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)

A 17-year-old female weighing 37 kg and 140 cm in height was referred to our hospital for evaluation of dwarfism and primary amenorrhea. She was delivered with 3350 g in weight and 50 cm in height after a ten month pregnancy without complications. No abnormal findings were revealed in physical appearance except critomegaly. Episodes of nausea, vomiting and dehydration were rare throughout her childhood, but she had a tendency to salt craving. At the age of 14, her height was 140 cm. On admission, her physical development was markedly retarded for her age, except external genitalia. Diffuse pigmentations on the trunk and extremities were observed. Her blood pressure was normal (112/62 mm Hg). Serum potassium concentration was 2.9 mEq/L. Arterial-blood gas analysis revealed metabolic alkalosis. Both of renin activity (PRA) and aldosterone concentration (PAC) in plasma at rest were markedly elevated to 15.5 ng/ml/h and 107.1 ng/dl, respectively. The plasma concentrations of pregnenolone (1449 ng/dl), progesterone (178 ng/dl), 17-OH-pregnenolone (1613 ng/dl), 17-OH-progesterone (180 ng/dl), dehydroepiandrosterone (3706 ng/dl), androstendione (824.6 ng/dl) and testosterone (900 ng/dl) were high, whereas deoxycorticosterone (15.7 ng/dl), corticosterone (0.65 microgram/dl) and cortisol (6.8 micrograms/dl) were within normal limits. Urinary 17-KS excretion showed high levels between 65.7 and 109.4 mg/day, while urinary 17-OHCS excretion was normal (5.7-7.0 mg/day). Vascular response to angiotensin II (A-II) was attenuated. Distal fractional chloride reabsorption was decreased (CH2O/CH2O+CCl = 0.62, normal: 0.92 +/- 0.04). Moderate hyperplasia of the juxtaglomerular cells was demonstrated in biopsy specimen of the kidney. Cytogenetic studies showed a 46, XX chromosome constitution with translocation of the long arm of chromosome 6 to the short arm of chromosome 9. Her mother as well as younger brother and sister, whose electrolytes and arterial-blood gas analysis showed normal values, had chromosomes with the same translocation. Treatment with dexamethasone (2 mg/day) reduced every adrenal steroids to normal range, but PRA and PAC remained high levels. Furthermore, neither hypokalemic alkalosis nor vasoreactivity to exogenous A-II was improved. Indomethacin (75 mg/day) decreased urinary excretion of prostaglandin E2 from a high level of 738.4 ng/day to 433.4 ng/day and normalized metabolic alkalosis. Vascular response to A-II was moderately improved. However, serum potassium remained low.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A case of 21-hydroxylase deficiency and Bartter's syndrome associated with a balanced 6-9 translocation]. 349 Oct 9

Thirty four beagle dogs, male and female were orally given 10, 30, 100 and 200 mg/kg/day of captopril, an angiotensin converting enzyme inhibitor, for 3 months followed by a recovery test for 4 weeks. One of 4 female dogs which were treated with the highest dose of 200 mg/kg/day throughout the experimental period died of bronchial pneumonia. Hypersalivation and occasionally vomiting was observed in dogs treated with 100 and 200 mg/kg/day. Skin eruption such as erythema and papules was observed mostly at the ventral surface of the neck, chest and upper abdomen in dogs in these two experimental groups. Histological examination of the lesion revealed cellular infiltration with edema and expansion in the dermis and slight hyperkeratosis with parakeratosis and acanthosis. Changes in erythrocyte counts, hematocrit values and hemoglobin contents during the course of administration were variable among dogs but these were obvious in animals treated with higher doses. An increase in erythropoiesis of the bone marrow, extramedullary hematopoiesis and slight hemosiderosis in liver and spleen were revealed by histological examination. Above histological observations suggest that captopril may cause hemolysis. Hypertrophy and hyperplasia of juxtaglomerular cells with increased number of JG granules were shown in the highest dosage group even 4 weeks after suspension of captopril administration. A distinct plasma renin activity supported the morphological changes. From the results of three months administration of captopril to beagle dogs, the maximum non-toxic dose may be around 10 mg/kg/day and toxic dose 100 mg/kg/day.
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PMID:[Three month subacute toxicity of captopril in beagle dogs]. 627 85

