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Biomedical subjects

M C Poon

Publications and source records attributed to M C Poon.

At least 91 records · Page 5Linked to original sources
PubMed1986

Coagulation testing of Hickman catheter blood in patients with acute leukemia.

We quantified coagulation parameters in vitro using standard automated methods in 12 adult patients with acute leukemia who also had Hickman catheters (HC). Test results from simultaneously obtained HC blood and control peripheral venous blood (PB) samples were compared in the respective patients. Heparin solutions (100 U/mL, US Pharmacopoela) used to prevent the formation of clots within the HC appeared to cause, to a significant degree, spuriously elevated levels of fibrin degradation products (FDP), decreased levels of fibrinogen (FBG), and prolongations of the prothrombin time (PT) and activated partial thromboplastin time (PTT) in the first 10 mL of HC blood. The second 10 mL sample from the HC showed that FBG levels were comparable with those demonstrable in PB samples, as were levels of FDP in eight of 12 cases. Both PT and PTT times, however, remained significantly prolonged. An alternative maneuver for obtaining HC blood studied in four patients showed significant prolongation of PTT values in the second 10-mL sample despite levels of FDP, FBG, and PT similar to those in the PB. Because heparin contamination of HC blood can mimic the laboratory findings of disseminated intravascular coagulation or other coagulopathies in patients with acute leukemia, we suggest that only values obtained from PB be used for interpretation of coagulopathy in these patients.

Acute Disease↗
PubMed1985

Immune hemolytic anemia following administration of antithymocyte globulin.

Antithymocyte globulin is commonly used as a therapy for rejection of transplanted organs. Its use can be associated with many side effects. We report a significant hemolytic anemia following therapy with horse-derived antithymocyte globulin. Several commercial Coombs' sera failed to yield a positive Coombs' test with the patient's erythrocytes; however, we were able to detect horse immunoglobulin on the patient's cells as well as on control red cells incubated with this particular preparation of antithymocyte globulin.

Adolescent↗
PubMed1985

Pulmonary angiomatoid vascular changes in mitomycin C-associated hemolytic-uremic syndrome.

Angiomatoid vascular changes in lungs and pulmonary hemorrhage are described in a woman in whom mitomycin C-associated hemolytic-uremiclike syndrome developed. These changes represent part of the spectrum of vascular damage that may complicate mitomycin therapy. Patients receiving mitomycin C chemotherapy require careful monitoring for possible development of these complications.

Female↗
PubMed1985

Hepatitis B virus DNA is enriched in polymorphonuclear leukocytes.

DNA hybridization and cell separation techniques were used to determine which blood components contained hepatitis B viral DNA sequences. Free monomer-length hepatitis B virus was found in large amounts in the polymorphonuclear leukocyte cell fraction in two of five HBsAG-positive patients. In these two patients, viral DNA sequences were not detected in the plasma or platelet fraction, whereas the mononuclear cell DNA contained small amounts of a 7.2 kb size unintegrated hepatitis B genome. These studies indicate that the major reservoir of unit-length viral DNA in the asymptomatic hepatitis B carriers studied here was in the polymorphonuclear leukocyte fraction. The basis for the presence of the viral DNA within these cells is presently unknown, but may relate to viral replication within, or phagocytosis of virus by, these cells.

Carrier State↗
PubMed1984

Detection of hepatitis B virus DNA in mononuclear blood cells.

The Southern transfer hybridisation technique was used to test mononuclear blood cells for hepatitis B virus DNA. Viral DNA sequences were detected in mononuclear cells of 10 out of 16 patients with hepatitis B virus infection and in none of 21 normal controls. Blood contamination was excluded by the absence of hepatitis B virus DNA in the corresponding serum samples in all cases. Free monomeric hepatitis B virus DNA was found in three patients positive for hepatitis Be antigen (HBeAg) and one positive for anti-HBe, and integrated hepatitis B virus DNA was present in four patients positive for anti-HBe. In two other patients the small size of the samples did not allow a distinction between free and integrated viral DNA. The state of the virus in the mononuclear cells seemed to correlate with the HBeAg or anti-HBe state, as has been noted in the liver. These results indicate that hepatitis B virus may infect mononuclear blood cells, thereby expanding the tissue specificity of this agent beyond the liver, as has been reported for pancreatic, kidney, and skin tissue. They also suggest that hepatitis B virus infection of mononuclear cells might be related to immunological abnormalities observed in carriers of the virus.

