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)

Thirty patients of acute or acute on chronic renal failure (ACRF) were randomly divided into two group of 15 cases each. Group A patients received 36 cycles of intermittent peritoneal dialysis (PD) with an exchange volume of one litre and duration of one hour per cycle. The 36 cycles of PD were divided into 12 clearance periods of 3 cycles each. Sodium Nitroprusside (SNP) was added in a dose of 4 mg/litre of dialysate in alternate clearance periods. Group B patients were given 4 hours of haemodialysis (HD) to compare the efficacy of two modes of dialysis. Symptomatic relief was observed in various uraemic signs and symptoms like vomiting, level of consciousness, fluid overload, hiccough and asterexis in most of the patients in both the groups. The percentage fall in blood urea and serum creatinine was 57.02 Vs 58.04 mg% and 46.9 Vs 47.8 mg% in group A and B respectively (P 70.5 each). Total dialysate urea removal following PD and HD was 118.8 +/- 57.3 gm and 98.5 +/- 37.0 gm respectively and also there was no significant difference in total creatinine removal. No untoward effects were observed with PD. However, following HD, 5 patients developed hypotension, supraventricular tachycardia was observed in one and disequilibrium syndrome in 8 of them. Therefore, it can be concluded that SNP added PD is comparable to 4 hours of haemodialysis both clinically as well as biochemically and in situations where facilities for HD do not exist or it is contraindicated, PD may be preferred mode of therapy.
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PMID:Comparison of sodium nitroprusside added peritoneal dialysis and standard haemodialysis. 925 52

Esophageal involvement is a common situation found in 50 to 80% of patients with scleroderma, but Boerhaave's syndrome is rare in this context. The authors report the first case of spontaneous esophageal rupture occurring in a chronic renal failure patient treated by continuous ambulatory peritoneal dialysis. In this observation, sclerodermal esophageal dyskinesia, chronic renal failure which is a classical cause of vomiting and the peritoneal dialysis which play an increasing role in the intraabdominal pressure are potential contributing factors to Boerhave's syndrome. In such patients presenting risk factors, even if they are asymptomatic, it seems reasonable to propose esophageal explorations with manometry or/and endoscopy looking for dyskinesia or other complications of gastro-esophageal reflux.
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PMID:[Spontaneous rupture of the esophagus (Boerhaave syndrome) in a patient with scleroderma treated by continuous ambulatory peritoneal dialysis]. 925 75

In 25 patients with chronic renal failure treated by haemodialysis with acetate-37 mEq/l containing fluid, plasma free, total carnitine and acetate concentration before and after HD were assessed. The concentration of acetate was high-12 mmol/l in 4 patients in which carnitine concentration was low. In these patients the incidence of the so-called "dialysis intolerance" or "acetate intolerance" such as acute hypotension, nausea, vomiting and headache were increased. The correlation between the serum acetate level and carnitine level and the symptoms suggest that the acetate overload during acetate dialysis affects acetate metabolism and administration of L-carnitine decreases the amount of accumulated acyl-CoA in the cytosol, and consequently--the citrate cycle function increases and diminish the intolerance symptoms.
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PMID:[Protective role of carnitine in acetate metabolism of patients with uremia treated by hemodialysis]. 944 Dec 89

A 49 year old female patient with anorexia nervosa was admitted to the hospital because of treatment-refractory hyperuricemia and gout. Medical history and clinical findings were compatible with primary gout and uric acid nephropathy. The patient stated that she regularly took allopurinol. In the hospital she initially received 300 mg allopurinol daily after breakfast. In order to ensure allopurinol ingestion and absorption the plasma concentrations of both allopurinol and its active metabolite oxipurinol were determined in addition to serum uric acid and further clinical chemistry data. Despite allopurinol treatment no decrease of serum uric acid was observed for three days. Therefore the head nurse was instructed to supervise the intake of allopurinol carefully. During the following days serum uric acid decreased and plasma oxipurinol concentrations rose. On day 9 of treatment serum uric acid fell into the upper normal range. Therefore the patient was allowed to leave the hospital within a few days. However serum uric acid thereafter increased again while plasma oxipurinol declined. Later on it became evident that the patient had vomited self-induced approximately 15 minutes after allopurinol intake. In the meantime her husband had urged her to return home. Starting with day 18 benzbromarone treatment was added. Combined therapy with 400 mg allopurinol and 50 mg benzbromarone daily finally resulted in a serum uric acid concentration of 4.5 mg/dl at discharge from the hospital. About three weeks later the private physician again diagnosed hyperuricemia with serum uric acid values between 10 and 12 mg/dl. Meanwhile the patient needs to be dialysed due to end stage renal disease. Our observations show that self-induced vomiting to prevent effective treatment may be a disease-specific pattern of noncompliance with drug therapy in anorexia nervosa.
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PMID:Disease-specific noncompliance with drug treatment as a cause of persistent hyperuricemia and gout in anorexia nervosa. 951 72

