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Query: UMLS:C0042963 (vomiting)
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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

Hypokalemia and hyperkalemia are common problems that may be artifactual, iatrogenic, or due to altered body homeostatic mechanisms. ECG may help one to recognize hyperkalemia but not hypokalemia. Excessive K supplementation is a common iatrogenic cause of hyperkalemia whereas fluid therapy is a common cause of iatrogenic hypokalemia. The most common causes of spontaneous hyperkalemia are renal failure and hypoadrenocorticism whereas the most common causes of spontaneous hypokalemia are vomiting, diarrhea, and renal wasting. Symptomatic therapy is usually done until the underlying cause(s) is resolved.
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PMID:Disorders of potassium homeostasis. 264 65

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

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.
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PMID:Canine hypoadrenocorticism: report of 37 cases and review of 39 previously reported cases. 703 23

We report the case of a 6-year-old boy with X-linked adrenoleukodystrophy (ALD). In view of the acute onset of vomiting, fever, and coma, encephalitis was initially suspected. However, brain magnetic resonance imaging demonstrated a pattern of demyelination that was consistent with ALD; this diagnosis was confirmed by the finding of elevated plasma very long-chain fatty acids levels. At presentation, the patient was hyponatremic. That this metabolic disturbance and the coma resolved within hours of the initiation of corticosteroid therapy suggests that the presenting symptoms were secondary to adrenal cortical insufficiency. Primary adrenal failure was confirmed by endocrinologic evaluation. Thrombocytopenia, hepatic transaminase abnormalities, anemia and leukopenia developed during the subsequent course of therapy with oleic acid and erucic acid.
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PMID:Acute onset of X-linked adrenoleukodystrophy mimicking encephalitis. 794 11

We reported a case of Addison's disease, caused by adrenal tuberculosis. The patient was female, seventy four years old. She complained cough and body weight loss. She complained cough from June, 1989, but her home doctor didn't take care of her symptoms. September 1989, she felt appetite loss, and easy fatigue, so her home doctor suspected her disease as pulmonary tuberculosis, so he introduced our hospital, and she admitted. When she admitted, her chest roentogenogram revealed bIII2. Sputum smear examinations were negative. Laboratory data on admission, we observed slightly eosinophilia, severe iron deficiency anemia, and accenturation of blood sedimentation rate. Immediately after admission, she complained nausea, vomiting, coldness, and powerless. On 25 days after admission, she lost her senses suddenly, and her blood pressure fell 5 days after, she fell in shock state, too. We found out her blood sugar data was 29. After blood examinations, we found out that ACTH was high, cortisole, 17-KS, 17-OHCS were low. So we thought she got acute hypoadrenocorticism. We found her abdominal CT revealed calcification in her right adrenal gland. We diagnosed her disease as Addison's disease caused by adrenal tuberculosis so we began to give prednisolone, 7.5 mg per day. After giving, her state made better. We thought her disease as Addison's disease caused by adrenal tuberculosis, revealed acute hypoadrenocorticism.
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PMID:[A case of Addison's disease caused by adrenal tuberculosis, and revealed acute hypoadrenocorticism]. 826 25

Fourteen dogs diagnosed with Addison's disease and having atypical serum electrolyte levels are described. Seventy-eight percent were female, and most showed signs of inappetence, weakness, or vomiting. Ninety-three percent of the cases had either hyponatremia without hyperkalemia or normal serum electrolyte concentrations. Hemogram features were variable and were not useful in suggesting a diagnosis of hypoadrenocorticism. The results of this study show that normal or mild serum electrolyte changes in a dog with clinical signs compatible with Addison's disease should not exclude this diagnosis from consideration. Definitive diagnosis depends on the demonstration of inadequate adrenocortical response to adrenocorticotropic hormone (ACTH) stimulation.
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PMID:Atypical Addison's disease in the dog: a retrospective survey of 14 cases. 868 Sep 23

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


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