymocytes to metabolize cortisol was found to be 11 times lower than that of peripheral lymphocytes. Inhibition of CCL with an ethanol extract of plasma from AIDS/ARC patients made the cells vulnerable to cortisol, causing them to die at a rate seven times greater than that of control samples. It is suggested that these findings may have important implications with regard to the nature of lymphocyte depletion in AIDS/ARC patients or in people at risk of developing the syndrome.

Hematopoietic cell surface markers on metastatic small cell carcinoma detected with monoclonal antibodies.

Using a panel of monoclonal antibodies, cells from lymph node biopsies have been examined in three patients with small cell carcinoma presenting with cervical lymphadenopathy. Two patients had small (oat) cell carcinoma of the lung; in the third patient, a primary tumor was not found. Two lymph node biopsies showed typical small (oat) cell carcinoma, and one was an intermediate cell variant; in the last, lung biopsy showed small (oat) cell carcinoma. Electron microscopy demonstrated desmosomes in all three tumors. In each case, lymph node cell suspensions were examined by indirect immunofluorescence with the use of a panel of monoclonal antibodies to antigens usually associated with lymphoid or myeloid cells. In two of the three cases malignant cells were positive with the lymphoid marker BA-2; in two cases malignant cells were positive with OK1a1, a marker for the Ia-like antigen (HLA-DR); and in one case malignant cells were positive with My-1. Caution is needed in the interpretation of cell surface marker studies in the differential diagnosis of small round cell tumors.

Myelodysplastic syndrome with prolonged reticulocyte survival mimicking hemolytic disease.

A patient with myelodysplastic syndrome (refractory anemia) with marked and persistent reticulocytosis is presented. A referring diagnosis of hemolytic disease had been made. However, the 51Cr red cell survival was normal (T1/2 24 days). Reticulocyte morphology, red cell creatine content, and in vitro reticulocyte survival studies have suggested that the reticulocytosis arose as a consequence of delayed maturation of the reticulocytes. Two patients with myelodysplastic syndrome and delayed reticulocyte maturation have previously been described; in both patients, however, red cell survival was also shortened. Anemia with reticulocytosis, mimicking hemolytic disease, may be an unusual presentation of myelodysplastic syndrome.

Sensitivity of routine blood bank methods for the detection of anti-D as determined during proficiency testing.

A proficiency testing program in immunohematology, involving over 240 laboratories, was used to assess the detection of anti-D in six concentrations ranging from 11 to 8,500 ng/mL. Using the indirect antiglobulin test, more than 98% of laboratories reporting detected anti-D at all concentrations. Enzyme and albumin antiglobulin methods as routinely practiced did not clearly increase sensitivity, and the direct agglutination methods used were much less sensitive than indirect antiglobulin methods. If proficiency testing truly reflects performance in practice in Ontario, Canada, the sensitivity of manual indirect antiglobulin methods in routine use for the detection of anti-D appears to meet reasonable expectations of these technics.

Proficiency testing in immunohematology in Ontario, Canada, 1975-1977.

Since April 1975 the proficiency of laboratories in Ontario that perform immunohematology tests has been assessed. While the majority of test samples have required only ABO and Rh(D) typing, others have posed problems. The error rate in uncomplicated ABO typing was 1.3/1,000 in 17,479 tests and that in straightforward Rh(D) grouping, 6.6/1,000 in 17,757 tests. False-negative (36/1,000) and false-positive (1.4/1,000) direct antiglobulin tests occurred. Errors in detection of strong alloantibodies (e.g., anti-D) were 19.7, 10.2 and 5.1/1,000 in three test samples. A2B or A2 cells with anti-A1 in serum were sent out in two surveys; error rates in ABO interpretation were 189 and 52/1,000, respectively. Laboratories also experienced difficulty in interpreting the Rh(D) type of cells with positive antiglobulin tests. These surveys have had several effects: (1) laboratories with poor performance have been identified, (2) patterns of practice have been influenced, (3) areas of ignorance have been identified, and (4) a stimulus has been provided for continuing education in immunohematology.

Lazy leucocyte syndrome--disorder of the granulocyte membrane?

An adult with long-standing neutropenia had the functional granulocyte abnormalities typical of the lazy leucocyte syndrome. Scanning electron microscopy of the patient's neutrophils showed alteration in the surface configuration of the cell with coarsening of the normal fine ruffles and the appearance of knob-like projections. Similar functional and anatomical changes were induced in normal neutrophils by treatment with vinblastine. The lazy leucocyte syndrome may be a consequence of altered membrane microfilamentous protein structure or function, and undue rigidity of the affected neutrophils may explain the clinicopathological features of the disease.

Idiopathic acquired sideroblastic anaemia transforming to acute myelosclerosis.

A case of idiopathic acquired sideroblastic anaemia transforming to acute myelofibrosis is reported. The appearance of atypical megakaryocytic proliferation in idiopathic acquired sideroblastic anaemia may presage the development of an acute myelofibrotic phase of this usually chronic disease.

Proficiency testing in immunohaematology in Ontario, Canada, and in the United Kingdom: a comparative study.

A comparative study of proficiency testing models in immunohaematology has been carried out between the United Kingdom National External Quality Assessment Scheme and the Laboratory Proficiency Testing Program of the Ontario Medical Association, using material supplied by both programmes to laboratories in the United Kingdom and Ontario. The results suggest that the general standard of performance in immunohaematology practice is similar in the two jurisdictions and that, where clear differences are seen, these reflect differences in technique or in educational emphasis.

