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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included lethargy (n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5), collapse (n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

Nine dogs with primary gastrointestinal disease had clinical and laboratory findings resembling hypoadrenocorticism. The dogs had histories of anorexia, weakness or lethargy, diarrhea, vomiting, and weight loss. Hypothermia, dehydration, and emaciation also were detected on physical examination. Hyponatremia, hyperkalemia, and abnormally low Na/K ratios were found on laboratory evaluation, but results of ACTH-response tests were not compatible with hypoadrenocorticism. The primary diagnoses were trichuriasis and salmonellosis in 2 dogs, trichuriasis in 5 dogs, and perforated duodenal ulcer in 2 dogs. Most dogs responded to medical or surgical treatment of their primary gastrointestinal disease, and the original electrolyte abnormalities resolved. These findings emphasize the importance of the ACTH-response test in the diagnostic evaluation of dogs with clinicopathologic findings similar to those of hypoadrenocorticism.
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PMID:Clinicopathologic findings resembling hypoadrenocorticism in dogs with primary gastrointestinal disease. 299 Nov 78

Three dogs with hypoadrenocorticism did not have characteristically abnormal serum concentrations of sodium, potassium, and chloride and had not been treated with glucocorticoids. Diagnosis was based on lack of adrenocortical response to exogenous adrenocorticotropic hormone. Clinical signs included lethargy, weakness, anorexia, vomiting, and weight loss. The case demonstrated that the diagnosis of canine hypoadrenocorticism should not be excluded on the basis of normal serum electrolyte values.
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PMID:Atypical hypoadrenocorticism in three dogs. 626

The most common cause of hypoadrenocorticism in dogs is idiopathic immune-mediated destruction of the adrenal cortex. Other causes include anterior pituitary insufficiency, pituitary or adrenal neoplasia, acute withdrawal of exogenous corticosteroids, and mitotane toxicity. Females are affected more often than males; only 1 feline case has been documented. Animals 2-5 years old are most commonly affected. Clinical signs include lethargy, weakness, weight loss, anorexia, vomiting, diarrhea and bradycardia. Hematologic and biochemical changes can include eosinophilia, lymphocytosis, anemia, hyperkalemia, hyponatremia and hypercalcemia. Diagnosis is by finding negligible resting levels of plasma cortisol and no response to ACTH administration, and a serum Na:K ratio of 20:1 or less. Treatment involves restoring fluid volume, correcting acidosis, and supplementing salt and glucocorticoids. Daily oral use of prednisone at 0.05 mg/kg can safely maintain most affected dogs. Some dogs only require glucocorticoids in stressful situations. Iatrogenic secondary adrenocortical insufficiency (iatrogenic Cushing's disease) may result from a single injection of long-acting glucocorticoids or from long-term use. Clinical signs are the same as for natural hyperadrenocorticism, but endogenous cortisol release is suppressed. Treatment is gradual withdrawal of the offending glucocorticoid and elimination of the cause that initially prompted glucocorticoid therapy.
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PMID:Diseases of the adrenal cortex of dogs and cats. 674 17

Adrenal insufficiency was diagnosed in a 9-year-old American Quarter Horse gelding that had received monthly injections of stanozolol for 8 years. After the injections were abruptly discontinued, the horse developed anorexia, lethargy, weight loss, and bilateral forelimb lameness. Secondary hypoadrenocorticism was diagnosed on the basis of clinical signs, lack of high endogenous plasma ACTH concentration, and lack of cortisol response to administration of ACTH. Because the medical history did not include glucocorticoid administration, the cause was determined to be excessive administration of an anabolic steroid. Treatment consisted of physiologic glucocorticoid replacement for 9 months until adrenal function returned. Findings in this horse indicate that anabolic steroids influence the hypothalamic-pituitary axis in horses.
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PMID:Adrenal insufficiency associated with long-term anabolic steroid administration in a horse. 815 Jun 80

