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)

Recently introduced chloroquine resistant malaria has altered the clinical picture and complicated the overall management of malaria. 113 adults with proved malaria admitted at Harare Central Hospital, Zimbabwe, were evaluated to determine the incidence, nature, relationship to morbidity and mortality and response to treatment of the complications due to malaria. 47.7 pc (52 of 109) patients had relatively chloroquine resistant malaria. 87.4 pc (99 of 113) had complications whose percentage frequency of occurrence were: Anaemia 51.2 pc, diarrhoea and/or vomiting 42.2 pc, cerebral malaria +/- fits 39.2 pc, renal insufficiency +/- hyperkalaemia 26.4 pc, hypoglycaemia 15.6 pc, jaundice 15.2 pc, neuro-psychiatric 15.0 pc, shock 10.6 pc, concurrent sepsis 8.9 pc, pulmonary oedema 3.5 pc and hyperpyrexia 1.7 pc. Multiple complications in the same patient were common. The combination of cerebral malaria and renal insufficiency had the worst mortality (p less than 0.001). All patients dialysed, however, survived. Non-iron deficiency anaemia, 91.7 pc (51 of 55) and diarrhoea and/or vomiting, were common, worsened morbidity but not mortality (p = 0.555). A seriously-ill patient with malaria should be suspected of having complications and chloroquine resistance and should be referred promptly to a centre with facilities for dialysis. Anti-malaria drugs should be mixed in a dextrose solution and iron supplements should not be given routinely.
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PMID:Complications of seasonal adult malaria at a central hospital. 209 79

The purpose of this study was to investigate the prevalence and type of lesions in the upper gastrointestinal tract and to identify characteristics associated with ulcer disease among geriatric inpatients with positive faecal occult blood test and/or iron deficiency anaemia. Two thousand five hundred and four patients aged 60-98 (mean, 82) years admitted to a geriatric clinic for rehabilitation were screened by faecal occult blood test, for B-haemoglobin, and, in a case of anaemia, analyses of serum levels of mean corpuscular volume, mean corpuscular haemoglobin concentration, iron, and total iron-binding capacity. One hundred and seventy patients were included in the study. A high prevalence of ulcer disease (22%) was found. Significantly higher proportions of non-steroidal anti-inflammatory drugs and steroid users and of patients with rheumatoid arthritis and osteoarthrosis were found among ulcer patients than among patients without ulcerative upper gastrointestinal lesions. The clinical picture of ulcer disease differed from the classic presentation: abdominal pain occurred in only 7 of 38 patients (18%), whereas appetite and weight loss and nausea/vomiting were common. It is important to be aware of the high prevalence and the clinical picture of ulcer disease among geriatric inpatients with iron deficiency anaemia and/or occult gastrointestinal bleeding.
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PMID:Ulcer disease among geriatric inpatients with positive faecal occult blood test and/or iron deficiency anaemia. A prospective study. 235 77

A review of 339 treated acute iron ingestions was conducted to define treatment guidelines better. According to the poison center protocol, ingestions of 20-40 mg/kg of elemental iron required only home treatment, and ingestions of greater than or equal to 40 mg/kg required hospital referral. Gastrointestinal symptoms developed in 23% of patients. There were no seriously ill patients. No serious toxicity developed in patients ingesting 40-60 mg/kg. In 199 cases in which the dose ingested was known, the mean dose was 39.5 mg/kg. The peak measured serum iron levels ranged from 12 to 539 micrograms/dl. In 129 cases with serum iron levels reported, increasing serum iron levels were associated with vomiting (p = 0.006). Of 88 patients who received deferoxamine, 14 had urine color change. Urine color change was associated with symptoms (p = 0.005) but not with iron dose or peak serum iron level. The poison center protocol was changed to home management for ingestions of 20-60 mg/kg unless significant symptoms developed and hospital referral for ingestions greater than or equal to 60 mg/kg.
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PMID:Assessment of management guidelines. Acute iron ingestion. 236 39

