Canadian university students' perceptions of COVID-19 severity, susceptibility, and health behaviours during the early pandemic period.

OBJECTIVES: We surveyed university students to assess their demographic factors, perceived severity, personal susceptibility, and the adoption of health behaviours in relation to COVID-19. STUDY DESIGN: Ethics approval was obtained from the University of Toronto's Research Ethics Board (#39169). Responses were collected between March 20 and April 17, 2020, capturing the first month of government-mandated social distancing in Ontario, Canada. METHODS: We distributed the online survey to the University of Toronto student population, yielding a total convenience sample of 592 participants. We summarised the results and conducted Mann-Whitney U and Kruskal-Wallis tests to explore relationships between demographic data and perceived severity of COVID-19. Pearson's Chi-square tests were used to explore the relationship between demographic variables and perceived susceptibility, with phi being used to explore the strength of the association. A value of p â€‹< â€‹0.05 was used to determine significance. RESULTS: The majority of participants (60.1%) judged COVID-19 to be Very Severe; there was a significant relationship between being female and the adoption of new health behaviours. 57.4% indicated they felt susceptible to COVID-19, while 40.9% did not. Feeling susceptible was associated with studying a healthcare field or being personally affected by COVID-19. Individuals who stated they were not susceptible to COVID-19 declared mitigating factors such as new health behaviours to be a major driver in their perception. CONCLUSION: University students believe COVID-19 is a severe disease and have adopted new and increased health behaviours to mitigate the spread. While this study demonstrates differing health behaviour adoption rates based upon demographic factors, overall this research finds young adults supportive and accepting of government policy as a protective and susceptibility-mitigating measure.

Abnormal function of B lymphocytes from peripheral blood of multiple myeloma patients. Lack of correlation between the number of cells potentially able to secrete immunoglobulin M and serum immunoglobulin M levels.

Multiple myeloma patients are deficient in normal polyclonal serum immunoglobulins. To determine the reasons for this decrease, we quantitated and compared the number of surface IgM+ B lymphocytes, and the number of B cells susceptible to transformation by Epstein-Barr virus (EBV) with the concentration of IgM in serum. Serum IgM levels varied considerably in individual patients, temporally shifting from undetectable to normal amounts and then dropping again to undetectable levels. A transient rise to normal serum IgM concentrations was seen in 42% of patients assessed at two or more time points. Of 44 patients, 52% showed a lack of correlation between the number of surface IgM+ (sIgM+) B cells and serum IgM concentration. One subset of patients (25%) had detectable to normal numbers of sIgM+ B cells in blood but undetectable levels of serum IgM. Transformation of B cells from these patients indicated a block in IgM secretion that was extrinsic to the B cells that were fully able to transcribe, translate, and secrete IgM after EBV transformation. A second subset of patients (27%) had undetectable numbers of sIgM+ B cells but near normal levels of serum IgM, suggesting abundant secretion by few clones of B cells. Of 18 patients with monoclonal gammopathy of undetermined significance (MGUS), 26% showed a lack of correlation between the numbers of sIgM+ B cells and serum IgM concentration. We suggest that in patients with multiple myeloma, and in some with MGUS, there exists a mechanism(s) extrinsic to the B cell that mediates an arrest in terminal B lymphocyte maturation.

Severe deficiency of B lymphocytes in peripheral blood from multiple myeloma patients.

A major problem in the assessment of circulating B lymphocytes in multiple myeloma is the extent to which cells with passively absorbed Ig contribute to the assay. We have analyzed peripheral blood B cell numbers in 51 patients in various treatment categories by using an assay that is not subject to artifacts involving cytophilic Ig. We have defined a B lymphocyte by three different criteria (a) expression of a high surface density of Ig (b) expression of a high density of HLA.DR and (c) expression of a marker exclusive to surface Ig+ B cells. By these criteria, normal individuals have an average of 6% B cells. In multiple myeloma patients, B cell levels in purified mononuclear cell preparations are severely reduced. Untreated patients and the majority of patients on intermittent chemotherapy have 20-600-fold fewer B cells than do normal donors (average = 0.3%). This decrease was even greater in whole blood of patients as compared with normal donors (100-1,000-fold fewer B cells). The number of B cells did not correlate with disease status or paraprotein concentration. We found no evidence to support the idea that B lymphocytes in patients include a substantial monoclonal subset.