Hypoadrenocorticism was diagnosed in 42 dogs over a two-and-a-half-year period. The disease occurred more commonly in young to middle-aged dogs, with a female:male ratio of 2:1. Most dogs had chronic intermittent signs (eg, poor appetite, lethargy and vomiting), but more than a third were in acute adrenal crisis at the time of diagnosis. Serum biochemical testing revealed azotaemia, hyperphosphataemia, hyperkalaemia and hyponatraemia in almost all the dogs. In all dogs, results of adrenocorticotrophic hormone (ACTH) stimulation testing revealed a low to low-normal serum baseline cortisol concentration that failed to increase after ACTH administration. In two dogs with persistently normal serum electrolytes concentration, one had a markedly high plasma ACTH concentration diagnostic for primary hypoadrenocorticism, whereas the other had a low concentration confirming secondary hypoadrenocorticism. Fludrocortisone acetate was initially used for mineralocorticoid replacement in 33 of the 37 treated dogs with primary hypoadrenocorticism (final median dosage, 27.0 micrograms/kg/day), but supplementation was changed to desoxycorticosterone pivalate (DOCP) in four dogs because of poor response or adverse effects. Seven dogs with primary hypoadrenocorticism were treated with DOCP (final median dosage, 2.02 mg/kg/month). Prednisone, initially administered to 36 dogs, was discontinued in 11 dogs because of side effects. Of the dogs treated with fludrocortisone, the response was considered good to excellent in 26 dogs (78.8 per cent), fair in three, and poor in four. All dogs treated with DOCP responded well.
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PMID:Diagnosis and treatment of naturally occurring hypoadrenocorticism in 42 dogs. 880 97

An 11-month-old, neutered female miniature schnauzer presented with a severe head injury. The dog was treated for the acute effects of craniocerebral trauma and was hospitalized for just over a week. Several weeks later, she became weak and lethargic. A diagnosis of hypoadrenocorticism was confirmed with an adrenocorticotropin hormone (ACTH) stimulation test. An endogenous ACTH assay confirmed secondary hypoadrenocorticism. The dog was tested for hypopituitarism with canine thyroid-stimulating hormone and thyroxine serum assays and an insulin-like growth factor assay. These tests could not confirm panhypopituitarism in this dog. The hypoadrenocorticism was treated with prednisone, and the dog remains controlled adequately three years later.
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PMID:Secondary hypoadrenocorticism associated with craniocerebral trauma in a dog. 1010 79

Hypoadrenocorticism secondary to bilateral lymphomatous invasion of adrenocortical tissue was diagnosed in 2 adult castrated domestic shorthair cats. In both cats, findings during initial physical examination (ie, lethargy, anorexia, weight loss, and severe weakness) were consistent with severe hypoadrenocorticism. Hyperkalemia, hyponatremia, and azotemia were also detected, which were consistent with hypoadrenocorticism. Hypoadrenocorticism was documented on the basis of finding low baseline and ACTH-stimulated serum cortisol concentrations. The cats initially responded well to treatment, but both owners chose to have the cat euthanatized. Multicentric lymphoma with infiltration and destruction of the adrenal glands was confirmed during necropsy.
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PMID:Hypoadrenocorticism as the primary manifestation of lymphoma in two cats. 1021 85

A 3-year-old mixed-breed dog was evaluated for lethargy, weakness, anorexia, and vomiting. The dog was dehydrated, hyponatremic, hypochloremic, and hypoglycemic. Results of an ACTH stimulation test indicated hypoadrenocorticism. Treatment to restore cardiovascular stability and serum electrolyte balance caused serum sodium concentration to increase by 32 mEq/L within 48 hours, and the dog developed severe neurologic signs that persisted for approximately 3 weeks. Magnetic resonance imaging revealed cerebrocortical lesions on day 6 and more severe lesions, including diffuse atrophy of the cerebral hemispheres, at 23 weeks after initial evaluation; however, the dog recovered complete neurologic function. Serum sodium concentration should be monitored during treatment for hypoadrenal crisis to avoid rapid increases that can cause CNS damage.
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PMID:Severe neurologic sequelae in a dog after treatment of hypoadrenal crisis. 1041 76

Primary hypoadrenocorticism was diagnosed in an eight-year-old neutered male cat. The predominant presenting complaint was dysphagia. Other historical signs included lethargy, weight loss, polydipsia, polyuria, muscle weakness and occasional vomiting. The signs had waxed and waned over the two months before presentation and had improved when the cat was treated with enrofloxacin and prednisolone by the referring veterinarian. On referral, dehydration, depression and poor bodily condition were found on physical examination. Results of initial laboratory tests revealed mild anaemia, hyperkalaemia, hyponatraemia, hypochloraemia and elevations in serum creatinine and creatine kinase. The diagnosis of primary adrenocortical insufficiency was established on the basis of results of an adrenocorticotropic hormone (ACTH) stimulation test and endogenous plasma ACTH determination. Initial therapy for hypoadrenocorticism included intravenous administration of 0.9 per cent saline and dexamethasone, and oral fludrocortisone acetate. Within one week the cat was clinically normal and two years later was still alive and well on fludrocortisone acetate treatment only.
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PMID:Hypoadrenocorticism in a cat. 1132 66


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