Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 63-year-old white woman was admitted to the hospital for bilateral total knee arthroplasty. She was given prophylactic subcutaneous heparin therapy postoperatively. Three days later, she had a brief hypotensive episode and an unexplained drop in hemoglobin level. Seven days postoperatively, she became confused and disoriented while complaining of pain in her right side and, later, under her left breast. She also had nausea, vomiting, anorexia, and a vague feeling of "illness." Her condition deteriorated progressively, with blood pressure falling to 65/40 mm Hg and a temperature of 39.7 degrees C. Blood, urine, and cerebrospinal-fluid culture samples showed no evidence of infection. A diagnosis of acute adrenal insufficiency was made. Following corticosteroid therapy, the patient's condition improved markedly. Of interest in our patient was that she had had no antecedent hypotension, sepsis, fever, or surgical complications. Acute adrenal hemorrhage is often overlooked because the symptoms are attributed to other conditions, especially to sepsis. Acute adrenal hemorrhage should be suspected in any stressed patient in whom an abrupt deterioration associated with back or abdominal pain, hypotension, and unexplained fever are noted. Suspicion should be raised regarding those patients who are receiving anticoagulant therapy (including subcutaneous heparin prophylaxis) at the time of deterioration. With increased awareness, more cases of acute bilateral adrenal hemorrhage and subsequent adrenal insufficiency can be recognized ante mortem and treated.
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PMID:Prophylactic subcutaneous heparin therapy as a cause of bilateral adrenal hemorrhage. 155 45

In eight (25%) of 32 consecutive AIDS patients between 1986 and 1989, Mycobacterium avium infection was diagnosed: in seven disseminated, in one as a local lymph node process. Six patients were treated as consistently as possible with a combination of ethambutol, rifabutine, clofazimine and protionamide (or cycloserine) in relatively large dosages. Median survival of treated patients was 15.5 (4-22) months. Protionamide inhibited most M. avium strains (7 of 8) in vitro, but often caused intolerance (nausea). Treatment of disseminated cytomegalovirus infection in our opinion was necessary in 5 of 6 patients during longterm M. avium therapy. HIV therapy (Zidovudine) during M. avium treatment was not possible due to bone marrow depression. A low maintenance dose of corticosteroids was necessary in 3 of 6 patients (one with adrenal insufficiency) to suppress symptoms such as fever and malaise.
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PMID:[Mycobacterium avium disease in AIDS patients; diagnosis and therapy]. 175 16

Patients receiving exogenous corticosteroids may develop iatrogenic adrenal insufficiency, with resultant nausea, emesis, and abdominal distension if perioperative "stress steroid" dosages are inadequate. To investigate these gastrointestinal disturbances, motility measurements were obtained using perfused catheters in 10 dogs before steroid treatment (control), during administration of high-dose corticosteroids, and daily during 5 days of abrupt withdrawal. Withdrawal was characterized by a significant disruption in normal antral, duodenal, and jejunal motility with a prolongation of the migrating motor complex (MMC) and phases I and II, but not III (I = quiescence, II = irregular activity, and III = regular activity). Retrograde giant contractions (RGCs), giant migrating contractions (GMCs), and/or "intestinal fibrillation" were also observed during the first two withdrawal days. Adrenal weights and morphology did not change. We conclude: (1) high-dose corticosteroids can induce profound adrenal suppression in dogs without morphologic changes within 3 weeks; (2) high-dose steroid administration enhances gastrointestinal motility; and (3) acute withdrawal causes disappearance or shortening of MMC and the development of RGCs and GMCs with associated emesis.
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PMID:Alterations in gastrointestinal motility during postoperative acute corticosteroid withdrawal. 192 86

Addison's disease is an uncommon endocrine condition manifested by a variety of nonspecific symptoms, such as malaise, anorexia and nausea. Symptoms usually do not occur until most of the adrenal gland has been destroyed. Autoimmune disease has surpassed tuberculosis as the primary cause of Addison's disease. Nevertheless, tuberculosis still accounts for a significant proportion of cases. The rapid adrenocorticotropic hormone (ACTH) stimulation test is useful for identifying adrenal insufficiency. Maintenance therapy consists of hydrocortisone and fludrocortisone.
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PMID:Addison's disease. 200 21

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.
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PMID:[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy]. 230 57

We reported the clinical results in 13 cases of hypercortisolism treated with amino-glutethimide (AG), which was developed by Tiantsin Research Institute of Medical Industry. Of the thirteen cases nine were confirmed by surgery and histology, and the others were diagnosed clinically. Clinical improvements have been achieved in ten of the thirteen cases over a therapeutic course of 8 to 12 wk with a daily dosage of 1.0 to 2.0 g of AG. Plasma and urinary corticosteroids, as well as plasma testosterone levels were significantly decreased after one-month treatment followed, however, by somewhat return and fluctuation. The high levels of blood glucose and serum insulin were declined after therapy consistent with the decrement of corticoids. Serum potassium levels in hypokalemic patients returned to normal after one month of therapy. Radial bone mineral contents in patients with low bone density returned or closed to normal after three-month treatment. The main side effects of AG are anorexia, nausea, drowsy, tierdness, skin rashes, etc, which are mild and transient. Adrenal hypofunction was seen in one case after treatment.
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PMID:[Clinical observation on hypercortisolism treated with amino-glutethimide]. 279 46