A syndrome of renal tubular resistance to aldosterone has been identified in infants with obstructive uropathy and urinary tract infection. Six infants (ages 9 days to 7 months) were seen with fever, vomiting, polyuria, dehydration, or failure to thrive. Urine cultures were positive for Escherichia coli. Radiologic studies demonstrated bilateral ureterohydronephrosis (four patients), left ureteral duplication with upper pole hydronephrosis (one), and left vesicoureteral reflux (one). The infants had hyponatremia, hyperkalemia, and metabolic acidosis. Plasma aldosterone concentration was markedly elevated, and plasma renin activity was similar to or higher than that reported in normal infants of comparable age. Fractional excretion of potassium was not significantly different from control values, both in absolute terms or when related to glomerular filtration rate, but fractional sodium excretion was significantly increased. The UK/UNa ratio was significantly lower in the patients. After medical or surgical therapy (when appropriate), all blood and urine determinations returned to normal, except for UK/UNa values, which although higher, remained significantly diminished. Our data indicate that a hyperkalemic salt-losing state can arise in infants with obstructive uropathy and urinary tract infection as a consequence of tubular unresponsiveness to aldosterone, and that the clinician should rule out such cause before establishing the diagnosis of primary pseudohypoaldosteronism.
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PMID:Transient pseudohypoaldosteronism secondary to obstructive uropathy in infancy. 635 May 53

The purpose of the present study was to develop a controllable experimental model in the dog that would consistently and predictably produce a malignant hypertensive crisis, and to determine the sequential changes in renal function, salt and water balance, and hormones that are involved in the transition from benign to accelerated hypertension. Norepinephrine (NE) was infused continuously into the renal artery of unilaterally nephrectomized dogs that were maintained on 50 mEq sodium/day. The infusion rate of NE was increased each day according to the following schedule: 0.05, 0.1, 0.2, 0.3, 0.4, and 0.5 microgram/kg/min. During the first 4 to 5 days of intrarenal NE infusion, there was a progressive decrease in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), and increases in plasma renin activity (PRA), mean arterial pressure (MAP), and filtration fraction. At the end of this period of benign hypertension, MAP had risen from a control value of 91 +/- 4 to 132 +/- 8 mm Hg, in association with approximately a 10-fold increase in PRA and a 40% reduction in renal function. Then, suddenly, during the subsequent 24-hour infusion period, the MAP increased abruptly in all animals (MAP = 156 +/- 8 mm Hg), and a hypertensive crisis occurred. This crisis was associated with the following: salt and water depletion, hyponatremia, hypovolemia and hemoconcentration, polydipsia, marked activation of the renin-angiotensin-aldosterone system, increased plasma cortisol concentration, hemolysis, marked impairment in renal function, lethargy, and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malignant hypertensive crisis induced by chronic intrarenal norepinephrine infusion. 637 96

An Amerindian girl with Friedreich's ataxia presented at the age of 14 years with intermittent bifrontal headaches and abdominal aching, often associated with nausea and recurrent vomiting and an evanescent pink, blotchy rash on the upper trunk. In these attacks she also had hypertension up to 210/160 mm Hg. Renal function studies, including intravenous pyelogram and angiography, were normal. Plasma renin activity (2.5 ng/ml/hr) was also normal. Total body CT scan was negative for phaeochromocytoma, and repeated estimations of 24-hour excretion of urinary VMA were normal or borderline high. Levels of total catecholamines in 24-hour urine were normal twice, but two random specimens during the paroxysmal episodes contained abnormally high levels of norepinephrine and dopamine. Plasma catecholamine concentrations were increased but not as high as with phaeochromocytoma. Blood pressure monitoring demonstrated marked fluctuations with position and temperature. A clonidine suppression test showed a substantial fall of plasma catecholamine levels, consistent with dysautonomia and not with phaeochromocytoma. It is concluded that the patient has dysautonomia of central origin, probably as a manifestation of Friedreich's ataxia. These findings are discussed in relation to the recent demonstration of increased levels of plasma catecholamines in that disease.
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PMID:Friedreich's ataxia with dysautonomia and labile hypertension. 670 98

The etiology of persistent hypokalemia and renal potassium loss was investigated in three children. Each had normal blood pressure but low plasma aldosterone values in relation to elevated plasma renin activity. None had a history of licorice abuse, laxative or diuretic use, persistent vomiting or diarrhea, pyelonephritis, or diabetes insipidus. Additional studies in one patient showed low prostaglandin E excretion and a normal platelet aggregation response to epinephrine and ADP. Although certain aspects of this condition resemble Bartter syndrome, the low concentrations of aldosterone and the absence of evidence for mineralocorticoid excess suggest a previously undescribed syndrome.
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PMID:Hypokalemia, normal blood pressure, and hyperreninemia with hypoaldosteronism. 702 99

