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)

The authors reported a case of niclofolan intoxication occurred during the trial of clonorchiasis treatment. The case, a 15 years old Korean schoolboy, took niclofolan(Bilevon(R)) of total 473 mg(11 mg/kg) in 11 divided doses during 20 days. And the case suffered from neurologic symptoms such as severe headache, dizziness, nausea, vomiting, blurred vision, papilledema, retinal hemorrhage, an epsiode of seizure attack and elevated intracranial pressure, and hepatotoxic symptoms such as hepatomegaly, increased serum transaminases, and shoulder pain, excessive sweating and weight loss. Therapy was concentrated to the management of the elevated intracranial pressure. Hepatotoxic manifestations subsided within one month. The clinical signs related to elevated intracranial pressure persisted two months. Body weight regained after 2 months. And the symptoms of headache, dizziness and vomiting were complained intermittently until 4 months after onset. However, no subsequent clinical problems related with this episode has been noted until this record.
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PMID:A Case Of Niclofolan (Bilevon(R)) Intoxication. 1290

A 67-year-old white woman developed severe nausea, vomiting, diffuse abdominal cramping pain, and blurred vision followed by a syncopal episode after taking 1 tablet of quinine for leg cramps. Examination was significant for fever, elevated blood pressure, and confusion without any focal neurological deficits. Laboratory studies showed markedly elevated liver enzymes, elevated lactate dehydrogenase, anemia, thrombocytopenia, and acute renal failure. Peripheral smear showed many schistocytes and burr cells. She later recalled taking quinine more than 40 years before while on a trip to the Philippines. The patient was treated with 7 sessions of plasmapheresis with a rapid normalization of her hematological parameters. Three weeks of dialysis support were required before return of renal function to baseline. Re-exposure to quinine can cause a rapid onset of hemolytic uremic syndrome-like syndrome. We are not aware of any cases of hemolytic uremic syndrome-thrombotic thrombocytopenic purpura in response to re-exposure to a single tablet of the drug 40 years after first use.
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PMID:Quinine induced HUS-TTP: an unusual presentation. 1467 3

Neurovestibular symptoms experienced by astronauts in the post-flight period were examined using data from medical debriefs contained in the NASA Longitudinal Study of Astronaut Health database. Ten symptoms were identified (clumsiness, difficulty concentrating, persisting sensation aftereffects, nausea, vomiting, vertigo while walking, vertigo while standing, difficulty walking a straight line, blurred vision, and dry heaves), of which eight were crossed with twelve demographic parameters (mission duration, astronaut gender, age, one-g piloting experience, previous space flight experience, g-suit inflation, g-suit deflation, in-flight space motion sickness, in-flight exercise, post-flight exercise, mission role, fluid loading). Three symptoms were experienced by a majority of subjects, and another two by more than a quarter of the subjects. Intensity of the symptoms was mild, suggesting that they are unlikely to pose a risk to the crew during landing and the post-flight period. Seven of the symptoms and eight of the parameters under study were found to be significantly associated with each other.
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PMID:Neurovestibular symptoms following space flight. 1475 12

This survey is part of a more comprehensive study on the health consequences of pesticide exposure. In the county (municipality) of Paty do Alferes, Rio de Janeiro State, Brazil, 55 agricultural workers were interviewed on the use of pesticides, use of personal protective equipment, data on health status, and symptoms related to pesticide exposure, disposal of agrochemical containers, and technical assistance. The most widely used pesticides were insecticides such as abamectin, organophosphate compounds, and pyrethroids, and fungicides such as mancozeb, chlorothalonil, and copper products. As a rule, pesticides are handled carelessly, and 92% of workers involved in the mixing, loading, and spraying of insecticides and fungicides used no protective clothing or equipment whatsoever. Some 62% of workers reported at least one illness associated with mixing or spraying pesticides. The most frequently reported symptoms were headache, nausea, vomiting, dizziness, skin irritation, and blurred vision, and 21% of affected workers required medical care. In more than half (51%) of the cases, workers reported using organophosphate insecticides from toxicological class I when they felt sick.
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PMID:[Pesticide use and poisoning among farmers from the county of Paty do Alferes, Rio de Janeiro, Brazil]. 1502 19

