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)

A 15-year-old girl with familial dysautonomia had acute corneal ulcerations while on a respiratory during a dysautonomic crisis. Within 18 days she developed irritating corneal ring calcifications. Subsequent corneal perforation in the left eye was treated successfully with a lamellar graft, followed later by a penetrating graft in the right eye under local anesthesia. Four days postoperatively, the patient died during a vomiting crisis. Neuropathologic studies showed marked cell reduction in the superior cervical and trigeminal ganglia, but slight in the ciliary. The foveas appeared immature and macular ganglion cells were mildly reduced. The corneal button and lamellar grafted cornea had severe thinning and superficial calcification. Keratoplasty in familial dysautonomia is considered hazardous because of the continual threat of vomiting crises, but with sufficient care may be worthwhile for corneal perforation or advanced corneal scarring.
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PMID:Corneal transplantation in familial dysautonomia. 39 Oct 49

Starved houseflies were held over a suspension of Aujeszky's virus (PRV-1) for 24-48 h. One group was rinsed in 70% ethanol to kill virus attached to the body surface. No virus was isolated from this group. For the other group the titre of virus decreased more rapidly on the body surface of flies than in the environment. Model experiments demonstrated that the Aujeszky's virus cannot survive in the body of the housefly but the body surface may be contaminated for a period of time depending on the initial viral titre. Experiments showed that susceptible pigs fed on flies contaminated with Aujeszky's virus may become infected. The quantity of virus (5 x 10(5) pfu ml-1) shed by a single housefly during biting and vomiting on the cornea or abraded skin proved to be sufficient to cause infection in susceptible pigs, rabbits and a lamb. It is possible that houseflies could play a role in transmission of infection within herds. Transmission between herds is much less likely.
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PMID:The role of the housefly, Musca domestica, in the spread of Aujeszky's disease (pseudorabies). 285 39

In the two weeks immediately after the Bhopal disaster a community based survey was carried out in a series of eight exposed and two non-exposed clusters of households. The primary concern was the effect of the gas (subsequently identified as methyl isocyanate) on the eyes of the victims but data were also sought on respiratory status and the first symptoms of the exposure. No case of blindness was encountered that could be attributed to the gas. The most frequent symptoms reported were burning of the eyes, coughing, watering of the eyes, and vomiting. Among these, the frequency of cough most closely followed the rate of death in the different clusters. Although much rarer overall, the frequency of reported diarrhoea appeared to bear a stronger relation to death rates. Reports of photophobia and the clinical finding of superficial interpalpebral erosion of the cornea were more frequent where the death rates were lower. This clinical and epidemiological picture is consistent with different effects of the gas at different doses (as estimated from distance from the factory).
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PMID:Exposure and response to methyl isocyanate: results of a community based survey in Bhopal. 339 82

Blasticidin S is an effective fungicidal aminocylonucleoside antibiotic against a rice blast disease. We presented the first 4 reported cases of acute poisoning from ingesting blasticidin S for suicidal attempts. Three of the patients were fatal. The symptoms observed in the patients included vomiting immediately after ingestion and severe, persistent, watery diarrhea. The toxic effects of blasticidin S were noted in ectodermal tissues including the skin, conjunctiva, cornea, and intestine. Massive loss of intestinal fluid resulted in progressively pronounced hypotension associated with tachycardia. The treatment of choice for the poisoning consists of intravenous fluid administration and the management of body water and electrolyte balance.
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PMID:Acute blasticidin S poisoning. 382 82

Epidermal growth factor (EGF) effects have been explored extensively in vivo in rodents, but little is known about trophic responses in nonhuman primates. A previous publication reports the hyperplastic epithelial/parenchymal changes noted in the digestive tract (tongue, esophagus, stomach, intestine, liver, gallbladder, pancreas, and salivary glands) of adult cynomolgus monkeys treated with recombinant human EGF(1-48) (rhEGF(1-48)). This report documents clinical findings and structural effects in the remaining epithelium-containing tissues of these animals. Two monkeys/sex/dose received rhEGF(1-48) by intravenous bolus at 0 (vehicle), 10, 100, 500 (females only), or 1,000 microg/kg/day (males only) daily for up to 2 weeks. Treatment- and dose-related clinical findings included emesis, fecal alterations (soft feces and diarrhea), lacrimation, nasal discharge, hypoactivity, transient hypotension, and salivation after dosing. Male monkeys administered 1,000 microg/kg became moribund after 5 days of treatment and were necropsied. All other monkeys completed the 2-week treatment period. Necropsy findings in nongastrointestinal tissues were: enlarged, pale kidneys at 100 microg/kg and greater; small thymuses seen sporadically at all doses; and enlarged adrenals and small thyroids in males at 1,000 microqg/kg. Respective organ-to-brain weight ratios at 500 and 1,000 microg/kg for kidneys were 1.5- and 2.6-fold greater and for heart were 1.7- and 1.3-fold greater than controls. Microscopically, pronounced dose-related epithelial hypertrophy and hyperplasia were evident in kidney, urinary bladder, skin (epidermis and adnexa), mammary gland, prostate, seminal vesicles, epididymis, uterus, cervix, vagina, thyroid, thymus, tonsillar crypts, cornea, trachea, and pulmonary airways. Epitheliotrophic effects were conspicuous in many tissues at 100 to 1,000 microg/kg. Changes to renal collecting ducts were present at 10 microg/kg, suggesting that kidneys were a relatively sensitive target. Proliferative alterations were not apparent in testes, intraocular structures, brain ependyma and choroid plexus at any dose. Aside from the noted exceptions, rhEGF(1-48) was a pantrophic epithelial mitogen in cynomolgus monkeys when used intravenously at suprapharmacologic doses.
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PMID:Systemic proliferative changes and clinical signs in cynomolgus monkeys administered a recombinant derivative of human epidermal growth factor. 1142 83

