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)

In the week of May 7, 1973, seven persons contracted botulism after eating together. The most common symptoms were vomiting, constipation, dry mouth, dysphagia, and dysphonia. All were treated with trivalent botulinal antitoxin, and none died. Serum specimens obtained from all seven patients were negative for botulinal toxin, but stool specimens from three patients were positive for type B toxin. Electromyographic studies performed on five patients documented the neurophysiologic abnormalities of botulism. Commercially canned peppers in oil were implicated epidemiologically, and type B toxin was identified in leftover peppers. The processor voluntarily recalled the pepper product, and no further cases were reported.
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PMID:Type B botulism outbreak caused by a commercial food product. West Virginia and Pennsylvania, 1973. 57 68

Thirty-eight emergency cricothyrotomies were performed over a 3-year period. This was the first airway control maneuver attempted in 5 patients, 3 of whom had facial and/or neck injury, one apneic with upper airway hemorrhage, and one with aortobronchial fistula. The remaining 33 procedures were performed only after other airway management failed. Five indications were identified among these cases: 1) excessive emesis or hemorrhage (11), 2) possible cervical spine injury with airway compromise (9), 3) technical failure (7), 4) clenched teeth (5), and 5) masseter spasm following succinylcholine administration (1). Fourteen immediate complications occurred in 12 patients (32%). The most frequent was incorrect site of tracheostomy tube placement (5), with 4 of 5 misplaced through the thyrohyoid membrane. Others included execution time greater than 3 minutes (4), unsuccessful tracheostomy tube placement (3), and significant hemorrhage (2). Twelve of the 38 patients were long-term survivors. There was one long-term complication, a longitudinal fracture of the thyroid cartilage during forceful placement of an oversized tube (8 mm inner diameter) through the cricothyroid membrane. This required operative repair and left the patient with severe dysphonia.
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PMID:Cricothyrotomy in the emergency department. 709 96

Parkinsonism as well as dystonic signs are rarely seen in central pontine myelinolysis and extrapontine myelinolysis. A 51 year old woman developed central pontine myelinolysis and extrapontine myelinolysis with parkinsonism after severe vomiting which followed alcohol and drug intake, even though marked hyponatraemia had been corrected gradually over six days. Parkinsonism resolved four months after onset, but she then exhibited persistent retrocollis, spasmodic dysphonia, and focal dystonia of her left hand. Although the medical literature documents three similar patients, this patient is different as dystonic symptoms only developed four months after parkinsonian signs had resolved.
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PMID:Parkinsonism and dystonia in central pontine and extrapontine myelinolysis. 966 73

Two siblings (one man, one woman), presenting with diarrhea, severe weight loss peripheral neuropathy, ophthalmoparesis, asymptomatic leukoencephalopathy were diagnosed as a new cases of Mitochondrial Neuro Gastro Intestinal Encephalomyopathy syndrome (MNGIE). Hirano (1994) defined four criteria for the diagnostic: peripheral neuropathy, ophthalmoparesis, gastro intestinal dysmotility, muscle biopsy with histologic features of mitochondrial myopathy (ragged-red fibers, muscle fibers with increased succinate deshydrogenase stain or ultra structurally abnormal mitochondria). In a review of the literature, we found 31 cases with MNGIE. With our two cases, we study this group of 33 patients. First symptoms begin about 13.5 years with a median of 10 years and extremes for 1 to 32 years. The first signs are gastro intestinal symptoms (recurrent nausea, vomiting or diarrhea with intestinal dysmotility) in 22 cases, an ophthalmoparesia in 4 cases, intestinal and ocular signs in 1 case, gait ataxia or peripheral neuropathy in 3 cases, hearing loss in 1 case, gait ataxia or peripheral neuropathy in 3 cases, hearing loss in 1 case. During the evolution, besides the cardinal signs, the following features have been observed with a variable frequency: hearing loss, short stature, facial palsy, dysphonia, dysarthria, sweating, orthostatic hypotension, bladder dysfunction, hepatomegalia, The laboratory features are: abnormal Nerve Condition Studies/EMG compatible with a sensory motor neuropathy, lactic acidosis, mitochondrial respiratory chain defect (essentially complex IV deficiency, complex I deficiency or multiple complex defect), MRI leukodystrophy, elevated CSF protein, heart block, ragged-red fibers or increased SDH stain. The prognosis is poor, due to a severe weight loss bordering on cachexia 13 patients died with a mean age of 28.5 years (median 24 years, extreme 3 years to 51 years). The prognosis seems to be worsened by a young age of onset. The 33 patients belong to 19 families with 7 cases of consanguinity. 25 patients had a brother, a sister or a cousin affected. The study of these families is compatible with an autosomic recessive transmission, suggesting a pathology of the nuclear genomi, probably impliying the control of the mitochondrial DNA replication. In fact, in 13 cases, a study of the mt DNA was realized: multiple deletions were founded in 6 cases, multiples mutations in one case, unique mutation in 1 case. In 5 cases ther was no evidence of abnormality. These precise etiology and pathophysiologic significance of the mt DNA deletions, and the heterogeneity of the modifications of the mt DNA remain unknown. However, the possibility of various phenotypes for a same genotype or inversely is known in mitochondriopathies.
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PMID:[MNGIE syndrome in 2 siblings]. 968 18

