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)

Nasopharyngeal stenosis as a postoperative complication following pharyngeal surgery (tonsillectomy/adenoidectomy) is rare and may be difficult to treat. All patients with severe nasopharyngeal stenosis treated at UCLA with a bilateral Z-pharyngoplasty procedure from 1999 to 2006 were studied (n = 6). Degree of pharyngeal stenosis preoperatively and following a bilateral Z-pharyngoplasty was graded 0-4 based on (1) symptomatology (snoring, hyponasal speech, difficulty with nasal breathing, difficulty breathing during exercise, obstructive sleep apnea, daytime fatigue, anosmia, rhinorrea, dysphagia, or difficulty in blowing nose) and (2) measurement of stricture at the time of direct nasolaryngoscopy. Nasopharyngeal stenosis after pharyngeal surgery (adenotonsillectomy--67%, uvuloplasty--17%, pharyngoplasty--17%) failed to be alleviated by a mean of 2.3 procedures (kenalog injection or scar excision) and required corrective bilateral Z-pharyngoplasty a mean of 9.2 months after the original surgery. Symptomatic grading of the nasopharyngeal stenosis improved from a mean score of 3.3 (severe stenosis) preoperatively to a score of 0.2 (minimal to no stenosis) in follow-up. Endoscopic stricture measurement improved from 6.1 x 6.3 mm preoperatively to 28.1 x 39.3 mm in follow-up. Bilateral Z-pharyngoplasty was effective in alleviating severe postsurgical nasopharyngeal stenosis.
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PMID:Amelioration of acquired nasopharyngeal stenosis, with bilateral Z-pharyngoplasty. 2048 3

The purpose of this retrospective analysis was to characterize the feasibility and tolerability of oxaliplatin/5-fluorouracil (5-FU) given concurrently with radiotherapy for patients with locally advanced esophageal cancer. Between July 2005 and March 2009, 15 patients with clinical stage T3/T4 and/or N1/M1a lower esophageal or gastroesophageal junction adenocarcinoma were treated with preoperative chemoradiotherapy using oxaliplatin every 2 weeks and continuous infusion 5-FU. The main treatment-related toxicities were oral mucositis and dysphagia. During the first 2 weeks of treatment, 20% of patients presented with grade 1-2 oral mucositis, and one patient developed grade 1 dysphagia. In weeks 3-4, 53% of the patients experienced grade 1-2 mucositis, and 40% experienced grade 1-2 dysphagia. One patient only experienced grade 3 mucositis in week 4. Three patients (20%) had grade 3-4 dysphagia in weeks 3-4 and were continued on intravenous fluids and pain medications. During the last 2 weeks of chemoradiotherapy, 53% of patients reported grade 1-2 oral mucositis, mostly grade 1 and 73% of patients experienced grade 1-2 dysphagia and 26% patients experienced grade 3-4 dysphagia. Other toxicities included fatigue, nausea, neuropathy, and diarrhea. Only one patient experienced > 10% weight loss. The whole group was treated with aggressive supportive care during radiotherapy. Five (33%) patients achieved a pathological complete response. No patients developed locoregional failure. Sixty percent of the patients developed distant metastases and the 2-year disease-free survival was 53%. The median survival was 3.2 years with the 2-year overall survival of 73%. Preoperative oxaliplatin/5-FU-based chemoradiotherapy for locally advanced esophageal cancer is feasible, but associated with substantial gastrointestinal toxicity. A careful attention to nutrition and hydration throughout the course of therapy is required.
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PMID:Toxicity data for preoperative concurrent chemoradiotherapy with oxaliplatin and continuous infusion 5-fluorouracil for locally advanced esophageal cancer. 2114 94

The stomach and small intestine are common sites for gut lymphomas, but oesophageal lymphomas are very rare. In mantle cell lymphoma (MCL), although multifocal gut involvement is seen, oesophageal involvement is uncommon. Gut involvement may be primary or secondary to systemic involvement. Multiple lymphomatous polyposis (MLP) is the intestinal form of MCL. Most cases of MLP occur in the elderly, usually over 50 years of age, and the presenting symptoms are abdominal pain, melaena, haematochezia and fatigue. In MCL, tumour cells typically express CD5 and cyclin D1 markers. Our patient presented with generalised lymphadenopathy, dysphagia and rapid weight loss. Upper gastrointestinal endoscopy revealed submucosal polypoid lesions in the oesophagus, stomach and duodenum. Histopathology and immunophenotyping confirmed MCL. Although MLP presenting as a primary MCL of the intestine has been described in the literature, our patient also had multiple intestinal polyposis (including the oesophagus) due to secondary involvement from systemic MCL.
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PMID:Oesophageal involvement in mantle cell lymphoma. 2122 93

