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Biomedical subjects

E C Feldman

Publications and source records attributed to E C Feldman.

At least 73 records · Page 4Linked to original sources

Primary hyperparathyroidism in cats: seven cases (1984-1989).

The medical records of 7 hypercalcemic cats with primary hyperparathyroidism were evaluated. Mean age was 12.9 years, with ages ranging from 8 to 15 years; 5 were female; 5 were Siamese, and 2 were of mixed breed. The most common clinical signs detected by owners were anorexia and lethargy. A cervical mass was palpable in 4 cats. Serum calcium concentrations were 11.1 to 22.8 mg/dl, with a mean of 15.8 mg/dl calculated from each cat's highest preoperative value. The serum phosphorus concentration was low in 2 cats, within reference limits in 4, and slightly high in 1 cat. The BUN concentration was greater than 60 mg/dl in 2 cats, 31 to 35 mg/dl in 2 cats, and less than 30 mg/dl in 3 cats. Abnormalities were detected in serum alanine transaminase, aspartate transaminase, and alkaline phosphatase activities from 2 or 3 cats. Parathormone (PTH) concentrations were measured in 2 cats before and after surgery. The preoperative PTH concentration was within reference limits in 1 cat and was high in 1 cat. The PTH concentrations were lower after surgery in both cats tested. A solitary parathyroid adenoma was surgically removed from 5 cats, bilateral parathyroid cystadenomas were surgically resected in 1 cat, and a parathyroid carcinoma was diagnosed at necropsy in 1 cat. None of the cats had clinical problems with hypocalcemia after surgery, although 2 cats developed hypocalcemia without tetany, one of which was controlled with oral administration of dihydrotachysterol and the other with oral administration of 1,25 dihydroxyvitamin D. All 5 of the cta that underwent removal of an adenoma were alive at least 240 days after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

Serum free thyroxine concentration in healthy dogs, dogs with hypothyroidism, and euthyroid dogs with concurrent illness.

Serum free thyroxine (fT4), thyroxine (T4), and 3,5,3'-triiodothyronine (T3) concentrations were determined in 62 healthy dogs, 51 dogs with hypothyroidism, and 59 euthyroid dogs with concurrent dermatopathy or concurrent illness for which hypothyroidism was a diagnostic consideration. Status of thyroid function was based on history, physical findings, results of thyrotropin response testing, requirement for thyroid hormone replacement therapy, and in 31 dogs, on results of histologic examination of a thyroid gland biopsy specimen. Serum fT4 concentration was determined, using a single-stage radioimmunoassay. Mean (+/- SD) serum fT4 concentration was significantly (P less than 0.05) greater in healthy dogs vs dogs with hypothyroidism (0.51 +/- 0.27 ng/dl vs 0.10 +/- 0.07 ng/dl). Significant difference in mean serum fT4 concentration was not evident between dogs with hypothyroidism and euthyroid dogs with hyperadrenocorticism (0.16 +/- 0.13 ng/dl) or peripheral neuropathy (0.19 +/- 0.10 ng/dl). Mean serum fT4 concentration in all other groups of euthyroid dogs with concurrent illness was similar to values in healthy dogs and was significantly (P less than 0.05) greater, compared with values in dogs with hypothyroidism. Similar results were found for mean serum T4 concentration. Comparison of serum fT4 vs T4 concentration revealed: sensitivity, 0.97 vs 0.98; specificity, 0.78 vs 0.73; predictive value for a positive test result, 0.79 vs 0.80; predictive value for a negative test result, 0.97 vs 0.97; and accuracy, 0.78 vs 0.86, respectively. Ten (17%) and 12 (20%) of 59 serum fT4 and T4 concentrations, respectively, were inappropriately low in euthyroid dogs with concurrent illness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocortical Hyperfunction↗

Serum glucose and insulin responses to an insulin-containing ophthalmic solution administered topically in clinically normal cats.

