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)

Functional laryngectomies permit a more or less ideal preservation of laryngeal functions whose recovery, especially in les conservative operations, occurs very slowly and depends on several conditions: post operative course, sensitivity and motility of the hypopharynx, patient's ability to restore swallowing mechanisms. The Authors relate their experience concerning use of a rehabilitative program partially based on the experiences of some French logopedic schools and partially original. They illustrate the steps and goals of this program which starts on the fifth post-operative day with respiration exercises immediately followed by eight days of exercises to re-establish arytenoid mobilization and swallowing movements. If deglutition is not completely recovered and important inhalation problems persist, the logopedic approach is integrated with surgical rehabilitation consisting of one or more injection of gax-collagen. It is possible to use the same surgical technique later, after hospital discharge, if a slight dysphagia is still present in spite of continuous logopedic rehabilitation. Voice restoration exercises are introduced in the last days of the hospital stay when the patient is tube-free and continues at the office or outpatient clinic for two or three times every week. Concerning removal priority (tracheotomy tube followed by nasogastric tube or vice versa), we propose a diversified strategy for each patient, depending on the anatomicofunctional postoperative situation. Up to now 25 patients have taken part in this rehabilitation program (14 cricohyoidopexy, 6 Cricohyoidoepiglottopexy, 5 supraglottic laryngectomies). The results with regard to the amount of time that nasogastric feeding as well as tracheal tube are kept and the length of the hospital stay, were compared to those ones of a similar number of consecutive cases operated at our institution (ENT Department of Modena University) before February 1990 but not rehabilitated. In the early rehabilitated group, we observe a quicker functional recovery with a shorter hospital stay (about a week).
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PMID:[The experience of early rehabilitation]. 129 52

The existence of specific, age-related changes in gastrointestinal motility with clinical significance is controversial. Beside the more infrequent primary motility disorders, secondary motility disturbances associated with collagen vascular diseases, endocrinopathies, and neuromuscular diseases are prominent in the older and often multimorbid patients. Especially in geriatric patients, motility associated symptoms are undesired side-effects of drug therapy. The pathophysiology, clinical syndromes, and therapeutic principles of motility disorders in the elderly are discussed. The major symptoms of esophageal dysfunction are dysphagia, chest pain, heartburn, and regurgitation. Oropharyngeal dysphagia, mostly caused by cerebrovascular accidents and other neurologic disorders, leads to disturbances in food intake, and is often complicated by broncho-pulmonary infections arising from recurrent aspiration of food or saliva. Gastrointestinal reflux disease and spastic motility disorders of the esophagus are regarded as possible causes of angina-like chest pain after exclusion of cardiac diseases. Motility disturbances of the stomach and small bowel are often related to systemic disease (i.e., diabetes mellitus, chronic intestinal pseudo-obstruction) of drug side-effects. Mental and physical decline, reduced fluid intake, and constipating drugs are the most relevant factors for idiopathic constipation in the elderly. Fecal incontinence means a great psychological strain for older patients and leads to social isolation.
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PMID:[Gastrointestinal motility in the elderly]. 144 9

Polymyositis is a rare disease entity belonging to the class of enigmatic disorders known as the collagen vascular diseases. It is characterized by proximal muscle weakness. More than 50% of the patients with this disease have development of head and neck manifestations, most commonly a heliotrope rash or dysphagia. Weakness and atrophy of neck muscles, and lolling of the neck have also been described. We report a case of polymyositis presenting as a neck mass, a heretofore undescribed manifestation of this disease in the head and neck. A review of the literature and an interdisciplinary approach to the diagnosis and management of this unusual disease will be described.
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PMID:Polymyositis presenting as a neck mass. 155 55

