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)

Hypernatremic dehydration is a fairly common and potentially very dangerous illness in infants and children. It occurs during the course of a wide variety of illnesses. Predisposing factors include central nervous system diseases, decreased fluid intake, increased fluid losses from hyperventilation, perspiring, diarrhea and emesis, increased aldosterone output (contributing to sodium retention), the infant's high obligatory renal water loss and the practice of feeding infants fluids with a comparatively high solute content. If the attending physician is aware of the predisposing factors and makes an early diagnosis and then rehydrates the patient slowly using solutions which contain some salt, the outcome will most likely be favorable. Even though the brain appears to be damaged during rehydration, the patient may make a complete recovery if proper supportive measures are instituted.
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PMID:Hypernatremia. Its significance in pediatric practice. 1386 86

In a double blind, 3x3 factorial (volumexdose) study, 70 adult females (18-60 years of age) at four different international sites (total pooled n=269) were given 100, 150, or 200ml of bottled drinking water with 0.4, 0.8, or 1.2mg of copper (Cu) as the sulfate salt once each week. Two additional doses (0 and 1.6mg Cu) were added at the 200ml volume to determine a dose-response relationship and corroborate previously reported results. All subjects completed a questionnaire at 0, 0.25, and 1h post-dosing that screened for positive gastrointestinal (GI) effects (nausea, vomiting, abdominal pain, and diarrhea). Nausea was the most prevalent symptom reported and was generally reported within the first 15min (water volume, p<0.032; copper dose, p<0.0001; and water volumexcopper interaction, p<0.97). As volume increased, the effect of Cu-induced nausea decreased; as Cu dose increased, the incidence of nausea increased. At 200ml, a significant increase in reported incidence of nausea at 0.25h occurred at 1.2 mg Cu (6mg Cu/L), indicating a NOAEL of 0.8mg Cu (4mg Cu/L) for adult females. These data confirm a previously determined human acute NOAEL for Cu added to distilled water, and provide additional, controlled human data for determining safe concentrations of Cu in drinking water.
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PMID:Confirmation of an acute no-observed-adverse-effect and low-observed-adverse-effect level for copper in bottled drinking water in a multi-site international study. 1462 88

Previous results indicate that pretreatment with lobeline attenuates methamphetamine (METH) self-administration in rats, but not by acting as a substitute reinforcer. Given these findings, it has been suggested that lobeline may serve as a useful pharmacotherapy for psychostimulant abuse. However, because lobeline produces emesis and nausea in humans, the present study examined whether lobeline has direct effects on taste avoidance behavior in rats within the same dose range shown previously to decrease METH self-administration. Two experiments utilized a Pavlovian conditioning procedure to determine if lobeline produces conditioned taste avoidance (CTA) in rats. In Experiments 1 and 2, rats consumed either novel milk or salt solutions, respectively, and within 10 min, were injected with lobeline (0.3-3.0 mg/kg) or METH (0.3-3.0 mg/kg). A single-bottle test conducted 48 h after flavor-drug pairings indicated that the dose of lobeline that reduced METH self-administration in a previous study (i.e., 3.0 mg/kg) also produced reliable CTA for milk and salt solution. These findings suggest a need to develop lobeline analogs that reduce METH self-administration, but do not produce CTA following the consumption of a novel solution.
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PMID:Lobeline produces conditioned taste avoidance in rats. 1515 28

Hyponatremia caused by an inappropriately high level of antidiuretic hormone secretion after spinal surgery is an uncommon and self-limiting phenomenon that resolves within 2 or 3 weeks. During the early postoperative period, the patient's urine output and serum level of sodium should be monitored closely to prevent possible serious complications of the syndrome of inappropriate secretion of antidiuretic hormone. Symptoms vary depending on the severity of the hyponatremia and can range from mild headache, muscle cramps, nausea, and vomiting to convulsions, coma, and death. Treatment options include fluid restriction, oral intake of salt, and hypertonic saline. It is important that spine surgeons recognize this phenomenon early and treat it appropriately and conservatively to prevent possible serious complications.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone and hyponatremia after spinal surgery. 1519 39

Although a plethora of reports on life-threatening complications of salt emesis has been published since the early 1960s, salt is still used to induce emesis in cases of intoxication in the clinical as well as in the domestic setting. We report three cases of fatal hypernatremia after salt was used as an emetic. All fatalities were subjected to medico-legal autopsy at the Institute of Legal Medicine in Hamburg, Germany. In all cases, symptoms of cerebral damage such as seizures, fever and somnolence developed within hours after salt ingestion. All individuals were admitted to hospital before their deaths. Here, severe hypernatremia (up to 245 mmol/l) was detected, and all patients died under the clinical picture of cerebral edema despite intensive medical treatment. At autopsy, unspecific signs of a central regulatory failure were present. Histology revealed crenated red blood cells and few venous microthrombi in internal organs. Neuropathological investigations yielded no specific results but confirmed fatal cerebral edema and excluded other cerebral causes of death. Viewing the results of clinical and post-mortem investigations together, death could clearly be attributed to excessive salt intake in all cases.
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PMID:Fatal hypernatremia after using salt as an emetic--report of three autopsy cases. 1555 15

