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Biomedical subjects

B F Feldman

Publications and source records attributed to B F Feldman.

At least 55 records · Page 3Linked to original sources
PubMed1985

Splenectomy as adjunctive therapy for immune-mediated thrombocytopenia and hemolytic anemia in the dog.

Splenectomy was done in 9 dogs having immune-mediated hematologic disorders refractory to medical therapy. These disorders were immune-mediated thrombocytopenia (n = 3), immune hemolytic anemia (n = 3), and Evan's syndrome (n = 3). The diagnoses were based on clinical observations, laboratory test data, and differential of other conditions. In the 12 months after splenectomy was done, the dogs reflected clinical improvement and return of platelet and/or erythrocyte counts to clinically acceptable limits; medical treatment was stopped or reduced in 8 of 9 patients. The exceptional patient had shown clinical improvement without change in the platelet count. At the end of 1 year, survival rate was excellent, and postsplenectomy complications, such as hemobartonellosis, did not appear. It is believed that splenectomy may be useful for treating immune-mediated thrombocytopenia, anemia, and Evan's syndrome that seem refractory to medication.

Anemia, Hemolytic↗
PubMed1985

Nephrotic syndrome: a platelet hyperaggregability state.

Nephrotic syndrome characterized by hypoalbuminemia and hyperlipidemia is associated with an increased incidence of thromboembolism and increased platelet hyperaggregability. Although plasma coagulation proteins are also abnormal, changes are too inconsistent to attribute thromboembolic complications to the coagulation cascade alone. Antithrombin III (ATIII) has been shown to be deficient in nephrotic syndrome. There is, however, an increase in alpha 2 macroglobulin. It is clear that platelet to platelet interactions require exposure of platelet fibrinogen receptors, the binding of fibrinogen to these receptors, platelet crossbridging, and subsequent platelet aggregation. Fibrinogen is consistently elevated in nephrotic syndrome. Hyperlipidemia and hypoalbuminemia in nephrotic syndrome increases the availability of thromboxane A2 (TxA2) by increasing the availability of TxA2 precursors and the removal of TxA2 inhibitors. Thromboxane A2 is a known inducer of platelet aggregation probably through the exposure of platelet fibrinogen receptors. Recently, fibronectins a group of adhesive proteins, were implicated in platelet to platelet interactions. Since thrombin increases the expression of platelet surface fibronectin, fibronectin may be involved in thrombus formation in nephrotic syndrome. Thromboembolic formation in nephrotic syndrome is a composite mechanism involving the coagulation cascade, platelet-platelet interactions, and platelet-surface interactions.

Blood Platelets↗
PubMed1985

Early phase components of the kallikrein kinin system in hemorrhagic ascitic fluid and plasma in the rat with induced acute pancreatitis.

Acute hemorrhagic pancreatitis (AHP) was induced in 43 anesthetized rats by retrograde injection of sodium taurodeoxycholic acid into the common pancreatic biliary duct. At postinjection hours 1, 3, 6, 12, and 18, samples of plasma and hemorrhagic ascitic fluid (HAF) were obtained from rats in which AHP was induced and from rats that were sham operated. Early phase components of the kallikrein kinin system, including kallikrein-like (KK) activity and prekallikrein (PKK) and kallikrein inhibitor (KKI) concentrations, were measured in plasma and HAF samples. In the rats with induced AHP, PKK concentrations were decreased significantly in 18-hour plasma samples (P less than 0.05) and in all HAF samples (P less than 0.001) from 1 to 18 hours after induction of AHP. The KK activity was significantly increased (P less than 0.001) in the 6- and 12-hour plasma samples. In the 1-hour HAF samples, KK activity was increased greater than 10 times over that in the plasma pool of rats and remained increased for 18 hours. The KKI concentrations were markedly decreased in all HAF samples. In the sham-operated group, no significant change was observed. Histopathologic changes included edema, extensive hemorrhage, focal necrosis of many acinar cells around the head of the pancreas, slight inflammatory cell infiltration, vascular thrombosis, and partial lysis of pancreatic ducts. The extent of the changes of PKK, KK, and KKI values in HAF was greater than the extent of those in plasma. Increasing KK activity in plasma and HAF is indicative of bradykinin generation and the participation of this system in local and systemic pathologic change.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1985

Plasma fibronectin concentrations in dogs with disseminated intravascular coagulation.

