Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After at least 6 months on conventional hemodialysis (cellulosic dialyzers, acetate dialysate, and a 3- to 4-hour treatment time), 56 patients were changed to short-time hemodialysis (less than 180 minutes) using polysulfone dialyzers and bicarbonate-containing dialysate. Treatment time decreased (191 +/- 5 v 147 +/- 5 min; P = 0.001), while Kt/V (1.22 +/- 0.04 v 1.29 +/- 0.06; P = NS) and normalized protein catabolic rate (pcr) (1.10 +/- 0.05 v 1.10 +/- 0.07 g/kg/d; P = NS) remained constant. When compared with the conventional period, 30 months of short-time hemodialysis resulted in no changes in predialysis blood pressure (BP) (151 +/- 2/84 +/- 1 v 151 +/- 2/86 +/- 1 mm Hg), postdialysis BP (144 +/- 2/81 +/- 1 v 143 +/- 3/84 +/- 1 mm Hg), interdialytic weight gain (2.4 +/- 0.1 v 2.7 +/- 0.2 kg), or blood urea nitrogen (BUN) (26.1 +/- 0.71 v 25.3 +/- 1.07 mmol/L [73 +/- 2 v 71 +/- 3 mg/dL]). Shorter treatment times were not associated with an increase in intradialytic complications. Actually, the frequency (%) of dialysis treatments associated with nausea (5.94 +/- 1.33 v 2.21 +/- 0.52), vomiting (3.12 +/- 0.87 v 0.54 +/- 0.14; P less than 0.05), headaches (5.60 +/- 1.13 v 2.03 +/- 0.52; P less than 0.05), and back pain (0.91 +/- 0.25 v 0.05 +/- 0.05; P less than 0.05) was decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Clinical experience with short-time hemodialysis. 173 82

From 65 reported cases of medium chain acyl-CoA dehydrogenase deficiency, we found an average presenting age of 13.5 months and a mean age at death of 18.5 months. One quarter of patients died of a Reye-like syndrome and/or sudden infant death. In half the cases there had been at least one sibling death. Asymptomatic cases were not uncommon (12% of cases). The crises were generally induced by a prolonged fast and after a viral prodromal phase in three quarters of cases. The crises consisted of somnolence progressing to lethargy which could lead to coma. Vomiting was frequent (60% of cases). Seizures, which were found in 29% of cases, represented a bad prognosis. The physical examinations revealed frequently a variable and regressive anicteric hepatomegaly. Blood and urine analysis revealed in most instances hypoglycaemia (96% of cases) with hypoketonuria and sometimes metabolic acidosis. Hepatic and muscular cytolytic enzymes were frequently raised, as were plasma ammonia, urea, and uric acid. Plasma total or free carnitine concentrations, especially non-fasting, were diminished in most cases. Plasma saturated medium chain fatty acids and particularly unsaturated cis-4-decenoate were on the other hand raised during the crises or during fasting. Urinary organic acid analysis revealed a characteristic profile of medium chain aciduria: C6-C10 dicarboxylic acids, hydroxy acids, glycine conjugates, and carnitine conjugates. Oral loading tests with carnitine or phenylpropionate allow a precise diagnosis. The diagnosis is confirmed by specific assays in various tissues. Avoidance of prolonged fasting seems to be the mainstay of treatment.
 ...
PMID:Medium chain acyl-CoA dehydrogenase deficiency. 173 32

Two male siblings presented in the first 6 weeks of life with emesis, diarrhoea, metabolic acidosis and lethargy. A male sibling had previously died at 14 months of age from liver failure of unknown aetiology. Both of the current cases had mild hyperammonaemia with normal orotic acid, organic acid and argininosuccinic acid levels. Citrulline and arginine levels were normal or mildly decreased. One of the brothers was biopsied and had no detectable N-acetylglutamate synthetase activity and normal values for other enzymes of the urea cycle in liver. Treatment with a low-protein diet and sodium benzoate/sodium phenylacetate resulted in near normal blood ammonia levels, except during viral illness. Subsequent neurological development has been normal to mildly delayed. These patients differ from those previously described with N-acetylglutamate synthetase deficiency in that their presentation and subsequent course were relatively benign.
 ...
PMID:N-acetylglutamate synthetase deficiency: clinical and laboratory observations. 177 15

