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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As most diet therapy texts provide little information about psychiatric illnesses and their treatment, this article is intended as a brief introduction for dietitians. Several psychiatric illnesses, including schizophrenia, mood disorders, eating disorders, and substance abuse, may adversely affect food intake and nutritional status. The drugs used to treat those disorders similarly have effects on appetite and gastrointestinal function and interact with food and nutrients. Antipsychotics, antidepressants, and monoamine oxidase inhibitors (MAOIs) cause dry mouth, constipation, and weight gain. Lithium may cause nausea, vomiting, diarrhea, polydipsia, and weight gain. MAOIs have well-known interactions with foods containing tyramine. Lithium interacts with dietary sodium and caffeine; decreasing dietary intakes of those substances may produce lithium toxicity. Despite claims to the contrary, major psychiatric illnesses cannot be cured by nutritional therapies alone. Dietitians can, however, play an important role as part of a multidisciplinary team in the treatment of patients with psychiatric illness. Such a role includes nutrition assessment and monitoring, nutrition interventions, patient and staff education, and some forms of psychotherapy, including supportive and behavioral therapies for patients with eating disorders.
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PMID:Nutritional aspects of psychiatric disorders. 267 98

Twentyfour patients treated with irradiation to either their pelvis or their chest for neoplastic disease were included in a randomized study of radioprotection with sodium meclofenamate (Meclomen) (SM). Seventeen patients received SM 100 mg, p.os, t.i.d., and seven received placebo. The long-range radiation related chronic gastrointestinal and urinary tract toxicity was diminished by SM. At 12 months post irradiation, SM treated patients experienced less gastrointestinal and urinary symptoms, as well as less measured bladder contraction, than the controls. Acute gastrointestinal signs of radiotoxicity, however, seemed to have been enhanced by SM. The treated patients suffered from nausea, vomiting, and diarrhea. These acute toxic effects were temporary and reversible.
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PMID:Radio-protective effect of sodium meclofenamate. A prospective clinical trial. 268 95

Potassium is one of the most abundant ions in the human body and yet it is difficult to assess potassium balance. Potassium chloride is extensively used as a potassium supplement, both by physicians as a therapeutic modality and by the general public, mostly in the form of salt substitute. Therapeutically, both the oral and intravenous forms of potassium are utilised. Overdose of potassium is not as frequently encountered in clinical practice as hyperkalaemia (excess potassium in the body) due to acute or chronic renal disease. Potassium homeostasis is maintained very delicately and is governed by the daily consumption of potassium and the renal excretion mechanisms. Any change in these or related factors can present as hyperkalaemia. However, potassium overdoses leading to serious consequences do occur. Orally, the dose of potassium has to be large enough so that the normal excretory mechanisms for potassium are overcome and clinical toxicity occurs. It takes a much bigger dose of ingested potassium to produce toxicity in a person with normal renal function than in patients with compromised renal function. Potassium toxicity manifests in significant, characteristic, acute cardiovascular changes with ECG abnormalities. Besides cardiovascular effects, neuromuscular manifestations in the form of general muscular weakness and ascending paralysis occur. Gastrointestinal symptoms manifest as nausea, vomiting, paralytic ileus, and local mucosal necrosis which may lead to perforation. It is imperative when treating hyperkalaemia that the whole clinical picture is taken into account rather than the numerical potassium values. Only the extracellular potassium can be measured in the laboratory, yet 98% of the body potassium is intracellular and cannot be measured. In acute overdose situations due to ingestion of potassium salt, the general principles of treatment for overdoses should be followed. Calcium chloride infusion, dextrose and insulin in water, and correction of acidosis with sodium bicarbonate are helpful in controlling the acute, life-threatening cardiac arrhythmias. These modalities do not remove the excess potassium from the body. That is achieved either by utilising ion-exchange resins or by mechanically removing potassium via haemodialysis. To curtail inadvertent or accidental potassium overdoses, physicians should prescribe any potassium supplements very carefully to their patients and monitor the plasma potassium periodically.
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PMID:Clinical features and management of poisoning due to potassium chloride. 268 36

