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)

Poisoning is a significant problem in the elderly. The majority of poisonings in older people are unintentional and may result from dementia and confusion, improper use of the product, improper storage or mistaken identities. Depression is also common in the elderly and suicide attempts are more likely to be successful in this age group. The elderly patient's recuperative abilities may be inadequate as a result of numerous factors including impaired hepatic or renal function as well as chronic disease processes. General management of poisoning in the elderly parallels management of younger adults, but it is especially important to ascertain underlying medical conditions and concurrent medications. In most poisonings, activated charcoal and cathartic are sufficient. Haemodialysis or haemoperfusion may be required at lower plasma drug concentrations in elderly patients. While the specific indications for antidotes are the same for all age groups, dosage alterations and precautions may need to be considered in the elderly. Drugs most often implicated in poisonings in the elderly include psychotherapeutic drugs, cardiovascular drugs, analgesics and anti-inflammatory drugs, oral hypoglycaemics and theophylline. Cardiovascular and neurological toxicities occur with overdoses of neuroleptic drugs and, more frequently and severely, with cyclic antidepressants. Patients with pre-existing cardiovascular disease are at particular risk of worsening ischaemic heart disease and congestive heart failure. Benzodiazepines only appear to produce significant toxicity during long term administration or in combination with other CNS depressants. Digoxin can cause both chronic and acute intoxication, most seriously cardiac toxicity including severe ventricular arrhythmias, second or third degree heart block or severe refractory hyperkalaemia. Immune Fab antibody is indicated for the management of digoxin toxicity, although patients dependent on the inotropic effect of digoxin may develop heart failure after digoxin Fab antibody administration. Nitrates can cause toxicity including headache, vomiting, hypotension and tachycardia from excessive sublingual, transdermal or intravenous doses. Conduction disturbances and hypotension occur with overdoses of antihypertensive drugs; these effects are mild with angiotensin converting enzyme (ACE) inhibitors, occasionally severe with beta-blockers and of significant concern with calcium channel antagonists. The elderly commonly use aspirin and other salicylates, are more likely to develop chronic intoxications to these agents, and are more susceptible to severe complications such as pulmonary oedema. Salicylate poisoning, recognition of which is often delayed, should be considered in elderly patients with neurological abnormalities or breathing difficulties, especially in the setting of acid-base abnormalities. The clinical effects of NSAID overdose are mild and usually involve the central nervous system and gastrointestinal tract.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Poisoning in the elderly. Epidemiological, clinical and management considerations. 179 7

A fatal yellow oleander herbal poisoning is reported in a 2 1/2-year-old Melanesian boy, who had persistent vomiting,bradycardia caused by complete heart block, hyperkalemia and cardiac glycosides detected in his serum. This is one of the few recognized clinical pictures of illness from herbal poisoning, yet herbal poisoning in infants in some Pacific and African countries is common and has a high mortality.
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PMID:Herbal poisoning: a case report of a fatal yellow oleander poisoning from the Solomon Islands. 243 39

A total of 20 patients with histologically proven primary hepatocellular carcinoma (PHC) received mitoxantrone IV at a dose of 10-16 mg/m2 every 3 weeks. All patients had previous hepatitis B infection. None underwent remission after treatment; 2 had stable disease and 18 progressive disease. The median overall survival was 13 weeks (range, 1-59 weeks). There was no evidence of significant antitumor activity for mitoxantrone in our patients with PHC. Hematotoxicity occurred in 100% of the patients with grades 2-4 leukopenia, 89% of those with grades 1-4 anemia, and 26% of those with grades 2-3 thrombocytopenia. Cardiotoxicity occurred in 20% of the patients after 14-30 mg/m2 mitoxantrone; these included complete heart block with fatal outcome in one case, decreased ventricular ejection fraction in one, and sinus tachycardia in two. Nausea, vomiting, fever, diarrhea, and alopecia were mild and occurred in 15%-45% of the patients Therefore, patients with PHC following hepatitis B infection may be less tolerant to mitoxantrone, resulting in the apparent increase in toxicities.
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PMID:Phase II study of mitoxantrone in unresectable primary hepatocellular carcinoma following hepatitis B infection. 253 94

