Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From June 1975 to August 1977, 19 patients with distant metastases of malignant melanoma of the skin that were no longer responsive to chemotherapy were treated with BCG given intravenously. A single dose of lyophilized Pasteur BCG ranging from 2 X 10(7) to 3 X 10(8) viable units was given in 500 ml of saline infused in 5 to 6 h. Seven of the 16 evaluable patients benefited from treatment; 3 showed an objective regression of more than 50% of the original tumor volume, and 4 an arrest of tumor growth. The objective regressions lasted from 2 to 5 months, and 1 case had an arrest of tumor growth for 29 months. The regression rate was related to the BCG dosage: 2 X 10(8) viable units appears to be the dosage that gives severe but reversible toxicity and is able to induce objective regression. The most responsive lesions were skin and subcutaneous deposits (5 of 7) and lung metastases (1 of 4). Toxic effects seem to be related to the number of bacilli injected. In the group of 10 cases treated with less than 10(8) units, toxicity was modest: 4 patients had fever (up to 38.5 degrees C) that lasted a few days, and in 3 cases it was associated with shivering during the infusion period and weakness. One case only had vomiting and jaundice. Toxicity was severe in the 9 patients that were treated with a dosage higher than 10(8): patients had fever and weakness for at least 4 days and shivering during the infusion. Two had adrenal insufficiency and 7 had liver enlargement and jaundice with return to normality by day 21. In the whole series 8 patients had leucopenia and 5 thrombocytopenia for 2 to 3 days: only 1 patient required blood and platelet transfusion. No significant variations in immunoglobulin levels were observed. No variations of PPD or BCG skin tests were observed after treatment. Three patients expired; the first treated with 6 X 10(7) unit, had an intercurrent disease (autopsy showed a heart infarction); the second, treated with 1.8 X 10(8), showed a rapid growth of lung metastases and died 15 days after treatment; the death of the third patient was probably due to anaphylactic shock. All 3 patients had been previously treated with BCG, given by scarification or intranodular injection.
 ...
PMID:Intravenous administration of BCG in advanced melanoma patients. 68 66

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.
 ...
PMID:Prophylactic subcutaneous heparin therapy as a cause of bilateral adrenal hemorrhage. 155 45

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.
 ...
PMID:Alterations in gastrointestinal motility during postoperative acute corticosteroid withdrawal. 192 86

A 68-yr-old man had developed intractable vomiting soon after recovering from a flu-like illness. The use of Compazine as an antiemetic produced classic dystonic manifestations which resolved rapidly after discontinuation and treatment with Artane. However, he later developed a variety of neurobehavioral disturbances which led to his admission to the hospital. Extensive diagnostic procedures failed to identify any gastrointestinal or neurological causes. His condition unceasingly worsened until hypocortisolemia was serendipitously discovered, and all of his symptoms disappeared rapidly and completely with glucocorticoid replacement. Over the course of hospitalization, other than a single episode of orthostatic hypotension, the patient did not manifest any signs of adrenal insufficiency or endocrinopathy. Although detectable, his plasma ACTH level was markedly low in the presence of hypocortisolemia. His adrenal function was subnormal in the cortisol response to ACTH stimulation. His renin-angiotensin-aldosterone system and catecholamine levels were normal. He had normal pituitary responses to GnRH, TRH, and insulin, with rises in plasma levels of LH, FSH, TSH, PRL, and GH, but no stimulation of ACTH. Repeated CRH tests revealed no stimulation of ACTH and cortisol. No circulating anti-ACTH, antiadrenal, or antipituitary antibody was detected. We conclude that this elderly patient had a rare syndrome of selective corticotroph dysfunction which resulted in secondary adrenal failure and exacerbated his mental and neuromuscular abnormalities. To our knowledge, these symptoms, which clearly relate to hypocortisolism, have not been previously reported.
 ...
PMID:Delirium and neuromuscular symptoms in an elderly man with isolated corticotroph-deficiency syndrome completely reversed with glucocorticoid replacement. 255 16

