Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Starting August 2006, a major epidemic of bluetongue (BT) was identified in North-West Europe, affecting The Netherlands, Belgium, Germany, Luxembourg and the North of France. It was caused by BT virus serotype 8 (BTV-8), a serotype previously unknown to the European Union (EU). In this outbreak, the virus caused clinical disease in a few individual animals within cattle herds, whereas overt clinical disease was usually restricted to sheep. Investigations in Belgium suggested that the first clinical signs of BTV-8 appeared mid July 2006 in a cattle herd, while the first suspicion of a BT-outbreak in Belgium was reported on 17 August 2006. In the first 10 BTV-8 outbreaks in the Netherlands, the owners indicated that the first clinical signs started approximately 12-17 days before a suspicion was reported to the veterinary authorities via a veterinary practitioner. In BTV-8 affected sheep flocks, erosions of the oral mucosa, fever, salivation, facial and mandibular oedema, apathy and tiredness, mortality, oedema of the lips, lameness, and dysphagia were among the most frequent clinical signs recorded. The most prominent clinical signs in BTV-8 affected cattle herds were: crusts/lesions of the nasal mucosa, erosions of lips/crusts in or around the nostrils, erosions of the oral mucosa, salivation, fever, conjunctivitis, coronitis, muscle necrosis, and stiffness of the limbs. Crusts/lesions of nasal mucosa, conjunctivitis, hyperaemic/purple coloration and lesions of the teats, and redness/hypersensitivity of the skin were relatively more seen on outbreak farms with cattle compared to sheep. Mortality, oedema of the head and ears, coronitis, redness of the oral mucosa, erosions/ulceration of tongue mucosa, purple coloration of the tongue and tongue protrusion and dyspneu were relatively more seen on outbreak farms with sheep compared to cattle.
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PMID:Field observations during the bluetongue serotype 8 epidemic in 2006. I. Detection of first outbreaks and clinical signs in sheep and cattle in Belgium, France and the Netherlands. 1862 Jul 67

The aim of this study was to investigate the prevalence of gastroesophageal reflux disease (GERD) in patients with laryngopharyngeal symptoms, the relationship between laryngopharyngeal reflux (LPR) and Helicobacter Pylori infection and treatment response to proton pump inhibitors. Forty-five patients with suspected gastroesophageal reflux diseases related symptoms (sore throat, throat burning, throat clearing, globus sensation, cough, halitozis, dysphonia, dysphagia, postnasal dripping, vocal fatigue, and sputum) were included in this study. For pre-therapeutic and post-therapeutic comparison, symptoms and laryngological findings were graded on a 4-point scale. The patients underwent upper gastrointestinal system endoscopy. During endoscopy, antral biopsies from the stomach were obtained to detect H. Pylori. Antireflux medication with proton pump inhibitors (PPI) and H. Pylori eradication therapy if present were prescribed to the patients. The improvement in symptoms and laryngological findings were evaluated after treatment. By means of esophagogastroduodenoscopy (EGD), reflux was detected in only 11% of patients. But there can be reflux patients other than the detected ones. Although, H. Pylori was present in 62% of patients, no correlation was found between H. Pylori positivity and symptoms. All patients responded well to antireflux treatment and H. Pylori eradication therapy. Laryngopharyngeal symptoms and findings can be predictors of gastroesophageal diseases when response to reflux treatment is taken into account.
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PMID:Association of laryngopharyngeal manifestations and gastroesophageal reflux. 1864 36