We present a case of prolonged hoarseness after tracheal intubation in a 62-year-old woman with bronchial asthma who underwent a pylorogastrectomy under a combination of epidural and general anesthesia. After the induction of anesthesia, the patient was carefully intubated using a 7.5-mm cuffed endotracheal tube without a stylet to avoid causing an asthma attack; the patient was extubated approximately 6 hours after the tracheal intubation. On the first postoperative day, the patient complained of hoarseness, vocal fatigue, and dysphagia. A direct laryngoscopy performed by an otorhinolaryngologist revealed dyskinesia of the left vocal cord and sufficient arytenoid cartilage mobility. The poor vocal fold mobility was probably caused by the force exerted on the left arytenoid by the convex curvature of the endotracheal tube, which had been inserted from the right side of the mouth, or a backward pressure on the thyroid cartilage during intubation. Early treatment is crucial in such cases, since the cricoarytenoid joint can become fibrosed in an unfavorable position. Fortunately, all the symptoms disappeared after one month in the present case. Although the trigger responsible for the spontaneous healing remains unknown, natural recovery might be associated with proper use of the vocal cords.
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PMID:[Prolonged hoarseness and arytenoid dislocation after endotracheal intubation]. 2122 88

Symptoms management in multiple sclerosis is an integral part of its care. Accurate assessment and addressing the different symptoms provides increased quality of life among patients with multiple sclerosis. Multiple sclerosis symptoms may be identified as primary, secondary, or tertiary symptoms. Primary symptoms, such as weakness, sensory loss, and ataxia, are directly related to demyelination and axonal loss. Secondary symptoms, such as urinary tract infections as a result of urinary retention, are a result of the primary symptoms. Tertiary symptoms, such as reactive depression or social isolation, are a result of the social and psychological consequences of the disease. Common multiple sclerosis symptoms include fatigue and weakness; decreased balance, spasticity and gait problems; depression and cognitive issues; bladder, bowel, and sexual deficits; visual and sensory loss; and neuropathic pain. Less-common symptoms include dysarthria and dysphagia, vertigo, and tremors. Rare symptoms in multiple sclerosis include seizures, hearing loss, and paralysis. Symptom management includes nonpharmacological methods, such as rehabilitation and psychosocial support, and pharmacological methods, ie, medications and surgical procedures. The keys to symptom management are awareness, knowledge, and coordination of care. Symptoms have to be recognized and management needs to be individualized. Multiple sclerosis therapeutics include nonpharmacological strategies that consist of lifestyle modifications, rehabilitation, social support, counseling, and pharmacological agents or surgical procedures. The goal is vigilant management to improve quality of life and promote realistic expectations and hope.
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PMID:Therapeutics for multiple sclerosis symptoms. 2142 63

Paroxysmal nocturnal hemoglobinuria (PNH) is a hematological disorder characterized by complementmediated hemolytic anemia, thrombophilia and bone marrow failure. The clinical hallmark of PNH is evident chronic hemolysis due to the absence of the complement regulators CD55 and CD59 on PNH erythrocytes. Intravascular hemolysis drives the major clinical features of PNH, including anemia, hemoglobinuria, fatigue and other hemolysisrelated disabling symptoms, such as painful abdominal crises, dysphagia and erectile dysfunction. A peculiar thromboembolic risk has been associated with the hemolysis in PNH, but its pathophysiologic cause remains unclear. The treatment of PNH has remained supportive until a few years ago, when the first complement inhibitor, designated eculizumab, became available. Chronic treatment with eculizumab results in sustained control of intravascular hemolysis, leading to hemoglobin stabilization and transfusion independence in half of the patients. However, residual anemia may persist in a substantial fraction of patients. Recent observations by different groups, including our own, have demonstrated that residual hemolysis may be due to persistent activation of the early phases of the complement cascade, leading to progressive C3-deposition on PNH erythrocytes and possible subsequent extravascular hemolysis through the reticuloendothelial system. Here we critically review the available clinical results of eculizumab treatment for PNH patients, pointing out the recent insights into the pathophysiology of the disease. We discuss the role of the different components of the complement cascade leading to hemolysis, in both the absence and presence of the terminal effector pathway inhibition by eculizumab. Finally, we provide a theoretical rationale for the development of novel strategies of complement inhibition which could in the future further improve on the already substantial efficacy of eculizumab.
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PMID:Achievements and limitations of complement inhibition by eculizumab in paroxysmal nocturnal hemoglobinuria: the role of complement component 3. 2156 3

