Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of 1 h intravenous infusions of equimolar amounts of two putative 5-hydroxytryptamine (5-HT) renal prodrugs, 5-hydroxy-L-tryptophan (5-HTP, 10 micrograms kg-1 min-1) and gamma-L-glutamyl-5-hydroxy-L-tryptophan (glu-5-HTP, 16.6 micrograms kg-1 min-1) were examined in five healthy male volunteers in a randomised, placebo-controlled, cross-over study. 2. Both compounds increased urinary excretion of 5-HT and there was greater extra-renal formation of 5-HT following 5-HTP administration than after glu-5-HTP. 3. Glu-5-HTP was significantly antinatriuretic. 5-HTP reduced mean urinary sodium excretion but this effect was not statistically significant. 4. 5-HTP, but not glu-5-HTP, significantly increased plasma aldosterone. There was no increase in plasma renin activity with either compound. 5. There were no significant changes in pulse rate or blood pressure. Two subjects complained of nausea at the end of 5-HTP infusion but none had any adverse reactions with glu-5-HTP. 6. The results of this study suggest that both prodrugs generate 5-HT in man and that glu-5-HTP is antinatriuretic. The glutamyl derivative may have greater renal specificity than 5-HTP and, as a result, causes less systemic side effects.
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PMID:A comparison of the effects of two putative 5-hydroxytryptamine renal prodrugs in normal man. 769 May 83

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

Pseudo-hypoaldosteronism (PHA) is due to mineralocorticoid resistance and manifests as hyponatremia and hyperkalemia with increased plasma aldosterone levels. It may be familial or secondary to abnormal renal sodium handling. We report the case of a 54-year-old woman with multifocal cancer of the colon, who developed PHA after subtotal colectomy, ileal resection and jejunostomy. She was treated with 6 g of salt daily to prevent dehydration, which she stopped herself because of reduced fecal losses. One month later she was admitted with signs of acute adrenal failure, i.e. fatigue, severe nausea, blood pressure of 80/60 mmHg, extracellular dehydration, hyponatremia (118 mmol/l); hyperkalemia (7.6 mmol/l), increased blood urea nitrogen (BUN) (200 mg/dl) and creatininemia (2.5 mg/dl), and decreased plasma bicarbonates level (HCO3-: 16 mmol/l; N: 27-30). However, the plasma cortisol was high (66 microg/100 ml at 10:00 h; N: 8-15) and the ACTH was normal (13 pg/ml, N: 10-60); there was a marked increase in plasma renin activity (>37 ng/ml/h; N supine <3), active renin (869 pg/ml; N supine: 1.120), aldosterone (>2000 pg/ml; N supine <150) and plasma AVP (20 pmol/l; N: 0.5-2.5). The plasma ANH level was 38 pmol/l (N supine: 5-25). A urinary steroidogram resulted in highly elevated tetrahydrocortisol (THF: 13.3 mg/24h; N: 1.4+/-0.8) with no increase in tetrahydrocortisone (THE: 3.16 mg/24h; N: 2.7+/-2.0) excretion, and with low THE/THF (0.24; N: 1.87+/-0.36) and alpha THF/THF (0.35; N: 0.92+/-0.42) ratios. The number of mineralocorticoid receptors in mononuclear leukocytes was in the lower normal range for age, while the number of glucocorticoid receptors was reduced. Small-bowel resection in ileostomized patients causes excessive fecal sodium losses and results in chronic sodium depletion with contraction of the plasma volume and severe secondary hyperaldosteronism. Nevertheless, this hyperaldosteronism may be associated with hyponatremia and hyperkalemia suggesting PHA related to the major importance of the colon for the absorption of sodium. In conclusion, this case report emphasizes 1) the possibility of a syndrome of acquired PHA with severe hyperkalemia after resection of the ileum and colon responding to oral salt supplementation; 2) the major increase in AVP and the small increase in ANH; 3) the strong increase in urinary THF with low THE/THF and alpha THF/THF ratios; 4) the normal number of lymphocytic mineralocorticoid receptors outside the acute episode.
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PMID:Transient pseudo-hypoaldosteronism following resection of the ileum: normal level of lymphocytic aldosterone receptors outside the acute phase. 1019 79

