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Biomedical subjects

W D Schall

Publications and source records attributed to W D Schall.

At least 19 recordsLinked to original sources
PubMed1988

Adrenal function in 15 dogs with insulin-dependent diabetes mellitus.

Pituitary-adrenal function was assessed by a combined dexamethasone suppression-ACTH stimulation test in 15 diabetic and 9 healthy dogs. In both groups, plasma cortisol concentrations decreased (P less than 0.001) after dexamethasone administration and increased (P less than 0.001) after ACTH administration. Differences between groups (P greater than 0.05) and group-by-time interactions were not significant (P greater than 0.05). Seemingly, adrenal function was not altered in well-regulated diabetic dogs.

Animals↗
PubMed1987

Severe hypophosphatemia associated with diabetes mellitus in six dogs and one cat.

Severe hypophosphatemia was found in 6 diabetic dogs and in one diabetic cat. The cat suffered from hemolysis, and one dog had seizures, both apparently as a result of the severe hypophosphatemia. Clinical signs were not determined solely by the serum concentration of phosphorus, as seen in 5 other patients that did not have signs of disease despite similar serum phosphorus concentrations.

Animals↗
PubMed1987

Effect of nonadrenal illness on adrenal function in the cat.

Adrenal function was assessed by a combined dexamethasone suppression-ACTH stimulation test in 18 healthy cats, 17 diabetic cats, and 19 sick nondiabetic cats. In all groups, plasma cortisol concentrations decreased after dexamethasone was administered and increased after ACTH was administered. There were no significant (P greater than 0.05) differences among groups in time trend changes in cortisol concentration. There was considerable variation in adrenal response between cats in each group. Diabetic cats had more variation in base-line and postdexamethasone plasma cortisol concentrations (P less than 0.05) than did other groups. In sick, nondiabetic cats, cortisol concentrations tended to be higher in cats with hyperthyroidism (P = 0.06) than in cats with other diseases.

Adrenal Cortex Function Tests↗
PubMed1986

Cyclosporine pharmacokinetics in normal and pancreatectomized dogs.

Oral and i.v. cyclosporine (Cs) pharmacokinetics determined from radioimmunoassay (RIA) data were compared in normal and pancreatectomized dogs. An altered pharmacokinetics of Cs was observed in the pancreatectomized dogs that include: a 170% larger central compartment volume; a 34% greater total-body clearance; and lower steady-state average serum concentrations relative to the normals. Even though there were marked intersubject variations, both groups displayed a triexponential decline in Cs serum concentrations and disposition kinetics. Following 7 daily oral doses of commercial cyclosporine (CsA) (20 mg/kg) the Cs serum trough concentrations of the pancreatectomized dogs were consistently below 100 ng/ml, while those of the normal dogs were above 400 ng/ml. No alteration of CsA oral absorption was noted following pancreatectomy. This study suggests that frequent serum Cs concentration monitoring, with appropriate dosage adjustments, even in normals, is necessary to assure adequate drug levels. More significantly, the CsA dosage for pancreatectomized dogs should be several times greater to maintain serum concentrations comparable to normal dogs.

Animals↗
PubMed1986

Transplantation of pancreatic islets in dogs.

Dispersed pancreatic islet tissue, prepared by collagenase digestion without separation of exocrine and endocrine components, was transplanted into the splenic pulp of 12 dogs made diabetic by total pancreatectomy. Four dogs (group 1) were given autotransplants, and all became euglycemic 4.5 +/- 1.5 days (mean +/- SE) after the transplantation was done. Three of these dogs remained euglycemic until splenectomized 60 days after transplantation was done. Four dogs (group 2) given allogeneic transplants from histocompatible littermates within the same group were administered cyclosporine (40 mg/kg of body weight/day; starting 2 days before transplantation was done until dogs were splenectomized), and 3 of these dogs became euglycemic 8.0 +/- 2.0 days after the transplant was done. Two of the 3 dogs that became euglycemic remained so until splenectomized 60 days after transplantation was done, and the 3rd was euglycemic until 31 days after transplantation. Four dogs (group 3) given allogeneic islet transplants from nonrelated histocompatible donors within the same group were given cyclosporine (40 mg/kg/day; as described for group 2), and none became euglycemic.

Animals↗
PubMed1986

Adherence of neutrophils from dogs with diabetes mellitus.

Adherence of neutrophils from dogs with type I (insulin-dependent) diabetes mellitus controlled by insulin administration was compared with that from control dogs. Neutrophil adherence in whole blood decreased with increased serum glucose concentration, but was not different from normal cell adherence when isolated cells were examined. The decreased adherence in whole blood was considered to be the result of media factors and not dependent on altered neutrophil function.

Animals↗
PubMed1985

Chronic active hepatitis in 26 Doberman pinschers.

