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Biomedical subjects

B F Feldman

Publications and source records attributed to B F Feldman.

At least 73 records · Page 4Linked to original sources
PubMed1982

Myelomonocytic myeloproliferative diseases in a horse.

Myelomonocytic myeloproliferative disease in a horse was diagnosed on the basis of hematologic, enzymatic, and histopathologic findings. It was characterized clinically by depression, weight loss splenomegaly, lymphadenopathy, coagulopathy, and bacteremia. Hematologic findings included severe refractory anemia, thrombocytopenia, monocytosis, and pleomorphic leukocytes, with a left shift of the myeloid series. The serum lysozyme concentration was 14.5 microgram/ml (normal, less than 5 microgram/ml). The bone marrow contained many immature cells of the myeloid series and had a myeloid-to-erythroid ratio of 30.5 to 1. The horse died after brief hospitalization. Necropsy revealed generalized lymphadenopathy and hemorrhages throughout the body. Histopathologically, primitive cells were seen in several tissues. Cells that proliferated in the bone marrow were primarily myeloblastic, with some additional erythropoietic cells. Myeloblastic cells with evidence of normal erythropoiesis were seen in numerous lymph nodes and in the spleen, whereas primarily normal erythropoietic cells proliferated in the adrenal glands. Myeloid blast-type cells predominated in the lungs, myocardium, liver, and kidneys.

Animals↗
PubMed1982

Lymphosarcoma with leukemia in a horse.

A 17-year-old Arabian gelding was presented because of CNS depression and weight loss. Physical examination revealed generalized lymphadenopathy, pitting edema, and ascites. The diagnosis of lymphosarcoma with leukemic manifestations was based on cytologic and histopathologic examination of lymph node biopsy samples and a peripheral leukocyte count of 98,300/microliters, 94% of which were mature lymphocytes. These circulating lymphocytes lacked B-lymphocyte markers and did not respond to mitogenic stimulation, indicating functional incompetence. Though ultrastructural findings were equivocal, most morphologic changes indicated these cells were of T-lymphocyte lineage. Virus particles were not observed during transmission electron microscopy of these lymphocytes.

Animals↗
PubMed1982

Coagulation, fibrinolysis, and kinin generation in adult cats.

Screening coagulation tests, coagulation factors, and components of fibrinolysis and kinin generation were examined in 21 healthy adult cats. Observed ranges for screening tests were: prothrombin time, 7.3 to 11.4 s; activated partial thromboplastin time, 10.6 to 14.9 s; and thrombin time, 10.7 to 18.9 s. Functional coagulation factors II, V, VII, VIII, IX, X, XI, and XII were assayed and expressed as percentage of normal. Although individual factors varied, the observed range for factors assayed was 37% to 208% of normal. Fibrinogen ranged from 50 to 165 mg/dl. Plasminogen and antithrombin III ranged from 50% to 200% and 89% to 111% of normal, respectively. Plasma kallikrein ranged from 0.3 to 3.9 mukat/L. Fibrin(ogen) degradation products and fibrin monomers were examined with variable and inconsistent results.

Animals↗
PubMed1981

Disseminated intravascular coagulation: antithrombin, plasminogen, and coagulation abnormalities in 41 dogs.

An analysis was made of 41 cases of disseminated intravascular coagulation in dogs, with the objective of evaluating routine and nonroutine laboratory tests used in making the diagnosis. The dogs were grouped on the basis of underlying disease, which included neoplasia (39%), pancreatitis (30%), chronic active hepatitis (15%), heat stroke (12%), and sepsis (4%). Of the diagnostic tests evaluated, those for determination of activated partial thromboplastin time, antithrombin III activity, prothrombin time, and the platelet count were the most valuable. Of the clotting factors, factor V activity was decreased more frequently than the activity of factor VIII:C (factor VIII: procoagulant). The factor VIII:C activity was in conflict with prevailing dogma that reflects depression of this factor in disseminated intravascular coagulation. Factor VIII:C activity was decreased in only 29% of dogs studied. Activation of the fibrinolytic system was manifested by decreased plasminogen activity in 49% of the dogs studied. Sixty-one percent of the dogs had increased amounts of fibrin (ogen) degradation products.

Animals↗
PubMed1981

The anemia of inflammatory disease in the dog. I. The nature of the problem.