Adhesion of multiple myeloma peripheral blood B cells to bone marrow fibroblasts: a requirement for CD44 and alpha4beta7.

We have earlier described the presence of phenotypically unusual monoclonal B cells within the peripheral blood of multiple myeloma (MM) patients. To determine the biological properties of these B cells as compared to B cells from normal donors, we investigated the potential of CD19+ MM blood B cells to adhere to endothelial cell and bone marrow (BM)-fibroblast monolayers. We find that 30-60% of freshly isolated CD19+ MM blood B cells adhere to endothelial cell monolayers, and 50-80% adhere to BM fibroblast monolayers. The adhesion of MM blood B cells to either monolayer was not increased by in vitro activation, suggesting that these cells were activated in vivo. In contrast, fewer than 10% of CD19+ B cells from peripheral blood of normal donors adhered. Function-blocking monoclonal antibodies (mAbs) were used to determine which adhesion receptors were involved in CD19+ MM blood B cell interaction with BM fibroblasts. mAbs against very late antigen 4, the beta7-integrin subunit, and CD44, but not mAbs against very late antigen 5 and beta1, inhibited adhesion 61, 50, and 30%, respectively. The lack of inhibition with mAbs against beta1 implicates alpha4beta7 but not alpha4beta1 in adhesion of CD19+ MM blood B cells. To determine the alpha4beta7 ligand that mediated MM blood B cell adhesion, mAbs against vascular cellular adhesion molecule 1 and fibronectin, as well as CS1 and RGD peptides, were used as inhibitors. These were unable to reduce the adhesion of CD19+ MM blood B cells to BM fibroblasts, suggesting that fibronectin and vascular cellular adhesion molecule 1 are not involved in adhesion. Also, adhesion of MM blood B cells to mucosal addressin cell adhesion molecule 1-transfected Chinese hamster ovary cells was not enhanced compared to control-transfected Chinese hamster ovary cells, suggesting that mucosal addressin cell adhesion molecule 1 was not promoting adhesion of these cells. These data implicate CD44:HA interactions, as well as alpha4beta7 and an as yet unidentified ligand in the adhesion of in vivo activated MM blood B cell adhesion to BM fibroblasts. The adhesion properties of MM CD19+ B cells distinguishes them from normal B cells. Although the malignant status of these cells is as yet undefined, their adhesion properties implicate MM blood B cells in migratory spread of the disease.

In multiple myeloma, circulating hyperdiploid B cells have clonotypic immunoglobulin heavy chain rearrangements and may mediate spread of disease.

