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

Surgical treatment was applied to 18 patients for intrathoracic struma. Dyspnoea, dysphagia, recurrent palsy, and dilatated cervical veins with facial flushing were indications for surgery. Surgical access routes depended on localisation of the intrathoracic struma and its connection to the thyroid gland. Goitre located in the anterior mediastinum (substernal) can be extirpated, using the cervical approach (Kocher). Sternotomy was found to be necessary only in cases with tracheal resection. Goitres located in the posterior mediastinum were removed by means of right or left thoracotomy. Postoperative "collapse" of the posterior tracheal wall in patients with extreme dislocation of the trachea was successfully avoided by means of intratracheal intubation for 24 hours.
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PMID:[Surgical treatment of intrathoracic struma]. 363 Apr 55

The objectives of this study were to determine the dose limiting toxicity (DLT) and other major toxicities, the maximum tolerated dose (MTD) and the human pharmacokinetics of N1N11 diethylnorspermine (DENSPM), a new polyamine analog which in experimental systems inhibits the biosynthesis of intracellular polyamines and promotes their degradation by inducing the enzyme spermine/spermidine N-acetyl transferase. These objectives were incompletely achieved because of the occurrence of an unusual syndrome of acute central nervous system toxicity which forms the basis of the present report. Fifteen patients with advanced solid tumors were entered into a phase I study of DENSPM given by a 1 h i.v. infusion every 12 h for 5 days (10 doses). The starting dose was 25 mg/m2/day (12.5 mg/m2/dose) with escalation by a modified Fibonacci search. Doses of 25 and 50 mg/m2/day were tolerated with only minor side effects of facial flushing, nausea, headache and dizziness (all grade I). At doses of 83 and 125 mg/m2/day, a symptom complex of headache, nausea and vomiting, unilateral weakness, dysphagia, dysarthria, numbness, paresthesias, and ataxia, was seen in 3 patients, one after 2 courses of 83 and 2 after 1 course of 125 mg/m2/day. This syndrome occurred after drug administration was complete and the patients had returned home. Lesser CNS toxicity was seen in 2 other patients at lower daily doses. Preliminary pharmacokinetics of DESPM measured in plasma by HPLC in 8 patients showed linearity with dose and a rapid plasma decay with a t1/2 of 0.12 h. We conclude that great caution is warranted in administering DENSPM on this schedule at doses of > or = 83 mg/m2/day.
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PMID:Unusual central nervous system toxicity in a phase I study of N1N11 diethylnorspermine in patients with advanced malignancy. 938 45

A 45-year-old veteran runner, while on a summer vacation in Martha's Vineyard, went for his usual 5-mile jog in 80 degrees F weather. Two minutes after completing the run, his vision blurred and he became lightheaded. He had difficulty swallowing and noted tingling in his hands and arms and generalized flushing. He felt no chest pain, but his facial and arm muscles felt "distorted."
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PMID:ECG Quiz: Flushing, Paresthesias, and Difficulty Swallowing After a Run. 2008 62

Idiopathic anaphylaxis (IA) is defined as anaphylaxis without any identifiable precipitating agent or event. The clinical manifestations of IA are the same as allergen-associated (immunologic) anaphylaxis and include urticaria, angioedema, hypotension, tachycardia, wheezing, stridor, pruritus, nausea, vomiting, flushing, diarrhea, dysphagia, light-headedness, and loss of consciousness. Patients usually tend to have the same manifestations on repeated episodes. IA is a prednisone-responsive disease that is ultimately a diagnosis of exclusion. Approximately 40% of patients are atopic. Serum tryptase (or urine histamine or its metabolite) will be elevated acutely but if elevated in the absence of anaphylaxis, should suggest alternative diagnoses including indolent systemic mastocytosis. A focused history, examination, and follow-up will dictate whether a patient's symptoms may be attributable to disorders that mimic anaphylaxis, such as indolent systemic mastocytosis, carcinoid syndrome, pheochromocytoma, hereditary angioedema acquired C1 esterase inhibitor deficiency, or panic attacks. The presence of urticaria may help limit the differential because they do not usually accompany any of the aforementioned disorders, except for indolent systemic mastocytosis. IA is classified according to the symptoms as well as the frequency of attacks. Patients who experience six or more episodes in a year or two or more episodes in 2 months are classified as IA-frequent (IA-F). Patients who experience fewer episodes are classified as IA-infrequent (IA-I). This distinction is important because IA-F patients initially will require prednisone as disease-modifying therapy whereas most IA-I patients will not. Patients with IA must carry and know when and how to self-administer epinephrine.
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PMID:Chapter 25: Idiopathic anaphylaxis. 2279 98

The ingestion of cell batteries can cause serious complications (fistula, perforation or stenosis) at the esophageal level. The damage starts soon after ingestion (approximately 2 hours) and is directly related to the amount of time the battery is lodged in said location, the amount of electrical charge remaining in the battery, and the size of the battery itself. Injury is produced by the combination of electrochemical and chemical mechanisms and pressure necrosis. The ingestion of multiple cells and a size > = 20 mm are related with more severe and clinically significant outcomes. A female patient, 39 years old, with a history of previous suicide attempts, was admitted to the Emergency Room with chest pain and dysphagia after voluntary ingestion of 2 cell batteries. Two cell batteries are easily detected in a routine chest X-ray, presenting a characteristic double-ring shadow, or peripheral halo. Urgent oral endoscopy was performed 10 hours after ingestion, showing a greenish-gray lumpy magma-like consistency due to leakage of battery contents. The 2 batteries were sequentially removed with alligator-jaw forceps. After flushing and aspiration of the chemical material, a broad and circumferential injury with denudation of the mucosa and two deep ulcerations with necrosis were observed where the batteries had been. The batteries' seals were eroded, releasing chemical contents. Despite the severity of the injuries, the patient progressed favorably and there was no esophageal perforation. Esophageal impaction of cell batteries should always be considered an endoscopic urgency.
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PMID:Caustic esophageal injury by impaction of cell batteries. 2793 Nov 8

