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)

A 3-yr-old boy was investigated for numerous episodes of fatigue, irritability, pallor, and sweating, which began at 11 mo of age, when he had an episode of symptomatic hypoglycemia with ketonuria. He had euphoria, mental confusion, drowsiness, nausea, and vomiting 1-5 hr after oral administration of glycerol in doses of 0.5-1.0gm/kg. Orally administered MCT (1 gm/kg) had similar effects. On one occasion, oral glycerol also provoked hypoglycemia, as had a 16 1/2 hr fast. Intravenously administered glycerol (0.09 gm/kg) induced an immediate loss of consciousness from which he recovered spontaneously after 30 min; there were no changes in blood glucose values. Intravenously administered fructose (0.25 gm/kg) was tolerated normally. Leukocytes showed normal activities for FDPase, glycerol kinase, and glycerol phosphate dehydrogenase. The restriction of dietary intake of fat has been associated with a marked improvement in physical and mental activities. These observations suggest a unique, yet undifined intolerance to glycerol, which suggest caution in the diagnostic use of glycerol in the investigation of hypoglycemia as well as in the therapy of increased intracranial or intraocular pressure.
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PMID:Glycerol intolerance in a child with intermittent hypoglycemia. 16 54

The feasibility of furosemide test for the detection of endolymphatic hydrops has previously been discussed (Authors, 1973, 1975). The glycerol test also has been reported as being effective for the same purpose but only in Meniere patients with fluctuating hearing loss (Klockhoff & Lindblom, 1966). In 48 patients with Meniere's disease, both the furosemide test (F-test) and the glycerol test (G-test) were performed on 51 ears including 3 cases of bilateral involvement. The average value of urine volume in the F-test was significantly greater than that for the G-test. The decrease in tinnitus was 40% in the former, 45% in the latter. The F-test yielded a positive rate of 73%, and the G-test, 45%. The results were thus: positive in the both tests, i.e., F+: G+ were 17 (33%); F+: G-, 20 (39%); F-: G+, 6 (12%), and both negative, F-: G-, only (16%). The side effects of the F-test were nil, but those of the G-test were as follows: headache (29%), nausea (4%), and increase in tinnitus (9%). The response increase of the hydropic labyrinth caused by the two kinds of systemic dehydration over-lapped in part and differed in part, as a result of the differing diuretic mechanisms and their respective affinities to the cochlea and the vestibulum. The furosemide test may be based on the action of the vestibular response type, which is caused by natriuretic dehydration accompanying the more sensitive response increase in caloric-induced nystagmus, while the glycerol test may be based on the action of the cochlear response type, owing to osmotic diuresis manifested as hearing shift. The correlation between labyrinthine hydrops and dehydration was discussed and it was concluded that these double test were quite adequate methods for choice of treatment of not only unilateral Meniere's disease in its various stages but also in bilateral involvements.
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PMID:A comparison of the furosemide and glycerol tests for Meniere's disease. With special reference to the bilateral lesion. 85

The metabolic response to human growth hormone (HGH) was studied in five obese subjects in the fed state and during prolonged (5-6 wk) starvation. In the fed state (three subjects), HGH induced an elevation in basal serum insulin concentration, a minimal increase in blood and urine ketone levels, and a marked reduction in urinary nitrogen and potassium excretion resulting in positive nitrogen and potassium balance. In prolonged fasting (four subjects), HGH administration resulted in a 2- to 3-fold increase in serum insulin which preceded a 50% elevation in blood glucose. Persistence of the lipolytic effects of HGH was indicated by a rise in free fatty acids and glycerol. The response differed markedly from the fed state in that blood beta-hydroxybutyrate and acetoacetate levels rose by 20-40%, resulting in total blood ketone acid concentrations of 10-12 mmoles/liter, ketonuria of 150-320 mmoles/day, and increased urinary potassium loss. The subjects complained of nausea, vomiting, weakness, and myalgias. Despite a 50% reduction in urea excretion during HGH administration, total nitrogen loss remained unchanged as urinary ammonia excretion rose by 50% and correlated directly with the degree of ketonuria. It is concluded that in prolonged starvation (a) HGH may have a direct insulinotropic effect on the beta cell independent of alterations in blood glucose concentration, (b) persistence of the lipolytic action of HGH results in severe exaggeration of starvation ketosis and interferes with its anticatabolic action by necessitating increased urinary ammonia loss, and (c) failure of HGH to reduce net protein catabolism in starvation suggests that this hormone does not have a prime regulatory role in conserving body protein stores during prolonged fasting.
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PMID:Metabolic response to human growth hormone during prolonged starvation. 554 Jan 76