Sequential changes in hormone levels were assessed for one year in postmenopausal breast cancer patients administered the aromatase inhibitor fodrozole hydrochloride hydrate (Afema) in order to evaluate its efficacy and safety in long-term treatment. Forty patients received Afema alone as postoperative adjuvant therapy, while 30 received it with 5-FU. Plasma estrone and estradiol levels decreased significantly in both groups (p < 0.001) and were not affected by body mass index (BMI). Plasma androstenedione and testosterone levels increased within the normal range. Aldosterone levels hit bottom 3 months after treatment was started, and tended to return to the pre-treatment baseline thereafter. Plasma cortisol levels increased significantly within the normal range. FDP and alpha 2-PIPC, parameters related to blood coagulation and fibrinolysis, showed no significant change. Adverse reactions, mainly nausea and elevation of LDH levels, were all slight. Thus, long-term administration of Afema resulted in significant decreases in estrogen levels with few adverse reactions regardless of the BMI, suggesting that it can be safely used as effective postoperative adjuvant therapy.
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PMID:[Sequential changes in hormone levels in postmenopausal breast cancer patients under long-term treatment with an aromatase inhibitor. Kanagawa AI Study Group]. 1063 5

Exemestane was administered orally to postmenopausal women with advanced/recurrent breast cancer at a dose of 10 mg/day or 25 mg/day once daily for more than 8 weeks in order to evaluate the drug's anti-tumor effects and safety in a dose-finding study. The response rate (CR + PR) in the 10 mg and 25 mg group was 25.0% (8/32) and 31.4% (11/35), respectively, demonstrating no significant differences between the two groups, yet a higher efficacy rate was observed in 25 mg group. The efficacy rate in hormone-treatment-resistant patients within the 10 mg and 25 mg groups was 14.3% (3/21) and 26.1% (6/23), respectively, demonstrating more than a 20% response rate in 25 mg group. Incidences of the adverse events of which relevance to the drug could not be excluded were 30.6% (11/36) in the 10 mg group. 13.9% (5/36) in the 25 mg group and 22.2% (16/72) in the total group. The major adverse events were, hot flashes, numbness of the limbs, nausea, headache etc. Abnormal findings in clinical laboratory tests were as follows: ALP increase; GOT increase; GPT increase; gamma-GTP increase; total cholesterol increase; urinary sediment present. Abnormal findings in endocrine function were as follows: aldosterone decrease; testosterone.cortisol.DHEA-S decrease. But discontinuation due to abnormal laboratory findings was not found. No abnormal findings in physical tests were observed. A significant decrease in plasma estrogen concentration at week 4 was observed in both the 10 mg and 25 mg groups compared with baseline. These low levels were maintained throughout the study period. On the basis of these results, the efficacy of exemestane 25 mg/day was verified to be slightly higher than 10 mg/day. In addition the safety profile had no major adverse events to notice. In these patients with advanced/recurrent breast cancer, 25 mg/day was recommended as the most appropriate dose to be used clinically.
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PMID:[Early phase II dose-finding study of exemestane in postmenopausal patients with advanced/recurrent breast cancer]. 1214 1

