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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At the 1990 World Congresses of Gastroenterology, the Working Party on Helicobacter pylori (H. pylori) recommended that, in suitable patients, the bacterium should be eradicated using a therapeutic regimen comprising a bismuth salt, tetracycline and metronidazole for two weeks. We have treated 40 patients infected with H. pylori with 'triple' therapy consisting of 120 mg tripotassium dicitrato bismuthate q.d.s., 500 mg tetracycline q.d.s. and 400 mg metronidazole t.d.s. for two weeks. The success rate, in terms of bacterial eradication, was 19/21 (90.5%) in patients with metronidazole-sensitive organisms, compared with only 6/19 (31.6%) in patients whose H. pylori were resistant to metronidazole (P less than 0.01). Side effects, particularly diarrhoea and vomiting/nausea, were common: 23/40 patients reported such symptoms during the 14-day course of therapy. Fifteen of these 23 patients completed the entire 14-day course, although suffering from significant side effects, while the remaining eight patients had to discontinue the treatment because side effects became intolerable. If a form of triple therapy is going to be widely used to eradicate H. pylori infection, the regimen will have to be simpler, shorter, produce fewer side effects and be more effective in patients with metronidazole-resistant bacteria.
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PMID:Experience with 'triple' anti-Helicobacter pylori eradication therapy: side effects and the importance of testing the pre-treatment bacterial isolate for metronidazole resistance. 142 Jul 35

The authors observed 6 cases of brain pseudotumours in children aged from 3 to 15 years. All patients had been referred with the diagnosis of brain tumour, with headaches, eye fundus changes fundus changes. Some children had nystagmus, squint, vomiting and dizziness. One child had pharyngitis, two had sinusitis. Contrast brain examinations gave normal results. Diet with salt and fluid restriction and oedema-reducing drugs (glycerol, mannitol, decadron) were used. In all patients the neurological and ophthalmological signs regressed within 3 to 12 weeks.
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PMID:[Pseudotumor cerebri in children]. 145 58

In a case-control study we evaluated the role of maternal behaviour, as reflected in maintenance of breast feeding and the use of oral rehydration therapy (ORT) at home during acute diarrhoea, in preventing dehydration in infants and young children. A systematic 5% sample was taken of all children aged 1-35 months attending the treatment centre of the International Centre for Diarrhoeal Disease Research, Bangladesh, with acute watery diarrhoea of six days or less between August 1988 and September 1989. There were 285 children with moderate or severe dehydration as cases and 728 with no dehydration as controls in the study. In a multivariate analysis using a logistic regression model we showed that withdrawal of breast feeding during diarrhoea was associated with a five times higher risk of dehydration compared with continuation of breast feeding during diarrhoea at home. Lack of ORT with either complete formula or a salt and sugar solution at home was associated with 57% higher risk of dehydration compared with receipt of a reasonable amount of ORT after controlling for several confounders. The confounding variables--that is, lack of maternal education, history of vomiting, high stool frequency, young age and infection with Vibrio cholerae 01--were also shown to be risk factors of dehydration. Health education programmes should promote continued breast feeding and adequate oral rehydration therapy for infants with acute diarrhoea at home.
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PMID:Breast feeding and oral rehydration at home during diarrhoea to prevent dehydration. 152 6

Salt losing nephropathy, occurring predominantly in male infants, has been reported in association with a spectrum of urologic diseases including obstructive uropathy and massive, infected vesicoureteral reflux (VUR). This has been called pseudo-hypoaldosteronism (PHA) or alternatively, pseudo salt-losing congenital adrenal hyperplasia (CAH), and is thought to reflect a tubular unresponsiveness to aldosterone. We report our experience with six cases, discuss one case in detail and review the 39 cases previously reported. A one month old male infant presented with a left upper quadrant mass. Signs and symptoms included vomiting, dehydration, hyponatremia and hyperkalemia. This suggested the diagnosis of CAH for which therapy was instituted. Ultrasonographic examination subsequently revealed the mass to be a urinoma in an infant with posterior urethral valve (PUV) and obstructive hydronephrosis.
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PMID:Salt losing nephropathy simulating congenital adrenal hyperplasia in infants with obstructive uropathy and/or vesicoureteral reflux--value of ultrasonography in diagnosis. 174 73

Type I pseudohypoaldosteronism (PHA) is a hereditary disease characterized by salt wasting resulting from target organ unresponsiveness to mineralocorticoids. We have studied two kindreds including a total of nine patients with PHA. In kindred I, the propositus presented with renal salt wasting in infancy (vomiting, failure to thrive, short stature, hyponatremia, hyperkalemia) and responded dramatically to a high salt diet (2.5 g/day). Sodium supplementation was discontinued at the age of two. In seven additional family members from three generations, clinical expression of PHA varied from asymptomatic to moderate. In affected members (propositus, mother, and two brothers), hyperaldosteronism persisted over 13 yr; however, the PRA decreased gradually to near normal values. Persistent hyperaldosteronism in the face of a decrease in PRA indicated the development of tertiary hyperaldosteronism due to autonomously functioning zona glomerulosa. The pedigree was consistent with an autosomal dominant mode of transmission with variable expression. In kindred II, the propositus, who was the product of a consanguineous marriage, developed severe renal salt losing at age 9 days. She had also increased salivary and sweat electrolytes consistent with PHA resulting from multiple organ unresponsiveness to mineralocorticoids. Life threatening episodes of salt wasting recurred beyond the age of 2 yr. At 5 yr of age she still requires high amounts of salt supplements (14 g/day). A sister died at 9 days of age with PHA symptoms. Six close relatives (parents, three siblings, maternal uncle) showed no biochemical abnormalities. This pedigree was consistent with an autosomal recessive mode of inheritance. In view of the findings on these two kindreds and the analysis of those in the literature, we conclude that type I PHA includes two clinically and genetically distinct entities with either renal or multiple target organ defects.
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PMID:Type I pseudohypoaldosteronism includes two clinically and genetically distinct entities with either renal or multiple target organ defects. 193 32

