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)

Classic renal tubular acidosis is characterized by a primary defect in establishment of a large hydrogen ion gradient across the distal renal tubule. Thus the development of hyperchlorenic metabolic acidosis follows. In addition, hypokalemia results from renal potassium wasting secondary hyperaldosteronism from sodium wasting and contraction of the extracellular fluid. The presenting signs and symptoms are growth retardation, fatigue, periodic paralysis, polyuria, polydipsia, vomiting and constipation as well as nephrocalcinosis and nephrolithiasis. It is suggested that effective treatment with alkali therapy requires markedly higher doses than formerly recommended, and may related to a higher rate of endogenous acid production from (1) intermediary metabolism of sulfur amino acids and organic acids, (2) impaired tubular reabsorption of bicarbonate and (3) hydrogen ion release from hydroxyapatite formation. It is also suggested that acidosis may interfere with vitamin D metabolism and thus play an important role in the pathoetiology of the growth failure in children with this disorder.
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PMID:Acid-base, calcium, potassium and aldosterone metabolism in renal tubular acidosis. 3 60

In distal (type 1) RTA, renal acid excretion is impaired by the inability to establish adequate pH gradients between plasma and distal tubular fluid at any level of acidosis. Main clinical signs in infancy are anorexia, vomiting and failure to thrive. Despite low serum bicarbonate levels the renal threshold of bicarbonate is normal, while urinary pH levels are high even with values below the threshold. Under conditions of bicarbonate-induced systemic alkalosis urinary the pCO2 exceeds blood pCO2 in normal subjects. by contrast, the urinary pCO2 tension is not significantly greater in distal RTA, indicating a failure of the cells of the distal nephron to secrete hydrogen ions even without a gradient. Red cell carbonic anhydrase is within the normal range, whilst the inhibition of carbonic anhydrase activity has no effect on distal tubular function. Until now no histological or enzymatic defect could be detected to explain the ineffective acidification. Bicarbonate loading is followed by a lowering of calcium excretion to within the normal range and a decrease in the uncharacteristic renal hyperaminoaciduria.
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PMID:[Investigations on the pathogenesis of distal renal tubular acidosis (author's transl)]. 3 16

This study is a description of a patient who exhibited diabetic ketosis associated with an alkalosis rather than acidosis and a review of eight previously reported cases. Precipitating factors for this syndrome are severe vomiting with loss of hydrogen, potassium, and chloride ions, and dehydration. The ingestion of alkali may also result in this mixed acid-base disturbance. Treatment consists primarily of replacement of potassium and chloride. All reported patients had received large doses of insulin for initial therapy; however, limited insulin (20 U) therapy in this patient almost completely reversed the metabolic abnormality with 12 hours.
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PMID:Mixed acid-base abnormalities in diabetes. 10 96

The usual metabolic derangement in uncontrolled diabetes mellitus is metabolic acidosis, with an increase in the anion gap because of increased ketoacids and lactate. However, diabetic ketoalkalosis may occasionally be encountered, the prominent clinical feature of which is vomiting, with depletion of potassium, chloride, and hydrogen ions. Self-medication with absorbabe alkali may also contribute to the alkalosis. It would be dangerous to treat hyperlgycemic patients with alkali if their condition is ketoalkalosis instead of ketoacidosis.
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PMID:Diabetic ketoalkalosis. 45 54

The mechanisms underlying ethylmalonic-adipic aciduria were studied in a 5-yr-old girl. Oxidation of radioactive substrates by cultured skin fibroblasts from the proband and asymptomatic family members was also determined and compared to that by normal fibroblasts and that by cells from a patient with glutaric aciduria type II. Feeding medium-chain triglycerides promptly induced vomiting and lethargy accompanied by a pronounced increase of urinary ethylmalonate. Significant increases of serum isovalerate and urinary isovalerylglycine were observed after leucine feeding, but urinary glutarate increased only slightly after lysine feeding. Thus, the results from clinical investigation remained equivocal as to whether pathways other than fatty acid oxidation were blocked in our patient. Oxidation of [1-(14)C]butyrate by cultured skin fibroblasts from the proband was reduced to 14% of control. In vitro oxidation of [2-(14)C]lysine and [2-(14)C]leucine was also reduced to 28 and 23% of control, respectively. Much more severe reduction in oxidation of these three substrates (3, 9, and 9%, respectively) was observed in glutaric aciduria type II cells. These results indicated that in the proband, degradative pathways of fatty acids, lysine, and leucine are blocked at the steps of butyryl-CoA, glutaryl-CoA, and isovaleryl-CoA dehydrogenases, respectively, as in the case of glutaric aciduria type II. Because activities of multiple acyl-CoA dehydrogenases are reduced, a deficiency of electron-transferring flavoprotein, which serves as a hydrogen-acceptor for these dehydrogenases, is postulated as the underlying mechanisms of these two diseases, but a genetic heterogeneity was indicated by significant differences in the residual activities in these two types of cells. The hypothesis of more than one mutant allele of an autosomal recessive gene was also suggested by the study on cells from asymptomatic members of the family.
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PMID:Ethylmalonic-adipic aciduria. In vivo and in vitro studies indicating deficiency of activities of multiple acyl-CoA dehydrogenases. 50 Aug 26