We describe the case of a 10-year-old boy who had been admitted on several occasions with a diagnosis of gastroenteritis. He had been severely ill, and on one occasion lost consciousness. He had a metabolic acidosis on these occasions. Examination of the urine by gas chromatography-mass spectrometry showed a large peak, identified as glycerol. The concentration of glycerol in the urine was 40-280 mmol/L and the concentration in plasma about 2 mmol/L. He was subjected to a fast of 21 h, at the end of which he expressed feelings of discomfort and nausea, began vomiting, and became somnolent. During this period the blood glucose concentration was only slightly decreased, the plasma glycerol concentration increased to 4.9 mmol/L, and the plasma lactate concentration increased to 3.8 mmol/L. During work on a bicycle ergometer for 35 min (40 W) he complained of muscle pain and became nauseated, but there was no significant increase in the concentration of plasma glycerol. The activity of glycerol kinase (EC 2.7.1.30) in leukocytes and cultured fibroblasts was less than 1% of the value for healthy subjects.
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PMID:Deficiency of glycerol kinase (EC 2.7.1.30). 629 16

Forty-four patients with metastatic brain neoplasms received glycerol instead of corticosteroids during periods of brain irradiation. Headache, nausea, and vomiting were controlled in more than 90% of symptomatic patients, while paralysis, confusion, and papilledema improved in 55% to 80%. Patients with minimal or no symptoms remained stable. Patients with moderate or severe symptoms had significant improvement during the first week and substantial improvement during the second week of treatment. Glycerol did not induce immunosuppression when administered in combination with radiotherapy and chemoimmunotherapy. Patients with malignant melanoma had longer survival when treated with glycerol instead of corticosteroids.
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PMID:Glycerol: an alternative to dexamethasone for patients receiving brain irradiation for metastatic disease. 699 10