The anemia of inflammatory disease(AID) in the dog is an almost invariable complication of infection, inflammation and disseminated or necrotizing neoplastic disease. Clinically innocuous, it is important only in the greater understanding of the mechanisms controlling circulating erythrocyte quantity and quality. The etiology and pathogenesis include a shortened red cell life-span, disordered iron metabolism, depressed bone marrow response to the anemia and a disordered iron storage. The laboratory features of a moderate anemia, normal bone marrow cellular pattern, depression iron metabolism and reticuloendothelial iron sequestration make a final diagnosis of AID dependent on ruling out other etiologic mechanisms which may obscure or aggravate the anemia of the inflammatory disease in the dog.

Anemia↗
PubMed1981

Serum lysozyme (muramidase) activity in dogs with neoplastic disease.

The lysozyme (muramidase) activity was measured in the sera of 84 dogs with neoplastic disease. Neoplasms included 32 lymphomas, 13 primary bone neoplasms, 5 melanomas, 5 thyroid neoplasms, 9 soft tissue sarcomas, 5 mast cell sarcomas, and 15 carcinomas. The sera from 21 healthy dogs served as control. Dogs with neoplastic disease had significantly (P less than 0.005) higher serum lysozyme activity than did the healthy controls. For lymphosarcoma, dogs with clinical signs of systemic disease had significantly higher serum lysozyme activity than did dogs without clinical signs. For bone neoplasms, dogs with metastatic disease had higher serum lysozyme activity than did dogs without metastasis. Increased lysozyme activity may be a useful marker of macrophage-mediated host responses to neoplasms in dogs.

Animals↗
PubMed1981

Biochemical and coagulation changes in a canine model of acute necrotizing pancreatitis.

Acute necrotizing (hemorrhagic) pancreatitis was induced in 12 dogs by infusing oleic acid into their pancreatic ducts. There were decreases in blood pH, complement, antithrombin III, blood platelets, 24- and 48-hour plasminogen, and 24-hour haptoglobin and modest decreases in serum albumin. There were increases in fibrinogen, 48- to 120-hour haptoglobin, and 96-hour and 120-hour plasminogen and prolongations of prothrombin and activated partial thromboplastin times. The latter 2 changes together with decreases in antithrombin III, platelet numbers, and complement were indicative of consumption coagulopathy. A clinically innocuous but statistically significant decrease in serum total and ionized calcium despite significant acidosis was noted. This indicates that serum total and ionized calcium is helpful in making the diagnosis of acute necrotizing pancreatitis. Methemalbuminemia of 6 mg/dl at 24 hours and 7 mg/dl at 48 hours indicates that methemalbuminemia is a valuable diagnostic and prognostic finding in association with acute necrotizing pancreatitis.

Acute Disease↗
PubMed1981

Anemia of inflammatory disease in the dog: clinical characterization.

To characterize the erythroid homeostatic defect in canine inflammatory states, a single dose of Freund's complete adjuvant was injected subcutaneously to simulate naturally occurring infection and inflammation. After a latent period of 5 to 8 days, a generalized noninfectious inflammatory process was observed, followed by abscessation and drainage. This was accompanied by a modest anemia which decreased from base-line values by as much as 30%. In addition, a disordered iron metabolism was evidenced by depressed serum iron concentrations, total iron binding capacity (transferrin), percentage saturation of transferrin, and decreased numbers of bone marrow sideroblasts. Free RBC protoporphyrin concentrations were increased, as were serum copper, zinc, and ceruloplasmin. Bone marrow reticuloendothelial iron and hepatic nonheme iron were increased. Bone marrow myeloid-erythroid ratios were depressed. Throughout the course of the inflammatory period, the anemia remained normocytic and normochromic. A significant reticulocyte response was not observed.

Anemia↗
PubMed1981

Anemia of inflammatory disease in the dog: measurement of hepatic superoxide dismutase, hepatic nonheme iron, copper, zinc, and ceruloplasmin and serum iron, copper, and zinc.

Copper and iron are involved in protection of the aerobic cell from highly toxic oxygen by-products, one of which is the superoxide anion-free radical. This protection is associated with a copper-zinc enzyme, superoxide dismutase. Increased hepatic superoxide dismutase activity correlated directly with hepatic nonheme iron, serum zinc, and serum copper concentrations and inversely with hepatic copper, hepatic zinc, and serum iron concentrations (P less than 0.001). Decrease in hepatic ceruloplasmin concentration was correlated with the decrease in hepatic copper concentration (P less than 0.001).