Plasma fibronectin concentrations were significantly (P less than 0.001) below the reference range in dogs with disseminated intravascular coagulation (DIC) secondary to nonlymphomatous neoplasia, acute necrotizing pancreatitis, sepsis, chronic active hepatitis, and heat stroke. There was no statistical evidence of a group effect. Decrease in fibronectin concentration was associated with severe DIC, although no attempt was made to correlate fibronectin concentration with prognosis. These findings parallel those reported for severely ill human beings with diseases associated with DIC. They exemplify the potential of spontaneous diseases in animals as models for the study of human disease.

Acute Disease↗
PubMed1985

Measurement of canine plasma fibronectin by rocket immunoelectrophoresis.

Plasma fibronectin concentrations of 148 normal canine samples were measured by rocket immunoelectrophoresis. Electrophoresis was accomplished, using 2.0% rabbit anticanine fibronectin by volume in 0.7% agarose in buffer. Films were electrophoresed 18 hours in barbital buffer, 7.5 mA/film. The mean fibronectin concentration for normal citrated dog plasma was 290 micrograms/ml +/- 50 micrograms/ml.

Animals↗
PubMed1984

[Bone marrow depression following estrogen therapy].

The cases of three dogs are reported, in which administration of oestradiol resulted in bone marrow hypoplasia. These case reports gave rise to a discussion leading to the advice to seek other methods of treatment.

Anemia, Aplastic↗
PubMed1984

Practical toxicologic diagnosis.

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.

Animals↗
PubMed1984

Myeloproliferative disease in a cat.

Myeloproliferative disorders, a complex of cytologic abnormalities arising in the bone marrow, are among domestic animals most frequently recognized in cats but are relatively uncommon. A 4-year-old female Siamese, with splenomegaly and weight loss, was listless, anorectic, pale and dehydrated. A hemogram showed severe, macrocytic normochromic anemia, leukocytosis and reticulocytosis, with abnormally high numbers of nucleated RBC and undifferentiated blast cells. Bone marrow smears contained predominantly undifferentiated blast cells, RBC precursors and myeloblasts. The fluorescent antibody test for FeLV was positive. The cat died 66 days later despite a blood transfusion and chemotherapy. Necropsy confirmed a diagnosis of myeloproliferative disease, with hepatic and splenic invasion.

Animals↗
PubMed1984

Laboratory aspects of cancer.

Hematologic alterations unrelated to neoplastic bone marrow involvement include polycythemia, anemia, leukocytosis, leukopenia, thrombocytosis, thrombocytopenia and coagulopathies. Serum globulin levels may be increased or decreased, depending on the type of neoplasm. Plasma fibrinogen and fibrin degradation product concentrations are usually elevated in cancer patients, whereas cancer patients with DIC have low plasma fibrinogen concentrations. Hypercalcemia can be a sequel of osseous metastases. Neoplasia may cause the nephrotic syndrome in some patients. Effusions should be examined microscopically for signs of malignancy. Elevated serum enzyme levels are not specific in neoplastic disease.

Anemia↗
PubMed1984

Obtaining samples for the laboratory.

Mislabeling, incomplete or incorrect requisition forms, and in-vitro hemolysis are the most common problems related to specimen handling. Postprandial lipemia, administration of corticosteroids, and use of excess EDTA in the collecting tube may interfere with test results. Specimens for coagulation profiles should be collected in tubes containing EDTA or citrate. Most urinalysis errors result from improper sample collection, inappropriate storage, and delayed analysis.

Animals↗
PubMed1984

Examination of body fluids.

In dogs, the pericardial sac contains about 0.3 ml, and the pleural and peritoneal cavities 0-15 ml of clear, straw-colored fluid of pH 7.4, specific gravity 1.016, protein content less than 3.0 g/dl and cell count less than 3000/microliter. Fat can be cleared from chylous fluid with NaOH and ether. Inflammation is indicated by a cell count greater than 3000/microliter. Amylase levels in peritoneal fluid are elevated in necrotizing pancreatitis. The percentage of polymorphonuclear WBC exceeds 50% in bacterial inflammations. Normal joints contain less than 1 ml highly viscid, clear or straw-colored synovial fluid with less than 1000 nucleated cells/microliter. Synovial fluid becomes flocculent and less viscid in septic and occasionally in immune-mediated arthritis, often with cell counts greater than 75,000/microliter, with 75-90% polymorphonuclear WBC. Cerebrospinal fluid is normally acellular, clear and colorless but may be red, yellow or brown with intracranial hematomas. Viral or aseptic meningitis is characterized by mononuclear cell counts of less than 500/microliter. In acute bacterial meningitis, nucleated cell counts are greater than 1000/microliter, with most being polymorphonuclear WBC. Gram staining of cerebrospinal fluid is not useful.