Cardinal signs of red mold toxicosis in man and farm animals are vomiting, nausea, diarrhea, and food refusal. The red mold toxicosis has been suggested to be induced by trichothecenes, which are produced by Fusarium fungi. Fusarenon-X (F-X) is one of the trichothecene mycotoxins. The ip injection of F-X to rats causes an expansion of the small intestine and watery diarrhea. In this study, we measured the concentrations of protein, sodium, potassium, and calcium in the serum of rat treated with F-X for the sake of demonstrating the loss of serum protein and the decreases of serum sodium and calcium by F-X. Since it is well known that some diarrheal diseases are due to the increase of cyclic nucleotide level in the intestinal mucosa, we also measured cyclic AMP and cyclic GMP levels in the intestinal mucosa. It was demonstrated that F-X did not increase the cyclic AMP and cyclic GMP levels in the jejunal and the ileal mucosa at 8 and 24 hr after F-X treatment. The results obtained in this work suggest that F-X-induced diarrhea is not mediated by the cyclic nucleotide system.
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PMID:Studies on mechanisms of diarrhea induced by fusarenon-X, a trichothecene mycotoxin from Fusarium species: fusarenon-X-induced diarrhea is not mediated by cyclic nucleotides. 282 46

Cis-diamminedichloroplatinum II (CDDP; 52-169 mg/m2) mixed with angiotensin II (1.5-10 micrograms/min) was infused into the hepatic artery in 33 patients with hepatocellular carcinoma. Simultaneously, sodium thiosulfate (10-50 g) was administered intravenously in order to reduce the systemic toxicity of CDDP. Over 50 per cent reduction in tumor size was obtained in 18 patients (55%). Complete response was achieved in 4 patients (12%). Serum alpha-fetoprotein (AFP) levels decreased by more than 75 per cent in 10 of 18 patients in whom the previous AFP level was more than 200 ng/ml. The one year survival rate was estimated at 61 per cent by the Kaplan-Meier method. Alimentary symptoms (nausea, vomiting) were mild or non-existent in nearly 90 per cent of treatments. Peptic ulcer and abdominal pain were manifested in small numbers. Severe changes in the laboratory data were not observed. High dosage arterial infusion of CDDP and angiotensin II and intravenous injection of sodium thiosulfate was well tolerated and gave effective therapy in hepatocellular carcinoma.
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PMID:Intra-arterial cis-platinum infusion with sodium thiosulfate protection and angiotensin II induced hypertension for treatment of hepatocellular carcinoma. 283 19

Seventeen patients with primary or metastatic malignancy in the liver were treated with 'two-route chemotherapy' (TRC). One course of this TRC consisted of hepatic artery infusion of cisplatin, 120 mg/m2, in combination with concurrent intravenous administration of sodium thiosulfate, its neutralizing agent, at a dose of 9.0 g/m2 by a rapid push, followed by 1.2 g/m2/h by continuous infusion for 6 h. Five of 11 (45%) hepatocellular carcinoma and two of six (33%) metastatic tumors achieved partial response. Although almost all patients experienced nausea or vomiting, severe side-effects, including nephrotoxicity, peripheral neuropathy or ototoxicity, were not encountered. Myelosuppression was observed in one patient after seven courses of this TRC. The results indicate that TRC may be relatively effective against hepatic malignancies in patients without severe toxicity.
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PMID:'Two-route chemotherapy' using intra-arterial cisplatin and intravenous sodium thiosulfate, its neutralizing agent, for hepatic malignancies. 266 Dec 36

Apomorphine, a centrally-acting emetic, was administered subcutaneously (50 micrograms/kg) to nine normal subjects (four male, five female; aged 22-36 years) and four patients with idiopathic diabetes insipidus (DI) (one male, three female; aged 24-49 years). In the normal subjects this stimulus caused nausea (and vomiting in seven of nine) with a latency of 9.5 +/- 0.9 min which was followed by a large increase in plasma arginine vasopressin (AVP) concentration (from 0.9 +/- 0.2 pmol/l to 249 +/- 104 pmol/l at 15 min after the onset of symptoms; mean +/- SEM, P less than 0.01). There was a small but significant increase in plasma oxytocin (OXT) concentration (from 1.6 +/- 0.4 pmol/l to 6.2 +/- 3.4 pmol/l; P less than 0.05). Mean arterial pressure (MAP) fell slightly (from 87 +/- 1.9 mm Hg to 71 +/- 4.4 mm Hg; P less than 0.05) 15 min after the onset of nausea; there was no change in blood haematocrit or plasma osmolality and sodium concentration. In the DI patients apomorphine produced nausea (with vomiting in three of four) with a latency of 10.0 +/- 1.4 min but failed to cause an increase in either plasma AVP or OXT. In the DI patients the fall in MAP did not reach statistical significance (83 +/- 4 mm Hg to 71 +/- 11 mm Hg); there was also no change in haematocrit, osmolality or sodium concentration. Ipecacuanha, an emetic with both peripheral and central actions, was administered orally to seven normal subjects (three male, four female; aged 22-36 years) six of whom also underwent apomorphine tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of plasma oxytocin and arginine vasopressin to nausea induced by apomorphine and ipecacuanha. 290 23