During Ramadan, Moslems are required strictly to avoid fluids and nourishment from dawn to sunset. Heat stress during such abstinence represents a substantial health hazard. In the Federal Republic of Germany (FRG) where numerous Moslems, particularly of Turkish origin, perform heat work and other heavy labour, we observed moderate to severe health disturbances in such labourers during Ramadan, e.g.: tachycardia, severe headaches, dizziness, nausea, vomiting and circulatory collapse. The severe dehydration of these workers was demonstrated by substantial increases in their hematocrit, serum protein, urea, creatinine, uric acid and electrolyte imbalance. Because of the evidence of the substantial health hazard to Islamic workers in such situations, we have strongly urged employers to refrain from assigning Islamic workers to heat work or heavy daytime work during Ramadan; we have therefore limited systematic studies of health problems during Ramadan to persons performing only moderate work. Even under these conditions signs of dehydration were found in the 32 labourers monitored. Some of these labourers also had to interrupt their observance of Ramadan due to health problems, e.g.: acute gout due to serum uric acid increase, or circulatory insufficiency. In light of the observed potentially harmful pathophysiological effects, the danger of dehydration of Islamic workers due to heat work during Ramadan should be taken very seriously.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The health risks of occupational stress in islamic industrial workers during the Ramadan fasting period. 181 40

Severe hypercalcemia is a medical emergency requiring urgent treatment. It most commonly is caused by malignant tumors, as in the case study, but can also be caused by advanced hyperparathyroidism or high serum levels of vitamin D. The patient described in the case study shows clinical evidence of volume contraction due to hypercalcemia-related anorexia and vomiting. His elevated serum concentrations of urea nitrogen and creatinine reflect intravascular volume depletion and hypercalcemia-induced reduction of renal perfusion. He is also likely to have irreversible renal damage as a result of nephrocalcinosis. His central nervous system depression is most likely a result of hypercalcemia, but other central nervous system disorders such as cerebral metastases should be considered. Appropriate treatment would include intravenous fluids to correct volume depletion, dilute extracellular fluid calcium, and promote renal calcium excretion. Before waiting for the effects of volume expansion, the first dose of an inhibitor of bone resorption should be given. The agent of choice now (this may change when second-generation bisphosphonates become available) is plicamycin. Etidronate is a reasonable second choice. Because both drugs require at least 48 hours before their hypocalcemic action is manifest, calcitonin could be used to accelerate the rate of decline of the serum calcium. As the patient becomes more alert, weight-bearing and ambulation should be encouraged. With this combination of therapeutic modalities, this patient's serum calcium level should be corrected within 3 to 5 days. Intermittent injections of mithramycin or etidronate could be given on an outpatient basis approximately once a week in order to maintain the serum calcium within the normal range. One of the most important aspects of treatment in hypercalcemic patients is eradication of the underlying disease, which usually calls for specific antitumor therapy, including chemotherapy, radiation therapy, or surgery. Most of the agents currently available for the correction of hypercalcemia have cumulative toxicities or are only transiently effective and, therefore, their use should be considered a temporizing measure until specific treatment directed at the primary disease takes effect.
 ...
PMID:Management of severe hypercalcemia. 200 13

We report two cases of acute renal failure that followed the ingestion of jering. Features of jering poisoning included clinical presentation of bilateral loin pain, fever, nausea, vomiting, oligo-anuria, haematuria and passage of sandy particles in the urine. Blood urea (40.8 mmol/l; 21.9 mmol/l) and serum creatinine (1249 mumols/l; 693 mumols/l) were markedly elevated. With conservative therapy which included rehydration with normal saline and alkalinisation of the urine with sodium bicarbonate, the acute renal failure resolved.
 ...
PMID:Acute renal failure following jering ingestion. 204 77

In an open-label prospective study the safety, efficacy, and patient tolerance of an enterally administered isotonic intestinal lavage solution containing polyethylene glycol-3350 was evaluated in 20 pediatric patients (ages 1 1/2 to 19 years) undergoing diagnostic colonoscopy. After an oral dose of metoclopramide, lavage solution was administered by mouth or nasogastric tube at a rate of 40 ml/kg per hour until stools were clear. Emesis occurred in 4 patients, nausea in 11, and abdominal distension in 5. Clear stools were produced in a mean (+/- SE) time of 2.6 +/- 0.3 hours. The volume of lavage solution delivered, which ranged from 15.6 to 183.3 ml/kg, varied inversely with the weight (and age) of the patient. Preparation of the colon was considered optimal in 11 patients, satisfactory in 7, and suboptimal in 2. Small but significant decreases in urine osmolality, blood urea nitrogen, serum glucose, and potassium values were noted at the termination of perfusion. Postperfusion serum glucose concentration in the smallest patient (11.4 kg) was 61 mg/dL (3.4 mmol/L). Mean (+/- SEM) change in weight after perfusion was 0.14 +/- 0.05 kg (range -0.2 to +0.6 kg). Of 20 patients, 11 required or requested nasogastric administration of the lavage solution because of its unpleasant taste. We conclude that whole intestinal perfusion with a balanced electrolyte solution containing polyethylene glycol is safe, acceptable, and efficacious in children.
 ...
PMID:Safety, efficacy, and tolerance of intestinal lavage in pediatric patients undergoing diagnostic colonoscopy. 206 47

