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

Acute digoxin poisoning, its recognition and management, are reviewed. The uses of syrup of ipecac, gastric lavage, activated charcoal, cholestyramine, colestipol, edetate sodium and cathartics as measures to terminate the drug exposure are discussed. Measures to hasten digoxin elimination, such as the use of furosemide, hemodialysis and digoxin-specific antibodies are reviewed. Supportive management may include treatment with atropine, phenytoin, lidocaine, propranolol, glucose, insulin and sodium polystyrene sulfonate. Proper management of digoxin poisoning involves the use of standard decontamination procedures (emesis or gastric lavage). Activated charcoal is strongly recommended, followed by rapidly acting cathartics. Antiarrhythmic therapy usually involves atropine sulfate and phenytoin sodium.
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PMID:Acute digoxin poisonings: review of therapy. 34 83

Twenty-one patients with locally advanced breast cancer which had failed to respond to conventional therapy have been treated by infusion of C. parvum (strain CN 6134, Wellcome Research Laboratories) in 5% Dextrose. Thirteen patients had a single dose of 15 mg. C. parvum over 4 h and 8 patients received 5 daily infusions of 4 mg C. parvum over 1 h. In 3 patients there was some evidence of tumour regression. Pyrexia, often associated with rigors, headaches, vomiting and variations in blood pressure occurred in most patients receiving either schedule, although the severity of the side effects decreased daily in those receiving 5 treatments. One patient became comatose within 24 h of treatment and died two weeks later. Progressive swelling of the arm on the side of the tumour and inflammation of the primary lesion were prominent in those receiving 5 daily treatments. These results show that caution must be exercised in the clinical use of C. parvum and the search for an ideal schedule should continue.
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PMID:Clinical experience in the use of C. parvum in the treatment of locally advanced carcinoma of the breast. 34 4

Acute and chronic starvation is often associated with childhood cancer. Total parenteral nutrition (TPN) with 20% glucose and 3.0% amino acids, and minerals and vitamins was instituted to treat or prevent malnutrition in 41 children with cancer, ages three months to 18 years. TPN was required for anorexia, vomiting and diarrhea associated with anti-cancer therapy in 33 patients for intestinal complications or surgery in nine, and for preoperative correction of malnutrition in two. During TPN, general nutrition and appearance improved in all patients. Weight gain was noted in most. Despite gastrointestinal complications which usually require the interruption of chemotherapy and irradiation, in 21 children treatment could be continued at full dose with nutritional support by TPN. TPN was discontinued in six patients when blood cultures became positive. Sepsis was treated successfully by removal of the central venous catheter in all six and administration of antibiotics in three. No metabolic complications were noted. TPN appears to be a safe and effective means of combating the malnutrition which may occur with cancer and its therapy.
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PMID:Parenteral nutritional support in children with cancer. 40 34

In an attempt to obviate the need for intravenous fluids by preventing dehydration, 57 adult volunteers who experienced induced clinical cholera during a vaccine development programme were treated from the onset of diarrhoea with oral glucose-electrolytes therapy. 44 individuals with mild to moderately profuse diarrhoea (less than 8 L. total volume) were maintained in normal water and electrolyte balance with oral therapy alone. 13 individuals with severe diarrhoea (greater than 8 L. total volume) could not be maintained in balance with oral therapy alone, due chiefly to emesis during the first day of illness. Emesis occurred in the absence of significant dehydration or acidosis. Since emesis precludes effective early oral therapy in severe cases, domiciliary oral therapy is unlikely to eliminate cholera mortality. Rural diarrhoea treatment centres using oral therapy with limited amounts of intravenous fluids when needed, could reduce case fatality from cholera and related diarrhoeas virtually to zero with least expense.
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PMID:The problem of emesis during oral glucose-electrolytes therapy given from the onset of severe cholera. 44 66

Hypophosphatemia is common in hospitalized patients and occurs under a variety of circumstances other than parathyroid hormone excess. Charts of 100 inpatients with hypophosphatemia were reviewed and the patients divided into five groups on the basis of serum phosphate level: 18, 2.1 to 2.4 mg/dL; 49, 1.6 to 2.0 mg/dL; 20, 1.1 to 1.5 mg/dL; 12, 0.6 to 1.0 mg/dL; 1, 0.1 to 0.5 mg/dL. The effect of glucose ingestion on serum phosphate level was shown in one normal patient. Whenever carbohydrate was administered intravenously (45 cases), this was considered the primary cause of the hypophosphatemia. Other causes were as follows: diuretics, hyperalimentation, alcoholism, respiratory alkalosis, dialysis, insulin, corticosteroids, diabetic ketoacidosis, vomiting, phosphate-binding antacid, Gram-negative sepsis, primary hyperparathyroidism, saline, epinephrine, gastrointestinal malabsorption, and unknown. Hypophosphatemia in hospitalized patients may have multiple causes.
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PMID:Hypophosphatemia in hospitalized patients. 44 90