Elevated blood pressure is a risk factor for a variety of cardiovascular disorders, including coronary heart disease, peripheral vascular disease, cardiac failure and cerebrovascular disease. The prevailing view is that an elevated systolic rather than diastolic blood pressure is the major contributor in mortality and morbidity attributed to cardiovascular disorders. Isolated high systolic blood pressure, especially in the elderly, is a major risk factor and should undoubtedly be a target for drug treatment. In the general population, systolic and diastolic blood pressure are highly correlated, and thus it is difficult to dissociate the effects of these two components of the blood pressure and specifically ascribe cardiovascular risk factors to just elevated systolic blood pressure. Therefore, the goal in therapy of an individual with hypertension must be to reduce elevated systolic and diastolic blood pressure in order to reduce mortality and morbidity. ACE and neutral peptidase inhibitors are a new class of drugs that may be beneficial in the treatment of patients with hypertension and heart failure. They may also be useful in the treatment of diabetic patients with hypertension and/or heart failure. Drugs of this class are dual inhibitors of ACE and neutral endopeptidase, and are capable of affecting vascular tone and fluid balance. They are capable of producing vasodilatation by virtue of inhibiting the production of angiotensin II, degradation of natriuretic peptides and bradykinin. They also appear to promote natriuresis and diuresis by amplifying the actions of natriuretic peptidase and reducing aldosterone effects. In addition, they should also attenuate trophogenic actions of the renin angiotensin system and the sympathetic nervous system. Omapatrilat is one drug that appears to be at the advanced stages of clinical development. This drug has been shown to be quite effective in the treatment of hypertension. Evidence also seems to indicate that treatment with omapatrilat results in a higher tendency towards preventing death and worsening heart failure when compared with treatment with a pure ACE inhibitor in patients with advanced heart failure. Overall safety with omapatrilat appears to be good, but like other ACE inhibitors the incidence of cough is higher when compared with placebo. Other common adverse effects noted are headaches, facial flushing/warm sensation, dizziness, nausea and dyspnoea. Of greater concern is the occurrence of angio-oedema, the true incidence of which remains to be fully established as part of the published medical literature.
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PMID:Dual ACE and neutral endopeptidase inhibitors: novel therapy for patients with cardiovascular disorders. 1501 94

Bartter's syndrome is characterized by hypochloremia, hypokalemia, metabolic alkalosis associated with renal potassium leakage, and normal blood pressure despite increased plasma renin activity. Although association of empty sella with Gitelman syndrome has been reported, no association has been reported with Bartter's syndrome. Here we report a patient with Bartter's syndrome and empty sella. A 12 month-old male patient presented with a history of nausea, vomiting, abdominal distension, constipation, and edema in the lower extremities that had begun in the early postnatal period. The patient was born at 32 weeks gestation by operative delivery for polyhydramnios. Blood pressure was normal. Serum sodium, potassium, calcium, phosphate, chloride, albumin and alkaline phosphatase levels were 129 mEq/l, 2.5 mEq/l, 9 mg/dl, 3.8 mg/dl, 72 mg/dl, 4.2 g/dl and 1285 IU/l, respectively. Serum magnesium level was normal. Arterial blood gas levels revealed pH 7.55 (normal, 7.35-7.45), PCO2 33.6 mm/Hg (36-46), base excess +7.1 (+/- 2.3), and total CO2 33.6 mmol/l (23-27). Renin and aldosterone levels were elevated. Urine had pH 8.0 and specific gravity 1.010. Urinary calcium excretion was 22.8 kg/day (urine calcium/creatinine ratio 0.46). Urinary potassium and chloride levels were elevated. MRI of the brain was normal except for partially empty sella. We present the first pediatric patient with the association of Bartter's syndrome and empty sella.
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PMID:Association of Bartter's syndrome and empty sella. 1451 87