To investigate whether there are differences in the frequency of ADRs (adverse drug reactions) to parenteral iron preparations, we compared the results of 4 different data collections which contain observations in particular on i.m. or i.v. iron dextran and i.v. iron hydroxide sucrose complex, primarily in relation to anaphylactic/anaphylactoid reactions and common exanthemas. 1. In 206 patients of the department of general internal medicine in a city/teaching hospital (in association with the Swiss Foundation for Comprehensive Hospital Drug Monitoring--CHDM), 4 probably allergic reactions to i.m. iron dextran were found, one with acute severe dyspnea, cyanosis and flush, 3 with slight generalized, probably allergic reactions. Data from the USA on i.v. iron dextran do not show marked differences in the frequency of ADRs as compared with our data with i.m. administration. 2. A group of 400 otherwise healthy patients of the obstetric department of Zurich University Hospital were treated with i.v. iron sucrose for anemia due to iron loss during pregnancy or following childbirth. Seven generalized skin reactions, 4 in the form of flush and 3 of common exanthema, occurred. 3. In a retrospective study on patients on maintenance hemodialysis with chronic renal insufficiency and anemia, a questionnaire was answered by the medical heads of 17 selected hemodialysis units in Switzerland. Response was 100%. During around 8100 patient-years with approximately 160,000 ampoules of iron sucrose (with 100 mg elementary iron), not a single life threatening reaction was observed; only 5-7 situations of rapidly reversible blood pressure fall occurred, some 10 with flush, and one each with urticaria and vomiting/diarrhea. 4. The relatively good tolerance of i.v. iron sucrose in patients with chronic renal failure may be due either to reduced immune competence in patients with chronic renal insufficiency and/or to the use of the preparation itself, or probably both. 5. In ADRs of allergic appearance to iron sucrose, the 7 generalized skin reactions occurred on the first day of the injections, as did those under iron dextran. Preexisting hypersensitivity must be taken into consideration. 6. If our experience is confirmed, preventive measures with i.v. iron sucrose, mainly in patients with chronic renal insufficiency, could be reduced.
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PMID:[Parenteral iron therapy: problems and possible solutions]. 959 94

Benign intracranial hypertension (BIH) is reported in three children from Australia and one from New Zealand, who were being treated with recombinant human growth hormone (rhGH). Three males and one female, aged between 10.5 and 14.2 y, developed intracranial hypertension within 2 weeks to 3 months of starting treatment. A national database, OZGROW, has been prospectively collecting data on all 3332 children treated with rhGH in Australia and New Zealand from January 1986 to 1996. The incidence of BIH in children treated with growth hormone (GH) is small, 1.2 per 1000 cases overall, but appears to be greater with biochemical GHD (<10 IU ml(-1)), i.e. 6.5/1000 (3 in 465 cases), relative risk 18.4, 95% confidence interval 1.9-176.1, than in all other children on the database. The incidence in patients with Turner's syndrome was 2.3/1000 (1 in 428 cases). No cases in patients with partial GHD (10-20 IU ml(-1)) or chronic renal failure were identified. Possible causative mechanisms are discussed. The authors' practice is now to start GH replacement at less than the usual recommended dose of 14 IU m(-2) week(-1) in those children considered to be at high risk of developing BIH. Ophthalmological evaluation is recommended for children before and during the first few months following commencement of rhGH therapy and is mandatory in the event of peripheral or facial oedema, persistent headaches, vomiting or visual symptoms. The absence of papilloedema does not exclude the diagnosis.
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PMID:Benign intracranial hypertension and recombinant growth hormone therapy in Australia and New Zealand. 962 91