The physiologic effects of habitual vomiting mimic the metabolic abnormalities seen in Bartter's syndrome, ie, hypokalemic metabolic alkalosis and increased plasma renin and aldosterone levels with kaliuresis. However, in habitual vomiting, the 24-hour urine chloride level will be lss than 10 mEq/liter owing to gastrointestinal loss and in Bartter's syndrome it will be greater than 20 mEq/liter owing to defective chloride reabsorption. The case is reported of a young woman whose self-induced vomiting caused metabolic abnormalities consistent with a diagnosis of Bartter's syndrome. The absence of urinary chloride wasting, ie, level less than 10 mEq/liter, was the only finding distinguishing her condition from Bartter's syndrome and leading to the correct diagnosis.
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PMID:Self-induced vomiting presenting as Bartter's syndrome. 714 83

Application of the common marmoset to pharmacological studies was reviewed, especially employment of the animal as a model of Parkinson's disease were presented. The common marmoset is one of the New World monkeys with a body weight of 300-350 g. It is small enough to be easily handled and to be kept as a group in a room. In the fields of pharmacology, it has been used in studies of plasma renin activity inhibitors, lipoprotein, memory/learning, obstetrics, transplantation, toxicology, anxiolytic agents and virology/immunology. We showed that the common marmoset was a useful animal for studies on Parkinson's disease, dopamine metabolism by microdialysis and nausea/vomiting. The common marmoset was sensitive to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and developed permanent parkinsonism after MPTP injection. MPTP-treated common marmosets showed tremor and akinesia, and it remarkably responded to antiparkinsonian agents. A dopamine D1 agonist, which caused stereotyped behavior in rats, did not reverse parkinsonism in humans. We showed this agent did not have any antiparkinsonian effects on MPTP-treated common marmosets. MAO has subtypes, A and B, that have differences of distribution in different species. MAO type B inhibitors were applied for the treatment of Parkinson's disease. MAO subtype B inhibitors do not cause any change in behavior or extracellular concentration of dopamine or its metabolites in rodents. In MPTP-treated common marmosets, however, administration of a MAO type B inhibitor increased the antiparkinsonian effects of levodopa and decreased dopamine metabolites. The common marmoset is a suitable animal for the study of MAO type B inhibitors.
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PMID:[Application of the common marmoset to pharmacological studies]. 759 May 19

Sodium chloride deficiency (SCD) was observed within the 1st year of life in 12 of 46 cystic fibrosis (CF) patients between July 1989 and September 1992. All patients showed sweating, loss of appetite, fever, vomiting, irritation, dehydration, weakness, and cyanosis during an attack. Mean plasma sodium, potassium and chloride levels were 122.9 (range 106-135), 2.5 (range 1.6-3.5), and 73.3 (range 60-90) mEq/l respectively. Alkalosis and elevated plasma renin activity were detected in all patients. Of the patients, 50% showed microscopic haematuria, and hypercalciuria was detected in two out of four patients. Low urinary sodium and high urinary potassium were observed in the four examined patients. Increased creatinine, BUN and uric acid values returned to normal with treatment. All the patients were treated initially with intravenous fluids and electrolyte solutions. All patients were less than 7 months of age during the first attack, five received only breast milk and the others breast milk with formula milk. Their oral salt supplement was 2-4 mEq/kg per day, which is recommended for CF patients, but could be deficient in excessively sweating infants. The genotype of these patients might be cause of high salt losses. F508 is the most common mutation with the frequency of 38% in our CF patients with SCD, but the frequency of unknown mutations is high (54%).
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PMID:Sodium chloride deficiency in cystic fibrosis patients. 784 98

The effect of carmoxirole, a presynaptic dopamine (DA2) receptor agonist, on blood pressure, plasma catecholamines, renin-aldosterone and atrial natriuretic peptide and the intracellular concentration and transmembrane fluxes of Na+ and K+, in erythrocytes and platelets was studied in 24 normal men, using a double-blind, parallel study design. After a run-in period of 1 week, the subjects were treated with either placebo (n = 8) or 0.5 mg carmoxirole (n = 16) once daily for 1 week. Blood pressure and heart rate were not changed during carmoxirole administration in these normal men. Surprisingly, no significant effect of carmoxirole was found on the circulating plasma concentration of noradrenaline, adrenaline or dopamine. Other hormones such as renin, aldosterone and atrial natriuretic peptide were also not changed during carmoxirole administration. No significant effect of carmoxirole could be demonstrated on the intracellular concentration of Na+, K+, Mg2+ and Ca2+ and on the transmembrane fluxes of Na+ and K+ in erythrocytes and platelets. In the carmoxirole-treated subjects (n = 16), 6 subjects reported spontaneously adverse events such as syncope, dizziness and vomiting tendencies and/or fatigue.
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PMID:Erythrocyte and platelet cationic concentrations and transport systems in normal volunteers treated with carmoxirole. 790 90


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