Numerous drugs have been recommended for the treatment of systemic sclerosis, but without any significant effect on the fibrotic stage of this disorder. Because recombinant gamma-interferon (gamma-IFN) is a potent and selective inhibitor of fibroblast proliferation and collagen production by human dermal fibroblasts in vitro, we assessed the effects of gamma-IFN treatment on the skin and on pulmonary function in patients with systemic sclerosis. Fourteen patients entered the study, and nine completed the 12-month trial. Fifty micrograms/day of gamma-IFN was administered subcutaneously 3 days per week. At the end of the 12-month treatment period a significant improvement was observed in total skin score, and blood gas analysis showed a significant increase in Pa O2 during therapy with gamma-interferon. Other clinical parameters (dysphagia, Raynaud's phenomenon, cardiac involvement) were not altered significantly. No serious adverse effects were noted. These results suggest a beneficial effect of gamma-IFN on the cutaneous fibrotic abnormalities and on lung fibrosis in systemic sclerosis.
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PMID:Treatment of systemic sclerosis with gamma-interferon. 161 Jun 90

Epidermolysis bullosa acquisita (EBA) is a well-characterized, subepidermal blistering disorder associated with autoimmunity to type VII collagen, which is the collagen localized to anchoring fibrils within the dermoepidermal junction of skin. Although the full clinical spectrum of EBA is still being defined, it is known that the clinical features of EBA may be reminiscent of hereditary dystrophic epidermolysis bullosa, a scarring blistering disease of children that is commonly associated with esophageal stenosis. We describe a patient with EBA who had both an acral-predominant mechanobullous disease akin to dystrophic epidermolysis bullosa and an inflammatory, widespread bullous eruption reminiscent of bullous pemphigoid in association with esophageal webs and dysphagia. Although esophageal involvement is common in dystrophic epidermolysis bullosa, a review of the literature shows that this is the first bonafide case of EBA with symptomatic esophageal disease.
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PMID:Epidermolysis bullosa acquisita and associated symptomatic esophageal webs. 199 68

A patient presented with dysphagia, arthralgias, and a peculiar skin eruption characterized by histopathologic features of sarcoidal granulomas and lupus erythematosus occurring in the same lesion. Sarcoidal granulomas were also found in skeletal muscle. The unique histopathologic features of this case suggest that coexistence of sarcoidosis with autoimmune collagen vascular diseases may be more than coincidence. A review of the immunologic status of patients with sarcoidosis and autoimmune collagen vascular disorders is presented with speculations on the relevance of potential disease-sustaining immunologic patterns of both groups of diseases.
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PMID:A unique case of sarcoidosis with coexistent collagen vascular disease. Possible result of a compatible disease-sustaining immunologic environment. 406 28

Congenital esophageal stenosis (CES) is a rare disorder with narrowed esophageal lumen that presents as dysphagia from childhood and that is often associated with tracheobronchial remnants or webs. The pathogenesis of CES is unknown. The aim of this study was to examine the histological and immunohistochemical features of CES. Esophagi from 2 young adults with CES and 3 controls with no motility disorders underwent routine H&E staining, trichrome staining for collagen, and detailed immunocytochemical studies for general neuronal markers (protein gene product 9.5, neuron-specific enolase, and S-100) and neurotransmitters (vasoactive intestinal polypeptide, substance P, and galanin) and nitric oxide synthase by beta-nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase and a specific NO synthase antibody. Quantitative experiments compared the numbers of myenteric neurons and amounts of fibers at the circular muscle. CES esophagi showed infiltration of neutrophils in the myenteric plane, without any increase in collagen. NADPH-diaphorase histochemistry showed a significant reduction of myenteric nitrinergic neurons (7 +/- 3.4 vs. 2.7 +/- 1.8 neurons per high-power field) and fibers at the circular muscle. Other peptidergic neurons studied were not significantly reduced in CES. The specific total lack of NO inhibitory innervation may be an important mechanism in the pathogenesis of stenosis and aperistalsis of the esophagus in this disorder.
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PMID:Peptidergic and nitrinergic denervation in congenital esophageal stenosis. 754 Oct