Autoradiography↗
PubMed1984

A lymphoproliferative disorder of granular lymphocytes with a novel phenotype and suppressor function.

In this study we have identified and characterized an expanded granular lymphocyte population in a patient with anemia and granulocytopenia. Granular lymphocytes were identified through the presence of cytoplasmic azurophilic granules, the dispersed granular pattern of cytochemical staining for acid hydrolases, and the ultrastructural localization of acid phosphatase within the granules. The surface phenotype of the granular lymphocytes was E+, FcR-, Leu 4+, Leu 2+, D 12+ (Leu 15+), OKM1+, and Leu 7+. This phenotype has not been reported previously in patients with similar features. Functional studies on FACS-purified populations showed that the patient's granular lymphocytes responded poorly to T-cell mitogens and were inefficient in NK and ADCC assays but exerted a potent suppressor effect on both T-cell proliferation and B-cell differentiation. The phenotype and functions of the expanded granular lymphocyte population correspond to those of a subset of normal E rosette-forming granular lymphocytes.

Adult↗
PubMed1984

Translocation (9;11)(p21;q23) in a case of acute myeloblastic leukemia (AML-M2).

A patient with acute myeloblastic leukemia (AML-M2) and a balanced translocation, t(9;11)(p21;q23), is described. The translocation appears to be the same as that previously reported in some patients with acute monoblastic leukemia (AMoL-M5). This suggests that, although t(9;11)(p21;q23) frequently may be associated with AMoL, the translocation may not be specific for that disorder.

Bone Marrow↗
PubMed1984

Human T-cell leukemia virus in lymphocytes of two hemophiliacs with the acquired immunodeficiency syndrome.

Fresh and cultured peripheral blood cells from two patients with hemophilia A and the acquired immunodeficiency syndrome were examined for markers of infection with human T-cell leukemia virus (HTLV) type 1. Neither patient had antibody to membrane antigens of HTLV-infected cells at the time of culture. Electron microscopy of peripheral blood cells from Patient 1 and cultured cells from Patient 2 showed type C retrovirus-like particles. Examination of peripheral blood lymphocytes showed other smaller virus-like particles in circulating mononuclear cells from both patients. Indirect immunofluorescence of peripheral mononuclear cells from both patients and of cultured cells from Patient 2 showed staining with antibodies to purified HTLV and to HTLV core proteins p24 and p19.

Acquired Immunodeficiency Syndrome↗
PubMed1984

A unique precipitating autoantibody against plasma thromboplastin antecedent associated with multiple apparent plasma clotting factor deficiencies in a patient with systemic lupus erythematosus.

A 42-yr-old woman with systemic lupus erythematosus without bleeding diathesis developed a prolonged activated partial thromboplastin time that was not corrected by normal plasma. An inhibitor that acted rapidly and inactivated 0.5 U/ml plasma thromboplastin antecedent (PTA, factor XI) at a 1:200 plasma dilution was demonstrated. In addition to a low titer of PTA (less than 0.01 U/ml), plasma assayed at 20-fold dilution also showed low titers of Hageman (factor XII, 0.02 U/ml), Fletcher (plasma prekallikrein, 0.02 U/ml), and Fitzgerald (high molecular weight kininogen, less than 0.01 U/ml) factors. The titer of these factors, except PTA, returned to normal upon further plasma dilution or upon removal of the inhibitor by protein A adsorption. Thus, the inhibitor appeared to interfere with these clotting factor assays, possibly by inactivating PTA in the substrate plasmas in the test system. Its specificity was further confirmed. The inhibitor did not interfere with surface-induced proteolytic cleavage of Hageman factor. Surface-induced generation of plasma kallikrein activity (amidolysis of H-D-pro-phe-arg-pNa and cold-promoted factor VII activity enhancement) requires only Hageman, Fletcher, and Fitzgerald factors and was normal. Reactions requiring all 4 contact phase factors, including PTA, such as surface-induced generation of plasmin activity (amidolysis of H-D-val-leu-lys-pNa) and activated Christmas factor (factor IXa) activity, were defective. Furthermore, the inhibitor bound to agarose-protein A inactivated and removed PTA selectively from normal plasma. The inhibitor was an IgG-lambda autoantibody that precipitated PTA. The inactivated activated PTA (factor XIa) without the requirement for an additional cofactor. Furthermore, it inhibited surface-induced activation of PTA by interfering with its proteolytic cleavage upon glass surface exposure and with its binding onto the reactive surfaces.