The mechanisms of acid base balance in digestive organs, including stomach, intestine as well as liver, have been described in the present paper. The stomach secrets large amount of acid as well as sodium bicarbonate, so that hydrogen ion would be lost in the severe vomiting state such as pyloric stenosis, resulting in metabolic alkalosis and hypokalemia. In the diarrheal condition, sodium bicarbonate would be lost in large amount, causing metabolic acidosis and hypokalemia. Hepatic failure induces the respiratory alkalosis of which mechanisms have not been clarified yet. In any case, urgent correction of acid base imbalnce would be crucial. It is, however, obscure to date how the systemic acid base imbalnce affects the function of the digestive system. This issue would be promising field in the investigation of digestive diseases.
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PMID:[Acid base balance in the digestive system]. 143 24

Synthesis and pharmacological evaluation of a series of 1,2-dihydro-1-[(5-methyl-1-imidazol-4-yl)methyl]-2-oxopyridine 5-HT3 antagonists are described. The key pharmacophoric elements were defined as a basic nitrogen, a linking group capable of hydrogen bonding interactions, and an aromatic moiety. 1,2-Dihydro-2-oxopyridine moiety could be a good linking group because of its nicely planar structure. The steric limitations of the aromatic moiety were investigated by X-ray analysis and computer analysis and shown to be optimal when the aromatic moiety was constrained within an arched planar system, which could be successfully replaced by 3-(2-thienyl)-2-oxopyridine function or 6-amino-7-chloro-1-isoquinolinone function without any loss of the activity. Among the synthesized compounds, 42 showed the most potent activity in the inhibition of Bezold-Jarisch reflex in rats. Compounds 44a and 64 were orally active in the protection against cisplatin-induced emesis in dogs or ferrets. Structure-activity relationships are discussed.
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PMID:Novel 5-HT3 antagonists. Isoquinolinones and 3-aryl-2-pyridones. 152 80

The ingestion of hydrogen peroxide is usually benign. However, the ingestion of greater than 10% hydrogen peroxide can result in significant pathology. Two fatalities are reported in the literature involving children who ingested 27% and 40%. We report a case involving the ingestion of one mouthful of 35% hydrogen peroxide by a 26-month-old female. The child vomited spontaneously. In the Emergency Department the child was lethargic and had an episode of bright red emesis. Several hours later the child experienced a fainting episode followed by a brief respiratory arrest after which she began drooling bright red blood. The initial oral evaluation was negative. Endoscopic evaluation performed 16 hours postingestion revealed erosion of the cardia of the stomach, erythema of the lower esophageal sphincter, and an additional gastric burn. The child was observed for six days and discharged. Follow-up endoscopy performed 12 days postingestion showed only minimal hyperemia in the cardia of the stomach. Exposures to concentrated hydrogen peroxide should be managed aggressively.
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PMID:Ingestion of 35% hydrogen peroxide. 238 Oct 26

Apart from the classic distal renal tubular acidosis (RTA), the proximal RTA, and a few cases of distal RTA and renal bicarbonate wasting we know only 2 cases of infantile transient distal RTA with bicarbonate wasting. A 3 month-old male patient is admitted because of deficient suction, vomiting and dehydration. Despite a strong metabolic acidosis (pH 7,09, bicarbonate 8,6 mMol/l, chloride 110 meq/l) the urine is constantly alkaline; clinically the disease manifests itself in the form of an alkali-resistant RTA. Accompanying troubles such as inner ear deafness, G6PDH deficiency, hyperparathyroidism and vitamin D intoxication are to be excluded. A bicarbonate study carried out with care so as to prevent extracellular fluid expansion reveals the lack of excretion of titratable acid (-2.4 to +4.7 mueq/min/1.73 m2), an reduced excretion of ammonium (5 to 24.8 mueq/min/1.73 m2) with regard to GFR (42.4 ml/min/1.73 m2), and a constant loss of bicarbonate (FE HCO3- about 10%) covering most of the bicarbonate plasma concentration, which results in a constantly negative net acid excretion. Even with alkalosis there is no urine minus blood pCO2 increase. The renal excretion of gamma GT is significantly reduced. On substitution with high quantities of bicarbonate (10 meq/kg BW/day) the defect heals up at the age of 13 months. The pathogenesis of this disease is not quite clear, but is similar to that of the Lightwood infantile RTA. The acidification defect may be explained by a deficient hydrogen ions--secretion in the distal tubule; as for kinetics, it is not in the proximal tubule that the bicarbonate wasting occurs but it may be due to increased sodium delivery to the distal nephron.
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PMID:[Infantile transitory distal renal tubular acidosis with bicarbonate loss]. 286 14

Idarubicin (IDA) is an anthracycline analog which differs from the parent compound by the substitution of a C4 methoxyl group with an hydrogen atom in the aglycone moiety. This drug has shown greater potency and activity in experimental and human leukemias and lymphomas by intravenous and oral routes of administration together with less cardiotoxicity than doxorubicin (DX) and daunorubicin (DNR). We have treated 15 patients with advanced multiple myeloma (MM) refractory or relapsed to standard chemotherapy regimens. The treatment schedule consisted of idarubicin 40 mg/m2 orally on day 1 every 3 weeks for 6-8 months. We obtained 8/14 partial response, 4/14 minor response and 2 progressions. One patient was not evaluable for the response because of liver toxicity not related to IDA administration. The median duration of response was 8 months with a minimum of 2 and a maximum of 12 months. Hematologic toxicity occurred in about 20% of patients and no treatment was delayed. Cardiotoxicity, defined as impairement of left ventricular ejection fraction (LVEF), was observed in one case. The major systemic toxicity observed was nausea in 80% of patients and vomiting in 40%. Hair loss resulting was socially acceptable. These results indicate that IDA is useful as a single agent, easy to administer, not cross resistant with DX and recommended for a combination regimen.
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PMID:A phase II study of idarubicin (4-demethoxydaunorubicin) in advanced myeloma. 316 69


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