Genetic factors are known to play an important role in the variations in blood pressure levels. However, genetic factors that explain the higher average blood pressure levels of western hemisphere blacks when compared with African blacks have not been seriously considered. Because the genetic makeup of a population is largely determined by biological and ecological forces in the past, an examination of the biohistory of blacks, specifically the slavery era, was conducted. An overview of the salient findings of that investigation is included in this article. The published historical evidence on the transatlantic slave trade and New World slavery (from the 16th century to the 19th century) reveals that conditions existed for "natural selection," and therefore, genetic changes were virtually inevitable in the slave populations. During this period of history, mortality was extremely high, and fertility (or reproductive success) was so low among the survivors that most plantation societies in the western hemisphere depended on a constant importation of captives (over 12 million) from Africa for the viability of the plantation communities. Because the major causes of death were salt-depletive diseases such as diarrhea, fevers, and vomiting, it is argued that individuals with an enhanced genetic-based ability to conserve salt had a distinct survival advantage over others and were, therefore, more likely to bequeath their genotype to subsequent generations of Western hemisphere blacks. Thus, it is predicted that blacks in the Americas have a greater frequency of individuals with an enhanced genetic-based ability to conserve salt than African blacks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biohistory of slavery and blood pressure differences in blacks today. A hypothesis. 198 89

Acute barium salt poisoning may cause acute hypokalemia and result in respiratory paralysis and ventricular tachyarrhythmias. The early nonspecific gastrointestinal symptoms of barium poisoning due to food contamination could be confused with other benign food poisonings. Early diagnosis and initiation of intensive supportive care is essential. We report an outbreak of acute barium carbonate poisoning, occurring at a family reunion party, which resulted in 9 hospital admissions. All of the victims initially developed nausea, vomiting, abdominal colic, dizziness and watery diarrhea followed by numbness of the face and distal extremities 1-2 h after ingesting fried flour-coated sweet potatoes. The flour was later confirmed to be contaminated with barium carbonate. One person died in the emergency room with a serum potassium level of 0.8 mEq/L. Two other victims developed ventricular tachycardia and respiratory paralysis but completely recovered with the treatment advice provided by the poison center. The poison center was successful in helping to make the correct diagnosis in a timely manner, immediately distribute the treatment protocol, and coordinate the laboratory confirmation of barium carbonate poisoning.
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PMID:The essential role of a poison center in handling an outbreak of barium carbonate poisoning. 203 49

Two brothers, patient 1 with fever and vomiting, and patient 2 with failure to gain weight were studied. After 4 hr of water deprivation test, the urinary osmolality of the patient 1 was only 105 mOsm/liter and his body weight showed a 4.6% reduction. In response to desamino-8-D arginine vasopressin intranasal administration, no significant elevation of urinary osmolality of patient 1 occurred. After low dose vasopressin tests, the maximal urinary osmolality of their father was in the normal range, but that of their mother was below the normal range. Moreover, the patients showed no significant increase of urinary osmolality after the same tests. The brothers were diagnosed as nephrogenic diabetes insipidus (NDI) and their mother was diagnosed as a carrier. An early diagnosis of NDI is important, since adequate managements such as low-solute diet with restricted protein and salt intake or such as water intake at frequent intervals can prevent the hyperosmolality which would develop the delayed mental and physical developments. The usefulness of the combination of indomethacin with thiazide diuretics is described.
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PMID:A family case of nephrogenic diabetes insipidus. 209 13

Metabolic alkalosis is defined as a primary increase in plasma bicarbonate concentration. As a consequence of this increase, systemic alkalemia and secondary hypercapnia develop. In most instances metabolic alkalosis arises from loss of acid through the kidney or gastrointestinal tract. The causes of metabolic alkalosis can be separated into two groups. Those forms of alkalosis responsive to chloride salt administration (e.g., vomiting), are associated with extracellular fluid volume and chloride depletion. In contrast, alkalosis resistant to administration of chloride salt (e.g., primary aldosteronism), is usually associated with extracellular fluid volume expansion and a urine chloride above 20 mEq/L (mmol/L). Metabolic alkalosis; causes; diagnosis; clinical manifestations.
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PMID:[Water-electrolyte and acid-base disorders. VII. Metabolic alkalosis]. 222 26

The propensity to prefer and to consume salty foods varies considerably from person to person, and excessive salt intake has been linked to a number of pathological conditions. Extracellular dehydration occurs in humans after vomiting or diarrhea and is commonly observed during pregnancy. Because the hormonal responses to extracellular dehydration are known to increase salt appetite, we tested the hypothesis that extracellular dehydration during pregnancy increases the propensity of offspring to consume salt. Pregnant rats were treated with polyethylene glycol, which is known to produce extracellular dehydration and to exaggerate sodium appetite. The offspring of these treated pregnant rats showed an increase in salt appetite as compared with the offspring of control untreated dams. These results demonstrate that extracellular dehydration during pregnancy can enhance the natriophilic propensity in offspring and suggest that gravidic vomiting may contribute to the epidemiological factors of hypertension and other pathologies.
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PMID:Extracellular dehydration during pregnancy increases salt appetite of offspring. 230 41


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