DNA aneuploidy characterizes a proportion of malignant bone marrow (BM)-localized plasma cells in multiple myeloma (MM). This analysis shows that for most MM patients, circulating clonotypic B cells in MM are also hyperdiploid. Although all normal B cells and some malignant B cells are diploid, hyperdiploidy is likely to be exclusive to those that are malignant. Hyperdiploid MM B cells express CD34 and have clonotypic IgH transcripts, confirming them as part of the malignant clone. For MM, 92% (70/76) of patients had a DNA hyperdiploid subset [5-30% of peripheral blood mononuclear cells (PBMCs)] of CD19+ B cells. All CD19+ PBMCs in MM expressed CD19 and IgH variable diversity joining (VDJ) transcripts, confirming them as B cells. DNA aneuploid cells were undetectable in T or B lymphocytes from normal blood, spleen or thymus, or in blood from patients with B chronic lymphocytic leukemia. In MM, untreated patients had the highest DNA index (1.12). DNA hyperdiploid PBMCs were most frequent among untreated patients and were significantly reduced after chemotherapy. Diploid B cells were significantly more frequent after chemotherapy than at diagnosis. Of the hyperdiploid PBMCs, 81 +/- 3% expressed CD34 and CD19. In contrast to circulating CD34+ B cells, CD34- B cells in MM are diploid. In MM, unlike hyperdiploid PBMC B cells, hyperdiploid BM plasma cells lack both CD34 and CD19, suggesting that loss of CD34 correlates with differentiation and BM anchoring. In situ reverse transcription-PCR of the CD34+ (hyperdiploid) and CD34- (diploid) PBMC B-cell subsets was performed using patient-specific primers to amplify clonotypic IgH VDJ transcripts. Confirming previous work, CD34+ hyperdiploid MM PBMCs were clonotypic (86 +/- 5%). In contrast, CD34- diploid MM PBMCs had few monoclonal cells (4.8 +/- 2%). The lack of hyperdiploidy, together with the relative absence of cells having clonotypic transcripts, suggests these polyclonal CD34- B cells are normal. After culture in colchicine to arrest mitosis, hyperdiploid B cells were reduced and MM B cells accumulated in a diploid G2-M, suggesting that hyperdiploid in MM may represent a transient S-phase arrest rather than an aneuploid G0 phase. The DNA hyperdiploidy of CD34+ clonotypic B cells suggests these cells may be clinically important constituents of the myeloma clone and that they may play a direct role in the spread of myeloma.

Lithium carbonate therapy in severe Felty's syndrome. Benefits, toxicity, and granulocyte function.

Lithium carbonate was administered to six patients with severe Felty's syndrome, five of whom had problems with infection. Two patients had granulocyte increments that persisted after therapy was discontinued; in one of them problems with infections resolved. In another patient a transient granulocyte rise accompanied treatment. There was no response in three patients. Granulocyte function was measured in three patients during treatment. It was normal except for subnormal hexose monophosphate shunt activity in two patients. Although serum lithium levels were less than 1.5 mmole/L, serious toxic effect occurred in one patient and significant side effects in the other five. These results support a short trial of lithium carbonate therapy in patients with severe symptomatic Felty's syndrome. Potentially beneficial granulocyte increases occur in a minority of patients only, however, and side effects and toxic effects are common.

Diagnostic leg scanning for deep venous thrombosis in the recently heparinized patient.

Leg scanning with fibrinogen I 125, either alone on in combination with other procedures, has been proposed as an alternative to venography for diagnosis of deep venous thrombi. Clinical circumstances may necessitate anticoagulation before scanning can be performed, which could alter its reliability. We have compared the results of scanning with venographic findings in heparinized patients with venous thromboembolism. Different criteria for an abnormal leg scan gave different sensitivities and specificities. During the first four days of scanning with a requirement for a persistently abnormal result, five of eight criteria had high specificity (greater than 92%). However, sensitivities did not exceed 55%. With the use of transiently abnormal results and six days of scanning, higher sensitivities were obtained but specificities were reduced. No criterion gave results considered acceptable for a diagnostic test for deep venous thrombosis. Leg scanning should therefore not be used for this purpose in patients who have received anticoagulants. Our results also suggest that duration of symptoms has little effect on the sensitivity of leg scanning and that the test is more reliable for establishing the presence of thrombus than at defining its location.

Low-molecular-weight heparin prophylaxis using dalteparin in close proximity to surgery vs warfarin in hip arthroplasty patients: a double-blind, randomized comparison. The North American Fragmin Trial Investigators.

