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Biomedical subjects

C B Chastain

Publications and source records attributed to C B Chastain.

At least 19 recordsLinked to original sources
PubMed1996

Use of orally administered succimer (meso-2,3-dimercaptosuccinic acid) for treatment of lead poisoning in dogs.

OBJECTIVE: To determine whether succimer (meso-2,3-dimercaptosuccinic acid) would be effective in reducing blood lead concentration in dogs with naturally acquired lead poisoning and whether treated dogs would develop clinically important adverse effects. DESIGN: Prospective case series. ANIMALS: 13 dogs with moderate-to-high blood lead concentrations (39 to 120 micrograms/dl) and clinical signs of lead poisoning. PROCEDURE: Dogs were treated with succimer (10 mg/kg of body weight, PO, q 8 h) for 10 days. Blood and urine samples were analyzed for lead concentration before, during, and after treatment with succimer. RESULTS: Mean blood lead concentrations on days 0, 3, 7, and 20 were 70.6, 32.7, 16.8, and 27.6 micrograms/dl, respectively. Mean blood lead concentrations decreased 53.6, 76.2, and 60.9% from pretreatment value on days 3, 7, and 20, respectively. Mean urine lead concentrations on days 0, 3, 7, and 20 were 70.0, 485.4, 254.3, and 28.3 micrograms/dl, respectively. CLINICAL IMPLICATIONS: In dogs with naturally acquired lead poisoning, succimer administered orally for 10 days effectively reduced blood lead concentrations and eliminated clinical signs of lead poisoning.

Administration, Oral↗
PubMed1990

Canine pseudohypothyroidism and covert hypothyroidism.

Primary hypothyroidism is perhaps the most common endocrinopathy of the dog. Unfortunately, a paradox exists. Many cases of mild to moderately severe hypothyroidism are unrecognized, while many euthyroid dogs are misdiagnosed as having hypothyroidism. Uncommon manifestations resulting from earlier stages of primary hypothyroidism, from secondary/tertiary hypothyroidism, or from a unique interplay between thyroid hormone deficiency and the age, sex, or breed affected can obscure the clinical suspicion of hypothyroidism. Conversely, nonthyroidal diseases and drug therapy can alter thyroid hormone metabolism in ways that mimic hypothyroidism and can lead to an erroneous diagnosis. Misinterpretation of clinical signs and laboratory findings are also causes for an incorrect diagnosis of hypothyroidism. The level of confidence in the diagnosis of hypothyroidism should be reflected as "suspected," "probable," and "definitive" hypothyroidism. Screening laboratory evaluation should be serum T4 and free T4 levels. The most reliable current evaluation for equivocal cases is the thyroid-stimulating hormone (TSH) stimulation test. Intramuscular or subcutaneous administration of TSH provides a greater separation between normal and abnormal post-TSH response. A definitive diagnosis of hypothyroidism in an adult dog is a retrospective assessment based on complete recovery after appropriate thyroid hormone replacement.

Animals↗
PubMed1989

Anti-triiodothyronine antibodies associated with hypothyroidism and lymphocytic thyroiditis in a dog.

A 5-year-old spayed Shetland Sheepdog had clinical signs consistent with hypothyroidism. Laboratory findings, including subnormal serum T4 concentration, also were suggestive of hypothyroidism; however, the apparent serum T3 concentration, as determined by a solid phase assay, was extremely high. Thyroid scintigraphy revealed ectopic radionuclide uptake in the neck and thyroid biopsy revealed lymphocytic thyroiditis. Determination of T3 autoantibody titer confirmed that the previously measured high serum T3 concentration was spuriously high because of autoantibodies to T3.

Animals↗
PubMed1988

Benign cutaneous mastocytomas in two litters of Siamese kittens.

Histiocytic-like cutaneous mast cell tumors were found in related Siamese cats less than 6 months old. The 2- to 5-mm diameter tumors developed only on the head and regressed within 4 months of diagnosis. Attempts to treat 2 of 4 affected kittens with topically or parenterally administered corticosteroids did not speed tumor regression, and the cause of the tumors was not determined.

Animals↗
PubMed1988

Eosinophilic granuloma of the nasal skin in a dog.

A recurrent mass removed surgically from the dorsocaudal aspect of the planum nasale in a 12-year-old dog was identified histologically as eosinophilic granuloma. The dog was treated orally with prednisone for 15 days, and the granuloma has not recurred.

Animals↗
PubMed1985

Congenital hypotrichosis in male basset hound littermates.

Four Basset Hound littermates, each 4 weeks old, with predominantly mahogany coats, had congenital focal alopecia especially affecting the head and dorsal pelvic region. Two predominantly black-coated female littermates were clinically normal. Histologic diagnosis was hypotrichosis.