After 5 years of cyclic vomiting an 8 year old boy was presented with coma and hyponatremia. ACTH and renin plasma concentrations were elevated, cortisol concentrations did not rise after ACTH-stimulation. Behavioural abnormalities including secondary enuresis and dysarthria drew attention to the possibility of an association of adrenal insufficiency with leucodystrophy. NMR tomography of the brain showed symmetrical demyelinated areas in the parieto-occipital regions. Very long chain fatty acids were elevated. The mother showed discrete neurological symptoms and elevated long chain fatty acids. Cyclic vomiting might suggest adrenoleukodystrophy.
 ...
PMID:[Differential acetonemic vomiting diagnosis--recurrent Addison crises as an early sign of adrenoleukodystrophy]. 282 90

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.
 ...
PMID:Suramin therapy in AIDS and related disorders. Report of the US Suramin Working Group. 365 Mar 39

Adrenal pathology was examined in 41 autopsied patients with the acquired immune deficiency syndrome. This represents the largest series and the first study with quantitation of adrenal cortical necrosis. In 32 cases clinical data were analyzed for features of adrenal insufficiency. Common clinical findings included vomiting, diarrhea, fever, hypotension, and hyponatremia. None of the 32 patients showed characteristic skin hyperpigmentation. Two patients were suspected premortem to have adrenal insufficiency. In one of these patients, adrenocorticotrophic hormone (ACTH) stimulation resulted in an adequate rise in plasma cortisol values. In the other patient, the baseline plasma cortisol value was elevated and failed to rise significantly after ACTH stimulation. Pathologic findings included widespread lipid depletion, infection by cryptococcus, and acid-fast organisms consistent with Mycobacterium avium-intracellulare, involvement by Kaposi's sarcoma, and necrotizing adrenalitis due to cytomegalovirus (CMV). A point-counting method was used to quantitate adrenal cortical and medullary necrosis. Necrosis due to CMV was greater in the medulla than the cortex. The maximum amount of adrenal cortical necrosis in any case was 70%. The degree of cortical necrosis was less than that usually associated with adrenal insufficiency.
 ...
PMID:Adrenal pathology in the acquired immune deficiency syndrome. 390 1

Acute adrenal insufficiency may present only with nonspecific symptoms and signs. Hyperpigmentation is not a feature of secondary adrenal insufficiency and is absent in patients with primary adrenal failure of recent or acute onset. Similarly, characteristic electrolyte disturbances may be obscured by concomitant vomiting and diarrhea as well as by parenteral electrolyte replacement. A high index of suspicion must therefore be maintained to make the diagnosis of acute adrenal insufficiency in patients without a recognized history of autoimmune adrenal insufficiency or of other diseases or therapeutic regimens known to result in pituitary-adrenal failure. Timely intervention with volume and glucocorticoid replacement rapidly reverses all symptoms and signs of adrenal insufficiency. Guidelines are presented for glucocorticoid replacement in the treatment of adrenal crisis as well as for the prevention of acute adrenal insufficiency in patients with known or suspected pituitary-adrenal disease. In addition, recommendations are given for the simultaneous diagnosis and treatment of adrenal insufficiency in patients without previously established disease.
 ...
PMID:Acute adrenal insufficiency: recognition, management, and prevention. 628 75

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)
 ...
PMID:[Central pontine and extrapontine myelinolysis following rapid correction of hyponatremia--report of an autopsy case]. 646 6

We report the case of a boy with adrenal insufficiency diagnosed at the age of 2.5 months. He required immediate therapy with corticosteroids. His two brothers and a cousin died in infancy with vomiting and dehydration. Aged 17.5 years (bone age 13 years), he showed no signs of puberty, a testicular volume of 2 ml, an infantile penis, and no axillary or pubic hair. There was no evidence of a pubertal growth spurt. The low plasma levels of cortisol, 17-OHP, delta-4-A, LH and FSH did not increase after stimulation with ACTH or LHRH respectively. Urinary testosterone levels before and after HCG were extremely low. These factors strongly suggest the diagnosis of a sex-linked type of adrenal insufficiency (cytomegalic form), associated with gonadotropin deficiency.
 ...
PMID:Congenital adrenal hypoplasia in a male with gonadotropin deficiency. 654 50


1 2 3 4 5 6 7 8 9 10 Next >>