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)

We reported a unique case of myasthenia gravis in association with tuberculous mediastinal lymphadenitis. A 56-year-old man suffering from generalized myasthenia gravis underwent thymothymectomy followed by good clinical recovery for 2 years. Thereafter, the patient complained of acute onset of ptosis, diplopia, dysphagia and limb weakness with elevated titers of serum anti-acetylcholine receptor antibody. CT scans of the chest showed a mediastinal lymphadenopathy and the Thallium-201 SPECT revealed an abnormal mediastinal accumulation, suggesting recurrence of thymoma in the mediastinal lymphonode. Histologically, the re-operated mediastinal tumor was of tuberculous lymphadenitis. This patient gives us a caution that we must guard against errors in differentiation between thymoma and tuberculous mediastinal lymphadenitis, particularly when myasthenic patients with mediastinal tumors are expected to receive the corticosteroids therapy. (120 words).
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PMID:[Acute deterioration of myasthenia gravis in association with tuberculous mediastinal lymphadenitis, simulating recurrence of thymoma. A case report]. 761 72

A 64-year-old man with chronic renal insufficiency was hospitalized with dysphagia and inability to keep his head erect 11 months after beginning procainamide hydrochloride (PA) for control of atrial flutter. Evaluation revealed esophageal dysmotility, worsening renal function, and elevated serum PA and N-acetylprocainamide (NAPA) concentrations. No evidence of autoimmune myasthenia gravis was found. PA was discontinued and normalization of PA and NAPA concentrations was associated with a decrease in muscle weakness and resolution of dysphagia. The correlation between clinical findings and serum concentrations of PA and NAPA suggests that drug excess due to impaired clearance was the basis for this unusual adverse drug reaction.
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PMID:Procainamide-induced myasthenia-like weakness and dysphagia. 768 90

Ten patients with atrophy of the tongue, from a group of 752 with generalized acquired myasthenia gravis (MG), were studied. Tongue atrophy developed late in the majority of patients and was accompanied by tongue paresis (70% of the cases) and eventually associated to atrophy of other muscles of the palate, especially the uvula. All the patients exhibited severe forms of MG with bulbar involvement, mainly persistent dysphonia and dysphagia, almost always refractory to treatment. There is no correlation among atrophy of the tongue, sex, and thymus pathology. There is correlation between severeness of symptoms and early, persistent and treatment refractory dysphonia and dysphagia.
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PMID:Atrophy of the tongue with persistent articulation disorder in myasthenia gravis: report of 10 patients. 777 22

The potential causes of neurogenic oropharyngeal dysphagia in cases in which the underlying neurologic disorder is not readily apparent are discussed. The most common basis for unexplained neurogenic dysphagia may be cerebrovascular disease in the form of either confluent periventricular infarcts or small, discrete brainstem stroke, which may be invisible by magnetic resonance imaging. The diagnosis of occult stroke causing pharyngeal dysphagia should not be overlooked, because this diagnosis carries important treatment implications. Motor neuron disease producing bulbar palsy, pseudobulbar palsy, or a combination of the two can present as gradually progressive dysphagia and dysarthria with little if any limb involvement. Myopathies, especially polymyositis, and myasthenia gravis are potentially treatable disorders that must be considered. A variety of medications may cause or exacerbate neurogenic dysphagia. Psychiatric disorders can masquerade as swallowing apraxia. The basis for unexplained neurogenic dysphagia can best be elucidated by methodical evaluation including careful history, neurologic examination, videofluoroscopy of swallowing, blood studies (CBC, chemistry panel, creatine kinase, B12, thyroid screening, and anti-acetylcholine receptor antibodies), electromyography, and magnetic resonance imaging (MRI) of the brain, plus additional procedures such as lumbar puncture and muscle biopsy as indicated. Little is known about aging and neurogenic dysphagia, specifically the relative contributions of natural age-related changes in the oropharynx and of diseases of the elderly, including periventricular MRI abnormalities, in producing dysphagia symptoms and videofluoroscopic abnormalities in this population.
Dysphagia 1994
PMID:Neurogenic dysphagia: what is the cause when the cause is not obvious? 780 24