Alopecia↗
PubMed1983

Congenital hypothyroidism in a dog due to an iodide organification defect.

A 10-month-old dwarfed male pup born of large-breed parents with normal stature had congenital goiter. Hypothyroidism due to failure to form organic iodine was diagnosed based on low serum thyroxine and triiodothyronine assays, radiographic findings in the epiphyses, and an abnormal perchlorate discharge test. Replacement of thyroid hormone resulted in more than 450% increase in body weight and a 600% increase in shoulder height over an 8-month period of treatment. A relapse in mental and physical condition occurred when hormone replacement therapy was later withdrawn. Postmortem findings are described.

Animals↗
PubMed1981

Low-dose intramuscular insulin therapy for diabetic ketoacidosis in dogs.

Seven dogs with diabetic ketoacidosis were treated initially with lactated Ringer's solution or 0.45% NaCl solution subcutaneously or intravenously and low doses of regular (crystalline) insulin administered intramuscularly every hour until the blood glucose concentration decreased to less than 250 mg/dl. For dogs weighing less than or equal to 10 kg, the initial dose was 2 units and the hourly doses were 1 unit. For dogs weighing greater than 10 kg, the initial dosage was 0.25 units/kg of body weight, and the dosage for hourly injections was 0.1 units/kg. The mean hourly decrease of the blood glucose concentration for all 7 dogs was 87.6 mg/dl. The mean period of treatment required was 4.1 hours. Late hypoglycemia did not develop in any dog, but the serum potassium concentration decreased 0.4 to 1.0 mEq/L. The results suggested that low-dose intramuscular regular insulin therapy for treatment of diabetic ketoacidosis is an effective alternative to conventional regular insulin therapy in dogs.

Animals↗
PubMed1981

Adrenocortical suppression in cats given megestrol acetate.

Megestrol acetate was given orally to 8 cats at a dose of 2.5 mg every other day for 2 weeks and to 8 cats at a dose of 5.0 mg every day for 2 weeks. Four cats were designated nontreated controls. Pre-ACTH-stimulated plasma concentrations of cortisol (hydrocortisone) and ACTH-stimulated cortisol and tolerance to large-dose glucose infusion (IV) were determined on each of the 20 cats given megestrol acetate. Cats were restrained with acepromazine maleate and ketamine hydrochloride during blood sample collection and large-dose glucose infusion. Adrenocortical function and tolerance to large-dose glucose infusion were reevaluated for 4 weeks--after 1st and 2nd weeks of megestrol acetate treatment of the treated groups, and after 1st and 2nd weeks when treatment was stopped (ie, experiment weeks 3 and 4). Each week a cat from the control group and 2 cats from the 2 treated groups were selected to determine the changes occurring during the experiment for that week; after collection of plasma samples, each week's 5 selected cats were euthanatized and necropsied. Significant impairment of adrenocortical function and alteration of adrenocortical morphology occurred with both treated groups. The most severe adrenocortical alterations occurred in the cats 1 week after megestrol acetate was no longer given (ie, experiment week 3). Megestrol acetate-induced adrenocortical suppression contributed to the death of 1 cat. It was concluded that if stress occurs to cats on treatment or soon after treatment with megestrol acetate, glucocorticoids should be supplemented. The effects of megestrol acetate on glucose tolerance were overshadowed by the unforeseen intolerance caused by chemical restraint with acepromazine maleate and ketamine hydrochloride.

Adrenal Cortex↗
PubMed1979

Adrenocortical suppression in dogs on daily and alternate-day prednisone administration.

Three groups of eight normal dogs each were orally given prednisone at doses of 0.22 mg/kg of body weight/day, 0.55 mg/kg/day, or 1.1 mg/kg on alternate mornings. Four dogs served as nontreated controls. Samples were obtained from members of each group to determine baseline serum cortisol and ACTH-stimulated cortisol values and histologic features in the lateral thoracic skin before prednisone administration, and after 1, 2, 3, and 4 weeks of administration. Some animals from each group were necropsied after 1, 2, 3, and 4 weeks of prednisone administration. Each course of prednisone administration resulted in adrenocortical atrophy and hypofunction, but adrenocortical suppression was less severe and slower in onset in the group given prednisone on alternate days. Extra-adrenal effects observed were atrophy of the skin and focal, fatty change of the liver. These changes were most evident in dogs given daily pharmacologic doses of prednisone (0.55 mg/kg/day). Fewer extra-adrenal effects were observed in dogs given alternate-day therapy. There were no extra-adrenal lesions in the dogs given equivalent glucocorticoid replacement doses (0.22 mg/kg/day).

Administration, Oral↗