CASE STUDY KD is a 67-year-old man with a medical history of hypertension, asthma, and a 20-pack/year smoking history who developed progressive dysphagia 8 months ago. Upon consultation with his primary care provider, he underwent an esophagogastroduodenoscopy (EGD) for evaluation. A friable mass was visualized at the gastroesophageal junction, and biopsies confirmed adenocarcinoma of the esophagus. KD completed a staging evaluation with positron-emission tomography/computed tomography (PET/CT), which did not reveal distant metastatic disease. He also had an endoscopic ultrasound (EUS), which showed the tumor invading the muscularis propria and did not identify any enlarged regional lymph nodes (stage T3N0 disease). KD was referred to a medical oncologist and a radiation oncologist; he underwent concurrent chemoradiation therapy with docetaxel and fluorouracil and radiation therapy (50.4 Gy). KD was referred to thoracic surgery following restaging with PET/CT and EGD; there was no evidence of distant metastatic disease, and pathology findings revealed residual adenocarcinoma in one of the four esophageal biopsies. KD underwent Ivor Lewis esophagectomy and had a jejunostomy tube placed for nutritional requirements for 10 weeks as he adjusted to oral nutrition. Surgical pathology findings revealed residual adenocarcinoma with treatment effect; no malignancy was detected in the sampled regional lymph nodes. Four months later, KD presents with complaints of frequent postprandial diarrhea and reflux. He says he has been trying to lie down after meals due to palpitations and flushing. He is anxious about these symptoms and fearful about his long-term prognosis adjusting to the side effects of esophagectomy and would like to discuss lifestyle modifications.
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PMID:Symptom Management for Patients With Esophageal Cancer After Esophagectomy. 2967 Aug 9

The lingual tonsil (LT), located at the base of the tongue posterior to the circumvallate papillae, consists of aggregates of lymphoid tissue separated by a median glossoepiglottic ligament that splits the LT into right and left halves. Tonsillar tissue on either side of the ligament exhibits discrete round nodules that project upward. Each prominence is covered by nonkeratinized epithelium and has a central crypt formed by an invagination of the overlying epithelium. Ducts of adjacent mucous glands empty into the crypt, serving as a flushing mechanism to cleanse the crypt. A thin fibrous connective tissue capsule isolates the LT from the underlying tongue musculature. Lingual tonsillar tissue tends to regress with aging. Hypertrophy and pathologic changes of the LT can develop and cause subjective symptomatology. Patient complaints include sore throats, dysphagia, globus sensation, dyspnea, obstructive sleep apnea, dysgeusia, halitosis, and otalgia. Tonsilloliths in the palatine tonsil are often reported, but the LT also can develop a tonsillolith. Only 1 report of LT tonsilloliths was found in the English-language dental literature. Because of its literary rarity, this report presents a case of an incidental finding of a lingual tonsillolith. Diagnostic skills are sharpened when such cases are brought to the attention of the profession.
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PMID:Lingual (Not Palatine) Tonsillolith: Case Report. 3098 Aug 10

Idiopathic anaphylaxis (IA) is defined as anaphylaxis without any identifiable precipitating agent or event. The clinical manifestations of IA are the same as allergen-associated (immunologic) anaphylaxis and include urticaria, angioedema, hypotension, tachycardia, wheezing, stridor, pruritus, nausea, vomiting, flushing, diarrhea, dysphagia, light-headedness, and loss of consciousness. Patients usually tend to have the same manifestations on repeated episodes. IA is a prednisone-responsive disease that is ultimately a diagnosis of exclusion. Approximately 40% of patients are atopic. Serum tryptase (or urine histamine or its metabolite) will be elevated acutely, but, if elevated in the absence of anaphylaxis, should suggest alternative diagnoses, including indolent systemic mastocytosis. A focused history, examination, and follow-up will dictate whether a patient's symptoms may be attributable to disorders that mimic anaphylaxis, such as indolent systemic mastocytosis, carcinoid syndrome, pheochromocytoma, hereditary angioedema or acquired C1 esterase inhibitor deficiency, or panic attacks. The presence of urticaria may help limit the differential diagnosis because urticaria does not usually accompany any of the above-mentioned disorders, except for indolent systemic mastocytosis. IA is classified according to the symptoms as well as the frequency of attacks. Patients who experience six or more episodes in a year, or two or more episodes in 2 months are classified as having IA-frequent (IA-F). Patients who experience fewer episodes are classified as having IA-infrequent (IA-I). This distinction is important because patients with IA-F will initially require prednisone as disease-modifying therapy, whereas most patients who with IA-I will not require prednisone. Patients with IA must carry and know when and how to self-administer epinephrine.
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PMID:Idiopathic anaphylaxis. 3169 Mar 94