We investigated a Japanese pedigree with oculopharyngeal muscular dystrophy (OPMD) which included the probands of two sisters and a brother. Case 1 (Fig. 1): A woman born in 1940 at Fuji City, Shizuoka prefecture (Pacific coast side, which located about 80 miles west from Tokyo) was insidiously suffering from dysphagia and eye lid ptosis since her age of 40. She was admitted to Shizuoka Red Cross Hospital when 48 years old, because of difficulty of going upstairs. Neurological examination revealed severe eye lid ptosis without eye movement disorders, dysphagia, and moderate weakness on neck and proximal muscles of extremities without definite atrophy and fasciculation. In the laboratory data, serum creatine kinase level was slightly elevated to 215 U/l. Electromyographic findings showed myogenic pattern on the extremities but no evidence of the existence of myasthenia gravis and neurogenic involvement. Intranuclear tubular filaments were found in 3% of muscle fibers from her left biceps muscle. Case 2: The elder sister of the case 1 was suffering from eye lid ptosis without eye movement disorder and severe dysphagia since the age of 44. Case 3: The younger brother of the case 1 was suffering from dysphagia and proximal muscle weakness since the age of 40. We found eye lid ptosis, dysphagia and/or proximal muscle weakness in 24 cases (men: 12 cases, women: 12 cases) out of 50 examined members of this pedigree after their ages of 40 (Fig.3; family tree). It was concluded that this pedigree had cases of oculopharyngeal muscular dystrophy with autosomal dominant inheritance which was quite rare in Japanese.
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PMID:[A Japanese pedigree with oculopharyngeal muscular dystrophy]. 792 58

We report myasthenia gravis presenting as dysphagia of acute onset in a 56-year-old female who had no other stigmata of the disease and who was generally well despite rheumatoid arthritis and hypothyroidism. She recovered respiratory function following a general anaesthetic for oesophagoscopy only when antimyasthenic treatment was instituted. She remains well to date. In patients who are known to have autoimmune diseases and who present with dysphagia, features of myasthenia gravis should be specifically sought.
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PMID:Myasthenia gravis presenting during general anaesthesia for oesophagoscopy--a cautionary tale. 793 Sep 2

Myasthenia gravis is an autoimmune disorder of the neuromuscular junction that causes muscle weakness. Involvement of oropharyngeal musculature is not uncommon, which leads to dysphagia. Timely consideration of myasthenia gravis in evaluating dysphagia is crucial to prevent complications and to improve the quality of life of these patients. We report four patients who underwent extensive investigations for dysphagia, by gastroenterologists as well as otolaryngologists, before the diagnosis of myasthenia gravis was established.
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PMID:Myasthenia gravis presenting as dysphagia: clinical considerations. 801 68

The patient was a 79-year-old male. On CT of the chest, a mass shadow of the anterior mediastinum was found. He did not complain of symptoms, and there were no clinical signs of myasthenia gravis (MG) before surgery. The tumor and the thymus was completely resected. The pathological diagnosis was non-invasive thymoma, and his postoperative course was satisfactory. However, 2 months after the operation, the patient complained of ptosis, diplopia, dysphagia, and muscle weakness, which deteriorated rapidly. The titer of anti-acetylcholine receptor antibody was high at 91.0 nmol/l. By medication of anti-cholinesterase drug and predonin, the symptoms of MG improved. After resection of thymoma, postoperative follow-up with considering the possibility of postoperative MG is necessary.
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PMID:[A case of myasthenia gravis developing after resection of non-invasive thymoma]. 846 68

Eight elderly men whose primary symptoms of myasthenia gravis were decreased speech and swallowing ability were seen for speech pathology evaluations and videofluoroscopic swallow studies. All patients had fatigable flaccid dysarthria and greater than expected pharyngeal phase dysphagia on videofluoroscopy; eight had decreased pharyngeal motility as demonstrated by residual material in the valleculae and pyriform sinuses bilaterally; seven had episodes of laryngeal penetration secondary to overflow of residual material; and five experienced silent aspiration despite gag reflexes and the ability to cough to command. Five patients required feeding tubes because their dysphagia responded poorly to treatment. Videofluoroscopic swallow studies revealed a common swallowing profile with pharyngeal phase dysphagia greater than expected from patient symptoms. Dysphagia did not improve at the same rate as other manifestations of myasthenia gravis.
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PMID:Dysphagia in elderly men with myasthenia gravis. 879 Dec 38

A 49-year-old man, who developed generalized symptoms of myasthenia gravis at the age of 30 and had thymomectomy, was recently admitted to our hospital for myasthenic crisis after alpha-interferon (IFN) therapy for his chronic hepatitis C. He had shown only mild ocular symptoms before the start of the IFN intramuscular injection therapy. Three months after the IFN therapy (900MU three times a week after 2 weeks of daily injection), he developed generalized weakness, dysarthria, and dysphagia. After the cessation of his IFN therapy, his conditions became worse in parallel with the increase in the titer of anti-acetylcholine receptor antibody. He required artificial ventilation for 2 weeks during myasthenic crisis and he received food and medication through nasogastric tube. He recovered from myasthenic crisis and could eat orally 4 months after the cessation of interferon therapy, but he still suffered from mild bulbar symptoms 8 months after the IFN cessation. IFN therapy should be avoided for the patients with myasthenia gravis, since it may cause myasthenic crisis, and may aggravate myasthenic symptoms for a long period.
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PMID:[A case of myasthenia gravis which developed myasthenic crisis after alpha-interferon therapy for chronic hepatitis C]. 895 52


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