Serum glucose and immunoreactive insulin concentrations were monitored after topical administration of an insulin-containing ophthalmic solution in 20 clinically normal cats. Three ophthalmic surface-acting agents, benzalkonium chloride, dimethyl sulfoxide, and proparacaine hydrochloride, were evaluated individually for their effectiveness in enhancing absorption of topically applied insulin. The ophthalmic effects of insulin-containing ophthalmic preparations were assessed by complete ophthalmic examination before and at the conclusion of each test period. Withholding of food overnight (12 hours) preceded each topical application of insulin-containing ophthalmic solution (12.25 to 26.4 U/cat), either alone or in combination with surface-acting agents, after which blood samples were drawn serially from an indwelling IV catheter over a period of 8 hours. Baseline serum insulin concentration, after food was withheld for 12 hours, in nonstressed cats was 6.0 microU/ml (geometric mean), and an exponentiation of the logarithmic quantity (mean +/- SD) yielded values of 1.5 to 23.0 microU/ml. All ophthalmic solutions tested failed to significantly lower serum glucose concentration or increase serum insulin concentration. Solutions used did not induce deleterious effect on ocular structures. Results indicate that topical administration of insulin-containing ophthalmic solution, either alone at the concentrations used or in combination with surface-acting agents, did not result in effective absorption of insulin across the conjunctival and lacrimal nasal mucosa in biologically relevant quantities. Thus, this route of insulin administration, under these specific conditions, is not an effective alternative or adjunct to SC administration of insulin for treatment of cats with insulin-dependent diabetes mellitus or severe noninsulin-dependent diabetes mellitus.

Absorption↗

Comparison of two low-dose dexamethasone suppression protocols as screening and discrimination tests in dogs with hyperadrenocorticism.

Two low-dose dexamethasone suppression test protocols were evaluated in 18 dogs with hyperadrenocorticism (14 dogs with pituitary-dependent hyperadrenocorticism [PDH] and 4 dogs with adrenocortical tumor) and in 5 healthy control dogs. Blood was obtained immediately before and 2, 4, 6, and 8 hours after IV administration of either 0.01 mg of dexamethasone sodium phosphate/kg of body weight or 0.015 mg of dexamethasone polyethylene glycol/kg. At 8 hours after dexamethasone administration, 18 of 18 (100%) dogs with hyperadrenocorticism given the sodium phosphate preparation and 16 of 18 (89%) affected dogs given the polyethylene glycol preparation failed to have suppression of plasma cortisol concentration (less than 1.4 micrograms/dl). Plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl at 2, 4, and/or 6 hours after administration of either dexamethasone preparation in 5 of 14 dogs with PDH and to less than 50% of baseline cortisol concentration in 10 of 14 dogs with PDH. Suppression, as identified by these 2 criteria, was not observed at 2, 4, 6, or 8 hours after administration of either dexamethasone preparation in dogs with adrenocortical tumor. For both protocols, the 8-hour plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl and to less than 50% of baseline in the 5 control dogs. Both protocols were comparable for use as screening tests in establishing a diagnosis of hyperadrenocorticism. Suppression of plasma cortisol concentration to less than 50% of baseline (or less than 1.4 micrograms/dl) during the test was consistent with diagnosis of PDH. Failure to have such suppression, however, was observed in dogs with PDH as well as in those with adrenocortical tumor.

Adrenal Cortex Function Tests↗

Plasma cortisol response to ketoconazole administration in dogs with hyperadrenocorticism.

The effect of orally administered ketoconazole on plasma cortisol concentration in dogs with hyperadrenocorticism was evaluated. Every 30 minutes from 0800 hours through 1600 hours and again at 1800 hours, 2000 hours, and 0800 hours the following morning, 15 clinically normal dogs and 49 dogs with hyperadrenocorticism had plasma samples obtained and analyzed for cortisol concentration. The mean (+/- SD) plasma cortisol concentration for the initial 8-hour testing period was highest in 18 dogs with adrenocortical tumor (5.3 +/- 1.6 micrograms/dl), lowest in 15 control dogs (1.3 +/- 0.5 micrograms/dl), and intermediate in 31 dogs with pituitary-dependent hyperadrenocorticism (PDH; 3.4 +/- 1.2 micrograms/dl). Results in each of the 2 groups of dogs with hyperadrenocorticism were significantly (P less than 0.05) different from results in control dogs, but not from each other. The same cortisol secretory experiment was performed, using 8 dogs with hyperadrenocorticism (5 with PDH; 3 with adrenocortical tumor) before and after administration at 0800 hours of 15 mg of ketoconazole/kg of body weight. Significant (P less than 0.05) decrease in the 8-hour mean plasma cortisol concentration (0.9 +/- 0.2 microgram/dl) was observed, with return to baseline plasma cortisol concentration 24 hours later. Twenty dogs with hyperadrenocorticism (11 with PDH, 9 with adrenocortical tumor) were treated with ketoconazole at a dosage of 15 mg/kg given every 12 hours for a half month to 12 months. The disease in 2 dogs with PDH failed to respond to treatment, but 18 dogs had complete resolution of clinical signs of hyperadrenocorticism and significant (P less than 0.05) reduction in plasma cortisol responsiveness to exogenous adrenocorticotropin (ACTH).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗