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

The only venomous reptile that naturally occurs in Poland is the adder or common viper (Vipera berus). Its bites are not of great epidemiological importance, but in some cases serious life-threatening symptoms may appear. The most common symptoms of adder envenomation are: local edema, reddening and pain of the bitten site and also the general symptoms coming from the alimentary tract (vomiting, diarrhoea, abdominal pain), the circulatory system (hypotension, shock, ECG abnormalities), the central nervous system (sleepiness, vertigo, disorientation, loss of consciousness), hematological symptoms (leukocytosis, hemolysis, coagulopathy) and allergic symptoms (fever, urticaria, angio-oedema). In the present study we described the case of a twenty-year-old patient hospitalized at the Toxicology Department of the Collegium Medicum UJ after a viper bite. Except for some above-mentioned symptoms he also developed ocular symptoms like ptosis and blurred vision. Such symptoms after the common viper bite have not been described in the literature till now. The cause of them seems to be an intense allergic reaction in the region of the orbit and eyelids all the more so because the patient had the positive allergy history. However, taking into account the latest reports from the literature, a neurotoxic action of some components of the Vipera berus venom may also play a role. Because of the developing general symptoms a specific equine antivenom was administered to the patient, apart from the supportive care, without any serious side effects that usually are observed after the use of such a kind of sera. It is thought that the sheep antivenom is better than the equine one considering a lack of allergic side effects. As a result of applied treatment the local and general symptoms including ocular symptoms subsided.
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PMID:[Envenoming by common viper (Vipera berus)--subject still exists...]. 1552 21

A 34-year-old man had a history of short-lasting episodes of rotatory vertigo followed by severe headache, provoked by sudden movements of the head and body. MRI of the brain revealed hydrocephalus secondary to a colloid cyst at the level of the foramen of Monro. The patient underwent microsurgery, after which he remained without symptoms. Colloid cysts are rare, benign tumours accounting for 0.5-1.0% of all primary brain tumours. They are attached by a stalklike appendage to the roof of the third ventricle between the fornices. Typical symptoms include intermittent headache, vomiting, occasional dizziness and blurred vision. These symptoms may be secondary to intermittent obstruction of cerebrospinal-fluid outflow through the foramen of Monro. The results of clinical and neurological examination are usually normal. In any patient with short-lasting episodes of severe headache, provoked by changes in position, an MRI of the brain should be done to exclude a colloid cyst. In general, these patients do not fulfil the criteria of the International Headache Society for migraine because of the short-lasting nature of the pain.
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PMID:[Transitory headaches caused by a colloid cyst of the third ventricle]. 1581 39

A 42-year-old pregnant woman (26 weeks of gestation, G(4)P(0+3)) presented at the emergency department with a two-hour history of dizziness, blurred vision and repeated vomiting. These symptoms started during the use of an undiluted insecticide liquid (diazinon 60 EC) while cleaning a small non-aired bathroom. After clinical and laboratory confirmation for organophosphate poisoning (plasma pseudocholinesterase levels 161 U/l), treatment with atropine and pralidoxime was started. She recovered within 7 days and delivered a healthy baby 12 weeks later (Apgar score 9 and 10) by elective cesarean section. The child showed no signs or symptoms of organophospate, atropine or pralidoxime exposure.
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PMID:Organophosphate poisoning in pregnancy: a case report. 1585 33