A red eye is mostly a relatively harmless sign of simple conjunctivitis. Viral conjunctivitis may be extremely contagious. If no improvement is seen after ten days of treatment, referral to an ophthalmologist is indicated. Local corticosteroids and local anesthetics must not be prescribed. The patient should also be referred to an ophthalmologist when the red eye is chronic or recurrent, and when a unilateral red eye is associated with severe pain and vomiting (suspicious for acute glaucoma!), or generally when severe pain or impairment of sight, indicative of corneal infiltration or a hypopyon, presents. The diagnostic use of fluorescein to stain the cornea and any alteration of corneal transparency also belong in the hands of the ophthalmologist.
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PMID:[From conjunctivitis to glaucoma. When is a red eye an alarm signal?]. 1206 6

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

A 16-month-old boy was admitted to the clinic because of vomiting and growth failure. His weight and height measurements were under the fifth percentile. He had fair hair and skin, enlarged wrists and rachitic rosaries. The presence of metabolic alkalosis, hypokalemia, hypochloremia, and high renin and aldosterone levels were suggestive of Bartter syndrome. However, in view of the growth failure, fair hair and skin, proteinuria, polyuria and active rickets, cystinosis was considered. Bone marrow smear examination was normal, despite the existence of suspicious crystals in the cornea. Cystine crystals were seen in the conjunctiva biopsy and increased leukocyte cystine level was measured; therefore, definitive cystinosis diagnosis was made. Renal Fanconi syndrome with metabolic acidosis is prominent in cystinosis; however, in rare instances, if sodium-dependent trans-tubular transport defect is present, patients could have Bartter syndrome findings such as hypochloremic metabolic alkalosis. Our case is a good example demonstrating that metabolic alkalosis should not exclude cystinosis and the other signs and symptoms of the patient should be thoroughly evaluated.
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PMID:A patient with cystinosis presenting transient features of Bartter syndrome. 1717 73

Cystinosis is a rare autosomal recessive lysosomal storage disorder characterized by excessive accumulation of cystine within the lysosome. Cystinosis is caused by mutations in the lysosomal cystine transporter, cystinosin (CTNS). The CTNS gene consists of 12 exons and encodes for an integral lysosomal membrane protein with seven transmembrane domains. A majority of cystinotic patients are of European descents, and only a few cases have been reported from other ethnic groups. Here we report a case of nephropathic cystinosis in an Indian boy born to consanguineous parents. Major symptoms of the patient include weight loss, vomiting, dehydration, and cystine crystals in the cornea. Ichthyosis on the arms and legs is also observed. Sequencing analysis of all the CTNS exons revealed that the proband is homozygous for a 3-bp in-frame deletion in exon 10 (c.809_811delCCT), resulting in the loss of a conserved p.Ser270del within the fifth transmembrane domain of CTNS. His parents are both heterozygous for the same mutation. This work represents the first molecular characterization of cystinotic patients from India. Interestingly, a p.Ser270del resulting from c.809_811delCCT in CTNS had been identified in a European patient. Therefore, it appears that this mutation arose independently in the two different continents.
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PMID:An Indian boy with nephropathic cystinosis: a case report and molecular analysis of CTNS mutation. 1958 Apr 42

Bacillus cereus is ubiquitous in nature and thus occurs naturally in a wide range of raw materials and foodstuffs. B. cereus spores are resistant to desiccation and heat and able to survive dry storage and cooking. Vegetative cells produce several toxins which on ingestion in sufficient numbers can cause vomiting and/or diarrhoea depending on the toxins produced. Gastrointestinal disease is commonly associated with reheated or inadequately cooked foods. In addition to being a rare cause of several acute infections (e.g. pneumonia and septicaemia), B. cereus can also cause localized infection of post-surgical or trauma wounds and is a rare but significant pathogen of the eye where it may result in severe endophthalmitis often leading to loss of vision. Key risk factors in such cases are trauma to the eye and retained contaminated intraocular foreign bodies. In addition, rare cases of B. cereus-associated keratitis (inflammation of the cornea) have been linked to contact lens use. Bacillus cereus is therefore a microbial contaminant that could adversely affect product safety of cosmetic and facial toiletries and pose a threat to the user if other key risk factors are also present. The infective dose in the human eye is unknown, but as few as 100 cfu has been reported to initiate infection in a susceptible animal model. However, we are not aware of any reports in the literature of B. cereus infections in any body site linked with use of personal care products. Low levels of B. cereus spores may on occasion be present in near-eye cosmetics, and these products have been used by consumers for many years. In addition, exposure to B. cereus is more likely to occur through other routes (e.g. dustborne contamination) due to its ubiquity and resistance properties of spores. The organism has been recovered from the eyes of healthy individuals. Therefore, although there may be a perceived hazard, the risk of severe eye infections as a consequence of exposure through contaminated near-eye cosmetics is judged to be vanishingly small. It is unlikely that more stringent microbiological standards for near-eye cosmetics will have any impact on the risk of severe eye infections caused by B. cereus, as these are not linked to use of personal care products.
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PMID:Bacillus cereus in personal care products: risk to consumers. 2548 51


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