Dysphagia is related to the impairment of food passage from the mouth to the stomach. Globus pharyngis implies the frequent and often painful sensation of a lump in the throat that usually does not interfere with swallowing and may even be relieved by food intake. The diagnosis is based upon a careful history, clinical examination, endoscopy, dynamic imaging (videofluoroscopy, cinematography, videosonography) and electrophysiologic procedures (including pharyngoesophageal manometry, electromyography and pH determinations). Structural lesions of the cervical spine such as diffuse idiopathic skeletal hyperostosis are rare causes of dysphagia. Dysphagia following anterior cervical fusion as well as globus and dysphonia due to dysfunction of the vertebral joints are more likely. Symptoms with swallowing fluids indicate a neurogenic origin. Dyscoordinated swallowing, nasal reflux, dysphonia or general weakness may also occur. Chronic aspiration with respiratory compromize is the main consequence in a variety of neurological disorders as well as in cases of postsurgical dysphagia. Relaxation of the upper esophageal sphincter indicates coordinated muscle movement between the pharynx and esophagus. Dysfunction of the pharyngoesophageal segment may lead to cricopharyngeal achalasia. A dyskinetic sphincter commonly represents an extrapharyngeal cause: i.e., disease associated with gastroesophageal reflux. Disorders of the esophageal phase of deglutition can produce retrosternal pain, heartburn, regurgitation and vomiting, as well as laryngeal and respiratory signs. Esophageal motility disorders include lower achalasia, tumors, peptic strictures, inflammatory diseases, drug-induced ulcers, rings and webs. Motility disorders present with aperistaltic, spontaneous contractions, diffuse esophagospasm, or a hypermotile esophagus. Gastroesophageal reflux with esophagitis must always be excluded, especially in patients with a globus sensation. The multiple features of the appearance of the symptoms of dysphagia and globus makes multidisciplinary approach necessary in order to establish a diagnosis and begin effective treatment.
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PMID:[Deglutition disorders]. 977 28

In this study we tested the hypothesis that the initial cuff volume of the laryngeal mask airway influences emergence characteristics and postoperative laryngopharyngeal morbidity. One hundred and sixty adult patients undergoing minor surgery were randomly assigned for airway management with the laryngeal mask airway with either a fully inflated cuff (LMA-High) or a semi-inflated cuff (LMA-Low). Anaesthesia was with propofol, nitrous oxide, oxygen and isoflurane. Following insertion, the cuff was inflated with either 15 or 30 ml for the size 4 (females) and 20 or 40 ml for the size 5 (males). At the end of surgery, a blinded observer documented the presence or absence of adverse airway events (hypoxia, hypercapnea, coughing, retching, regurgitation/vomiting, airway obstruction, hypoventilation, hiccupping, biting, body movement or shivering) during every 1 min epoch and cardiorespiratory variables (heart rate, mean blood pressure, arterial oxygen saturation, end-tidal carbon dioxide and respiratory rate) every 5 min until the patient was awake and the laryngeal mask airway removed. Patients were interviewed about pharyngolaryngeal morbidity (sore throat, dysphonia and dysphagia) immediately before leaving the postanaesthesia care unit and 18-24 h following surgery. Analysis by epoch showed more partial airway obstruction in the LMA-High group, but analysis by patient numbers revealed no difference. Heart rate was slightly higher in the LMA-High group upon arrival in the postanaesthesia care unit, but otherwise there were no differences in cardiorespiratory responses. Sore throat and dysphagia were more common in the LMA-High group. We conclude that, in general, emergence characteristics with the laryngeal mask airway are not influenced by the volume of air used to inflate the cuff, but that postoperative sore throat and dysphagia are more likely at high initial cuff volumes.
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PMID:Emergence characteristics and postoperative laryngopharyngeal morbidity with the laryngeal mask airway: a comparison of high versus low initial cuff volume. 1078 Nov 19

