Search PubMed⌕ Search

Biomedical subjects

H Messmore

Publications and source records attributed to H Messmore.

At least 19 recordsLinked to original sources
PubMed2000

Differential effects of unfractionated heparin and low-molecular-weight heparins on tissue thromboplastin inhibition test.

Circulating anticoagulants are endogenously produced substances that interfere with in vitro tests of coagulation like activated partial thromboplastin time (APTT), and cause prolongation of the clotting times. Evaluation of the abnormal APTT involving various factor assays and mixing studies may provide inconclusive and ambiguous results. Tissue thromboplastin inhibition test (TTIT) is one of the screening assays for detection of circulating anticoagulants. However, this test is influenced by the presence of unfractionated heparin (UFH) from concentrations 0.2 U/mL and higher. Since low-molecular-weight heparins (LMWHs) are increasingly used for the prevention of thrombotic disorders and may replace UFH in the future, in this study the authors studied the influence of LMWHs on the performance of TTIT and compared the results with UFH. UFH and LMWHs showed a prolongation of TTIT in the concentration range of 0.25-1.0 U/mL. The marked prolongation of the TTIT with UFH and different LMWHs is in decreasing order of UFH > ardeparin > tinzaparin > dalteparin > enoxaparin. Patients with circulating anticoagulants who are given LMWHs may have false-positive results of TTIT and this influence should be kept in mind during patient management.

Anticoagulants↗
PubMed1999

Safety of warfarin anticoagulation in patients with heparin-induced thrombocytopenia.

OBJECTIVES: Venous limb gangrene has been reported to occur after high warfarin doses in heparin-induced thrombocytopenia (HIT), and this observation has been used to exclude warfarin management in this condition. The outcome of patients receiving modest doses of warfarin was studied. DESIGN: Retrospective study of 114 consecutive HIT patients who received diagnoses by platelet aggregometry; 51 of the 114 patients received warfarin. SETTING: Tertiary-care medical center. RESULTS: Thirty-five patients received warfarin for non-HIT indications, and 16 received warfarin for heparin-associated thrombosis. Warfarin was given to 23 patients (47%) 2.4 +/- 0.4 days prior to the onset of HIT, in 19 while receiving IV heparin for an overlap of 2.7 +/- 0.4 days. Twenty-eight patients (53%) received warfarin 2.8 +/- 1.0 days after the diagnosis of HIT. Patients received 11 +/- 1 doses of warfarin over 16 +/- 2 days, with a mean daily dose of 3.5 +/- 0.5 and a maximum dose of 9 +/- 0.5 mg. Prothrombin time at discharge was 17.3 +/- 0.4 s with a maximum of 22.8 +/- 0.8. The final international normalized ratio was 2.9 +/- 0. 3, and the maximum was 7.5 +/- 1.4. The minimum therapeutic range was reached in 59% of determinations. When compared to the 63 patients who did not receive warfarin, warfarin patients received more IV heparin (86% vs 41%; p < 0.001), open heart surgery (78% vs 43%; p < 0.001), and had a lower mortality (8% vs 43%; p < 0.001), but had no differences in thrombosis. CONCLUSIONS: Modest doses of warfarin were not associated with a worse outcome in patients with HIT.

Anticoagulants↗
PubMed1995

Successful treatment of heparin-associated thrombocytopenia and thrombosis using Hirulog.

Heparin-associated thrombocytopenia is a serious medical problem, especially when the patient requires continued anticoagulation. Hirulog is an immediate-acting intravenous anticoagulant that can be substituted for heparin. A new use of Hirulog in the treatment of life-threatening heparin-associated thrombocytopenia with thrombosis (HATT) is presented. Two patients suffering from the HATT syndrome were successfully treated with Hirulog to prevent further thrombosis. A third patient had developed heparin-associated thrombocytopenia after coronary artery bypass surgery in the past and was subsequently treated with Hirulog during a peripheral angioplasty procedure. Hirulog was an effective and predictable anticoagulant for these patients and was free from adverse effects.

Aged↗
PubMed1992

Scleredema and smoldering myeloma.

A 46-year-old white man had classic findings of scleredema; subsequently, a monoclonal immunoglobulin G lambda light chain was detected in his serum. Findings of a bone marrow biopsy specimen revealed that he had an increased percentage of plasma cells, some of which were atypical. A diagnosis of scleredema and smoldering myeloma was made.