BACKGROUND: Based on the current understanding that venous thrombosis starts perioperatively, administration of just-in-time low-molecular-weight heparin immediately before or in close proximity after hip arthroplasty may be more effective than usual clinical practice. METHODS: We performed a randomized, double-blind trial comparing subcutaneous dalteparin sodium given once daily immediately before or early after surgery with the use of postoperative warfarin sodium in 1472 patients undergoing elective hip arthroplasties. The primary end point was deep vein thrombosis detected using contrast venography performed after surgery (mean, 5. 7 days) in each group. RESULTS: The frequencies of deep vein thrombosis for patients with interpretable venograms receiving preoperative and postoperative dalteparin for all deep vein thrombosis were 36 (10.7%) of 337 (P<.001) and 44 (13.1%) of 336 (P<.001), respectively, vs 81 (24.0%) of 338 for warfarin; for proximal deep vein thrombosis, 3 (0.8%) of 354 (P =.04) and 3 (0.8%) of 358 (P =.03), respectively, vs 11 (3.0%) of 363. Relative risk reductions for the dalteparin groups ranged from 45% to 72%. Symptomatic thrombi were less frequent in the preoperative dalteparin group (5/337 patients [1.5%]) vs the warfarin group (15/338 patients [4.4%]) (P =.02). Serious bleeding was similar among groups. Increased major bleeding at the surgical site was observed for patients receiving preoperative dalteparin vs warfarin (P =.01). CONCLUSIONS: A modified dalteparin regimen in close proximity to surgery resulted in substantive risk reductions for all and proximal deep vein thrombosis, compared with warfarin therapy. Such findings have not been observed with low-molecular-weight heparin therapy commenced 12 hours preoperatively or 12 to 24 hours postoperatively vs oral anticoagulants. Increased major but not serious bleeding occurred in patients receiving preoperative dalteparin. Dalteparin therapy initiated postoperatively provided superior efficacy vs warfarin without significantly increased overt bleeding.

Low-molecular-weight heparin prophylaxis using dalteparin extended out-of-hospital vs in-hospital warfarin/out-of-hospital placebo in hip arthroplasty patients: a double-blind, randomized comparison. North American Fragmin Trial Investigators.

BACKGROUND: No randomized trials have directly evaluated the need for extended out-of-hospital thromboprophylaxis for patients who have hip arthroplasty in the United States or Canada. The uncertainty as to the need for extended prophylaxis in North American patients is complicated by early hospital discharge, resulting in a short thromboprophylaxis interval. METHODS: To resolve this uncertainty, we performed a randomized double-blind trial in 569 patients who underwent hip arthroplasty comparing the use of dalteparin sodium started immediately before surgery or early after surgery and extended out-of-hospital to an overall interval of 35 days with the use of warfarin sodium in-hospital and placebo out-of-hospital. RESULTS: For patients with interpretable venograms in the preoperative, postoperative, and combined dalteparin groups, new proximal vein thrombosis out-of-hospital was observed in 1.3%, 0. 7% (P =.04), and 1.0% (P =.02) of patients, respectively, compared with 4.8% in the in-hospital warfarin/out-of-hospital placebo group. The respective overall cumulative frequencies of all deep vein thrombosis were 30 (17.2%) of 174 patients (P<.001), 38 (22.2%) of 171 (P =.003), and 68 (19.7%) of 345 (P<.001) in the dalteparin groups compared with 69 (36.7%) of 188 for the in-hospital warfarin/out-of-hospital placebo group. For proximal deep vein thrombosis, the respective frequencies were 5 (3.1%) of 162 (P =.02), 3 (2.0%) of 151 (P =.007), and 8 (2.6%) of 313 (P =.002) compared with 14 (9.2%) of 153. No major bleeding occurred during the extended prophylaxis interval. CONCLUSIONS: Extended dalteparin prophylaxis resulted in significantly lower frequencies of deep vein thrombosis compared with in-hospital warfarin therapy. Despite in-hospital thromboprophylaxis, patients having hip arthroplasty in the United States and Canada remain at moderate risk out-of-hospital. The number needed to treat provides a public health focus; only 24 to 28 patients require extended prophylaxis to prevent 1 new out-of-hospital proximal vein thrombosis. Recent studies demonstrate that asymptomatic deep vein thrombi cause the postphlebitic syndrome; thus, extended out-of-hospital prophylaxis will lessen the burden to both the patient and society.

Chronic consumptive coagulopathy due to intracardiac thrombus.