Adult↗
PubMed1983

Platelet function abnormalities in response to arachidonic acid in the acute phase of myocardial infarction.

The aggregation of platelets to arachidonic acid was studied serially in patients admitted to the hospital with suspected acute myocardial infarction (MI) and no history of platelet-altering drug ingestion. Of 17 patients studied within the first 48 hours after MI, 16 had a marked decrease in aggregation, to 0.5 mM arachidonic acid (15 +/- 12% compared with 64 +/- 15% for control subjects, p less than 0.01). The exception was a patient with documented coronary artery spasm who was receiving nifedipine at the time of MI. He had a delayed but normal final percent aggregation. The aggregation response returned to normal at 2 to 4 days and was slightly above normal at 6 to 10 days (change not statistically significant). Thromboxane B2 formation correlated with the response of patients' platelets to arachidonic acid (38 +/- 15 ng in the low responders versus 161 +/- 30 ng/3 X 10(8) platelets/4 min in the normal responders, p less than 0.05). Low responding platelets after washing had normal adenosine diphosphate and adenosine triphosphate contents and aggregated and formed thromboxane B2 normally with arachidonic acid. The plasma of patients with MI was found to inhibit platelet aggregation and thromboxane B2 formation to arachidonic acid.

Adenosine Diphosphate↗
PubMed1983

Antibodies to human T-cell leukemia virus membrane antigens (HTLV-MA) in hemophiliacs.

Along with homosexual men, Haitians, and intravenous drug abusers, hemophiliacs are at high risk of contracting acquired immunodeficiency syndrome (AIDS). An earlier study revealed that 36 percent of a group of the AIDS patients had antibodies to cell membrane antigens associated with the human T-cell leukemia virus (HTLV-MA), whereas only 1.2 percent of matched asymptomatic homosexual controls had these antibodies. In the present experiments, serum samples from 172 asymptomatic hemophiliacs were examined for the presence of antibodies to HTLV-MA. Such antibodies were detected in 5 to 19 percent of the hemophiliacs examined from four geographical locations, but in only 1 percent or less of laboratory workers, normal blood donors, donors on hemodialysis, or donors with chronic active hepatitis.

Antibodies, Viral↗
PubMed1983

Acid-labile alpha interferon. A possible preclinical marker for the acquired immunodeficiency syndrome in hemophilia.

Many homosexual men with the acquired immunodeficiency syndrome (AIDS) have an unusual acid-labile form of human leukocyte, or alpha, interferon in their serum. Male patients with classic hemophilia treated with lyophilized clotting-factor concentrates are also at high risk for the development of AIDS. To determine whether the level of alpha interferon may be a preclinical marker of early subclinical disease, we examined stored plasma and serum from three hemophilic patients with AIDS. Persistently elevated levels of the acid-labile form of alpha interferon were found in all three patients. In two patients the appearance of circulating alpha interferon preceded the onset of clinical disease by 3 to 10 months. In contrast, alpha-interferon levels were not elevated in 43 of 46 unselected patients with hemophilia; three of these patients had transient elevations. These results suggest that acid-labile alpha interferon may be a marker that can be used to identify affected asymptomatic members of high-risk groups before the onset of clinical disease.

Acids↗
PubMed1983

Febrile transfusion reaction following initial transfusion in a man with immunoblastic lymphadenopathy and granulocyte autoantibodies.