Glucose tolerance and insulin response in normal-weight and obese cats.

Glucose tolerance and insulin response were evaluated in 9 normal-weight and 6 obese cats after IV administration of 0.5 g of glucose/kg of body weight. Blood samples for glucose and insulin determinations were collected immediately prior to and 2.5, 5, 7.5, 10, 15, 30, 45, 60, 90, and 120 minutes after glucose infusion. Baseline glucose concentrations were not significantly different between normal-weight and obese cats; however, mean +/- SEM glucose tolerance was significantly impaired in obese vs normal-weight cats after glucose infusion (half time for glucose disappearance in serum--77 +/- 7 vs 51 +/- 4 minutes, P less than 0.01; glucose disappearance coefficient--0.95 +/- 0.10 vs 1.44 +/- 0.10%/min, P less than 0.01; insulinogenic index--0.20 +/- 0.02 vs 0.12 +/- 0.01, P less than 0.005, respectively). Baseline serum insulin concentrations were not significantly different between obese and normal-weight cats. Insulin peak response after glucose infusion was significantly (P less than 0.005) greater in obese than in normal-weight cats. Insulin secretion during the first 60 minutes (P less than 0.02), second 60 minutes (P less than 0.001), and total 120 minutes (P less than 0.0003) after glucose infusion was also significantly greater in obese than in normal-weight cats. Most insulin was secreted during the first hour after glucose infusion in normal-weight cats and during the second hour in obese cats. The impaired glucose tolerance and altered insulin response to glucose infusion in the obese cats was believed to be attributable to deleterious effects of obesity on insulin action and beta-cell responsiveness to stimuli (ie, glucose).

Animals↗

Pituitary macroadenomas and macroadenocarcinomas in dogs treated with mitotane for pituitary-dependent hyperadrenocorticism: 13 cases (1981-1986).

Pituitary macroadenoma/macroadenocarcinoma (PMA; tumor size greater than or equal to 1 cm in diameter) was diagnosed in 13 dogs after 0.5 to 24 months of mitotane treatment for pituitary-dependent hyperadrenocorticism (PDH). The diagnosis of PDH was established on the basis of results of common tests of the pituitary-adrenocortical axis in conjunction with results of x-ray computed tomography or necropsy. Initial clinical findings and clinicopathologic test results were typical of PDH. Signs referable to the CNS developed in 7 of the 13 dogs. The most common neurologic sign was stupor. Pituitary macroadenoma/macroadenocarcinoma was an unexpected finding in the other 6 dogs, because none had clinical signs of disease referable to the CNS at the time that pituitary tumor was documented. In the 13 dogs, strong correlation existed between tumor volume, compression/invasion of the surrounding nervous tissue, and development of neurologic signs, ie, neurologic signs were most frequently associated with larger tumors. The size of the tumor, however, was not always an indication of whether neurologic signs would be observed. All 7 dogs with neurologic signs were euthanatized because of the deleterious effects of the PMA. Of the 6 dogs without neurologic signs, 2 died of unrelated cause. Alternative treatment (ie, hypophysectomy, 60Co-teletherapy) was used successfully in 2 other dogs. Alternative treatment would seem indicated if PMA is documented in a dog with PDH. However, identification of PMA is dependent on evaluation of x-ray computed tomographic images. Signalment, history, physical examination, and alterations in routine clinicopathologic findings in these 13 dogs of our study were similar to previously reported findings in dogs with PDH but apparently without large pituitary tumors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗

Diagnostic approach to polydipsia and polyuria.

