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Biomedical subjects

D H Hild

Publications and source records attributed to D H Hild.

9 recordsLinked to original sources
PubMed1990

The role of cellular maturation in neutrophil heterogeneity.

Previous studies have shown that many neutrophil (PMN) characteristics are heterogeneous but the origin of PMN heterogeneity is unknown. It is unclear if PMN functional heterogeneity is secondary to maturational differences or due to distinct subpopulations of cells that possess different functional capacities. The PMN 31D8 antigen is a useful probe for evaluation of PMN subpopulations. The majority of PMNs (approximately 85%) exhibit a high intensity fluorescence after 31D8 monoclonal antibody (MoAb) labeling (31D8 enriched or "bright" PMNs) as determined by flow cytometric analysis. These cells are more functional than cells with low intensity fluorescence (31D8 diminished or "dull" PMNs). Various immunologic, clonogenic and functional techniques were used to study the expression of the 31D8 antigen in HL-60 cells and myeloid cells in order to evaluate antigenic and functional heterogeneity during morphologic maturation. The results of this study indicate that the percentage of 31D8 antigen positive (31D8 antigen enriched and diminished) bone marrow cells increases from 20 +/- 11% in myeloblast cells to 68 +/- 10% in promyelocytes, 93 +/- 2% in myelocytes and 99 +/- 1% in bands and PMNs. 31D8 antigen enriched cells first appear at the myelocyte stage (32 +/- 10%) and increase in bands (52 +/- 13%), marrow PMNs (62 +/- 13%) and peripheral blood PMNs (88 +/- 4%). These data indicate that the heterogeneous expression of 31D8 antigen in PMNs is due, at least in part, to maturational differences within the PMN population and raise the possibility that other heterogeneously expressed PMN characteristics are also maturationally derived. They also suggest that 31D8 antigenic expression may be a more precise indicator of myeloid functional maturation than maturation as identified by cellular morphology.

Antigens, Surface↗
PubMed1983

Respiratory failure due to pulmonary leukostasis following chemotherapy of acute nonlymphocytic leukemia.

Four patients with acute nonlymphocytic leukemia and leukocyte counts of more than 200,000/mm3 developed respiratory distress due to pulmonary leukostasis within 10-48 hours after initiation of chemotherapy. Clinically, the patients manifested fever, dyspnea, tachypnea, diffuse pulmonary rales, pleural effusions, and severe hypoxemia. Chest roentgenograms displayed diffuse pulmonary infiltrates, vascular engorgement, cardiomegaly, and pleural effusions. Three patients died from progressive respiratory failure despite ventilatory support. Pulmonary histology revealed thrombi composed of leukemic blast cells which obstructed and distended the lumens of pulmonary arterioles, capillaries, and venules. Electron microscopy studies of lung tissue showed pulmonary alveolar endothelium and basement membrane damage and interstitial edema. The pathophysiologic basis of pulmonary leukostasis and potential treatment modalities are discussed.

Acute Disease↗
PubMed1981

Coexistence of a primary immunodeficiency disorder and Hodgkin's disease: evidence against a B-lymphocyte origin for the Reed-Sternberg cell.

A 44-year-old woman with a life-long history of recurrent sinopulmonary infections developed Hodgkin's disease with characteristic Reed-Sternberg cells in a biopsy specimen of a mediastinal lymph node. Hypogammaglobulinemia was documented on several serum determinations and plasma cells were absent from biopsy specimens of the lymph node and bone marrow. Immunochemical studies failed to demonstrate any B lymphocytes bearing surface immunoglobulin or Fc-receptors for IgG in the peripheral blood. Pokeweed mitogen stimulation of the patient's peripheral blood lymphocytes in vitro resulted in the development of virtually no plasma cells. Peripheral blood T-lymphocyte number and function were defective initially. Following chemotherapy and radiotherapy, peripheral blood E-rossette-forming cells returned to normal, but T-cell function remained defective and B lymphocytes remained undetectable. These findings are compatible with the presence of two separate immune disorders: a primary hypogammaglobulinemia and Hodgkin's disease. The absence of lymphocytes bearing surface Ig or Fc-receptors for IgG in this patient adds further support against a B-lymphocyte origin for the Reed-Sternberg cell.

Adult↗
PubMed1980

Hyperviscosity in chronic granulocytic leukemia.

A patient with chronic granulocytic leukemia (CGL) initially presented with ischemic necrosis of three fingers. His peripheral white blood cell count (WBC) of 256,000/cu mm was associated with an elevated whole blood viscosity. These factors seemed related to his vascular insufficiency. In a further study of 10 patients with CGL, a direct correlation was found between an increasing WBC (or cytocrit) and whole blood viscosity. In CGL an elevated WBC causing an increased whole blood viscosity may be associated with vascular insufficiency, leukostasis, and the hyperviscosity syndrome.

Blood Viscosity↗
PubMed1978

Hemolytic anemia associated with heterograft replacement of the mitral valve.

The first case of overt hemolytic anemia following mitral valve replacement with a porcine heterograft is reported. Cardiac catheterization failed to reveal a paravalvular leak or valvular incompetence to account for the hemolysis. Red cell traumatization by the Dacron-covered Stellite ring and stent is suggested as the cause of hemolysis with the porcine heterograft.

Anemia, Hemolytic↗
PubMed1977

Consumption coagulopathy and microangiopathic hemolytic anemia with an axillo-femoral graft.

Consumption coagulopathy and microangiopathic hemolytic anemia occurred as a complication of insertion of an axillofemoral, preclotted dacron graft. Treatment with heparin followed by dipyridamole and aspirin normalized the hematologic and coagulation abnormalities over a two month period. The mechanism of consumption coagulopathy associated with prosthetic grafts is discussed and a possible role for treatment with antiplatelet agents is suggested.

Aged↗
PubMedDate not supplied

Pure red cell aplasia and the syndrome of multiple endocrine gland insufficiency.

A 26-year-old female with the syndrome of multiple endocrine gland insufficiency developed pure red cell aplasia. A clinical remission of the pure red cell aplasia was induced with prednisone and cyclophosphamide therapy. The occurrence of these two disorders in a single patient allows speculation on a possible defect in immune surveillance leading to multisystemic immune dysfunction in this patient.

Adolescent↗