We report a 64-year-old woman who developed nausea, headache, and consciousness disturbance. She was well until four years before the onset of her neurologic illness when (April of 1990 at her 59 years of the age) she was found to have an early cancer in her anterior wall of the lower stomach. Subtotal gastrectomy was performed and the operative result was reported as curative. Four years after the surgery (December of 1994 at her 64 years of the age), she noted suboccipital headache and nausea which had become progressively worse and she was admitted to our service on May 24, 1995. On admission, she appeared chronically ill but general physical examination was unremarkable with normal vital signs. Neurologically she was alert and not demented, and the higher cerebral functions were intact. Cranial nerves were also unremarkable. She was able to walk in tandem and on heels. No motor weakness or ataxia was noted. Deep tendon reflexes were moderately increased, however, no Babinski sign was noted. Although she had headache, no meningeal signs were seen. Slight superficial and vibratory sensory loss was noted in both feet. Routine blood work was again unremarkable except for slight increase in CEA to 8.3 ng/dl (N < 5 ng/dl). The opening pressure of lumbar CSF was 180 mm H2O and the CSF contained 39 cells/microliter, 79 mg of protein, and 10 mg/dl of glucose. Approximately half of the cells were atypical malignant cells. Plain CT was unremarkable, however, tentorial border showed enhancement after contrast infusion. FGS showed no malignant tumors in the stomach. She was treated with intravenous glycerol and whole brain radiation, however, she continued to complain of severe headache, and her sensorium started to be disturbed one month after the admission. Follow-up cranial CT scan revealed enlargement of the lateral and the third ventricles. Her consciousness progressively deteriorated and she became comatose three months after the admission. Repeated cranial CT scan showed enlargement of the ventricles, but no mass lesions were seen within the brain. She developed respiratory arrest on September 25 of the same year. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had a gastric cancer with meningeal seeding developing meningeal carcinomatosis. The cause of deep coma was ascribed to damage of cerebral cortical areas secondary to metastatic carcinoma cells and fibrinous materials in the surface of the brain. Postmortem examination revealed thickening and clouding of leptomeninges of the cerebral convexity. On histologic observation, patchy areas of fibrous thickening were seen in the cerebral leptomeninges; in such areas, adenocarcinomatous cells were seen scattered. The basal meninges were free of carcinoma cells, however, leptomeninges of the cerebellum and brain stem tegmentum contained scattered carcinoma cells. The lateral and the third ventricles were enlarged, however, insides of the brain were free of pathologies; the ependymal layer were intact. In the stomach no carcinoma cells were remaining. Pneumonic changes were seen in the right upper and the left lower lobes which appeared to be the direct cause of her death. No evidence of tentorial herniation was noted. The cause of her deep coma was not clearly determined, however, combination of hydrocephalus and cortical malfunction due to leptomeningeal carcinoma cell infiltration and fibrinous material accumulation appeared to have played a role.
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PMID:[A 64-year-old woman with severe headache and progressive disturbance of consciousness]. 919 1

CELL INJURIES DURING FREEZING AND THAWING: The aim of various cryopreservation procedures is to minimize cell injuries during the freeze-thaw cycle (cryoinjuries). Generally, the cell damage during freezing and thawing procedures may be the results of: (a) extensive cellular dehydration (solution effect) and/or (b) intracellular ice crystallization/recrystallization (mechanical cell damage). Two independent mechanisms are involved. They can act simultaneously, leading to cytolysis. The first one is expressed primarily during low rate freezing, and the second one during rapid freezing. Thus, determination and use of the optimal cooling velocity, specific for each type of isolated cells, should be considered. Finally, a higher degree of cell destruction has been documented when the transition period from liquid to solid phase (release of the fusion heat) is prolonged. CRYOPROTECTIVE AGENTS: For successful cell cryopreservation, cryoprotectants are needed. They decrease the osmotic gradient and the vapor pressure difference between the intra- and extracellular area. Adequate choice of the most suitable type and concentration of cryoprotective agent is important for the required cell recovery after thawing. There are several well known protocols for obtaining cryopreservation of isolated cells using different cryoprotectants. Glycerol, dimethyl sulfoxide (DMSO) and propanediol sucrose are commonly used as cryoprotectants, though in different concentrations. Glycerol, a trihydric alcohol, is a clear, colorless fluid. Pharmacologically, it is relatively inert. DMSO is a colorless liquid with a sulphur-like smell and has several medical uses. It is highly polar and dissolves many water- and lipid-soluble substances. DMSO given intravenously may cause nausea, vomiting, local vasospasm and an objectionable garlic-like odor and taste. HUMAN SPERM, OVA AND EMBRYOS CRYOPRESERVATION: Despite the fact that cryopreservation procedures of spermatozoa, ova and embryos are already in routine clinical use, some questions related to the optimal cooling velocity during controlled-rate freezing and the choice of the most effective, either penetrating (glycerol, dimethyl sulfoxide) and/or non-penetrating (hydroxyethyl starch) cryoprotective agent at the appropriate concentration are not resolved.
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PMID:[Current knowledge on cryopreservation of spermatozoa, ovum cells and zygotes]. 953 71