A variety of metabolic disturbances account for the majority of cases of polydipsia and polyuria. This chapter presents guides to differential diagnosis as well as a discussion of the etiology and clinical features of the primary causes--central diabetes insipidus, nephrogenic diabetes insipidus, and psychogenic polydipsia.

Animals↗

Effects of cyclosporin on insulin and C-peptide secretion in healthy beagles.

Plasma glucose, C-peptide, and insulin responses to intravenous glucose (intravenous glucose tolerance test [IVGTT], 0.5 g/kg), glucagon (1 mg i.v.), and oral glucose (oral glucose tolerance test [OGTT], 1 g/kg) were assessed in six normal beagles before, during, and 1 and 4 mo after the administration of cyclosporin A (CsA) in doses previously shown to be required for uniform prevention of canine islet-allograft rejection (20 mg/kg; mean trough radioimmunoassay serum levels greater than or equal to 500 ng/ml). Insulin secretion in response to intravenous glucose and glucagon was significantly inhibited during the administration of CsA (areas under insulin-response curves, pmol.min-1.L-1; IVGTT, pre-CsA, 11,127 +/- 1285; during CsA, 5954 +/- 1147, P less than .05; glucagon tolerance test, pre-CsA, 18,617 +/- 2807; during CsA, 4401 +/- 486, P less than .05 vs. pretreatment levels). These secretory defects persisted 4 mo after CsA was discontinued (IVGTT, 4358 +/- 659; glucagon tolerance test, 10,567 +/- 2479, P less than .05). C-peptide responses paralleled these changes. Plasma glucose disposal in response to these secretagogues, however, returned to normal 1 mo after discontinuation of CsA. In contrast to the findings for IVGTT and glucagon, insulin-response curves to OGTT were not statistically different during CsA administration. We conclude that, although glucose disappearance rates are normal after discontinuation of the CsA administration, CsA causes irreversible impairment in islet secretory responses detectable with IVGTT and glucagon but not with OGTT. These results suggest that short-term CsA in doses required to prevent islet-allograft rejection in dogs can result in permanent loss of functionally competent beta-cells.

Animals↗

Effect of dry, soft moist, and canned dog foods on postprandial blood glucose and insulin concentrations in healthy dogs.

The effect of dry, soft moist, and canned dog foods on immediate postprandial plasma glucose and insulin concentrations was evaluated in clinically normal dogs. Dogs were fed either dry (10 dogs; group I), soft moist (10 dogs; group II), or canned (8 dogs; group III) dog food for 5 consecutive days. On the fifth day, plasma glucose and insulin concentrations were determined in each dog prior to, during, and at 5, 10, 15, 30, 45, 60, 90, 120, 180, and 240 minutes after ingestion of the food. The alterations in plasma glucose concentrations were not significantly different from prefeeding values until 240 and 180 minutes after feeding for groups I and III, respectively. In contrast, the increments in plasma glucose were significantly (P less than 0.01) increased from basal concentrations at 30 and 45 minutes after feeding in group-II dogs. The maximal mean postprandial plasma glucose concentration was significantly (P less than 0.0001) less for group III, compared with concentrations for groups I and II, but there was no significant difference between concentrations for groups I and II. Although a biphasic insulin secretory response was found in all 3 groups of dogs, the patterns of phase-2 insulin secretion and the total amount of insulin secreted during the study were significantly different. There was a rapid increase in the plasma insulin concentration immediately after phase 1 in group II, with maximal plasma insulin concentrations occurring 30 minutes after feeding, followed by a gradual decrease in concentrations throughout the remainder of the study.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗

Advances in canine diabetes mellitus research: etiopathology and results of islet transplantation.