A patient with a consumptive coagulopathy of 11 months' duration that was due to a large left atrial mural thrombus is described. Bleeding occurred only with the hemostatic challenge of surgery. Heparin was used perioperatively to facilitate two surgical procedures. The coagulopathy was reversed by removal of the thrombus.

Effects of tsetse (Glossina morsitans morsitans Westw.) (Diptera: Glossinidae) salivary gland homogenate on coagulation and fibrinolysis.

The saliva of the tsetse, Glossina morsitans morsitans Westwood, has antithrombin anticoagulant activity and inhibits thrombin's esterolytic activity. It has no other detectable anticoagulant properties. The anticoagulant elutes in a single peak on Sephadex fraction, is immediately acting, heat and storage stable, and has a molecular weight of 11-13,000. Unlike heparin it is not neutralized by protamine sulphate or toluidine blue and does not require the co-factor, antithrombin III, for optimal anticoagulant activity. It has similar properties to hirudin, but does not elute with a protein peak upon Sephadex fractionation and has a slightly different molecular weight. Salivary gland homogenates contained neither a plasminogen activator nor fibrinolytic activity. The sera of rabbits used to maintain tsetses, which contained precipitating antibodies against saliva, did not neutralize the salivary anticoagulant in vitro. The properties of this anticoagulant suggest that it might be a potentially useful antithrombotic agent in man.

Drug resistance in multiple myeloma: novel therapeutic targets within the malignant clone.

Myeloma is incurable because the malignant stem cell is not eradicated by treatment. Thus, identification of the malignant hierarchy of B lineage cells in myeloma is required to identify potentially generative components and to evaluate their drug resistance properties. BM plasma cells are usually depleted by chemotherapy, but clonotypic B cells survive melphalan/prednisone as well as combination chemotherapy. In vitro, circulating and bone marrow-localized myeloma plasma cells show defective drug export, despite their phenotypic expression of P-glycoprotein, the mdr1 gene product. In contrast to plasma cells, circulating myeloma clonotypic B cells exhibit very efficient drug export. This suggests that circulating clonotypic MM B cells comprise a reservoir of drug resistant disease in myeloma although their stem cell potential remains to be confirmed. The malignant clone in each myeloma patient is defined by a unique IgH VDJ gene rearrangement. Using methods that exclude the possibility that a frequent but non-malignant clone has inadvertently been identified, and after confirming that the sequence identified is expressed by nearly all bone marrow plasma cells, we show that the drug resistant set of myeloma B cells is clonally related to the malignant plasma cells in myeloma. Clonotypic MM B cells survive chemotherapy, persist during clinically defined "minimal residual disease" and remain after autologous transplantation. Thus their malignant status is an important consideration. If malignant, they must be considered in the design of therapy. If non-malignant, they would be expected to have minimal impact on the disease process. A variety of evidence provides strong support for the view that clonotypic drug resistant B cells are malignant and may include the generative compartment of myeloma. The P-gp+ set of clonotypic B cells is extensively DNA aneuploid, an attribute of malignancy. All clonotypic B cells overexpress RHAMM, a novel oncogene involved in malignant spread. Finally, the population of clonotypic B cells lacks intraclonal heterogeneity. Since intraclonal heterogeneity is driven by the response to antigens, its absence in these cells indicates that they are no longer antigen-responsive. Since antigen-independent clonal expansion is characteristic of lymphoid malignancies, these observations provide further proof that clonotypic B cells in myeloma are malignant. Thus, the drug resistance of these cells is highly relevant to understanding why myeloma remains incurable despite the initial chemosensitivity of most bone marrow plasma cells.

Circulating clonotypic B cells in the biology of multiple myeloma: speculations on the origin of myeloma.