We present a case of a 79-year-old woman with periods of syncope, complete heart block (CHB), and ventricular standstill during periods of increased vagal tone following sublingual nifedipine for hypertension. The syncopal episodes were associated with periods of elevated vagal tone (micturition and vomiting) with one monitored episode showing a clear time course of emesis; CHB then ensued, progressing to ventricular standstill with loss of consciousness that resolved over several minutes. Although nifedipine is not thought to affect conduction at current clinical dosages, it seems likely that the additive effects of nifedipine and elevated vagal tone produced the observed conduction abnormalities. This is the first case report of nifedipine administration followed by syncope and conduction disturbances.
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PMID:Syncope and conduction disturbances following sublingual nifedipine for hypertension. 403 65

Aclacinomycin A (ACM-A), an anthracycline analog, was given to 17 patients with solid tumors and to one patient with multiple myeloma, in a phase I clinical trial. A single dose of 60-120 mg/m2 was given every 3 weeks. Dose-limiting toxicity was myelosuppression, especially thrombocytopenia. Granulocytopenia was variable and did not always recover by Day 21 in time for the next ACM-A treatment. Other toxic effects were nausea, vomiting, urticaria, and elevation of hepatic enzymes. Alopecia was not a side effect, even in patients receiving multiple courses of ACM-A. Nine patients were monitored with 24-hour continuous ECG recordings (Holter) on 19 ACM-A treatment days. The incidence of premature atrial and ventricular beats was significantly increased following ACM-A administration. In addition, one patient developed episodes of high-degree atrioventricular block and complete heart block after each of four ACM-A doses, necessitating the insertion of a pacemaker. No antitumor responses were seen in the ten patients who had measurable disease and who had received two or more courses of ACM-A. The recommended doses for solid tumor phase II studies are 100 mg/m2 as a single dose every 4 weeks for patients with high performance status and minimal prior chemotherapy and 60 mg/m2 every 4 weeks for all other patients. Until the acute cardiac effects of ACM-A are further understood, we recommend that all patients receiving ACM-A be monitored by ECG recordings.
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PMID:Phase I trial of aclacinomycin A. 695 61

The prognostic significance of various clinical and biochemical factors was investigated in 179 patients who had ingested more than 2 mg digitoxin. The mortality rate in this series was 17%. Supraventricular arrythmias had no influence on prognosis, but the death risk was higher in males and in patients with AV block. It increased with age, with digitoxin and potassium serum levels and even more with persistent hyperkalemia. Two other factors--previous heart disease and vomiting--were also significant in patients without heart block. Calculated on the basis of 4 clinical factors, the mortality rate varied from 2 to 74%. The death risk in acute digitalis poisoning can therefore be easily assessed simply from clinical criteria.
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PMID:[Prognostic factors in acute digitalis poisoning]. 713 39

The prognostic significance of various clinical and biochemical factors was investigated in 179 patients who had absorbed more than 2 mg of digitoxin. The mortality rate in this series was 17%. Supraventricular arrythmias had no influence on prognosis, but the death risk was higher in males and in patients with A-V block. It increased with age, with digitoxin and potassium serum levels and even more with persistent hyperkalemia. Two other factors, previous heart disease and vomiting, were also significant in patients without heart block. Calculated on the basis of 4 clinical factors, the mortality rate varied from 2 to 74%. The death risk in acute digitalis poisoning can therefore be easily assessed from simple clinical criteria.
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PMID:[Prognostic factors in acute digitalis poisoning (author's transl)]. 726 27