Earlier studies of the effect of 6 weeks of the Shaker Exercise have shown significant increase in UES opening and anterior excursion of larynx and hyoid during swallowing in patients with upper esophageal sphincter (UES) dysfunction, resulting in elimination of aspiration and resumption of oral intake. This effect is attributed to strengthening of the suprahyoid muscles, as evidenced by comparison of electromyographic changes in muscle fatigue before and after completion of the exercise regime. The effect of this exercise on thyrohyoid muscle shortening is unknown. Therefore the aim of this study was to determine the effect of the exercise on thyrohyoid muscle shortening. We studied 11 dysphagic patients with UES dysfunction. Six were randomized to traditional swallowing therapy and five to the Shaker Exercise. Videofluoroscopy was used to measure deglutitive thyrohyoid shortening before and after completion of assigned therapy regimen. Maximum thyrohyoid muscle shortening occurred at close temporal proximity to the time of maximal thyroid cartilage excursion. The percent change in thyrohyoid distance from initiation of deglutition to maximal anterior/superior hyoid excursion showed no statistically significant difference between the two groups prior to either therapy (p = 0.54). In contrast, after completion of therapy, the percent change in thyrohyoid distance in the Shaker Exercise group was significantly greater compared to the traditional therapy (p = 0.034). The Shaker Exercise augments the thyrohyoid muscle shortening in addition to strengthening the suprahyoid muscles. The combination of increased thyrohyoid shortening and suprahyoid strengthening contributes to the Shaker Exercise outcome of deglutitive UES opening augmentation.
Dysphagia 2009 Mar
PMID:Augmentation of deglutitive thyrohyoid muscle shortening by the Shaker Exercise. 1868 91

The purpose of this study was to determine the frequency of obstructive sleep apnea in patients with inflammatory myopathy. An observational and prospective study was performed on a cohort of adult patients with inflammatory myopathy followed at a specialized outpatient clinic. Sixteen consecutive adult patients were evaluated by the Epworth Sleepiness Scale (ESS) and by complete polysomnography study. Disease activity and severity were assessed using the Myositis Disease Activity Assessment Tool (MDAAT) and Myositis Damage Index (MDI), respectively. Associations between sleep parameters and other factors were calculated using the chi-square test, Fisher's exact test, Mann-Whitney U-test, and Wilcoxon's test. A serum autoantibody profile was determined for all patients. The mean apnea-hypopnea index was 28.7 (23.8), and 14 patients (87%) had an apnea-hypopnea index >5. The mean frequency of respiratory arousals was 20.1 (12.5). Eleven (68%) patients reported frequently-always snoring, and 3 (19%) had excessive daytime sleepiness (ESS >10). Seven patients were offered continuous positive airway pressure (CPAP) therapy; 4 tolerated the procedure well and reported a clear improvement in daytime sleepiness and/or sleep quality. No significant association was observed between the apnea-hypopnea index and clinical or immunological groups. Dysphagia, disease activity, and disease severity were not significantly associated with any sleep parameters. The frequency of obstructive sleep apnea in adult patients with inflammatory myopathy is high. The possibility that these alterations play a role in persistent fatigue in these patients cannot be ruled out.
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PMID:Obstructive sleep apnea in patients with inflammatory myopathies. 1914 52

Although denial in cancer patients is often seen in clinical practice, studies relating denial to physical outcomes are lacking. The present study aims to investigate patterns of denial among lung cancer patients and connect these to their physical outcomes. Denial was measured longitudinally in 195 consecutive newly diagnosed lung cancer patients. Four assessments were conducted over an 8-month period. Patient-reported physical outcomes were measured with a generic and disease-specific quality of life measure. Medical data were provided by the patients' chest physicians. Three patterns of denial over time were identified in lung cancer patients: patients displayed either low, moderate or increasing denial. Male lung cancer patients were found to deny at a moderate level more often. A moderate or increasing level of denial was consistently related to improved patient-rated physical outcomes. Lung cancer patients displaying more denial reported a better overall perception of health and better physical functioning. They complained less about fatigue, nausea and vomiting, appetite loss, dysphagia and pain in arm and shoulder than low deniers. Other symptoms did not differ among denial classes. Denial in lung cancer patients may well be an adaptive mechanism and have to be respected in clinical practice.
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PMID:Denial and physical outcomes in lung cancer patients, a longitudinal study. 2072 36

A 36-year-old man was admitted to our hospital because of general fatigue and dysphagia. He had experienced progression of thyrotoxic symptoms of weight loss, palpitation and sweating for several months. On admission, he showed thyroid storm associated with dysphagia and aspiration pneumonia. Dysphagia was restored completely with 2 months after intensive treatment with anti-thyroid agent, beta-blocker, potassium iodide and glucocorticoid for thyroid storm. Although dysphagia is an uncommon manifestation, we should keep in mind that dysphagia may be one of symptoms of thyrotoxic myopathy.
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PMID:Thyrotoxicosis complicated with dysphagia. 1960 94