The recognition that inflammatory events in the airways play a key role in the pathogenesis of asthma has led to a relentless search for pharmacological agents which modify these processes. Nedocromil sodium (Tilade) represents one such agent. Nedocromil sodium, when inhaled by patients with asthma (0.05-0.50% nebulized, 0.5-4.0 mg m.d.i.), has been shown to inhibit immediate bronchoconstriction provoked by challenges with allergen (10 studies), exercise (five studies), isocapnic hyperventilation, fog and sulphur dioxide (one study each) and adenosine (two studies). With these challenges, inhibition of bronchoconstriction exhibited dose-dependency up to 4 mg, with nedocromil sodium being up to four times more potent than sodium cromoglycate. When inhaled prior to allergen provocation, nedocromil sodium inhibited the late asthmatic reaction; when taken regularly during the pollen season, it attenuated the allergen-induced increase in non-specific bronchial responsiveness. The efficacy of nedocromil sodium (4 mg q.i.d.) in the treatment of clinical asthma was initially shown in four open studies and subsequently confirmed in nine double-blind, placebo-controlled 4-12 week studies on patients with seasonal and perennial asthma. Further clinical trials (eight studies) identified some difficulty in replacing inhaled corticosteroids with nedocromil sodium, especially if the corticosteroids were reduced rapidly (four studies). However, two studies have shown that nedocromil sodium produced further improvement in asthma symptoms when used in addition to bronchodilators and inhaled corticosteroids. Treatment with nedocromil sodium (4 mg q.i.d.) for up to 52 weeks demonstrated a progressive reduction in bronchodilator usage throughout the whole treatment period. During clinical assessment, nedocromil sodium was well tolerated, side-effects being unpleasant taste, nausea and headache. In most cases the adverse reactions were mild and transient, although in approximately 3% of patients they resulted in withdrawal from clinical trials. Thus, nedocromil sodium is a novel drug of proven efficacy in the treatment of asthma. Its position in the therapeutic armamentarium is likely to be as an adjunct to bronchodilators and inhaled steroids, to produce improvement in symptoms beyond that achieved with the already established drugs.
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PMID:Clinical evaluation of nedocromil sodium in asthma. 302 89

The efficacy of intramuscular methylprednisolone acetate in maintaining the antinauseant effect of intravenous methylprednisolone sodium succinate was assessed in a prospectively-randomized, double-blind, crossover-design trial. Of 150 patients entered, 127 were evaluable. There was no statistically significant difference between methylprednisolone acetate and saline placebo, although patient preferences slightly favoured the methylprednisolone acetate for nausea, vomiting, and overall effectiveness.
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PMID:Failure of methylprednisolone acetate to prolong the antinauseant effect of intravenous methylprednisolone sodium succinate in patients receiving chemotherapy. 305 74

The plasma concentration of arginine vasopressin (AVP) is increased in diabetic ketoacidosis (DKA) in man and the rat. Although haemodynamic changes and nausea/emesis may account for the increased secretion of AVP in severe human DKA, they appear not to be responsible in moderate DKA. Streptozotocin-treated rats were studied to investigate other factors possibly involved in the secretion of AVP in DKA. Wistar rats were injected i.p. with streptozotocin (150 mg/kg body weight). Diabetic rats were maintained on 3-4 units protamine-zinc insulin (PZI)/day for 11 days, after which PZI was withdrawn for 3 days in half the rats. The plasma concentration of AVP was greater in rats with DKA than in normal controls (mean 11.4 pmol/l compared with 1.6 pmol/l; P less than 0.05). Rats with DKA had higher plasma osmolality and concentrations of blood glucose, beta-hydroxybutyrate and acetoacetate, but lower plasma carbon dioxide content than diabetic and normal controls (P less than 0.05). There were no differences in plasma levels of sodium, urea or haematocrit between rats with DKA and controls. In a separate study involving the same procedures, daily systolic blood pressure was measured using a tail cuff to occlude arterial inflow to the tail, and subsequent detection of the cuff pressure at which the first arterial pulsation appeared. No significant differences were detected between normal and diabetic rats and rats with DKA. Exponential relationships between plasma osmolality and plasma AVP (correlation coefficient, r = + 0.75; P less than 0.01), and plasma ketone bodies and plasma AVP (r = +0.60; P less than 0.05) were obtained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Possible mechanisms responsible for the rise in plasma vasopressin associated with diabetic ketoacidosis in the rat. 312 19


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