The leaves of Phytolacca americana (pokeweed), when ingested, typically produce a self-limited but severe gastroenteritis characterized by intense vomiting and frothy diarrhea. Although cardiac effects have been reported in previous cases of pokeweed ingestion, no cardiac toxin has ever been identified in pokeweed. We report the case of a family who ingested raw and/or cooked pokeweed leaves, and 1 member who developed a Mobitz type I heart block associated with vomiting which resolved after i.v. promethazine. This suggests the possibility that some cardiac effects of pokeweed are secondary to the increased vagal tone seen with severe gastrointestinal colic.
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PMID:Mobitz type I heart block after pokeweed ingestion. 770 98

Medetomidine and fentanyl-droperidol (Innovar-vet) were assessed over a three hour period in 80 healthy dogs. Following physical examination, electrocardiogram (ECG), arterial blood sample analysis, and dynamometer pressure threshold (analgesia score), the dogs were randomly assigned to one of four treatments: Miv--medetomidine (750 micrograms/M2) administered intravenously (IV), Mim--medetomidine (1000 micrograms/M2) administered intramuscularly (IM), Iiv--Innovar-vet IV (0.05 mL/kg) or Iim--Innovar-vet IM (0.1 mL/kg). All assessments were carried out by a single individual unaware of the treatment used. Objective assessments included temperature, heart and respiratory rates, analgesia score, arterial blood gases, acid-base and lactate levels. Subjective evaluation included degree of sedation, response to various clinical procedures, noise responsiveness, posture, and the incidence of side effects. Onset and duration of effect were also recorded. The ECG strips were assessed for arrhythmias. Data was analyzed using a 3-way analysis of variance for continuous variables and a Chi-square analysis of frequencies. A p value < or = 0.05 was considered significant. Medetomidine-treated animals had a decreased respiratory rate, longer duration of analgesic effect, increased incidence of bradycardia, vomiting and twitching, were less noise responsive and shivered less throughout the study. An increased incidence of second degree heart block with Miv (15 min), a delayed onset and recovery with Mim and increased lactate levels following Iiv (15 min) were observed. No differences were found in other measurements and good to excellent chemical restraint was produced with all treatments in 65% or more cases.
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PMID:Comparison of medetomidine and fentanyl-droperidol in dogs: sedation, analgesia, arterial blood gases and lactate levels. 849 Aug 14

We report a 56-year old female with mitochondrial neurogastrointestinal encephalomyopathy (MNGIE), presenting with protein-losing gastroenteropathy and serum copper deficiency. There was no neuromuscular disease in her family members. Three years prior to admission, she developed severe gastrointestinal symptoms including diarrhea, nausea, vomiting and ascites, and was diagnosed as having protein-losing gastroenteropathy based on alpha(1)-antitrypsin clearance and other tests. She was referred to our department when neurological symptoms were apparent. Neurological examinations revealed bilateral ptosis, ophthalmoplegia, hearing loss, facial and limb muscle weakness, mild sensory deficit of vibration on her feet and hypoactive deep tendon reflexes. Pigmentary retinopathy, cerebellar ataxia and heart block were not seen. Serum copper level was decreased to 45 micrograms/dl (normal: 83-155). Chronic intestinal pseudo-obstruction was proven by X-ray studies, and diffuse leukoencephalopathy demonstrated on brain MRI. On EMG, motor nerve conduction velocities were prolonged with temporal dispersion. Her muscle biopsy from biceps brachii muscle showed both neuropathic and myopathic changes, scattered ragged-red fibers and focal cytochrome c oxidase deficiency. Southern blot and polymerase chain reaction analysis on mitochondrial DNA showed no deletions nor point mutations. The clinical and pathologic findings of the present patient fulfilled the diagnostic criteria of mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) proposed by Hirano et al. There are few reported patients with MNGIE in Japan, but none presented with protein-losing gastroenteropathy and serum copper deficiency. Since the copper is a cofactor of cytochrome c oxidase, decreased serum copper level may aggravate the respiratory chain enzyme metabolism in mitochondria. Therefore, treatment for gastrointestinal tract disturbance and copper administration may be necessary to prevent disease progression.
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PMID:[Mitochondrial neurogastrointestinal encephalomyopathy presenting with protein-losing gastroenteropathy and serum copper deficiency: a case report]. 949 Sep 4


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