A 19-year-old girl had headaches, blurred vision and vomiting for 2 weeks. Neurological examination revealed only bilateral papilloedema and left abducens palsy. Neuroimaging of the brain was normal. Cerebrospinal fluid study showed intracranial hypertension (IH), hypoglycorrhachia, hyperproteinorrhachia, and a negative cytology study. Eight months after the onset, paraparesis occurred. Spinal magnetic resonance imaging showed intramedullary masses at the cervical and thoracic cords with extensive seeding. Biopsy of the mass showed primitive neuroectodermal tumor (PNET). IH rarely occurs in patients with spinal cord neoplasms. Its incidence is low and the condition is always associated with signs of myelopathy. We report a patient whose initial manifestation of spinal PNET was IH only. Spinal tumor should be considered in IH patients whose intracranial examinations are negative.
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PMID:Intracranial hypertension as an initial manifestation of spinal neuroectodermal tumor. 1602 36

The first pyrethroid pesticide, allethrin, was identified in 1949. Allethrin and other pyrethroids with a basic cyclopropane carboxylic ester structure are type I pyrethroids. The insecticidal activity of these synthetic pyrethroids was enhanced further by the addition of a cyano group to give alpha-cyano (type II) pyrethroids, such as cypermethrin. The finding of insecticidal activity in a group of phenylacetic 3-phenoxybenzyl esters, which lacked the cyclopropane ring but contained the alpha-cyano group (and hence were type II pyrethroids) led to the development of fenvalerate and related compounds. All pyrethroids can exist as at least four stereoisomers, each with different biological activities. They are marketed as racemic mixtures or as single isomers. In commercial formulations, the activity of pyrethroids is usually enhanced by the addition of a synergist such as piperonyl butoxide, which inhibits metabolic degradation of the active ingredient. Pyrethroids are used widely as insecticides both in the home and commercially, and in medicine for the topical treatment of scabies and headlice. In tropical countries mosquito nets are commonly soaked in solutions of deltamethrin as part of antimalarial strategies. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. In addition, mammals are protected by poor dermal absorption and rapid metabolism to non-toxic metabolites. The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with either piperonyl butoxide or an organophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of pyrethroids are on sodium and chloride channels. Pyrethroids modify the gating characteristics of voltage-sensitive sodium channels to delay their closure. A protracted sodium influx (referred to as a sodium 'tail current') ensues which, if it is sufficiently large and/or long, lowers the action potential threshold and causes repetitive firing; this may be the mechanism causing paraesthesiae. At high pyrethroid concentrations, the sodium tail current may be sufficiently great to prevent further action potential generation and 'conduction block' ensues. Only low pyrethroid concentrations are necessary to modify sensory neurone function. Type II pyrethroids also decrease chloride currents through voltage-dependent chloride channels and this action probably contributes the most to the features of poisoning with type II pyrethroids. At relatively high concentrations, pyrethroids can also act on GABA-gated chloride channels, which may be responsible for the seizures seen with severe type II poisoning. Despite their extensive world-wide use, there are relatively few reports of human pyrethroid poisoning. Less than ten deaths have been reported from ingestion or following occupational exposure. Occupationally, the main route of pyrethroid absorption is through the skin. Inhalation is much less important but increases when pyrethroids are used in confined spaces. The main adverse effect of dermal exposure is paraesthesiae, presumably due to hyperactivity of cutaneous sensory nerve fibres. The face is affected most commonly and the paraesthesiae are exacerbated by sensory stimulation such as heat, sunlight, scratching, sweating or the application of water. Pyrethroid ingestion gives rise within minutes to a sore throat, nausea, vomiting and abdominal pain. There may be mouth ulceration, increased secretions and/or dysphagia. Systemic effects occur 4-48 hours after exposure. Dizziness, headache and fatigue are common, and palpitations, chest tightness and blurred vision less frequent. Coma and convulsions are the principal life-threatening features. Most patients recover within 6 days, although there were seven fatalities among 573 cases in one series and one among 48 cases in another. Management is supportive. As paraesthesiae usually resolve in 12-24 hours, specific treatment is not generally required, although topical application of dl-alpha tocopherol acetate (vitamin E) may reduce their severity.
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PMID:Poisoning due to pyrethroids. 1618 Sep 29


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