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)

The behaviour of some urinary metabolites of tryptophan/nicotinic acid pathway was studied in 7 patients with Parkinson's disease during a 24-day period of levodopa treatment. Corresponding to the appearance of side-effects (agitation, anorexia, dysphagia, glossitis, abdominal pains) in 5 patients there was an increase in urinary Ky, AA, AAG, o-AHA, and 3-HK, while 3-HAA excretion fell. Since no other drugs were given, it was presumed that this effect was due to levodopa administration.
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PMID:Tryptophan/nicotinic acid pathway during levodopa treatment of Parkinsonism. 124 93

Six horses with dysphagia (attributable to botulism, glossitis, or guttural pouch mycosis) were given a commercially available liquid diet as the sole source of nutrition. Seven horses with hypophagia caused by severe bacterial pleuropneumonia or peritonitis were given the liquid diet to supplement food consumed voluntarily. The liquid diet was administered through a nasogastric tube 2 or 3 times daily. Body weight did not change significantly, and pertinent laboratory values remained at satisfactory concentrations throughout the feeding period. Serious complications were not encountered. Three horses developed loose, low-volume feces, but did not require treatment.
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PMID:Use of a liquid diet as the sole source of nutrition in six dysphagic horses and as a dietary supplement in seven hypophagic horses. 212 65

Plummer-Vinson syndrome (PVS) is characterized by iron deficiency anemia, upper esophageal stricture, cervical dysphagia, and glossitis. The precise role of iron deficiency in PVS has yet to be defined and remains a subject of much debate. A 29-year-old woman with PVS is presented. The patient had a 4-year history of severe iron deficiency anemia, a 2-year history of progressive dysphagia and weight loss, and a greater than 90% benign upper esophageal stricture. Iron therapy alone resolved her dysphagia and anemia, and a follow-up esophagram 1 year later showed a residual stenosis of less than 30%. The development of severe iron deficiency anemia in this patient 2 years before the onset of dysphagia, as well as the response of the stricture to iron repletion, supports the theory that iron deficiency can cause dysphagia and upper esophageal strictures. The occurrence of glossitis, gastritis, and esophagitis in iron deficiency demonstrates the adverse effects of iron depletion on the rapidly proliferating cells of the upper alimentary tract.
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PMID:Importance of iron repletion in the management of Plummer-Vinson syndrome. 229 34

Plummer-Vinson syndrome is a clinical entity associated with dysphagia, sideropenic anemia and atrophic glossitis. Using rabbits with iron deficiency anemia, the author investigated the cause of dysphagia in this syndrome. Iron deficient animals were produced by bolus feeding without iron and intramuscular injection of an iron-chelating agent. The fibers of swallowing muscles (the thyro-pharyngeal, cricopharyngeal and cervicoesophageal muscles) were classified into three types (Type 1, 2A and 2B fibers) by actomyosin ATPase staining. No significant difference between the muscles of sideropenic rabbits and those of normal rabbits were found in the composition and distribution of their muscle fibers. By NADH-TR staining, however, the disturbance of the intermyofibrillar network and/or a "Moth Eaton" appearance, known to be caused by leakage of mitochondria, were observed in Type 1 fibers of the swallowing muscles of sideropenic rabbits. These morphological changes are similar to those observed in progressive muscular dystrophy. The quantity of iron in the swallowing muscles of sideropenic rabbits was significantly reduced in comparison with that in the sternothyroid and femoral muscles. This finding suggests that a selective decrease in myoglobin occurs in the swallowing muscles of iron deficient animals. From these observations, it might be concluded that dysphagia in iron deficiency anemia is caused by a myogenic disorder.
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PMID:[Disorder of swallowing muscles in iron deficient rabbits]. 845 10

We report the case of a 41-year-old woman with Plummer-Vinson syndrome and an esophageal motility disorder. She complained of dysphagia and odynophagia and had cheilitis, glossitis, and hypochromic anemia. An esophageal motility study showed low amplitude of contraction and high intrabolus pressure in the esophageal body. After iron replacement, the patient was free from symptoms, and a new motility study showed increased amplitude of contraction and decreased intrabolus pressure.
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PMID:Esophageal motility impairment in Plummer-Vinson syndrome. Correction by iron treatment. 848 99

Plummer-Vinson syndrome is characterized by dysphagia, iron deficiency, anemia and the presence of esophageal web or webs. Two cases of this syndrome are reported in middle-aged women, which were treated over the last eight years. Both patients presented with dysphagia, anemia, sideropenia, glossitis and cheilitis. Radiological examination of the pharynx showed the presence of webs in both cases. The patients were treated with iron supplementation, which resulted in elimination of the symptoms. Both patients remain in good general condition and without any dysphagic complaints, 5 and 8 years after the diagnosis, respectively.
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PMID:Plummer-Vinson syndrome. 1282 19