The low-protein diet (LPD) is used in patients with advanced chronic renal failure (CRF) to improve their symptoms and decrease the progression of CRF. LPD entails the risk for caloric malnutrition, which increases protein catabolism. Two groups were obtained from a total of 33 patients with CRF with LPD (0.6 g protein/kg/day): control group (group C), which went on with the same diet, and a group S, in which a portion of proteins and calories were provided through a low-protein and hypercaloric supplement (Suplena). During 6 months the protein intake and the evolution of the nutritional status and renal function were studied and compared between both groups. Additionally, tolerance and secondary effects of the supplement were studied in group S. Twenty-two patients (eleven in each group) completed the six month follow-up. At the end of the study, group S had the nutritional parameters better preserved, came closer to the low-protein diet objective, had a better compliance with therapy and had a less marked decrease in renal function--as measured by creatinine clearance--than group C. Tolerance to supplement was good in more than 70% of patients and secondary effects--nausea, vomiting and loss of appetite--occurred in 18% of patients at the end of the 6 months. We conclude that the use of this supplement in an LPD is usually well tolerated, enhances the compliance with the diet and can be of benefit for the mebacolic-nutritional status.
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PMID:[Treatment with low-protein diet and caloric supplements in patients with chronic kidney failure in predialysis. Comparative study]. 1111 1

Nephropathic cystinosis is a metabolic disease related to lysosomal cystine accumulation in almost all tissues of the body. The first symptoms set up from 5 or 6 months of age including anorexia vomiting polyurodipsia and failure to thrive associated with a proximal tubulopathy (glycosuria, tubular proteinuria, loss of bicarbonate, potassium, phosphorus, etc.) Treatment by cysteamine dramatically changed the prognostic. If started early this treatment allows to delay and possibly to prevent the spontaneous evolution towards end stage renal disease between 6 and 12 years of age and to avoid the growth failure. On the long term the disease involves other organs: eyes, thyroid endocrine pancreas, muscle and central nervous system. The diagnosis of cystinosis is based on the cystine leukocyte assay allowing also the follow up and the adjustment of the treatment. Prenatal diagnosis is possible on chorionic sample. The gene of this recessive disease, mapping on chromosome 17 was recently identified. This gene encodes a protein of the lysosomal membrane involved in the transport of cystine out of the lysosome. There is a juvenile, late onset, form of cystinosis its main symptom is proteinuria with variable tubular alterations. The so called adult form is asymptomatic its only symptom is corneal deposits most often found by chance examination.
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PMID:[Cystinosis from childhood to adulthood]. 1073 Feb 75

Renal involvement in amyloidosis leads to chronic renal failure. Prognosis is poor. Although amyloid deposits are frequent in adrenal glands, symptomatic adrenal dysfunction is uncommon. We report the case of a 63-year-old man with chronic renal failure (serum creatinine: 202 micromol/L) subsequent to amyloidosis who was referred to our unit for vomiting, dehydration despite a persistent nephrotic syndrome, acidosis, hyponatremia (121 mmol/l) and hyperkaliemia (7.1 mmol/l). A synacthen test was performed and disclosed adrenal insufficiency. Despite the initiation of substitution therapy, the patient died one month later from Addisonian crisis. Features of adrenal insufficiency may be masked by those of chronic renal failure, emphasizing the importance of adrenal explorations in patients with chronic renal failure due to amyloidosis.
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PMID:[Adrenocortical insufficiency in renal amyloidosis]. 1124 Apr 1

Methylmalonic acidemia (MMA) is an inborn error of organic acid metabolism that occurs in infancy with hypotonia, vomiting, dehydration, lethargy and failure to thrive and is biochemically characterized by metabolic ketoacidosis, hyperammonemia and sometimes hyperglycinemia. It results from deficiency of methylmalonyl-CoA mutase activity due to a defect in the mutase apoenzyme or to deficient function of one of the enzymes required for metabolism of its cofactor vitamin B12. Tubulointerstitial nephritis with progressive impairment of renal function is one of the most frequent long-term complications. We describe a case of a 17-year-old girl with methylmalonic acidemia unresponsive to vitamin B12 therapy. The clinical symptoms appeared at 4 months of life. She progressed into end stage renal disease and in January 1996 she started on hemodialytic treatment. In November 1996 we performed a kidney transplant. At present, urinary excretion of methylmalonic acid is normal and the renal function of the transplanted kidney is normal without any rejection episodes. We think that a kidney transplant could be a good therapeutic choice for the metabolic alterations in MMA with end stage renal disease. Indeed it would seem that the small methylmalonyl-CoA mutase activity present in the transplanted kidney could be sufficient to ensure normal metabolism of organic acids. Otherwise, the therapeutic goal can be achieved with a protein-restricted diet.
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PMID:Kidney transplantation in a girl with methylmalonic acidemia and end stage renal failure. 1168 86


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