Chronic active hepatitis with increased hepatic copper concentration was diagnosed in 25 female and 1 male Doberman Pinscher dogs. Common clinical signs included polyuria/polydipsia, weight loss, anorexia, icterus, and ascites. Increased liver enzyme activities and abnormal liver function test results were the most consistent clinicopathologic changes. The dogs were assigned to 3 groups on the basis of clinical course of the disease. Group 1 dogs (n = 12) had clinical signs of advanced liver failure and died within one week. Group 2 dogs (n = 7) had less severe clinical signs of liver disease and died within one month. Group 3 dogs (n = 5) did not have clinical signs of illness or had mild clinical signs of liver disease and died 1 to 42 months after initial evaluation. One dog could not be reevaluated and another dog was alive 3 months after initial examination. Treatments consisted of supportive care for dogs in group 1, and dietary manipulations and corticosteroids for dogs in groups 2 and 3. The association of increased liver copper concentration and chronic active hepatitis is not known.

Animals↗
PubMed1982

Hypoadrenocorticism following therapy with o,p-DDD for hyperadrenocorticism in four dogs.

Hypoadrenocorticism developed in 4 of 26 dogs treated with mitotane (o,p-DDD) for hyperadrenocorticism. Evidence of the hypoadrenocorticism was detected from 2-8 weeks after the beginning of weekly or bimonthly maintenance o,p-DDD therapy. The adversely affected dogs had hyponatremia plus hyperkalemia, and 3 of the 4 had severely diminished plasma cortisol concentrations at rest or after stimulation with ACTH given IM. One dog did not have detectable plasma aldosterone concentrations before or after ACTH administration. Clinically, 3 of the 4 dogs responded well to mineralocorticoid replacement. Electrolyte determinations after replacement therapy in 1 dog documented normal serum sodium and potassium concentrations. One dog died despite therapy and was determined to have adrenocortical destruction.

Addison Disease↗
PubMed1982

Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases.

Thirty-seven cases of canine hypoadrenocorticism were compared with 39 previously reported cases. The 2 series were compared because it was believed that a study of 37 consecutive cases diagnosed at 1 institution (Michigan State University) and compiled by 1 group of veterinarians would yield data that were more representative of the disease than multiple cases from various institutions. Age, sex, and breed data were similar in both series. The frequency of anorexia, vomiting, depression, and the mean values for the clinicopathologic data were similar for both series except for blood glucose concentration (P less than 0.025). The Michigan State University series was different in that it had a lower frequency of eunatremia, increased plasma total solids, and hypoglycemia but a higher frequency of lymphocytosis, lymphopenia, hyponatremia, hyperglycemia, and hypercalcemia. Further, 3 dogs in the Michigan State University series had azotemia plus near isosthenuric urine, suggesting renal disease, but they seemingly responded to therapy for hypoadrenocorticism. Only 1 such case was identified in the literature. Finally, we detected fewer instances of P waves not being evident in lead II of an electrocardiogram.

Addison Disease↗
PubMed1975

Pyruvate kinase deficiency anemia with terminal myelofibrosis and osteosclerosis in a beagle.

A 15-month-old male Beagle with chronic hemolytic anemia was found to have erythrocytic pyruvate kinase deficiency and, terminally, myelofibrosis and osteosclerosis. The dog's erythron was studied by procedures that enabled close comparison with congenital hemolytic anemia (pyruvate kinase deficiency) of Basenji dogs. The affected dog's sire, dam, and one littermate--each clinically and hematologically normal--were found to have 50% reduction in erythrocytic pyruvate kinase (PK) activity.

Ancylostomiasis↗
PubMed1975

Acetaminophen toxicosis in the cat.

Administration by the owner of three 325-mg (5-gr) tablets of acetaminophen (N-acetyl-p-aminophenol) to each of 2 adult Burmese cats was associated with severe illness of both cats and death of one. Administration of two 325-mg tablets to each of 2 experimental adult cats resulted in severe illness. Marked cyanosis was observed in experimental cats within 4 hours after administration of one 325-mg tablet. Cyanosis was apparently due to anoxia associated with conversion of hemoglobin to methemoglobin by acetaminophen or its metabolites. Anemia, hemoglobinuria, and icterus were subsequently observed in the cats. Anemia and hemoglobinuria were caused by intravascular hemolysis of red blood cells (RBC). Icterus was due to both lysis of RBC and hepatic necrosis. Facial edema developed in 3 of 4 cats, but the pathogenesis of this lesion was not determined. The doses of acetaminophen were extremely large; however, administration of comparable doses to cats by their owners is a potential hazard because the drug is available without prescription as a 325-mg tablet. From information available at present, it seems that acetaminophen administration to the cat causes more dramatic clinical signs and is more likely to be fatal than the same doses of salicylates. Because phenacetin is metabolized to acetaminophen, similar clinical signs may occur in cats given phenacetin.

Acetaminophen↗