Hyponatremia, albeit common in chronic renal insufficiency, necessitates a detailed search of the underlying hidden causes. We report on a 67-year-old woman with chronic kidney disease (creatinine 230 micromol/L) and hypertension who suffered from general fatigue, dizziness, nausea, vomiting and abdominal fullness off and on for 6 months. Hyponatremia (plasma Na(+) 106-125 mmol/L) on 4 occasions during the past 6 months was noticed. Her extracellular volume status was apparently normal. Plasma Na(+) concentration 110 mmol/L was the most striking laboratory abnormality with mild metabolic acidosis (HCO(3)- 19.8 mmol/L). Her urine Na(+) concentration and osmolality were inappropriately high. Her hyponatremia was refractory to normal saline, hypertonic NaHCO(3) and 0.1-microg 9 alfa-fludrocortisone. Despite normal plasma cortisol and thyroid hormone concentrations, a provocation test with cosyntropin (250 microg) showed a blunted cortisol (<579 nmol/L) but intact aldosterone response. Magnetic resonance imaging of her brain displayed a normal pituitary gland and hypothalamus. A history of intermittent intravenous steroid therapy to treat her allergic rhinitis for 3 years was uncovered. Steroid supplements induced water diuresis and corrected hyponatremia to 135 mmol/L in 5 days. With nonspecific clinical symptoms, glucocorticoid insufficiency must be kept in mind as a cause of hyponatremia even in patients with impaired renal function and normal plasma cortisol concentration.
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PMID:Recurrent hyponatremia in a patient with chronic kidney disease. 1687 5

Mercury intoxication is a rare cause of severe hypertension. A case of mercury intoxication presented with severe hypertension and erythromelalgia was reported. A 10-year- and -5-month-old girl presented with recurrent rash and painful hands for 2 months, with seizure attack and episodic loss of consciousness for one hand half months. The girl was found to have red painful hands, a blood pressure 170/120 mm Hg(1 mm Hg=0.133 kPa), tachycardia and hypokalemia (2.83-3.25 mmol/L, reference value 3.5-5.5 mmol/L). An extensive investigation ensued. Elevated renin-angiotensin and aldosterone were demonstrated in plasma. Cranial MRI T2 weighed images showed widespread white matter signal abnormalities, which particularly involved parietal, occipital and frontal lobes. With hypertension controlled, white matter signal abnormalities weakened. Other symptoms included insomnia, nausea and paroxysmal abdominal pain. The girl was found to have a raised concentration of mercury in urine (0.171 mg/L, reference value< 0.01 mg/L), and she had been exposed to elemental mercury for several days. After chelating therapy, the girl's blood pressure returned to normal, erythromelalgia ameliorated, all other symptoms disappeared. So, mercury intoxication should be considered in the differential diagnosis of hypertension with erythromelalgia.
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PMID:[Hypertension and erythromelalgia as prominent manifestations of mercury intoxication]. 1765 63

Evidence of the effect of dehydration on physiological responses to hypoxia is limited. The purpose of this study was to determine the effect of hypohydration severity on physiological, renal hormonal and psychological responses to acute hypoxia. Eight males completed intermittent walking tests under normobaric hypoxic conditions (FI O(2) = 0.13) after completing four separate hypohydration protocols, causing change in body mass of approximately 0% (EU), -1% (H1), -2% (H2) and -3% (H3). Physiological and psychological markers were monitored throughout the 125 min test. Fluid controlling hormones were measured pre and post exposure. Heart rate, core temperature, peripheral arterial oxygen saturation (SpO(2)), minute ventilation and urine osmolality were found to be significantly different between hydration conditions and correlated with Lake Louise Questionnaire score (LLQ) (P < 0.05). LLQ score increased with hypohydration severity above H2 (EU 1.3 +/- 1; H1 1.2 +/- 1; H2 2.7 +/- 2; H3 3.9 +/- 2) (P < 0.001). Antidiuretic hormone and aldosterone increased over the test, but were not different between hydration conditions (P < 0.05). Atrial natriuretic peptide showed no change over time, or with conditions. Therefore, renal hormones are not influenced by hypohydration severity during moderate intensity hypoxic exercise. Hypohydration less than -2% induces greater physiological strain during hypoxic exercise and may cause rise in symptoms such as, fatigue, headache, nausea and lightheadedness.
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PMID:The effect of hypohydration severity on the physiological, psychological and renal hormonal responses to hypoxic exercise. 1919 72


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