Salt appetite was investigated in 14 patients with congenital adrenal hyperplasia of the salt-wasting form (SW group), 12 patients with the simple virilized form who are not salt losing, and 18 healthy siblings. Salt appetite was evaluated by questionnaire, preference tests, and dietary analyses. The findings showed that SW who were not therapeutically normalized showed increased salt appetite but no change in sweet preference. Their salt appetite correlated with symptoms of salt wasting, namely, plasma renin activity, plasma K(+), and urine Na(+) and (inversely) with blood pressure. Sensitivity to the taste of NaCl was not altered. Factor analyses of a larger group confirmed the distinction between salt appetite and sweet preference, but intake of dietary Na(+) and sweet carbohydrates and intake of salty and sweet snacks did not reflect distinct salt or sweet preferences. We confirm that putative perinatal dehydration, due to maternal nausea and vomiting during pregnancy, childhood vomiting, and diarrhea with occasional saline infusion, was related to increased salt appetite in adolescence. The findings suggest that salt appetite in humans is determined by interdependent, innate, physiological, and acquired attributes. Salt appetite in SW patients is an adaptive response mediated by the renin-angiotensin system, an innate predisposition to acquire salt preference (in anticipation of both sodium loss and its consequence), and imprinting by perinatal hyponatremic occurrences. Our findings contribute to understanding human salt intake, provide insight into the motivation for salt in patients with congenital adrenal hyperplasia 21-OH deficiency, and may point the way to improvements in therapeutic compliance in these patients.
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PMID:Increased salt appetite in patients with congenital adrenal hyperplasia 21-hydroxylase deficiency. 1565 Jan 22

The purpose of this study was to investigate the relationship between salt taste perception and blood pressure (BP) in normotensive adolescents as modified by maternal fluid losses during the first trimester of gestation. Seventy-two healthy adolescents (42 boys) aged between 9.0-21.1 years, recruited from the population-based RICARDIN study, were included. A maternal questionnaire about the duration of pregnancy, birth weight and vomiting or diarrhoea in the first trimester of gestation was collected. The sample was categorized into: "vomiter descendents", those whose mother reported significant vomiting in the first trimester of gestation and "non-vomiter descendents" the remaining. Height, weight, and standardised BP measurement were recorded. Salt gustatory performance was assessed using a behavioral sensitivity test to determine the lower NaCl gustatory threshold, and a behavioral discrimination test, measuring the ability to distinguish among different saline solutions. Salt taste sensitivity showed a significant correlation with systolic BP (SBP) in "vomiter descendents" ( r = -0.66; P =0.003), but not in "non-vomiter descendents". Adjusted by gender, and actual height and weight, salt sensitivity performance remained significantly related to SBP. An association between descendents' SBP and maternal vomiting during gestation exists, adding a new element of evidence to the "Barker hypothesis".
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PMID:Maternal pregnancy vomiting and offspring salt taste sensitivity and blood pressure. 1586 54

A 17-month-old boy presented with failure to thrive, polyuria, and vomiting. He had been diagnosed clinically with nephrogenic diabetes insipidus and treated by amiloride and hydrochlorothiazide combination without a satisfactory outcome at another center since 1 year of age. The diagnosis was confirmed by genetic analysis (AVPR2mutation), and the treatment was modified to include rofecoxib (a selective cyclooxygenase-2 inhibitor) in addition to hydrochlorothiazide and amiloride. This combination along with a low-salt diet resulted in a dramatic decrease in urinary free-water loss, while no side effect was noted. Because of prohibition of rofecoxib, it had to be substituted first by indomethacin and then by ibuprofen. However, both drugs were ineffective in controlling water diuresis. Thus, we had to replace these drugs by celecoxib (another selective cyclooxygenase-2 inhibitor). We conclude that the combination hydrochlorothiazide/amiloride/cyclooxygenase-2 inhibitor could be successfully used to treat congenital nephrogenic diabetes insipidus.
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PMID:Efficacy of COX-2 inhibitors in a case of congenital nephrogenic diabetes insipidus. 1624 Jan 60