Patient L.A. (f., 20 yrs), affected by bulimia and self-induced vomiting, was hospitalized because of severe malnutrition (BMI 13.1), hypopotassemia (2.8 mEq/l) and prolonged QTc interval (0.469"). Intensive care treatment aimed to normalize mineral balance mainly serum potassium, consisted of administering e.v. potassium (mg 2346/day), magnesium (mg 72/day), calcium (mg 80/day), phosphorus (mg 769/day), chloride (mg 710/day), iron (mg 40/day). Dietary treatment was deliberately chosen to be slightly above minimum energy requirements in order to avoid possible side effects of forced hyperalimentation. The patient, immediately after hospitalization, interrupted vomiting and 2 wks later weight increased by 5 kg (from 34.9 kg to 40.0 kg). On the other hand normalization of serum potassium levels was slow and QTc interval reached normal range only after the 10th day of treatment (0.447"). This case supports the hypothesis that major ECG abnormalities may be present in severe malnutrition due to anorexia nervosa or bulimia with self-induced vomiting. The dangers of these complications were substantiated by the fact that intensive care treatment allowed prompt body weight recovery but normalization of electrolytic balance and cardiac function was very slow. For such patients, electrocardiographic monitoring should be routine.
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PMID:[Hypopotassemia and prolongation of the Q-T interval in a patient with severe malnutrition caused by bulimia and post-prandial vomiting]. 237 4

Although consequences of zinc deficiency have been recognized for many years, it is only recently that attention has been directed to the potential consequences of excessive zinc intake. This is a review of the literature on manifestations of toxicity at several levels of zinc intake. Zinc is considered to be relatively nontoxic, particularly if taken orally. However, manifestations of overt toxicity symptoms (nausea, vomiting, epigastric pain, lethargy, and fatigue) will occur with extremely high zinc intakes. At low intakes, but at amounts well in excess of the Recommended Dietary Allowance (RDA) (100-300 mg Zn/d vs an RDA of 15 mg Zn/d), evidence of induced copper deficiency with attendant symptoms of anemia and neutropenia, as well as impaired immune function and adverse effects on the ratio of low-density-lipoprotein to high-density-lipoprotein (LDL/HDL) cholesterol have been reported. Even lower levels of zinc supplementation, closer in amount to the RDA, have been suggested to interfere with the utilization of copper and iron and to adversely affect HDL cholesterol concentrations. Individuals using zinc supplements should be aware of the possible complications attendant to their use.
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PMID:Zinc toxicity. 240 97

Pneumatosis intestinalis (PI) is a well-recognized manifestation of necrotizing enterocolitis (NEC) in the newborn--a condition that often requires surgical intervention for infarcted bowel. However, little information is available concerning PI in older children or its management. Sixteen older infants and children (greater than 2 months) had x-ray findings of PI (intramural air). There were eight girls and eight boys ranging in age from 2 months to 8 years. Associated conditions included short bowel syndrome (SBS) (8), congenital heart disease (2), iron ingestion (1), nesidioblastosis (1), hemolytic anemia (1), rheumatoid arthritis (1), bronchopulmonary dysplasia (BPD) (1), and malrotation (1). Clinical presentation included abdominal distension (13), bloody diarrhea (12), bilious emesis (5), and lethargy (5). Two patients on steroids had unsuspected PI identified as an incidental operative finding during pancreatectomy for nesidioblastosis (1) and splenectomy for hemolytic anemia (1), respectively. Only four other children (iron toxicity, postcardiac catheterization, rheumatoid arthritis, and BPD required surgical intervention. Each manifested peritioneal irritation, acidosis, and hypotension or had pneumoperitoneum on abdominal x-ray. In ten of 14 patients, PI was managed nonoperatively with nasogastric suction, fluid resuscitation, intravenous (IV) antibiotics (seven to ten days), and repeated abdominal x-ray and physical examinations. Children with SBS comprised 50% of the total number of patients and eight of ten treated by observation. All had associated viral syndromes (rotavirus) or rhotozyme-positive stools and developed bloody diarrhea. There were two deaths (12.5%) in patients with iron toxicity and congenital heart disease who required resection of gangrenous bowel. All of the other patients survived.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pneumatosis intestinalis in children beyond the neonatal period. 267 35

To insure adequate nutrition, parents and pediatricians often advocate vitamin and mineral supplementation in young children. A retrospective review of 275 pediatric cases (6 mo-6 yr) involving multiple vitamins and vitamins with iron was conducted. Six cases with co-ingestants were excluded. The product ingested was the child's own dietary supplement in 93% of the cases. Fifty-six percent were children's multiple vitamins and 44% were children's multiple vitamins with iron. Adult vitamin preparations accounted for 7% of the ingestions. The average amount of vitamin A ingested by history was 43,300 IU (1,500-225,000) while the mean ingestion of iron was 16.8 mg/kg (0.9-77.5 mg/kg). Fifty ingestions (18.2%) involved more than one child. The mean time since ingestion was 15.8 min (0-150 min). Management data showed 246 (89.5%) being treated in the home setting with dilution (83%) or syrup of ipecac induced-emesis (10%). Medical intervention including emesis, serum iron/TIBC, and oral complexation was needed in 10.5% of the cases. The mean serum iron levels were 204.6 mcg/dl (81-414 mcg/dl). No patient needed admission. This review revealed 100% of patients showed no significant toxic effects. We conclude that early recognition and prompt treatment of pediatric overdoses involving multiple vitamins with and without iron significantly reduces morbidity.
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PMID:Multiple vitamins and vitamins with iron: accidental poisoning in children. 335 78