Humans↗
PubMed1992

Phase II trial of recombinant human interferon alpha in myelodysplastic syndromes.

Twenty patients with myelodysplastic syndromes were treated with daily subcutaneous injections of interferon alpha 2a, at the initial dose of 3 x 10(6) U/m2. Hemogram, chemistry profile, natural killer (NK) cell activity and lymphokine-activated killer (LAK) cell cytotoxicity were monitored serially. Bone marrow with cytogenetic analysis was done before therapy and every three months afterwards. Normalization to the complete blood count, and wherever applicable, decrease in blast count of 5% or less were defined as a complete response. Improvement in hemoglobin level to 12 g/dl, neutrophil count to 1000/mm3 and platelets to 100,000/mm3 was considered a partial response. The median age was 71 (range 59-83) years and 16 of the patients were males. Two patients withdrew from the treatment in the first week and were considered ineligible. Among the other 18, two had refractory anemia, two refractory anemia with ringed sideroblasts, four chronic myelomonocytic leukemia, eight refractory anemia with excess blasts, and two refractory anemia with excess blasts in transformation to acute leukemia. Twelve patients were treated for six months, the other six were taken off the treatment after six to eight weeks because of disease progression. Only one patient with chronic myelomonocytic leukemia had a partial response for two months. NK cell activity remained unchanged before (18.3 +/- 4.6 lytic units) and during interferon therapy (19.6 +/- 5.3 lytic units). LAK cytotoxicity was not detected in any patient before therapy and was seen in only one patient (not the responder) during therapy (5.7 lytic units). The toxicity of the interferon therapy was substantial. Seventeen patients required a dose reduction and fifteen lost greater than 10% of body weight. Eleven patients (61%) developed infections requiring antibiotic therapy, and eight (44%) required hospitalization. Seven patients developed neurologic toxicity. Interferon alpha 2a is an ineffective but toxic therapy in these elderly patients with myelodysplastic syndromes.

Aged↗
PubMed1990

Leukemic transformation in polycythemia vera: analysis of risk factors.

Forty-eight patients with polycythemia vera (PV) were retrospectively studied for incidence of acute leukemia over a 12 year period. Initial clinical features, hemogram, RBC mass, B12 levels, neutrophil alkaline phosphatase (NAP), and therapy given were studied for association with development of acute leukemia. There were 25 males and mean age at diagnosis was 61.4 years. Initial Hg was 18.38 +/- 1.86 g/dl, WBC 16.44 +/- 12.92 (x 1,000/mm3), platelets 632.94 +/- 303.81 (x 1,000/mm3), B12 1,030.93 +/- 445.20 pg/ml, and neutrophil alkaline phosphatase (NAP) score 136.63 +/- 55.14. Twenty-three patients were treated with phlebotomy alone and 25 received additional myelosuppressive therapy as follows--2 received p32 alone, 4 alkylating agents alone, 8 hydroxyurea (HU) alone, and 11 received 2 or more (multiple) of these agents. None of those treated with phlebotomy alone but 6 of 25 (24%) patients given myelosuppressive therapy developed acute leukemia (P = .03) after a mean period of 46.8 months from start of myelosuppressive therapy. Four of the 11 patients (36%) receiving multiple agent therapy developed acute leukemia (P = .019). Initial hemoglobin levels, but not the other clinical parameters, were significantly higher in patients who developed acute leukemia (P = .002), and this difference persisted in various subgroups receiving myelosuppressive therapy. Thus, high initial hemoglobin and use of any myelosuppressive therapy are associated with an increased risk of leukemic transformation in polycythemia vera. This risk becomes substantial with the use of two or more myelosuppressive agents. Since myelosuppressive therapy does not prolong survival, its role in the management of polycythemia vera should be reexamined.

Acute Disease↗
PubMed1990

Hemostasis in malignancy.