The population of circulating B cells in myeloma patients includes an apparently large but variable subset with the IgH VDJ rearrangement diagnostic for the malignant clone of plasma cells in individual myeloma patients. Although the biological significance is at present unknown, it is likely that they include both malignant and non-malignant clonal relatives of the myeloma plasma cells. This article presents speculations on the significance of these cells in the origin of myeloma and the relationship between monoclonal gammopathy of undetermined significance (MGUS) and frank myeloma. MGUS appears to represent the establishment of clonal dominance probably by a chronically antigen-stimulated B cell clone. It seems likely that malignant transformation event(s) occurring in a clonal daughter cell give rise to myeloma. If correct, this implies that in a myeloma patient, non-malignant antigen-responsive B cells expressing the patient-specific IgH rearrangement coexist in the circulation and probably all lymphoid tissues, with their malignant antigen-independent relatives. However, the significance one attributes to the clonotypic B cells detected in the blood of myeloma patients depends in part on the view one takes of the progression from MGUS to myeloma. An alternative perspective is that MGUS represents a dormant state of malignancy held in check by controlled apoptosis, arrested cell cycling, and/or by immunoregulatory networks. Although lacking in experimental support, if this interpretation were correct, myeloma would occur when the regulatory mechanisms fail, allowing uncontrolled malignant cell renewal. This alternative view would imply that the majority of circulating clonotypic B cells might be malignant. Thus, an analysis of the biology of these clonotypic circulating B cells, with an emphasis on measures of malignancy, is likely to shed considerable light on the events underlying myeloma genesis, progression and spread.

Es nucleoside transporter content of acute leukemia cells: role in cell sensitivity to cytarabine (araC).

Nucleoside analogs are important components of treatment regimens for acute leukemia in adults. Plasma membrane permeation of the nucleoside analog molecules, the initial event in the cellular conversion of nucleosides to active agents, is mediated by nucleoside-specific membrane transporters. The widely-expressed es nucleoside transporter accepts as substrates diverse nucleoside analogs, including cytarabine (araC), 2-chlorodeoxyadenosine, and fludarabine. The cellular content of es transporter sites has been measured in blasts from patients with acute lymphoblastic leukemia and acute myelogenous leukemia, by a sensitive, quantitative flow cytometry assay that employs the tightly-bound es ligand, SAENTA fluorescein. Values for es transporter expression varied ten-fold among samples from patients with acute myelogenous leukemia. In this article, we review current findings that document, in confocal fluorescence microscopy images and in flow cytometry assays of SAENTA fluorescein-stained cells, the patient-to-patient variance of es transporter expression in leukemic blasts from patients. Our data show a correlation between the expression of es transporters and the in vitro sensitivity to nucleoside drugs of blasts from acute leukemia patients. These findings show that the flow cytometry assay of es expression provides a facile means of predicting resistance of leukemia cells to the cytotoxicity of araC and other nucleosides.

The pregnant antithrombin III deficient patient: management without antithrombin III concentrate.

Pregnant patients with antithrombin III (AT III) deficiency have an unacceptably high risk of venous thromboembolism (VTE). Antithrombotic therapy is therefore recommended. The reported clinical experience of such prophylaxis is limited. Some authors have recommended the use of AT III concentrate in addition to heparin in the management of these patients. We report successful management with heparin alone during pregnancy and the postpartum period in two patients with AT III deficiency. Both patients had experienced VTE during a prior pregnancy; one also experienced VTE during the reported pregnancy. Both patients were therefore at particularly high risk of further VTE. Based on the good results in these two patients, and a review of previously reported cases, we propose that heparin alone, in a dose to maintain the APTT in a therapeutic range, provides adequate prophylaxis and treatment for VTE during pregnancy and delivery in many AT III deficient subjects.

Warfarin monitoring in patients with anticardiolipin antibodies, but without lupus anticoagulants.

Misleading international normalized ratios (INR) may be obtained from anticoagulated patients with lupus anticoagulants (LA). As a result, special precautions have been suggested for oral anticoagulant dosing. It is possible that plasma from subjects with an anticardiolipin antibody (ACA) without an LA could also affect the INR. We have studied nine such subjects who were anticoagulated and compared them with 11subjects who had neither antibody. The INR was performed, using local specific ISIs, with 11 different thromboplastins. No substantial difference was seen between the ACA-positive and ACA-negative patients, for either individual thromboplastins or patients. We similarly measured INRs in eight nonanticoagulated patients with ACAs. No effect on the INR results was observed. Thus, in these anticoagulated and nonanticoagulated patients we detected no evidence of any effect of an ACA on the INR.