Histopathologic and immunocytochemical alterations in the pancreas of 18 dogs with spontaneous diabetes mellitus were evaluated. In 5 of 18 dogs (28%), extensive pancreatic damage appeared to be responsible for the development of diabetes mellitus. In the other 13 dogs, there was substantial reduction in the number of well-granulated beta cells, but the number of well-granulated alpha and delta cells was normal in 70% and 85% of the dogs, respectively. Also, insulitis lesions composed of infiltrating mononuclear cells, predominantly lymphocytes, were observed in 6 of 13 dogs (46%), but evidence of islet-directed humoral autoimmunity was not detected. Each pancreas had dense Ia (class II antigen) expression on ductal epithelia but not on islet endocrine cells. The importance of the insulitis lesions and class II antigen expression on ductal epithelial cells remains unclear. Of the 18 dogs, 8 received multidonor intrahepatic islet allografts. Allograft rejection was prevented by administration of cyclosporin. Five dogs were administered cyclosporin continuously. One dog with an allograft failed to sustain euglycemia at 231 days after transplantation, and one dog with fasting euglycemia died of pneumonia at 186 days after transplantation. In the other dogs, euglycemia was sustained for periods that ranged from 253 to 716 days.

Animals↗

Thyroid carcinoma causing hyperthyroidism in cats: 14 cases (1981-1986).

The medical records of 14 hyperthyroid cats with thyroid carcinoma were analyzed retrospectively regarding historical, physical, laboratory, and thyroid scintiscan findings, treatment, and treatment outcome. Breed predilection was not detected, and older castrated male cats were most commonly affected. The most common clinical signs detected by owners were weight loss, polydipsia, polyuria, polyphagia, hyperactivity, and anorexia. Physical examination findings included tachycardia, palpable cervical mass, hyperactivity, cardiac murmur, and abnormal coat. Common abnormal laboratory findings were high serum thyroxine and triiodo-thyronine concentrations and high serum alanine transaminase, alkaline phosphatase, and aspartate transaminase activities. Azotemia, hyperphosphatemia, and hyperglycemia were noticed less frequently. The most common thyroid scintiscan findings were multiple nodular areas of high radionuclide uptake in the cervical region, thoracic inlet, and cranial mediastinum. The most common morphologic diagnosis was mixed compact and follicular carcinoma, with follicular and papillary carcinomas being less common. Most cats responded well to treatment of the thyroid tumor, with rapid resolution of the historical and physical examination findings. The most common necropsy findings were local tumor invasion, regional lymph node metastases, cardiomyopathy, and interstitial nephritis.

Animals↗

Hyperadrenocorticism in cats: seven cases (1978-1987).

Hyperadrenocorticism was diagnosed in 7 cats with concurrent diabetes mellitus. Four cats had pituitary adenoma with bilateral adrenocortical hyperplasia, 1 cat had pituitary carcinoma with bilateral adrenocortical hyperplasia, 1 cat had adrenocortical carcinoma, and 1 cat had adrenocortical adenoma of the left adrenal gland. One year later, adrenocortical adenoma involving the right adrenal gland also was diagnosed in this cat. Clinical signs included polyuria and polydipsia (n = 7), development of pot-bellied appearance (n = 5), dermatologic alterations (n = 5), lethargy (n = 3), weight loss (n = 3), dyspnea/panting (n = 2), and recurrent bacterial infections (n = 2). In 6 cats, the diagnosis of hyperadrenocorticism was established before death on the basis of results of the ACTH stimulation test (n = 3) and the dexamethasone screening test (n = 5). Pituitary-dependent hyperadrenocorticism was differentiated from adrenocortical neoplasia on the basis of results of the dexamethasone suppression test (n = 4), endogenous ACTH concentration (n = 3), results of abdominal radiography and ultrasonography (n = 3), and exploratory celiotomy (n = 1). Four cats died or were euthanatized without treatment attempts. Treatment with mitotane followed by 60Co teletherapy was ineffective in one cat with pituitary adenoma. One cat with pituitary carcinoma died one week after bilateral adrenalectomy. Bilateral adrenocortical adenomas were removed surgically in the affected cat.

Adenoma↗

Serial determination of thyroxine concentrations in hyperthyroid cats.