The term "microvesicular steatosis of the liver" refers to a variant form of hepatic fat accumulation whose histologic features contrast with the much more common macrovesicular steatosis. Microvesicular steatosis of the liver was originally described in association with conditions who share a number of biochemical and a limited number of clinical features: acute fatty liver of pregnancy, Reye's syndrome, Jamaican vomiting sickness, sodium valproate toxicity, high-dose tetracycline toxicity and certain congenital defects of urea cycle enzymes; they were thought to constitute an entity of "microvesicular fat diseases". In recent years the disease has been described in a wide variety of conditions: alcoholism, toxicity of several medications, delta hepatitis in South America and Central Africa, sudden childhood death, congenital defects of fatty acid beta oxidation, cholesterol ester storage disease, Wolman disease and Alpers syndrome. Not much is known regarding the pathogenesis of microvesicular steatosis but in many instances the primary defect could be a mitochondrial lesion, and inhibition of the mitochondrial beta oxidation of fatty acids has been the most frequently implicated defect. The different conditions associated with microvesicular steatosis are heterogenous in many aspects. Maintaining the concept of "microvesicular fat diseases" as a unique entity seems no longer justified.
 ...
PMID:Microvesicular steatosis of the liver. 217

Propionic acidemia is a rare hereditary disease which is an autosomal recessive disorder. Defect of propionyl CoA carboxylase results in abnormal accumulation of propionate and its metabolites which interfere the pathway of glycine cleavage and the urea cycle. This organic acidemia is characterized by a wide spectrum of clinical and biochemical findings, including recurrent vomiting, difficult feeding, lethargy, hypotonia, metabolic ketoacidosis, hyperglycinemia and hyperammonemia during the acute episodes. We present a male newborn infant who sustained this disorder and was managed successfully with blood exchange transfusion, peritoneal dialysis, supplemented with sodium benzoate and sodium bicarbonate therapy. Urine gas chromatography disclosed significant elevation of propionate and its metabolites which subsided 2 days after peritoneal dialysis. Special designed formula was then given with restriction of protein intake and supplement with sodium benzoate and sodium carbonate. Prenatal genetic counseling is necessary in further pregnancy. Diagnosis can be obtained when propionyl CoA carboxylase activity is low in cultured amniotic fluid cells or chorion villi sample or when there is abnormally high methylcitrate level in amniotic fluid.
 ...
PMID:[Propionic acidemia: report of a case that is successfully managed by peritoneal dialysis and sodium benzoate therapy]. 217 70

Intracranial pressure (ICP) was continuously monitored in a thirty-two-year-old female of acoustic neurinoma complicated with chronic renal failure. Severe headache with vomiting has begun to appear during hemodialysis for several months, prompting a diagnosis of an obstructive hydrocephalus. Continuous ventricular drainage was placed after admission and changes of ICP were monitored during hemodialysis. Dynamic changes of electrolytes, protein, sugar, urea nitrogen, and creatinine levels in the cerebrospinal fluid (CSF) as well as osmolarity were measured every one hour during the hemodialysis. An increment of ICP started to occur gradually after initiation of hemodialysis reaching the maximum value 23 minutes later. It was spontaneously decreased to the initial level 8 minutes later followed by fluctuations thereafter consisting of the changes of 20 to 30 mmHg. A remarkable rise in osmotic pressure in CSF has been observed corresponding to the rise of ICP which created a large difference from the blood osmotic pressure that consistently decreased following the onset of hemodialysis. Whereas, the absolute values of all measured factors including electrolytes and urea nitrogen in CSF have decreased consistently which did not seem to contribute intermittent increment of osmotic pressure of CSF. The cause of ICP increment in our case was considered mainly due to increase of water content in the brain tissue caused by the widening of osmotic gradient between the CSF and blood, although the substances responsible to the actual increase of CSF osmotic pressure remained unclear.
 ...
PMID:[Elevation of intracranial pressure during hemodialysis--continuous measurement of cerebrospinal fluid pressure in a patient with acoustic neurinoma]. 220 42


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>