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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary adrenocortical insufficiency is described in 3 dogs. Clinical signs included marked depression, vomiting, diarrhoea, weakness and bradycardia. Diagnosis was based on clinical signs and biochemical findings of hyperkalaemia, hyponatraemia and a lowered plasma Na+ : K+ ratio. Treatment during the acute illness consisted of intravenous fluids and hydrocortisone sodium succinate. Fludrocortisone acetate has maintained all dogs in good health. One dog was on treatment for 4 years.
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PMID:Adrenocortical insufficiency in the dog. 68 64

A patient with Addison's disease, treated with conventional hydrocortisone replacement, developed deep hyperpigmentation, headache and vomiting. Plasma adrenocorticotropin (ACTH) level was extremely high, showing abnormal diurnal rhythm. Suppression of ACTH with glucocorticoids was attenuated and the responses to ovine corticotropin-releasing hormone (oCRF) and lysine vasopressin (LVP) were absent. Magnetic resonance imaging (MRI) suggested an enlargement of the pituitary gland, while immunohistological examination of pituitary fragments obtained by transsphenoidal surgery revealed corticotroph hyperplasia without microadenoma. Postoperatively, plasma ACTH returned to normal and adequately responded to oCRF and LVP. Over the year since surgery, the symptoms have gradually improved and the patient has resumed normal activities.
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PMID:Inappropriate secretion of adrenocorticotropin from corticotroph hyperplasia in a case of Addison's disease. 217 Jul 22

Gastrointestinal symptoms are a common feature of Addison's disease, but the diagnosis may be delayed because of the nonspecific nature of the symptoms. This report describes nine patients with Addison's disease who presented to our unit over the past 3 yr. Eight had severe or unusual gastrointestinal symptoms at presentation. One, already known to have Addison's disease, required several admissions to the hospital because of unexplained abdominal pain and vomiting before inadequate glucocorticoid replacement was diagnosed. All but one had previously attended the hospital, but the diagnosis of Addison's disease had been overlooked. Five eventually presented in crisis. It is important to exclude Addison's disease in all patients with unexplained abdominal symptoms.
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PMID:Gastrointestinal manifestations of Addison's disease. 280 83

A young man with a long history of obsessional traits and food fads presented with anorexia, vomiting and marked weight loss. He showed little concern for his physical state and his vomiting was frequently witnessed as self-induced. A diagnosis of anorexia nervosa was made and he took his own discharge from hospital. He was readmitted one month later, severely cachectic and with biochemical abnormalities consistent with advanced Addison's disease which was subsequently confirmed. He responded dramatically, both mentally and physically, to corticosteroid therapy. It is likely that anorexia nervosa, relatively rare in males, was a manifestation of the psychological abnormalities commonly seen in severe Addison's disease.
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PMID:Addison's disease presenting as anorexia nervosa in a young man. 325 15

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

Dysphagia and vomiting are frequently present in untreated Addison's disease. These non-specific symptoms may be due either to the metabolic disorder and myopathy or to disorders associated with Addison's disease. We describe a patient with autoimmune adrenal failure as a feature of autoimmune polyglandular syndrome (APS) type II. This patient was referred initially because of megaoesophagus. The association of megaoesophagus with Addison's disease or any of the three types of APS has not previously been described in humans. The association of megaoesophagus and adrenal failure, however, is known to occur in Allgrove's syndrome, a disease with primary manifestation in childhood characterized by adrenal failure, achalasia and alacrimia. Moreover, there are several reports on the association of megaoesophagus with adrenocortical insufficiency and other autoimmune endocrine diseases in dogs. Vomiting and dysphagia usually resolve with hormone substitution in patients with isolated Addison's disease. In our patient these symptoms disappeared in spite of the radiological persistence of megaoesophagus, which might have been overlooked if the diagnosis of Addison's disease had been made earlier. The occurrence of megaoesophagus might be more common than previously suspected and we suggest a systematic search for similar findings in other patients with autoimmune Addison's disease, even when minor dysphagia is present.
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PMID:Megaoesophagus in a patient with autoimmune polyglandular syndrome type II. 895 91

Clinical features and the management of adrenal insufficiency are considered with reference to etiology, diagnosis, and treatment. Specifically considered are the management of patients with Addison's disease and metastases. Adrenal insufficiency may go unrecognized in the cancer patients because features such as nausea, vomiting, anorexia as well as orthostatic hypotension are not specific and may be mistakenly attributed to advancing malignancy or side effects of therapy. Prompt recognition and treatment of adrenal insufficiency can avert potentially life-threatening situations.
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PMID:[Adrenal cortex insufficiency caused by metastatic tumors]. 948 26

An 18-year-old white woman had nausea, vomiting, weight loss, and a diagnosis of anorexia nervosa. Copper-colored skin was noted on physical examination, and serum chemistry values were normal. Subsequent fever, disorientation, and confusion led to the discovery of Addison's disease, which responded well to corticosteroid replacement therapy. Addisonian and anorexic patients exhibit clinical similarities, including nausea, vomiting, weight loss, abdominal pain, cold intolerance, hypothermia, and orthostasis. Other commonalities include prolongation of electrocardiographic PR and QT intervals and generalized slowing on electroencephalogram. Important differences include a brown color to the skin in Addison's disease instead of a yellowish color in anorexia. Addisonian patients also display hypocortisolism, hypoglycemia, and hyperkalemia, in contrast to the hypercortisolism, hyperglycemia, and hypokalemia seen in anorexia.
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PMID:Prompt differentiation of Addison's disease from anorexia nervosa during weight loss and vomiting. 949 78

The patient was a 76 year-old female with tuberculous tendonitis, treated with anti-tuberculous drugs including rifampicin (RFP). About two weeks after the start of RFP, she noticed general malaise and started vomiting, and the laboratory data showed severe hyponatremia. Because of mild liver dysfunction, RFP was discontinued and her symptoms gradually improved. Abdominal X-ray and CT showed swellings and calcifications of adrenal glands bilaterally. Serum ACTH level was high and cortisole, 17-OHCS, and 17-KS levels were normal. Her response to rapid ACTH stimulation was blunted significantly. After another trial of RFP, she started to vomit and complain general malaise again. We diagnosed her as partial Addison's disease and administered hydrocortisone with RFP. After this treatment her improvement was rapid. It has been known that RFP causes induction of enzymes in hepatic microsomes which increase the catabolism of glucocorticoids. To avoid the risk of adrenal insufficiency, patients with insufficient adrenal hormone reserve should receive compensatory hydrocortisone while they are taking RFP.
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PMID:[A case of partial Addison's disease activated with the administration of rifampicin (RFP)]. 1019 4


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