From 1983 to 1991, iron caused over 30% of the deaths from accidental ingestion of drug products by children. An evidence-based expert consensus process was used to create this guideline. Relevant articles were abstracted by a trained physician researcher. The first draft of the guideline was created by the primary author. The entire panel discussed and refined the guideline before its distribution to secondary reviewers for comment. The panel then made changes in response to comments received. The objective of this guideline is to assist poison center personnel in the appropriate out-of-hospital triage and initial management of patients with suspected ingestions of iron by 1) describing the manner in which an ingestion of iron might be managed, 2) identifying the key decision elements in managing cases of iron ingestion, 3) providing clear and practical recommendations that reflect the current state of knowledge, and 4) identifying needs for research. This guideline applies to ingestion of iron alone and is based on an assessment of current scientific and clinical information. The expert consensus panel recognizes that specific patient care decisions may be at variance with this guideline and are the prerogative of the patient and the health professionals providing care, considering all of the circumstances involved. The panel's recommendations follow; the grade of recommendation is in parentheses. 1) Patients with stated or suspected self-harm or who are victims of malicious administration of an iron product should be referred to an acute care medical facility immediately. This activity should be guided by local poison center procedures. In general, this should occur regardless of the amount ingested (Grade D). 2) Pediatric or adult patients with a known ingestion of 40 mg/kg or greater of elemental iron in the form of adult ferrous salt formulations or who have severe or persistent symptoms related to iron ingestion should be referred to a healthcare facility for medical evaluation. Patients who have ingested less than 40 mg/kg of elemental iron and who are having mild symptoms can be observed at home. Mild symptoms such as vomiting and diarrhea occur frequently. These mild symptoms should not necessarily prompt referral to a healthcare facility. Patients with more serious symptoms, such as persistent vomiting and diarrhea, alterations in level of consciousness, hematemesis, and bloody diarrhea require referral. The same dose threshold should be used for pregnant women, however, when calculating the mg/kg dose ingested, the pre-pregnancy weight of the woman should be used (Grade C). 3) Patients with ingestions of children's chewable vitamins plus iron should be observed at home with appropriate follow-up. The presence of diarrhea should not be the sole indicator for referral as these products are often sweetened with sorbitol. Children may need referral for the management of dehydration if vomiting or diarrhea is severe or prolonged (Grade C). 4) Patients with unintentional ingestions of carbonyl iron or polysaccharide-iron complex formulations should be observed at home with appropriate follow-up (Grade C). 5) Ipecac syrup, activated charcoal, cathartics, or oral complexing agents, such as bicarbonate or phosphate solutions, should not be used in the out-of-hospital management of iron ingestions (Grade C). 6) Asymptomatic patients are unlikely to develop symptoms if the interval between ingestion and the call to the poison center is greater than 6 hours. These patients should not need referral or prolonged observation. Depending on the specific circumstances, follow-up calls might be indicated (Grade C).
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PMID:Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. 1625 38

A 39-yr-old male with hepatorenal syndrome type 1 and refractory ascites was treated with continuous renal replacement therapy (CRRT) resulting in clinical improvement. He was positive for antibodies to hepatitis B, C, and human immunodeficiency viruses, and had a history of chronic alcohol and iv drug abuse. The patient had 4 hospital admissions during a 12-wk period. He first presented with advanced liver disease including pedal edema and a serum ammonia level of 56 micromol/L (reference range: 11 - 35 micromol/L). In subsequent admissions, he had asterixis, nausea, vomiting, jaundice, and worsening pedal edema. On his 4th admission, there was lethargy, tense ascites, decreased urinary output, bilateral edema of the lower extremities and scrotum, serum creatinine of 6.2 mg/dl (reference range: 0.6 - 1.5 mg/dl), and weight gain of 16 kg during the prior 8 wk. During the first 3 hospitalizations, he was treated with lactulose with slight improvement. On the 4th admission, he was started on low-dose dopamine (3 microg/kg/min) and 25% salt-poor albumin without clinical improvement. A pulmonary artery catheter was placed and hemofiltration by CRRT was performed for 5 days, with removal of 26.7 L of fluid and a net reduction of 11 kg of body weight. Serum creatinine decreased to 4.2 mg/dl during CRRT and was 2.2 mg/dl at hospital discharge 2 weeks later. His PaO(2) improved from 66 to 78 mmHg and his systemic vascular resistance increased from 571 to 799 dyne.sec/cm(5). CRRT was effective in relieving severe fluid retention and producing marked clinical improvement. We suggest that CRRT should be considered for the treatment of refractory ascites including that caused by hepatorenal syndrome.
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PMID:Hepatorenal syndrome: resolution of ascites by continuous renal replacement therapy in an alcoholic coinfected with hepatitis B, C, and human immunodeficiency viruses. 1650 Dec 43


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