Systemic sclerosis is a collagen disease with high frequency of oesophageal affection, specially if we use manometry as an evaluation method that has a high rate of clinic complication in high rate of patients. The aim of the study was to evaluate the prevalence of the oesophageal affection through the clinical, radiological, endoscopical and manometrical studies and to compare the results with other authors. Between January 1978 and February 1993, we evaluated 101 patients with different clinical types of scleroderma 89 females and 12 males with ages between 16-83 (mean: 49, 19 years). In order to determine systemic sclerosis diagnosis following Masi Rodman criterion's we found from 101 cases 83 had dysphagia (82.2%) motor 66 (65%) organic 17 (34.7%) GER was seem in 41 cases (40.5%). According to Heitz's radiological classification: I: 26 patients (25%) II: 58 patients (52.4%) III: 19 patients (18.8%) IV: 17 patients (16.9%). In reference to Neschis manometric classification we found II 88 (76%) III 77 (76%) In accordance with endoscopical classification we found I: 16 (15.8%); II: 49 (48.5%); III: 19 (18.8%); IV: 17 (16.9%); Although this motor and organic oesophageal alterations have an evident diagnostic value, they have also been referred in another metabolic and collagen diseases but with lesser frequency than was found in the systemic sclerosis by us.
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PMID:[Esophageal involvement in progressive systemic sclerosis]. 770 9

Numerous materials have been used over the years for vocal fold augmentation. Early use of bioreactive compounds, such as paraffin, gave way to relatively inert substances, such as Teflon. More recently biocompatible materials, such as collagen and autologous fat, have gained wider acceptance. Autologous fat, in particular, is an easily obtainable source for potential rehabilitation of scarred, paralytic, and atrophic vocal folds. However, long-term systematic follow-up has been lacking. Since 1991 we at the University of Kansas Center for Voice and Swallowing Disorders have employed autologous fat for vocal fold augmentation, primarily for either paralysis or repair of a volume-deficient vocal fold segment. Twenty-two patients have completed > or = 1 year of follow-up studies, including graded video-laryngostroboscopy, electroglottography, computerized acoustic analysis, and blinded perceptual analysis by two speech-language pathologists. Statistically significant improvement was demonstrated in many parameters tested, frequently improving with time. Although the volume-deficient group had more "normal" values, the paralysis group had greater improvement in many variables using fat injection. We conclude that while autologous fat injections of the vocal fold may have long-term benefits, certain technical considerations and criteria of selection of patients are critical for success.
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PMID:Autologous fat injection into the vocal folds: technical considerations and long-term follow-up. 902 40

Here we present a 53-year-old woman with rheumatoid pachymeningitis. The subject had rheumatoid arthritis (RA) for 15 years. In April, 1996 she began to experience intermittent headaches. In September, her headaches became severe and continuous. In October, she suddenly developed ptosis of the left eye and diplopia. She also started to have dysphagia and she found it increasingly difficult to eat. She was admitted to our hospital on November 1, 1996. Neurological examinations revealed palsies of the left IIIrd, IVth, and VIth, and bilateral IXth, and Xth cranial nerves. Laboratory findings showed leukocytosis, elevated blood sedimentation rate, and positive CRP. Serum RA titer was positive (30x). The cerebrospinal fluid was normal and bacteriological examination was negative. T1-weighted MRI demonstrated hypertrophic cranial dura extending from the falx cerebri to tentorium cerebelli, which was enhanced markedly by Gd-DTPA. The dura adjacent to the cavernous sinus and the clivus were also thickened, which probably caused her cranial polyneuropathies. The dural biopsy showed massive infiltration of the inflammatory cells throughout the dura, proliferation of collagen fibers, and necrotic granuloma with neutrophilic infiltrations. Neither rheumatoid nodules, nor vasculitis were found. Despite the absence of rheumatoid nodules in the dural biopsy, the clinical features, pathologic specimens, and MRI findings of the thickened dura were most consistent with rheumatoid pachymeningitis. Administration of dexamethason ameliorated her headache on the 4th hospital day, and the cranial polyneuropathies completely disappeared on the 35th hospital day. The dural enhancement previously seen on the contrast T1-weighted MRI was diminished. Serum RA titer was also normalized (10x). Rheumatoid pachymeningitis is an extremely rare disease, and only 16 cases were reported in the literatures. Hypertrophic pachymeningitis should be considered as a diagnostic possibility in RA patients who have prolonged headache, and Gd-DTPA MRI is recommended to demonstrate the dural involvement.
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PMID:[A case of rheumatoid pachymeningitis]. 943 Oct


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