Arytenoid subluxation is a rare laryngeal injury that may follow instrumentation of the airway and present as hoarseness, vocal fatigue, stridor, dysphagia, odynophagia and sore throat. We report the case of an 88-year-old man with type 2 diabetes mellitus who developed this complication during a difficult intubation where a Macintosh laryngoscope and gum elastic bougie were used to facilitate intubation. Previously considered to play a minor role in treatment, voice therapy was used successfully in this patient to correct subluxation of the arytenoid, with prompt resolution of his symptoms.
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PMID:Arytenoid subluxation after a difficult intubation treated successfully with voice therapy. 1977 54

Infection of the central nervous system with Nocardia sp. usually manifests as supratentorial abscesses. Supratentorial and cerebellar abscesses from infection with Nocardia sp. following immunosuppression with long-term corticosteroids for idiopathic thrombocytopenia (ITP) have not been reported. An 83 years-old, human immunodeficiency virus (HIV)-negative, polymorbid male with ITP for which he required corticosteroids since age 53 years developed tiredness, dyspnoea, hemoptysis, abdominal pain, and progressive gait disturbance. Imaging studies of the lung revealed an enhancing tumour in the right upper lobe with central and peripheral necrosis, multiple irregularly contoured hyperdensities over both lungs, and right-sided pleural effusions. Sputum culture grew Nocardia sp. Neurological diagnostic work-up revealed dysarthria, dysphagia, ptosis, hypoacusis, tremor, dysdiadochokinesia, proximal weakness of the lower limbs, diffuse wasting, and stocking-type sensory disturbances. The neurological deficits were attributed to an abscess in the upper cerebellar vermis, myopathy from corticosteroids, and polyneuropathy. Meropenem for 37 days and trimethoprime-sulfamethoxazole for 3 months resulted in a reduction of the pulmonary, but not the cerebral lesions. Therefore, sultamicillin was begun, but without success. Long-term therapy with corticosteroids for ITP may induce not only steroid myopathy but also immune-incompetence with the development of pulmonary and cerebral nocardiosis. Cerebral nocardiosis may not sufficiently respond to long-term antibiotic therapy why switching to alternative antibiotics or surgery may be necessary.
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PMID:Cerebellar nocardiosis and myopathy from long-term corticosteroids for idiopathic thrombocytopenia. 2004 27

A 68-year-old man was referred with progressive dysphagia. During the course, the patient developed muscle fatigue and additional signs of myopathy such as high levels of creatine kinase. The dysphagia was a late-onset side-effect to the treatment with lipid-lowering drugs. Cessation of treatment gives quick remission of symptoms and normalization of creatine kinase. As an increasing number of patients are being treated with lipid-lowering drugs, it is important to recall that myopathy is a dangerous side-effect which may have either quick or delayed onset, and that dysphagia can be the initial symptom.
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PMID:[Statin-induced dysphagia]. 2043 66

Bulbar weakness and fatigue resulting in dysphagia and dysarthria is common in myasthenia gravis. In chronic MG it is often assumed that these symptoms herald an exacerbation of the patient's disease and doses of cholinergic agents and immunomodulatory therapies may be increased, along with initiation of plasma exchange. A case is presented in which dysphagia was refractory to standard MG therapy, leading to the subsequent discovery of cricopharyngeal sphincter achalasia as the primary cause of the patient's symptoms rather than an assumed myasthenia gravis exacerbation. The patient's dysphagia resolved after esophageal dilatation. Cricopharyngeal sphincter achalasia is a common disorder producing dysphagia in the elderly and needs to be considered in the evaluation of a myasthenic patient with worsening dysphagia when standard myasthenia gravis therapy fails. Discussion of myasthenia gravis, cholinergic therapy and cricopharyngeal sphincter achalasia is undertaken. Clinicians are encouraged to consider non-neurologic causes of worsening dysphagia in the myasthenic patient.
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PMID:Reversible oropharyngeal dysphagia secondary to cricopharyngeal sphincter achalasia in a patient with myasthenia gravis: a case report. 2018 78


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