Transcoronary platelet activation and consumption in coronary artery disease: studies at rest.

The platelet count(PC), plasma platelet factor 4 (PF4) and plasma beta-thromboglobulin(beta TG) have been measured in blood obtained from a peripheral vein, the aortic root and the coronary sinus in 7 patients with normal coronary arteries, 9 patients with lesser degrees of coronary artery disease(CAD) and in 13 patients with severe CAD under resting conditions. In each patient group values obtained in the peripheral venous blood were similar to those obtained in normal subjects. In each group values obtained in blood from the coronary sinus were similar to those obtained in blood from the coronary aortic root and in most instances these were similar to values obtained in peripheral venous blood. for example, in the 13 subjects with hemodynamically significant 3-vessel or 2-vessel CAD the mean values in blood from a peripheral vein, the aorta and the coronary sinus respectively were: PC-194, 205, and 208 x 10(9)/1; PF4-3.3, 3.7, and 3.5 ng/ml; and beta TG-15.5, 23.0 and 18.6 ng/ml. These findings provide no support for the occurrence of continuous platelet activation or platelet consumption in the coronary vessels or elsewhere in patients with stable CAD, under resting conditions, regardless of its severity.

Platelet activation caused by cardiac catheter blood collection, and its prevention.

The study of platelet changes occurring across the coronary circulation is important in the investigation of the platelet's role in ischemic heart disease. It requires blood sampling through cardiac catheters. This could activate platelets and alter the results of tests of platelet activation and reactivity. This study was designed to examine this problem and to devise satisfactory methods for obtaining blood for platelet studies through long catheters. Blood collected through catheters introduced with a guide-wire had a much higher plasma heparin neutralising activity (HNA), platelet factor 4(PF4) and beta-thromboglobulin (beta TG) than peripheral venous blood, and lower platelet count(PC). Blood collected through catheters introduced via a sheath, and kept filled with anticoagulant/antiplatelet solution until blood sampling, gave results similar to peripheral venous blood for the PC, platelet aggregate ratio, platelet fluorescent granule count, and for plasma HNA, PF4 and beta TG. It is concluded that platelets are activated during blood collection through cardiac catheters; however, with appropriate precautions, blood which is satisfactory for platelet studies can be obtained.

Plasma cell lesions of the thyroid: report of a case of solitary plasmacytoma and a review of the literature.

We report a case of a solitary plasmacytoma arising from a thyroid with longstanding Hashimoto's disease, and diagnosed by fine-needle aspiration cytology. Serum protein electrophoresis revealed an M-spike in the gamma-globulin region due to monoclonal IgG-lambda immunoglobulin. The thyroid tumor was treated with near-total thyroidectomy and irradiation, and the patient was well 6 years after surgery without evidence of multiple myeloma. The serum M-spike disappeared after the tumor resection and radiation therapy. Plasma cell lesions of the thyroid reported in the world literature are extensively reviewed. Solitary plasmacytomas occur most commonly in patients with Hashimoto's disease, and must be distinguished from plasma cell granulomas and involvement of the thyroid in multiple myeloma. Plasmacytomas should be considered in the differential diagnosis of a rapidly enlarging thyroid mass in a patient with known Hashimoto's disease.

Case report: successful treatment of an idiopathic acquired factor VIII inhibitor with unusual features.

A patient with an idiopathic acquired factor VIII inhibitor is described. Unusual features of this patient's illness were measurable factor VIII (4 to greater than 20%) despite the presence of inhibitor, and continued spontaneous bleeding despite these factor VIII levels. Successful treatment on both a short-term and a long-term basis--with neutralizing doses of human factor VIII concentrate and with chlorambucil, respectively--is reported. It is concluded that in patients with this type of inhibitor factor VIII, assays may not provide a reliable prediction of the potential for bleeding and that chlorambucil therapy warrants further study.