An 82-year-old woman was admitted with severe vomiting and progressive dysphagia mainly to solids. She gave a 3-month history of increasing heartburn, vomiting, tiredness, lethargy, anorexia and 13 kg weight loss. Her past medical history was unremarkable and she was a non-smoker. Physical examination revealed evidence of significant weight loss and dehydration only. Gastroscopy revealed mild oesophagitis, tongues of Barrett oesophagus and mild antral gastritis. CT scan of the thorax and abdomen was normal. Unfortunately her condition deteriorated rapidly and she died from aspiration pneumonia. Postmortem examination revealed thickening of the muscular wall of lower oesophagus and pylorus, but without any malignancy. The histological assessment of the oesophageal as well as gastric biopsies confirmed the diagnosis of gastrointestinal amyloidosis accounting for her symptoms of dysphagia and vomiting respectively.
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PMID:A rare cause of dysphagia and gastroparesis. 2168 44

In this article, we discuss clinical manifestations, laboratory results, and radiological findings in an old man with suppurative tender mass in the neck, accompanied by, fever, weight loss, malaise, fatigue, night sweat, cough, vomiting, and dysphagia. Pharyngeal exam revealed a huge retropharyngeal abscess.
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PMID:An old man with a mass in the retropharyngeal space. 2177 83

Iron-deficiency anaemia, the condition in which anaemia occurs due to a lack of iron, develops when the amount of available iron is insufficient to support normal red blood cell production. Iron deficiency and iron-deficiency anaemia, very prevalent conditions in premenopausal women, are often associated with menometrorrhagia (present in more than two-thirds of cases of iron-deficiency anaemia in premenopausal women). Appropriate identification and treatment of iron deficiency is imperative as iron deficiency can induce important specific clinical manifestations (including fatigue, atrophic changes in the epithelium, oral lesions, dysphagia, nail lesions, reduced immune response). Iron supplementation is the most common strategy used to control iron deficiency. Based on World Health Organisation recommendations, the most appropriate treatment is with an oral ferrous salt in a prolonged-release tablet form, to provide a dose of elemental iron equivalent to 60 mg per intake, in the range of 60 and 120 mg/day according to the severity of iron-deficiency anaemia. When haemoglobin levels have returned to normal, treatment should continue for about 3 months to fill iron stores. An extended-release formulation of ferrous sulphate with mucoproteose has been shown to be associated with a lower incidence of gastrointestinal adverse effects compared with other ferrous and ferric salts.
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PMID:The management of iron deficiency in menometrorrhagia. 2218 56

Fatigue is a common, under recognized, and poorly understood nonmotor symptom in Parkinson's disease (PD). Fatigue frequently presents early in PD, and its prevalence increases with disease progression, affecting up to 60% of patients. Fatigue has a negative impact on quality of life. Fatigue is often associated with other nonmotor symptoms, including sleep disturbance, excessive daytime sleepiness, and depression. Only a few reports have been published on the treatment of fatigue in PD (methylphenidate, levodopa, and pramipexole). Further well-designed studies, including physiotherapy, are necessary to develop more effective treatments for PD-associated fatigue. A number of patients with PD lose weight because of loss of fat. However, the evolution and determinants of weight loss are not well established. Possible determinants of weight loss in PD include loss of appetite, impaired hand-mouth coordination, difficulty in chewing and dysphagia, nausea, intestinal hypomotility, and increased energy requirements because of muscular rigidity and involuntary movements. Noticeable weight gain has repeatedly been reported after subthalamic or pallidal deep brain stimulation. Because low body weight is associated with negative health effects and a poor prognosis, monitoring weight and nutritional status should be part of PD management.
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PMID:[Fatigue and weight loss in Parkinson's disease]. 2248 11


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