A 69-year-old man with immunoblastic lymphadenopathy and autoimmune hemolytic anemia who had no previous exposure to blood products developed a severe febrile nonhemolytic transfusion reaction following the initial infusion of packed red blood cells. The reaction recurred with transfusion of packed red blood cells, but not when freeze-thawed red blood cells were used. Immunofluorescence techniques demonstrated granulocyte antibodies in his serum and on the surface of his granulocytes. Circulating immune complex, HLA, and platelet antibodies were not present. The granulocyte antibodies fluctuated in titers with disease activities, and could be completely removed from the serum by autologous granulocyte absorption. We conclude that our patient had granulocyte autoantibodies which probably produced febrile transfusion reactions.

Aged↗
PubMed1983

Immunologic studies in asymptomatic hemophilia patients. Relationship to acquired immune deficiency syndrome (AIDS).

Asymptomatic hemophilia patients receiving Factor VIII concentrate were found to have normal natural killer (NK) cells and B cells, and an inverted T helper/suppressor ratio due to an increase in cells of T suppressor phenotype. In contrast, a hemophilia patient with acquired immune deficiency syndrome (AIDS) exhibited nonfunctional NK cells, low B cells, and an inverted T helper/suppressor ratio due to very low numbers of T helper cells. Hemophilia patients on cryoprecipitate therapy exhibited normal immune parameters. A high percentage of hemophilia patients on both treatments had antibody to hepatitis B virus. The isolated finding of elevated levels of T suppressor cells in hemophilia patients receiving Factor VIII concentrate has not been recognized as an early indicator of impending AIDS, and longitudinal studies will be required to determine its clinical significance.

Acquired Immunodeficiency Syndrome↗
PubMed1983

Structure-activity relationships of heparin. Independence of heparin charge density and antithrombin-binding domains in thrombin inhibition by antithrombin and heparin cofactor II.

To better understand how heparin structure affects its activity the relationships between the functional domains for inhibitor binding and charge density were investigated to determine how these domains affect heparin-mediated thrombin inhibition by two different heparin-dependent protease inhibitors, antithrombin (AT) and heparin cofactor II (HC II). A series of heparins, fractionated systematically by charge density, was further fractionated on antithrombin agarose to isolate more homogeneous subfractions that were either inactive or highly active with respect to thrombin inhibition by AT. With AT, the activities of the AT-active subfractions increased sharply with heparin charge density, while those with little or no affinity for AT were virtually inactive. In contrast, with HC II inhibitor, the activities of the heparins depended only upon their charge densities and were independent of AT affinity. At any given charge density, the heparin before fractionation by AT affinity and the fractions that were highly active and inactive with AT were all equally active with HC II. The two inhibitors also differed in their reactivity with heparan sulfate and dermatan sulfate. A charge-density effect with the subfractions having similar high affinity for AT demonstrates that charge density represents a heparin functional domain that is independent of the AT-binding domain. The behavior of the AT-inactive heparins, being fully active with HC II, demonstrates the functional domain necessary for AT binding is not needed to produce HC II activity.

Animals↗
PubMed1983

Acquired immunodeficiency syndrome with Pneumocystis carinii pneumonia and Mycobacterium avium-intracellulare infection in a previously healthy patient with classic hemophilia. Clinical, immunologic, and virologic findings.

A previously healthy patient with classic hemophilia who was on a home infusion program with factor VIII concentrates developed an acquired immunodeficiency syndrome manifested by a dramatic weight loss (47 kg over 12 months), lassitude, transient thrombocytopenia, and opportunistic infections with Varicella zoster, Pneumocystis carinii, and Mycobacterium avium-intracellulare. The patient was not homosexual and had no history of intravenous drug abuse. Immunologic studies showed a persistent lymphopenia with reversal of helper/suppressor-cytotoxic T-lymphocyte ratios, depression of human natural killer cell function, and in-vitro lymphocyte proliferative responses to mitogens and viral antigens. Serum IgA levels were also elevated. Serum antibodies against cytomegalovirus, herpes simplex viruses 1 and 2, Epstein-Barr virus, Varicella zoster, and hepatitis B virus were shown, suggesting previous infection by these agents. Reactivation of cytomegalovirus infection was suggested by a rising titer of antibodies against cytomegalovirus concurrent with pneumocystis pneumonia, and was confirmed by the growth of this virus in a throat culture 2 months later.

Acquired Immunodeficiency Syndrome↗