Spontaneous retropharyngeal hematoma is an uncommon entity that is difficult to diagnose and may progress rapidly to airway obstruction. We report a case of a 53-year-old man with acute onset of retropharyngeal pain, dysphonia, and dysphagia after vomiting. On CT, a nonspecific retropharyngeal collection was seen. MR imaging demonstrated blood products, suggesting a diagnosis of retropharyngeal hematoma, and the patient was managed conservatively. MR imaging allowed specific diagnosis of a rare condition that is otherwise difficult to diagnose without surgical intervention.
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PMID:Spontaneous retropharyngeal hematoma: diagnosis by mr imaging. 1141 22

A 10-year-old boy presented with fever, headache, vomiting, and hypersomnolence. An akinetic-rigid syndrome with tremor, dysphagia, dysphonia, and sialorrhea, as well as pyramidal signs, developed. Slightly elevated protein content was found in the cerebrospinal fluid and serological investigations were suggestive of a primary Epstein-Barr virus infection. Magnetic resonance imaging (MRI) showed massive bilateral hyperintense striatal and punctiform periventricular lesions. After 2-month treatment with steroids and antiparkinsonian drugs, all features resolved without sequelae. Control MRI demonstrated only minimal residual lesions in both putamina. Strongly resembling the encephalitis lethargica-like syndrome, this case is an unusual presentation of parainfectious acute disseminated encephalitis.
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PMID:Acute reversible parkinsonism in Epstein-Barr virus-related encephalitis lethargica-like illness. 1625 20

C1 inhibitor (C1-INH) is a serine protease inhibitor (serpins) that inactivates several different proteases in the complement, contact, coagulation, and fibrinolytic systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds, and blocks the activity of its target proteases. The N-terminal end (nonserpin domain) confers to C1-INH the capacity to bind lipopolysaccharides and E-selectin. Owing to this moiety, C1-INH intervenes in regulation of the inflammatory reaction. The heterozygous deficiency of C1-INH results in hereditary angioedema (HAE). The clinical picture of HAE is characterized by bouts of local increase in vascular permeability. Depending on the affected site, patients suffer from disfiguring subcutaneous edema, abdominal pain, vomiting and/or diarrhoea for edema of the gastrointestinal mucosa, dysphagia, and dysphonia up to asphyxia for edema of the pharynx and larynx. Apart from its genetic deficiency, there are several pathological conditions such as ischemia-reperfusion, septic shock, capillary leak syndrome, and pancreatitis, in which C1-INH has been reported to either play a pathogenic role or be a potential therapeutic tool. These potential applications were identified long ago, but controlled studies have not been performed to confirm pilot experiences. Recombinant C1-INH, produced in transgenic animals, has recently been produced for treatment of HAE, and clinical trials are in progress. We can expect that the introduction of this new product, along with the existing plasma derivative, will renew interest in exploiting C1-INH as a therapeutic agent.
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PMID:C1 inhibitor: molecular and clinical aspects. 1626 49

Spontaneous pneumomediastinum is a presence of free air in the mediastinum without previous injury and without previously known lung disease. Spontaneous pneumomediastinum is infrequent and little known by physicians. Authors present a case report of three young men with spontaneous pneumomediastinum. There was no evident causation in two cases. In one case there was previous excessive sport activity. Main presenting symptoms were chest and neck pain, odynophagia, dysphonia, vomiting, and neck subcutaneous emphysema. Esophageal perforation was ruled out. All patients recovered spontaneously. Spontaneous pneumomediastinum is the benign disease. Its main importace is in differential diagnosis concerning especially esophageal perforation.
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PMID:[Spontaneous pneumomediastinum]. 1697 63


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