It is today's general medical opinion that children's diabetes mellitus was uncommon in the past. It was generally admitted at that time the initail stages were so sudden as to make difficut its early diagnosis. It's increased incidence is at present an alarming truth; however, a parallel increase of diabetic coma or of mulminant types has rather dropped. Diabetes may be diagnosed by just considering the main symptoms at the onset which are polydipsia, polyuria and weight loss. If an early diagnosis is not made, acidosis (abdominal pain, nausea, vomiting) may appear within a few days or weeks followed by coma (Kussamul's acidotic respiration and dehydration). Coma may be avoided by an early diagnosis and a life may be saved. It must be stressed that an important percentage of children and adolescents show a slow and gradual evolution (week or months) of their diabetes: gradual weight loss, sometimes with noticeable polyphagia, occasional enuresis, but without other associated symptoms. Asymptomatic, intermittent glucosurias are also frequent; they vary in magnitude an almost always they appear without ketonuria and with fasting normal glycemia. According to our experience they may precede in weeks or months the clinical manifestations of the disease. Postprandial glycemia is a sure diagnostic resource; it is of greater trustworthines than fasting glycemia; therefore we advise it as a routine diagnostic procedure which we recommend widely. In uncertain situations, the oral glucose tolerance test is advisable.
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PMID:[Diabetes mellitus in childhood and adolescence. Clinical types]. 48 58

Chronic alcoholism is a frequently unrecognized cause of ketoacidosis in nondiabetic patients. Seven episodes of alcoholic ketoacidosis were observed in three patients. No consciousness disturbances were present. Semi-quantitative tests for ketones were strongly positive in urine, weakly positive in serum. The anion gap was between 25 and 41 mEq/l; serum lactate was between 0.9 and 9.0 mEq/l, and, in all cases, below the anion excess. Blood glucose ammonia was increased. Massive fatty liver was documented in all patients. All ketosis episodes followed an increase of alcohol ingestion associated with one to four week-starvation and vomiting; however, at the time of admission, alcohol was weakly increased in blood. In the four episodes where diagnosis was correct, ketoacidosis was rapidly corrected without insulin administration. In conclusion, in some nondiabetic subjects, the occurence of alcohol prolongated ingestion together with starvation and vomiting is responsible for ketoacidosis; because alcoholic ketoacidosis has often a mild clinical expression, its true prevalence is underestimated; insulin administration is not required.
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PMID:[Alcoholic ketoacidosis (author's transl)]. 53 15

The potential toxicity of FE-S15, a soybean oil fat emulsion used in parenteral nutrition, was studied in dogs. Forty pure bred beagles, divided into two experimental groups (FE-S15 at 9 and 4 gm/kg BW/day) and two corresponding control groups (receiving Dextrose Ringer's Solution) were given daily infusions for 28 days via a central venous catheter. When compared with control groups no significant weight loss was observed in either experimental group; the food intake decreased only in animals receiving fat in high doses. Hemoglobin and hematocrit decreased in all groups, the greatest fall observed in the group receiving high dose fat infusion was the hematocrit decline from 43.9% to 31%. This decrease was significantly different from the control only during one observation period. The total serum lipids, triglyceride and phospholipid concentrations of the animals receiving fat in high doses increased 3-4 times in comparison to that of the control group; cholesterol increased 5 times. The serum protein level fell from 6.5 to 5.1 gm/dl in animals receiving 9 gm/kg BW/day while animals receiving 4 gm/kg BW/day had a significant increase to 8.4 gm/dl. Except for an overall decreased activity clinical sign such as lethargy, loss of appetite, vomiting, and diarrhea were infrequent and equally observed in experimental and control animals. The post mortem examination did not reveal changes that must be attributed to the administered fat. It is concluded that the fat emulsion FE-S15 is fairly well tolerated in dogs at a potentially toxic level.
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PMID:[Tolerance studies of an intravenous fat emulsion (FE-S15) with beagle dogs]. 57 61

Hypoglycin A(0.01--1.0 mmol/l) stimulated insulin release from pieces of rabbit pancreas in vitro in the presence or absence of extracellular glucose. The relevance of this finding to the hypoglycaemia of Jamaican vomiting sickness is discussed.
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PMID:Hypoglycin stimulates insulin secretion. 59 Jun 55

Histoplasma meningitis (HM) has been reported to occur primarily in association with disseminated histoplasmosis (DH). We report a case of histoplasma meningitis occurring in a patient with common variable hypogammaglobulinemia (CVH) in which no manifestations of DH were observed. L. L., a 66-year-old Caucasian male, clerical worker, developed occasional episodes of dizziness and tinnitus in mid-1971. During 1972, increasing frequency of these episodes and gradually progressive confusion were noted. In January 1973, vomiting, forther confusion, obnubilation, and a left central facial paresis developed and he was hospitalized. Physical examination revealed no pulmonary abnormalities, lymphadenopathy or hepatosplenomegaly. Over the ensuing 6-week evaluation, there was occasional fever to 38.5 degrees C. Chest roentgenogram was normal. Cerebral angiography suggested a mass in the left cerebellar hemisphere. EEG was diffusely slow. Multiple CSF examinations revealed: Glucose 7-18 mg/with a normal blood glucose, protein 109-256 mg/and cells 66-140 (95 + % mononuclear). Histoplasma capsulatum was cultured from CSF but not from sputum, urine, blood or bone marrow. Skin tests for PPD, histoplasmosis, coccidiodomycosis, blastomycosis, mumps, dinitrochlorobenzene and streptokinase-streptodornase were negative then and 6 months later. Histoplasma serum antibody was absent. Immunoglobulin analysis revealed IgG 430 mg %, IgA 46 mg %, and IgM 35 mg %, which with the history and skin test results suggested CVH. Treatment with 2.51 gm of amphotericin B given intravenously over a 3-month period resulted in complete reversal of all neurologic signs and clearing of the confusion. The remission has been maintained for two years. This case represents a primary infection of the CNS by histoplasma. The relationship between the HM and the CVH will be discussed.
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PMID:Histoplasma meningitis with common variable hypogammaglobulinemia. 61 43


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