Anemia↗
PubMed1981

Anemia of inflammatory disease in the dog: ferrokinetics of adjuvant-induced anemia.

Anemia of inflammatory disease induced by injection of adjuvant was characterized by decreases in hematocrit (mean +/- 1 SD, 37.5 +/- 2.7%, as compared with base-line values of 49.8 +/- 2.4%) and hemoglobin (12.54 +/- 1.22 g/dl, as compared with base line of 16.87 +/- 0.96 g/dl) and was classified as unresponsive, normocytic, and normochromic. Disordered iron metabolism was manifest by decreases in serum iron (62.3 +/- 13.6 g/dl, as compared with base line or 113.0 +/- 8.2 g/dl) and shortened mean radioiron clearance half-times (50.0 +/- 12.6 minutes, as compared with base line of 74.0 +/- 13.6 minutes) in the presence of increased bone marrow reticuloendothelial iron. Shortened radioiron clearance half-times reflected maximal extraction of iron from the plasma by the erythroid marrow due to suboptimal iron supply, since extraction of iron by other tissues is minor. Shortened mean marrow transit times (2.79 +/- 0.46 days, as compared with base line of 5.4 +/- 0.64 days) were indicative of adequate erythropoietin stimulation in the anemia of inflammatory disease. Increases in plasma iron turnover rate over base line (1.73 +/- 0.33 mg/dl/day to 1.51 +/- 0.34 mg/dl/day), erythron iron turnover rate (1.50 +/- 0.27 mg/dl/day, as compared with base line of 0.99 +/- 0.27 mg/dl/day), and RBC iron utilization (86 +/- 8.3%, as compared with base-line utilization of 65 +/- 9.3%) indicated erythroid marrow proliferation was effective. The magnitude of erythroid response appeared to be limited mainly by iron supply.

Anemia↗
PubMed1981

Anemia of inflammatory disease in the dog: availability of storage iron in inflammatory disease.

The iron-chelating agent deferoxamine (DF) was administered as a single dose and also daily over a prolonged period to evaluate availability of storage iron in dogs with induced anemia of inflammatory disease. In a 6-hour period, total urinary ferrioxamine (measured as urinary iron) excretion in controls was 251.22 +/- 119.68 microgram (mean +/- 1 SD), a 5.32 +/- 2.64-fold increase over prechelation values. In anemia of inflammatory disease-affected dogs, excretion was diminished to 115.67 +/- 34.86 microgram, a 2.87 +/- 1.10-fold increase, indicating a restricted iron excretion and sequestration of iron in a less soluble, less chelatable form. During prolonged DF administration, a pattern of increasing total urinary iron excretion was observed. This pattern is consistent with iron being stored as an insoluble polynuclear hydroxide in protein of ferritin and hemosiderin. The increase in hemoglobin and serum iron concentrations during prolonged DF administration indicates that increased iron stores are present, but in a less labile form. During the process of chelation, iron is converted to a more readily utilized state, and the increased availability of iron promotes hemoglobin synthesis. Thus, storage iron in the form of hemosiderin and ferritin is released to the metabolizable pool.

Anemia↗
PubMed1980

Coagulation abnormalities in dogs with neoplastic disease.

Conventional laboratory methods were used to screen untreated tumor-bearing dogs for hemostatic abnormalities. Excluded from study were dogs with clinical evidence of bleeding. The primary site for neoplastic disease in 100 dogs studied included hemolymphatic system, skin, bone, thyroid gland, oropharynx, mammary gland, and nasal cavity. Eighty-three percent of the dogs had one or more abnormal coagulation tests. Thrombocytopenia occurred in 36 dogs and 3 had thrombocytosis. Twenty-five dogs had hypofibrinogenemia, and 25 had hyperfibrinogenemia. There were 32 dogs with prolongation of the activated partial thromboplastin time, 10 dogs with shortened prothrombin time, and 6 dogs with prolongation of the thrombin time. Sixteen dogs had positive protamine sulfate (paracoagulation) reaction, and 8% had increased plasma fibrin degradation products. The euglobulin lysis time was accelerated in 24% of the dogs, and 15% had schistocytes on blood film. These data indicate that the majority of dogs with advanced neoplasms are likely to have abnormal coagulation tests.

Animals↗