Plummer-Vinson syndrome is characterised by dysphagia, anaemia, glossitis and oesophageal web. We report our findings in three patients with membranes in the upper oesophagus. All patients underwent endoscopic dilatation and iron replacement therapy, with good results. We review the literature of this syndrome.
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PMID:Plummer-Vinson syndrome: a report of three cases. 1452 74

Plummer-Vinson syndrome is known as the association of postcricoid dysphagia, upper esophageal web, and iron deficiency anemia. Although correction of iron deficiency may result in resolution of dysphagia and sometimes disappearance of the webs, dilation therapy is usually necessary to remove webs and relieve dysphagia. We report two cases of Plummer-Vinson syndrome. Both patients presented with significant and longstanding dysphagia, sideropenia, glossitis and koilonychia. Our two patients had occasional choking and aspiration episodes at eating and endoscope did not pass through at the level of the upper esophagus. Patients' esophagograms revealed the presence of webs in part of the post-cricoid region. Both patients were treated with esophageal bougienage or balloon dilation, and iron supplementation. The patients were examined periodically for two years after the initial treatment and found to be in good general condition.
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PMID:Plummer-Vinson syndrome and dilation therapy: a report of two cases. 1654 53

Plummer-Vinson or Paterson-Kelly syndrome presents as a classical triad of dysphagia, iron-deficiency anemia and esophageal webs. Exact data about epidemiology of the syndrome are not available; the syndrome is extremely rare. Most of the patients are white middle-aged women, in the fourth to seventh decade of life but the syndrome has also been described in children and adolescents. The dysphagia is usually painless and intermittent or progressive over years, limited to solids and sometimes associated with weight loss. Symptoms resulting from anemia (weakness, pallor, fatigue, tachycardia) may dominate the clinical picture. Additional features are glossitis, angular cheilitis and koilonychia. Enlargement of the spleen and thyroid may also be observed. One of the most important clinical aspects of Plummer-Vinson syndrome is the association with upper alimentary tract cancers. Etiopathogenesis of Plummer-Vinson syndrome is unknown. The most important possible etiological factor is iron deficiency. Other possible factors include malnutrition, genetic predisposition or autoimmune processes. Plummer-Vinson syndrome can be treated effectively with iron supplementation and mechanical dilation. In case of significant obstruction of the esophageal lumen by esophageal web and persistent dysphagia despite iron supplementation, rupture and dilation of the web are necessary. Since Plummer-Vinson syndrome is associated with an increased risk of squamous cell carcinoma of the pharynx and the esophagus, the patients should be followed closely.
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PMID:Plummer-Vinson syndrome. 1697 5

A 16-year old girl presented with rapid onset of muscular weakness and a history of severe dysphagia, dysphonia and significant wasting. On examination, she was dystrophic (BMI 15.7) and had signs of myopathy. Laboratory findings confirmed myopathy (CPK 106.4 microkat/L (6384 IU/L), AST 2.86 microkat/L (171.6 IU/L), myoglobin 1582 microg/L). There was profound hypokalaemia (S-K 1.8 mmol/L) suggesting hypokalaemic paralysis. Diagnosis of distal renal tubular acidosis (dRTA) was based on combination of hyperchloremic metabolic acidosis, severe hypokalaemia, high urinary pH and positive value of urinary anion gap. There was evidence of other signs of renal tubular impairment (urinary beta-2-microglobulin 213 mg/L, glomerulotubular proteinuria 1.01g/24h). Autoimmune tests (rheumatoid factor, antinuclear antibodies, autoantibodies to Ro/SSA and La/SSB) together with symptoms of xerostomia with swallowing difficulties and atrophic glossitis suggested primary Sjogren's syndrome (SS) as the underlying cause of dRTA. The renal biopsy confirmed chronic tubulo-interstitial nephritis compatible with this diagnosis. Full recovery of muscle weakness and hypokalaemia and acidosis followed after potassium and alkali replacement therapy. Corticosteroids were administered with subsequent addition of cyclosporine A because of disease activity. In conclusion, primary SS is a rare diagnosis in childhood and adolescence and should be considered in patients presenting with hypokalaemic paralysis, as this might be due to dRTA, even in the absence of apparent sicca syndrome.
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PMID:Hypokalaemic Paralysis Revealing Sjogren's Syndrome in a 16-Year Old Girl. 1927 13


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