Hemostatic abnormalities are present in a majority of patients with metastatic cancer. These abnormalities can be categorized as 1) increased platelet aggregation and activation, 2) abnormal activation of coagulation cascade, 3) release of plasminogen activator, and 4) decreased hepatic synthesis of anticoagulant proteins like Protein C and antithrombin III. The abnormal activation of coagulation cascade is mediated through release of Tissue Factor, Factor X activators, and other miscellaneous procoagulants from the plasma membrane vesicles of tumor cells. Macrophages of a tumor-bearing host also produce increased amounts of Tissue Factor. Production of Factor X activators and macrophage Tissue Factor is decreased by warfarin. The ability of the tumor cells to produce platelet-aggregating activity and plasminogen activator parallels their metastatic potential in animal and experimental systems. These studies also show that antiplatelet agents and antibodies against plasminogen activator can suppress the metastatic process. One or more laboratory abnormalities of hemostasis can be shown in up to 95% of patients with metastatic cancer. These abnormalities, however, are unable to predict subsequent development of thromboembolic or hemorrhagic complications. Clinical complications occur in 9-15% of the patients in the form of thrombotic or hemorrhagic disorders. The therapy of tumor-related coagulopathy should be guided by its clinical expression. Subclinical DIC should not be treated. Coumadin is generally ineffective for therapy of thrombosis in cancer patients. There is no consensus regarding the use of heparin in acute promyelocytic leukemia (APL). The defibrination in APL may be from disseminated intravascular coagulation as well as systemic fibrinolysis, as shown by decreased alpha 2 antiplasmin levels. In such cases, epsilon aminocaproic acid plus heparin therapy may be of benefit.

Antithrombin III↗
PubMed1983

CNS lesions in neonatal isoimmune thrombocytopenia.

We treated two siblings with classic neonatal isoimmune thrombocytopenia and porencephalic cysts in whom the CNS lesions occurred in a vascular distribution, for which there is no clear explanation. Whether the CNS vasculature is injured by the immune process at certain susceptible sites in larger vessels or whether there is a thrombotic process occurring at sites of vascular injury is speculative. This observation suggests that vascular factors are involved in the development of CNS lesions in this condition.

Brain Diseases↗
PubMed1983

Hairy cell leukemia and a fatal periarteritis nodosa-like syndrome.

We studied a patient with hairy cell leukemia (HCL) in whom periarteritislike lesions of multiple medium-sized arteries developed. There were many aneurysms distributed through the visceral organs. One ruptured into the abdomen, causing death. A previous study suggested that HCL may predispose to periarteritis nodosa, but recently a reversed temporal sequence of vasculitis and HCL was postulated. Our patient's course lends further support to the concept that HCL predisposes to vasculitis and periarteritislike lesions.

Adult↗
PubMed1983

Sinus histiocytosis with massive lymphadenopathy: remission with chemotherapy.

A case of sinus histiocytosis with massive lymphadenopathy (SHML) is reported, in which the patient had severe life-threatening complications resulting from SHML. The disease process was extensive involving the respiratory tract, skeleton, integument, orbit and eyelid, uveal tract, and the lymphatic system. Treatment with cytotoxic agents (chlorambucil, prednisone) resulted in resolution of the airway obstruction and was effective in managing these severe complications with minimal observed toxicity.

Biopsy↗
PubMed1982

Studies on a highly active anticoagulant fraction of high molecular weight isolated from porcine sodium heparin.

We have studied heparin fractionation using gel filtration and ion-exchange chromatographic methods. The starting material was commercial grade porcine mucosal sodium heparin (PSH). The fractionation was monitored employing synthetic substrates for assaying both antithrombin (with H-D-Phe-Pip-Arg-pNA ; S-2238) and anti-FXa (with Bz-Ileu-Glu-Gly-Arg-pNA ; S-2222) activities. The resulting fractions were evaluated in different amidolytic and coagulation methods used to determine heparin potency by comparison with PSH. By gel filtration of PSH on Ultrogel Aca 54, both strong anti-FXa and antithrombin activities were associated with the fractions eluted in the high molecular weight range (MW congruent to 20 x 10(3)). These fractions also had potent anticoagulant action when assayed by conventional clotting methods. PSH was also subjected to fractionation by an ion-exchange technique (DEAE-Sephacel) with increasing salt molarity. The patterns for antithrombin and anti-FXa activities were again closely related, if not identical. Four fractions were usually distinguished, with respectively negligible, intermediate, high and very high activities when compared to PSH. The very highly active fraction (HAF), approximately 15% by weight, was eluted at high salt molarity (greater than 0.8 M NaCl). On a weight basis its anticoagulant activity was congruent to 2-3 times that of PSH as determined by amidolytic as well as clotting methods. Intravenous injection of HAF to rabbits and dogs (1.0 and 2.5 mg/kg) produced a much stronger anticoagulant response than PSH, also showing an effect which persisted for a longer duration.

Animals↗