An assessment of the Coulter counter model S.

An assessment of the Coulter model S automatic blood counter has been carried out. The standard deviations for the haemoglobin concentration, haematocrit, red cell count, and white cell count are, respectively, +/- 0.15 g/100 ml, +/- 0.45%, +/- 0.04 m/c mm, and +/- 0.47 thous/c mm. These results are clearly more accurate than careful manual estimates, performed for comparison on the same samples. Details of the comparisons are presented. A comparison is also made with routine daily estimations.;Carryover' from one sample to the next was found to be about 2%, and tests in the ranges likely to be found in practice showed good linearity for the haemoglobin estimation, haematocrit, red cell count, and white cell count. A brief account of instrument failures is given.The performance of the Coulter model S compares well with that of other automated equipment for which detailed evaluations are available.

Chronic myeloid leukemia with a Philadelphia chromosome involving a t(21;22).

A second example of chronic myeloid leukemia showing translocation of material from the long arm of chromosome #22 to the long arm of chromosome #21, ( 21q +:22q-), is reported. The patient presented with the typical clinico-pathologic features of the disease.

A new translocation in chronic myeloid leukemia--t(4;9;22)--resulting in a masked Philadelphia chromosome.

A patient with chronic myeloid leukemia is described in whom a novel complex translocation was found among chromosomes #4, #9, and #22, resulting in a "masked" Philadelphia chromosome. The breakpoint in chromosome #4 (band q21) is in the same region as the breakpoint seen in the t(4;11), which is associated with some forms of acute leukemia.

A lineage-specific t(1;14)(q21;q32) as an early event in development of B-cell clonal expansion.

We report a patient in whom a cell line of 47,XY,+X,t(1;14)(q21;q32) constitution was found in a lymph node excised from the neck. Histologic examination and immunophenotyping both in situ and by flow cytometry failed to confirm a diagnosis of B-cell lymphoma, but Southern analysis indicated the presence of B-cell clonal expansion. These observations support the concept that primary chromosomal abnormalities occur in clonal expansions in the very earliest stages of tumorigenesis.

Deletion of the long arm of chromosome 5 in essential thrombocythemia.

A 51-year-old woman with no history of prior chemotherapy or radiation therapy was diagnosed with essential thrombocythemia (ET) according to the diagnostic criteria established by the Polycythemia Vera Study Group (PVSG). Cytogenetic analysis of bone marrow metaphases revealed both normal female karyotype and a single clonal abnormality, 46,XX,del(5)(q22q35). While chromosomal abnormalities have been reported in ET, their incidence is very low, and no specific abnormality has been found. Many of the reported cases of ET with chromosomal aberrations, including 5q-, do not meet the diagnostic criteria proposed by the PVSG, and may represent one of the other myeloproliferative disorders or a myelodysplastic syndrome. Furthermore, it is important to distinguish the 5q- syndrome, which may present with thrombocytosis and megakaryocytic hyperplasia, from ET. Our patient appears to be the first example of untreated ET clearly meeting the PVSG criteria in which 5q- was the only clonal abnormality seen at diagnosis.

Essential thrombocythemia with the Philadelphia chromosome and BCR-ABL gene rearrangement. An entity distinct from chronic myeloid leukemia and Philadelphia chromosome-negative essential thrombocythemia.

A 64-year-old woman presented with a platelet count of 3,225 x 10(9)/L. Bone marrow morphology showed massive megakaryocytic hyperplasia; cytogenetic studies showed the presence of the Philadelphia chromosome (Ph). The presence of a rearrangement involving the major breakpoint cluster region (mbcr) on chromosome 22 was confirmed by Southern blotting techniques. A diagnosis of Ph positive essential thrombocythemia (ET) was made. Such cases constitute less than 5% of patients with ET and it has been proposed that they be considered examples of chronic myelogenous leukemia (CML) because of a shared propensity to progress to blast crisis. An argument is presented for retaining Ph positive ET as an entity separate from Ph negative ET and Ph positive CML.

"Jumping" translocations involving band 3q13.3 in a case of acute monocytic leukemia.

We report a case of acute monocytic leukemia (FAB-5a) with a very aggressive clinical course and multiple chromosomal abnormalities. There were several sublines, each with trisomy 8 and a translocation involving 3q13.3 as a common breakpoint region. This region is an uncommon site of chromosomal breakage in malignancies and has not hitherto been reported as a breakpoint site in "jumping" translocations.

Breakpoints Involved in Deletions of the Long Arm of Chromosome 5 in Myelodysplasia and Acute Non-Lymphoblastic Leukemia do not Correlate with the Morphological Diagnosis.

Recent suggestions of a correlation between the extent of acquired deletions of the long arm of chromosome 5 [del(5q)] in association with myelodysplastic syndromes and acute non-lymphoblastic leukemia, and the morphological features, prompted us to review 34 patients with these conditions and del(5q). We found no correlation between the morphological diagnosis with which the patient presented and the extent of the deletion of 5q. All cases showed involvement of band 5q31, in common with most previously reported series. The consistent involvement of 5q31 is in keeping with the concept that a single gene at band 5q31 may be involved in the pathogenesis of these myeloid clonal expansions and that the deletion of genes in the long arm of chromosome 5, known to be involved in hemopoietic growth regulation, is unlikely to be the principal determinant of the hematological disorder.