Because of a projected pilot study with EDHPA in Cooley's anemia patients, animal studies with emphasis on reversibility of potential toxic signs were performed. Young dogs were treated iv with 6-18 mg/kg or orally with 30-240 mg/kg for 14 days followed by a 16-day recovery period. Drug-induced emesis, elevated BUN changes in kidney, spleen, and thymus weights diminished during recovery. One deceased dog exhibited nephrotoxicity consisting of tubular necrosis and deposition of the iron-EDHPA complex. The latter was observed in the excreta of survivors but kidney damage was not evident. Atrophy of the spleen and thymus in the deceased dog was consistent with less intense organ weight changes in recovered survivors. In the absence of morphologic changes after recovery, the precise effect on the immune system is unknown. The iv LD50 was 53 mg/kg for rats and mice. No rodent deaths occurred at an oral dose of 6000 mg/kg. An elevated BUN and changes in kidney, spleen, and thymus weights were confirmed in rodents given iv doses of 5-20 mg/kg or oral doses of 150-600 mg/kg for 5 days. It is cautioned that during the use of EDHPA derivatives that the functions of the renal and immune systems be monitored.
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PMID:Preliminary toxicity findings in dogs and rodents given the iron chelator ethylenediamine-N,N'-bis(2-hydroxyphenylacetic acid) (EDHPA). 369 19

Acute iron poisoning is most common in children below the age of 5 years. While there is no doubt that it may be fatal, recent surveys show that death occurs in only a very small percentage of cases and that iron salts are responsible for a small minority of fatalities due to overdosage with drugs. Similarly, the proportion of severe cases seems to have fallen over the last thirty years, possibly due to earlier and more aggressive treatment but more probably due to an increase in the number of minor exposures reported. Iron salts are directly toxic to the gastrointestinal tract causing vomiting, diarrhoea, abdominal pain and occasionally significant blood loss. They also cause metabolic acidosis by interfering with intermediary metabolism and producing shock and reduced tissue perfusion. The clinical course of acute iron poisoning is divided into 4 phases. Features of acute gastrointestinal irritation dominate the period up to 6 hours after ingestion and most patients do not develop other features or progress beyond this stage. Rarely, blood loss may be sufficient to cause hypotension. Severe poisoning is characterised by impairment of consciousness, convulsions and metabolic acidosis. The second phase, 6 to 12 hours after ingestion, is one of remission of features. Phase 3 comprises the period 12 to 48 hours from ingestion and is reached only by a small minority of patients. Recurrence or development of shock, and metabolic acidosis are usual and renal failure and features of extensive hepatocellular necrosis may develop. The last (fourth) phase, 2 to 6 weeks after ingestion, is only likely to develop in young children and is characterised by recurrence of vomiting due to gastric or duodenal stenosis caused by healing of iron-induced mucosal ulcers. Acute iron poisoning in humans has not been adequately studied and is unlikely to be so now because of the infrequent and sporadic occurrence of cases. The evidence for many conventional aspects of management is therefore unsatisfactory. Assessment of severity of poisoning is an essential prerequisite to optimum management but is difficult. The amount of elemental iron ingested is unacceptable since it is seldom known with accuracy and absorption is unpredictable because of vomiting and diarrhoea. The commonly encountered clinical features are also unreliable although it is generally accepted that coma, shock and metabolic acidosis indicate severe poisoning.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Management of acute iron poisoning. 378 42

Leukocytosis, blood glucose, vomiting, diarrhea, and abdominal radiograph have been reported as early indicators of toxic serum iron levels. To test the applicability of this battery of five variables, the charts of 64 patients admitted for toxic iron ingestion were reviewed. When these variables were subjected to tests of sensitivity, specificity, and predictive negative and positive values in 42 patients meeting study criteria, they failed to reach statistical significance. Only vomiting was found to approach statistical significance and, therefore, may serve as an early indicator of toxicity. In addition, several epidemiological issues relevant to the study population are discussed.
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PMID:Applicability of early indicators of iron toxicity. 379 82


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