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)

Maximal free-water clearance was measured in five patients with Bartter's syndrome and in five patients with the hypokalemic alkalosis of persistent psychogenic vomiting. Hypokalemic alkalosis, hyperreninemia, hyperaldosteronism and excessive renal production of prostaglandin E2 were present in the patients with both disorders. Maximal free water clearance was abnormally low, in association with a high clearance of chloride, in all the patients with Bartter's syndrome; it was normal in all the patients with psychogenic vomiting. In the patients with Bartter's syndrome, apparent distal delivery of proximal tubular fluid was inversely related to glomerular filtration rate and was excessive only in those patients with a low glomerular filtration rate. Patients with psychogenic vomiting showed mean distal fractional chloride reabsorption of 0.92 +/- 0.04 (standard error [SE]). In the patients with Bartter's syndrome, distal fractional reabsorption of chloride was 0.49 +/- 0.08 and was the same (0.46 +/- 0.06) during inhibition of prostaglandin synthesis with indomethacin therapy. Thus, a prostaglandin-independent defect in chloride reabsorption in the loop of Henle is the most proximal cause for the abnormalities in Bartter's syndrome thus far identified.
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PMID:Evidence for a prostaglandin-independent defect in chloride reabsorption in the loop of Henle as a proximal cause of Bartter's syncrome. 36 Aug 36

Bartter's syndrome characteristically exhibits the constellation of hypokalemic alkalosis with moderate kaliuresis, normotensive hyperreninemia, hyperaldosteronism, urinary hyperexcretion of prostaglandin E (PGE) and vascular hyporesponsivity to pressor agents. We describe precise biochemical mimicry of these metabolic abnormalities in a patient with surreptitious repetitive vomiting, in whom simple urinary chloride excretion data subsequently excluded the diagnosis of Bartter's syndrome.
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PMID:Metabolic mimicry of Bartter's syndrome by covert vomiting: utility of urinary chloride determinations. 42 77

The syndrome of bulimia is a common disorder and can be associated with serious psychological and physical morbidity. Unfortunately, many patients are reluctant to discuss their symptoms with their physicians and few clues can be found on physical examination to aid in the diagnosis. Possible physical signs include ulceration or scarring of the dorsum of the hand, salivary gland hypertrophy, and dental enamel erosion. In laboratory testing it is fairly common for patients with active bulimia to have fluid and electrolyte abnormalities, particularly hypokalemic alkalosis, and some also have elevated serum amylase levels. Rare complications include myopathies from misuse of ipecac, ruptured esophagus and pneumomediastinum associated with vomiting, and subtle abnormalities in neuroendocrine regulatory systems. Medical management including monitoring of fluid and electrolyte balance is essential during treatment.
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PMID:Medical complications and medical management of bulimia. 329

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

Bulimia is an episodic compulsive urge to overeat often followed by recurrent attempts to lose weight by self-induced vomiting. Seven young women with this eating disorder and associated benign bilateral painless parotid enlargement are described. The glandular swelling was generally intermittent, with parotid enlargement usually developing 2 to 6 days after a binge overeating episode had stopped. Several had hypokalemic alkalosis and a moderate elevation in serum amylase levels. None had clinical evidence of pancreatitis, and a parotid gland biopsy in one patient was normal. The clinician should be alerted to the association of benign parotid enlargement with this syndrome.
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PMID:Benign parotid enlargement in bulimia. 616 Jul 96

Batter's syndrome characteristically exhibits the constellation of hypokalemic alkalosis, normotensive hyperreninism, hyperalodosteronism, hyporesponsiveness to pressor agent and juxtaglomerular cell hyperplasia. Recently, metabolic mimicry of Batter's syndrome by vomiting, diarrhea, laxatives and diuretics abuse has been reported. We had a 30 year-old female patient who developed so-called pseudo-Bartter's syndrome as the result of surreptitious self-administration of furosemide for about six years. In this case, calcification of bilateral renal medulla was demonstrated. Such adverse reaction has not been reported to date. Moreover, a total 14 cases of pseudo-Bartter's syndrome reported in Japanese literature is reviewed.
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PMID:Pseudo-Bartter's syndrome due to furosemide abuse: report of a case and an analytical review of Japanese literature. 733 12

A patient with hypokalemic alkalosis, normotensive hyperreninism, hyperaldosteronism, increased levels of urinary and plasma prostaglandin E, and vascular hyporesponsivity to angiotensin II was thought to have Bartter's syndrome. Results of a kidney biopsy showed hyperplasia of the juxtaglomerular apparatus but no renomedullary cell hyperplasia. A 24-hour urine collection showed a low chloride level and no increase in the fractional chloride clearance, thus excluding Bartter's syndrome. Subsequent disclosure of surreptitious, habitual vomiting explained the hypokalemia.
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PMID:Surreptitious habitual vomiting simulating Bartter's syndrome. 735 67

Pseudo-Bartter syndrome presents the same clinical and biological characteristics as Bartter syndrome but without primary renal tubule abnormalities. We relate the case of a premature baby presenting at birth with severe hypokalemic metabolic alkalosis associated with hyponatremia and hypochloremia. Maternal blood at the time of delivery showed the same electrolyte perturbations. The baby's mother had suffered from anorexia and vomiting during pregnancy. A few weeks after birth the baby's blood abnormalities had almost returned to normal. Chloride depletion is at the origin of both maternal and fetal hypokalemic alkalosis.
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PMID:Pseudo-Bartter syndrome in a pregnant mother and her fetus. 1677 20

Although the diagnosis of Gitelman syndrome (GS) and Bartter syndrome (BS) is now feasible by genetic analysis, implementation of genetic testing for these disorders is still hampered by several difficulties, including large gene dimensions, lack of hot-spot mutations, heavy workup time, and costs. This study evaluated in a cohort of patients with genetically proven GS or BS diagnostic sensibility and specificity of a diuretic test with oral hydrochlorothiazide (HCT test). Forty-one patients with GS (22 adults, aged 25 to 57; 19 children-adolescents, aged 7 to 17) and seven patients with BS (five type I, two type III) were studied; three patients with "pseudo-BS" from surreptitious diuretic intake (two patients) or vomiting (one patient) were also included. HCT test consisted of the administration of 50 mg of HCT orally (1 mg/kg in children-adolescents) and measurement of the maximal diuretic-induced increase over basal in the subsequent 3 h of chloride fractional clearance. All but three patients with GS but no patients with BS and pseudo-BS showed blunted (<2.3%) response to HCT; patients with BS and the two patients with pseudo-BS from diuretic intake had increased response to HCT. No overlap existed between patients with GS and both patients with BS and pseudo-BS. The response to HCT test is blunted in patients with GS but not in patients with BS or nongenetic hypokalemia. In patients with the highly selected phenotype of normotensive hypokalemic alkalosis, abnormal HCT test allows prediction with a very high sensitivity and specificity of the Gitelman genotype and may avoid genotyping.
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PMID:A thiazide test for the diagnosis of renal tubular hypokalemic disorders. 1770 May 53

Ascariasis is one of the most common helminthic infestations in humans. Massive infestation can give rise to serious complications such as intestinal obstruction. We present a 4-year-old boy, who presented with acute flaccid quadriparesis due to the hypokalemic alkalosis induced by severe vomiting. Severe vomiting was due to intestinal obstruction caused by round worms.
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PMID:Hypokalemic paralysis following severe vomiting in a child with intestinal obstruction due to round worms. 1950


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