Six consecutive patients with Cushing's disease were treated with the broad spectrum antifungal drug ketoconazole. Urinary cortisol levels rapidly fell to within the normal range in five of the six patients. Acute hypoadrenalism occurred in one patient, and nausea and pyrexia in three. Our experience with hepatotoxicity was different from that reported by others in that reversible hepatotoxicity was demonstrated in three patients within 7 to 12 days of treatment. Further work is required before ketoconazole can be recommended as a standard primary therapy for patients with Cushing's syndrome. Continuing vigilance for both hypoadrenalism and hepatotoxicity is essential in any patient being treated with this drug either for hypercortisolism or for other reasons.
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PMID:Clinical experience with ketoconazole as a therapy for patients with Cushing's syndrome. 345 Apr 57

Fifteen consecutive patients with metastatic carcinoma who demonstrated bilateral adrenal metastasis on abdominal computed tomography (CT) were evaluated by the cosyntropin challenge test. Primary sites of tumors included lung, ten; colon, two; gastric, one; ovarian, one; and unknown primary, one. Bilateral adrenal enlargement was defined as greater than 1 cm on CT scan. Adrenal insufficiency was defined as a failure to increase serum cortisol by at least 5 micrograms/100 ml to a minimum of 15 micrograms/100 ml at either 30 or 60 minutes postcosyntropin. No patient had previously been on corticosteroids. All patients were questioned and examined for symptoms/signs of adrenal insufficiency. Five patients (33%) were found to have adrenal insufficiency based on the cosyntropin test. Of the clinical parameters evaluated, all five patients had nausea, anorexia, and orthostatic hypotension. The clinical onset of adrenal insufficiency was insidious; no patient experienced acute adrenal crisis. We conclude that adrenal insufficiency is not a rare occurrence in patients with metastatic cancer and bilateral adrenal involvement on CT scan.
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PMID:Prospective evaluation of adrenal insufficiency in patients with adrenal metastasis. 358 Oct 24

Suramin sodium is a reverse transcriptase inhibitor with in vitro activity against the human immunodeficiency virus (HIV), the causative agent of acquired immunodeficiency syndrome (AIDS). Ninety-eight patients with AIDS manifest as opportunistic infections (n = 38), AIDS with Kaposi's sarcoma (n = 38), AIDS-related complex (n = 20), or AIDS-associated non-Hodgkin's lymphoma (NHL) (n = 2) were treated with suramin sodium at 0.5, 1.0, or 1.5 g/wk for six weeks followed by maintenance therapy with 0.5 or 1.0 g/wk. Of 72 patients who were HIV culture positive before therapy and were assessable for subsequent HIV culture 40% became culture negative during treatment, with no apparent correlation between virus recovery and serum suramin concentration. No immunologic improvement was noted. One complete clinical remission was noted in a patient with Kaposi's sarcoma and stage IV NHL. Seven minor clinical responses were also noted. Toxic reactions were generally reversible, and included fever (78%), rash (48%), malaise (43%), nausea (34%), neurologic symptoms (33%), and vomiting (20%). Suramin-induced neutropenia was noted in 26%, thrombocytopenia in 12%, a serum creatinine level of 180 mumol/L or higher (greater than or equal to 2.1 mg/dL) in 12%, liver dysfunction in 14%, and clinical and/or laboratory evidence of adrenal insufficiency in 23%. Sixteen patients died while receiving suramin or within three weeks of discontinuation of drug therapy due to infection (n = 6), hepatic failure (n = 3), pulmonary Kaposi's sarcoma (n = 2), AIDS encephalitis (n = 2), AIDS-associated NHL (n = 1), iatrogenic hemo-pneumothorax (n = 1), or pulmonary disease of uncertain etiology. Suramin as currently administered cannot be recommended as effective therapy for AIDS.
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PMID:Suramin therapy in AIDS and related disorders. Report of the US Suramin Working Group. 365 Mar 39

A case of central pontine myelinolysis (CPM) following rapid correction of hyponatremia was reported and literatures were reviewed. The case was 61-year-old nonalcoholic female who had taken an operation of craniopharyngioma 23 years ago. Fifteen years later, she received re-operation for the recurrent tumor, followed by replacement therapy of corticosteroid and clofibrate. She was otherwise well until two weeks before entry, when she noticed abrupt onset of high grade fever, nausea, vomiting and general malaise. She was admitted to an emergency hospital because of weakness, disorientation and a slight impairment of consciousness, but she was able to speak and to take some food per os. Laboratory studies disclosed urinary tract infection and showed a serum sodium level of 117 mEq/l, potassium 2.9 mEq/l, a serum osmolarity 232 mO sm/l and urine osmolarity 141 mEq/l. She was diagnosed to have an exacerbation of adrenal insufficiency with hyponatremia and hypotonic dehydration triggered by urinary tract infection. Intravenous administration of vitamin B complex, electrolytes including KCL, 5% glucose solution and physiological saline with a large amount of corticosteroid was performed aggressively. Serum sodium concentration was raised to 161 mEq/l in two days, and the increased level had been maintained more than five days, resulting in coma and flaccid quadriplegia. During this period, there was no episode of hypotension, hypoglycemia, hypoxia nor hepatic failure which could have caused brain damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central pontine and extrapontine myelinolysis following rapid correction of hyponatremia--report of an autopsy case]. 646 6


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