A 62-year-old woman presented with rapidly developed visual disturbance without associated headache or nausea 3 weeks after head injury. Ophthalmologic examination revealed bilateral severe papilledema with retinal hemorrhage, and intracranial pressure (ICP) was 17.5 cmH2O estimated by lumbar puncture. Computed tomography and magnetic resonance (MR) imaging showed no evidence of increased ICP, except dilation of the subarachnoid space around the optic nerves with distortion of the nerves. Her visual acuity remarkably improved after steroid and glycerol treatment, and optic fundus examination revealed bilateral clear optic papillae without atrophic changes. Follow-up MR imaging demonstrated that the bilateral optic nerves had regained the normal appearance. These results indicate that the bilateral papilledema was caused by increased subarachnoid pressure around the bilateral optic nerves. We conclude that papilledema can occur with a mildly increased ICP and trapped subarachnoid cerebrospinal fluid around the optic nerves, and papilledema may progress after the ICP is normalized. Papilledema is a warning sign for increased ICP, associated with future visual loss from retinal hemorrhage. Therefore, repeated funduscopic investigation is necessary for the early diagnosis and treatment of papilledema.
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PMID:Severe papilledema identified 3 weeks after head injury. 1216 Mar 8

We report a case of hydrocephalus due to posterior cranial fossa subdural effusion. The patient was a 4-year-old boy, presenting headache and nausea, with a medical history of viral meningitis 2 months before. Cerebrospinal fluid provided no evidence of infection, and symptoms caused by increased intracranial pressure gradually deteriorated, although glycerol infusion was effective temporarily. Computed tomography revealed marked ventriculomegaly with subdural effusion in the right posterior cranial fossa. The subarachnoid space in the posterior fossa was very tight, and the cerebellum and brain stem were compressed anteriorly. Magnetic resonance imaging demonstrated stenosis of the aqueduct and foramens of Luschka and Magendie. The cerebeller tonsil was dislocated inferiorly, indicating impending herniation, so an emergency operation was performed. Ventriculoperitoneal shunt was undertaken after implantation of an Ommaya reservoir for the posterior fossa subdural effusion. The patient's postoperative course was uneventful, and the symptoms were improved. Although hydrocephalus and subdural effusion following viral meningitis is rare, neuroimaging studies such as CT and MRI should be examined when a young child suffers from symptoms of increased intracranial pressure.
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PMID:[A case presenting with hydrocephalus and posterior fossa subdural effusion]. 1451 82

Glycerol is used as a peroral treatment of increased intraocular and intracranial pressure due to its osmotic effect despite the potential increase in blood pressure and blood glucose. We examined the effects of peroral glycerol in diabetic patients and healthy individuals on blood pressure, capillary glucose, and plasma osmolarity. On two separate days, 15 diabetic patients ingested glycerol in doses of 855 and 1710 mg/kg body weight in a randomised, unmasked sequence. Five healthy individuals ingested a dose of 1710 mg/kg body weight. Mean arterial blood pressure (MAP), capillary glucose (CG) and plasma osmolarity (pOSM) were monitored for 180 min. At baseline, the MAP was comparable between the groups of healthy individuals and diabetic patients (p = 0.55), CG was marginal different (p = 0.06), and pOSM values were significantly different (p = 0.007). Following glycerol ingestion, a transient, non-significant increase occurred in blood pressure. Maximal DeltaCG was approximately 1 mM irrespective of the dose and presence of diabetes (p > 0.1). The pOSM response was analysed with a kinetic model and found independent of the presence of diabetes (p = 0.6). The maximal fitted DeltapOSM was 12.7 and 25.3 mOsm/l in the group of diabetic patients after the low and high dose, respectively, reflecting a dose-response relationship. Nausea, fatigue and headache were common side effects. In conclusion, peroral glycerol had similar effects on blood glucose, MAP and pOSM in the diabetic patients and healthy individuals. Specific precautions should not be implemented when treating diabetic patients with a single dose up to 1.7 g/kg body weight. A peak increase of 8% in the pOSM within 1 hr can be expected from this dose.
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PMID:The effects of peroral glycerol on plasma osmolarity in diabetic patients and healthy individuals. 1979 1


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