Serum thyroxine (T4) concentrations of 10 hyperthyroid cats were measured at hourly intervals between 9 AM and 4 PM. In 5 cats, blood samples were obtained by jugular venipuncture; the remaining 5 cats had blood samples obtained from jugular catheters. Over the 7-hour period, a significant temporal (diurnal) variation was not identified in the serum T4 concentrations of the cats (P greater than 0.01). The lowest mean serum T4 concentration (9.1 micrograms/dl) was measured at 3 PM and was 14.2% less than the highest mean serum T4 concentration (10.6 micrograms/dl) measured at 9 AM. Though there were fluctuations in serum T4 concentrations during the 7-hour period, the differences were not systematic. The maximal variation in serum T4 concentrations over the 7-hour period averaged less than 21%. Despite the random variations during the 7-hour period, none of the measured serum T4 concentrations was in the normal range. Measurement of serum T4 concentration from randomly obtained blood samples was determined to be reliable for diagnosing feline hyperthyroidism.

Animals↗

Transsphenoidal hypophysectomy in the clinically normal dog.

Pituitary function and short-term clinical effects after transsphenoidal hypophysectomy were investigated in clinically normal dogs. In study I, 8 dogs were given polyionic fluids IV during the first 12 hours after surgery. In study II, 4 dogs were given polyionic fluids IV and glucocorticoid supplementation for 7 days. Pituitary function was assessed by evaluating basal ACTH concentrations and results of a growth hormone stimulation test before and 1 and 12 weeks after hypophysectomy, an ACTH stimulation test, a thyrotropin-releasing hormone-stimulation test, and a modified water deprivation/vasopressin response test before and 1, 4, 8, and 12 weeks after hypophysectomy. Gross and histologic evaluations of the surgery site, thyroid and adrenal glands, and skin were done at 12 weeks after surgery. Four dogs from study I died within 27 hours after hypophysectomy. Postmortem examinations of these dogs revealed liver and lung congestion compatible with circulatory collapse. None of the dogs in study II died. For the surviving dogs in both studies, diabetes insipidus developed immediately after hypophysectomy and resolved within 2 weeks. Hypernatremia also developed immediately after hypophysectomy and resolved by 1 week. Production of ACTH was evident at 1 and 12 weeks after hypophysectomy in all dogs, and results of ACTH stimulation tests after surgery were not notably different from results obtained before surgery. Results of thyrotropin-releasing hormone stimulation and growth hormone-stimulation tests supported the diagnosis of hypothyroidism and hyposomatotropism attributable to hypophysectomy. Histologic examination revealed thyroid atrophy, epidermal and dermal atrophy, and normal adrenal glands in all dogs and remnants of the hypophysis in 2 dogs from study I.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

Use of pulsatile intravenous administration of gonadotropin-releasing hormone to induce fertile estrus in bitches.

The pulsatile IV administration of gonadotropin-releasing hormone (GnRH) was evaluated as a method to induce fertile estrus in 8 anestrous Beagle bitches. Bitches received 1.25 micrograms of GnRH every 90 minutes for 11 to 13 days. Gonadotropin-releasing hormone was delivered by use of an automatic pump. Reproductive history was known for all bitches, 4 of which, on the basis of 3 or 4 preceding cycles, had an interestrous interval of 219 +/- 14 days (mean +/- SEM). Estrus induction was attempted during early anestrus in 6 bitches (ie, 148 +/- 10 days since the preceding estrus) and late anestrus in 1 bitch (ie, 260 days since the preceding estrus); another bitch had not had an estrous cycle for nearly 2 years before GnRH administration. Signs of estrus were seen within 16 days after the start of GnRH administration in the bitches with regular estrous cycles (group 1, n = 7), and within 23 days in the bitch (group 2) with prolonged anestrus. All bitches were bred, and 7 of 8 (87.5%) became pregnant, with a mean litter size of 4.5 +/- 0.75. A normal hormonal response pattern was observed in group-1 bitches--a peak increase in plasma estrogen concentration of 22.3 +/- 2 pg/ml immediately before the onset of estrus. Peak plasma progesterone concentration (17.3 +/- 3 ng/ml) was observed 1 to 14 days after the onset of diestrus in the group-1 bitches that ovulated, and adequate plasma progesterone concentration was maintained throughout gestation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