Animals↗
PubMed1984

Interpreting absolute WBC counts.

The absolute count for a particular type of blood cell is the total white blood cell count multiplied by the differential percentage for that cell type. Neutrophilia is caused by increased marrow proliferation, redistribution among body neutrophil pools, stress and corticosteroids. Neutropenia is caused by decreased marrow proliferation, ineffective marrow production, reduced neutrophil survival and redistribution of neutrophils. Lymphocytosis is caused by chronic infections and allergic reactions, while lymphopenia is caused by increased lymphocyte destruction, neoplasia and lymphocyte loss. Monocytosis is associated with stress, infections, hematologic disorders, GI disease, necrosis and hemolysis. Eosinophilia is caused by allergic reactions, parasitism, skin diseases, neoplasia and adrenocortical insufficiency.

Anemia, Myelophthisic↗
PubMed1983

Hemorrhage in a cat caused by inhibition of factor XI (plasma thromboplastin antecedent).

A coagulation profile from a 5-year-old neutered male cat with severe epistaxis revealed an intrinsic coagulation defect characterized by prolonged activated partial thromboplastin time, with normal bleeding time, platelet count, and prothrombin time. Subsequent factor XI analyses, using bovine factor XI-deficient plasma, revealed factor XI deficiency. Hematologic and clinical studies on the cat failed to reveal an underlying disease process that might have resulted in acquired factor XI inhibition.

Animals↗
PubMed1983

Using red blood cell creatine concentration to evaluate the equine erythropoietic response.

Red blood cell creatine concentration was examined to determine its association with the equine erythropoietic response. Studies were conducted on 9 healthy horses, 4 healthy ponies, 24 anemia horses, and 2 horses in which anemia was experimentally induced. A modified Jaffe reaction was used to measure RBC creatine concentration. The mean RBC creatine concentration of the 9 healthy horses was 5.72 +/- 0.42 mg/dl, and that of the 4 healthy ponies was 2.59 +/- 0.31 mg/dl. Density-separation of erythrocytes from the healthy horses revealed significantly higher (P less than 0.001) creatine content (7.72 +/- 0.57 mg/dl) in the young RBC populations than in the old RBC populations (4.03 +/- 0.27 mg/dl). The RBC creatine content was assayed in 19 hot-blooded horses which were anemic due to a variety of causes. Of these anemic horses, 12 with PCV between 25% and 30% had a mean RBC creatine concentration of 6.12 +/- 0.46 mg/dl. The 7 other anemic horses with PCV less than 25% had a mean RBC creatine value of 6.07 +/- 0.12 mg/dl. Bone marrow films were examined from 5 anemic horses and in the 2 horses in which anemia was experimentally induced. The RBC creatine concentration correlated positively (P less than 0.001) with the reticulocyte count in the bone marrow and negatively with the myeloid-erythroid ratio (P less than 0.001).

Anemia↗
PubMed1983

Mechanism of diphacinone rodenticide toxicosis in the dog and its therapeutic implications.

Vitamin K1 (5 mg/kg of body weight/day divided for several 5-day regimens) was effective in preventing bleeding diathesis in diphacinone-poisoned dogs. Diphacinone, a vitamin K-inhibiting rodenticide, was given 2.5 mg of diphacinone/kg of body weight orally in divided doses 2 times daily for 3 days. One dog was given 5.0 mg of warfarin/kg in 2 divided doses for 3 days. Hemograms and biochemical profiles were performed every other day. A pancreatic exocrine function test was performed before and after administration of diphacinone and warfarin. All dogs were monitored, using routine coagulation screening tests and assays of coagulation factors II, VII, IX, and X. When laboratory results or clinical illness indicated hemorrhage, diphacinone-treated dogs were given 5.0 or 2.5 mg of vitamin K1/kg in divided doses 3 times a day for 5 days. The warfarin-treated dog was given 2.5 mg of vitamin K1/kg of body weight in divided doses 3 times a day for 5 days. Of the diphacinone-treated dogs, 1 dog (given 2.5 mg of vitamin K1/kg) required 3 vitamin K regimens and 2 dogs (given 5.0 mg of vitamin K1/kg) required only 2 vitamin K regimens. The warfarin-treated dog required only 1 vitamin K1 regimen. Bleeding was observed in the diphacinone-treated dogs up to 2 weeks after treatment. The vitamin K-enzyme complex was inhibited in diphacinone-treated dogs for approximately 30 days, as indicated by routine coagulation screening tests and coagulation factor inhibition. Hepatic dysfunction was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