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)

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

A patient with eosinophilia-myalgia syndrome developed progressive central nervosa system involvement that did not improve despite discontinuation of L-tryptophan therapy. Neurologic impairment was manifested initially by spastic monoparesis, which was improved by treatment with methyl-prednisolone and hydroxyurea. Recurrence of weakness was accompanied by gait ataxia, dysphagia, and complaints of a gradual decline in memory and concentration. Neuropsychological testing identified a broad pattern of cognitive deficits suggestive of a subcortical dementia, and magnetic resonance imaging demonstrated multiple high-signal lesions in the white matter. Cognitive deficits appear to be underrecognized in patients with the eosinophilia-myalgia syndrome. The response of our patient's initial symptoms to corticosteroid therapy suggests a possible role for autoimmune mechanisms in the pathogenesis of central nervous system involvement in the eosinophilia-myalgia syndrome. Neuropsychological evaluation should be performed in patients with cognitive complaints to delineate the full spectrum of central nervous system impairment associated with the eosinophilia-myalgia syndrome.
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PMID:Central nervous system involvement in the eosinophilia-myalgia syndrome. 141 16

Eosinophilia-myalgia syndrome (EMS) is a multisystemic disease that occurs in patients who have consumed products containing L-tryptophan. Prominent features include incapacitating myalgias, arthralgias, neuropathies, and eosinophilia. Despite the frequent association of dysphagia, dyspnea, and the potential for aspiration, the otolaryngology literature is devoid of information on EMS. In order to determine the frequency of otolaryngic symptoms, questionnaires were distributed to patients with EMS in 33 different US states. Among the 28 various head and neck manifestations studied, 70% of EMS patients complained of generalized muscle spasms, 66% xerostomia, 62% dyspnea, and 56% dysphagia. In addition, the epidemiology, clinical presentation, diagnostic criteria, and treatment options are discussed. This paper assesses the frequency of otolaryngic manifestations of EMS, as well as introduces this syndrome to the otolaryngologist-head and neck surgeon. It is important for the otolaryngologist to be aware of EMS and its manifestations and treatments so that patients with this potentially lethal disease can receive appropriate evaluation and expeditious treatment.
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PMID:Head and neck manifestations of eosinophilia-myalgia syndrome. 785 25

Glutaric aciduria type I (GA-I) is an inborn error in the degradation of lysine, hydroxylysine, and tryptophan due to a deficiency of glutaryl-CoA dehydrogenase. Glutaric, 3-OH-glutaric, and glutaconic acids are excreted in the urine, particularly during intercurrent illness. The enzyme may be assayed in leukocytes, cultured fibroblasts and chorionic villi. Twelve new cases, 9 months-16 years of age, are reported, comprising all known cases of GA-I in Sweden and Norway. Ten had a severe dystonic-dyskinetic disorder, one had a mild hyperkinetic disorder, and one was asymptomatic. Two children died in a state of hyperthermia. Carnitine deficiency and malnutrition developed in patients with severe dystonia and dysphagia, which necessitated substitution and gastrostomy. A slowly progressive dyskinetic disorder developed in spite of adequate early dietary treatment in one subject. Macrocephaly was found in three. Computed tomography and magnetic resonance investigations in 10 showed deep bitemporal spaces in 7. Neuropsychological testing of 8 of 12 subjects demonstrated receptive language function to be superior to expressive language and motor function. Cognitive functions were obviously less affected than motor functions. A review of 57 pooled cases showed that a severe dystonic syndrome developed in 77%, a mild extrapyramidal syndrome in 10%, and 12% were asymptomatic. This disorder may pass undetected in the cerebral palsy and mentally retarded child and adult populations. Repeated urine examinations of organic acids in the urine and enzyme assay may be necessary to confirm GA-I.
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PMID:Dystonia and dyskinesia in glutaric aciduria type I: clinical heterogeneity and therapeutic considerations. 813 2

The prevalence of gastroesophageal reflux disease (GERD) is increasing. GERD is a chronic disease and its treatment is problematic. It may present with various symptoms including heartburn, regurgitation, dysphagia, coughing, hoarseness or chest pain. The aim of this study was to investigate if a dietary supplementation containing: melatonin, l-tryptophan, vitamin B6, folic acid, vitamin B12, methionine and betaine would help patients with GERD, and to compare the preparation with 20 mg omeprazole. Melatonin has known inhibitory activities on gastric acid secretion and nitric oxide biosynthesis. Nitric oxide has an important role in the transient lower esophageal sphincter relaxation (TLESR), which is a major mechanism of reflux in patients with GERD. Others biocompounds of the formula display anti-inflammatory and analgesic effects. A single blind randomized study was performed in which 176 patients underwent treatment using the supplement cited above (group A) and 175 received treatment of 20 mg omeprazole (group B). Symptoms were recorded in a diary and changes in severity of symptoms noted. All patients of the group A (100%) reported a complete regression of symptoms after 40 days of treatment. On the other hand, 115 subjects (65.7%) of the omeprazole reported regression of symptoms in the same period. There was statiscally significant difference between the groups (P < 0.05). This formulation promotes regression of GERD symptoms with no significant side effects.
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PMID:Regression of gastroesophageal reflux disease symptoms using dietary supplementation with melatonin, vitamins and aminoacids: comparison with omeprazole. 1694 79

Anorexia is commonly present in persons with cancer and a major component of cancer cachexia. There are multiple causes of anorexia in cancer. Peripherally, these can be due to (i) substances released from or by the tumour, e.g. pro-inflammatory cytokines, lactate, and parathormone-related peptide; (ii) tumours causing dysphagia or altering gut function; (iii) tumours altering nutrients, e.g. zinc deficiency; (iv) tumours causing hypoxia; (v) increased peripheral tryptophan leading to increased central serotonin; or (vi) alterations of release of peripheral hormones that alter feeding, e.g. peptide tyrosine tyrosine and ghrelin. Central effects include depression and pain, decreasing the desire to eat. Within the central nervous system, tumours create multiple alterations in neurotransmitters, neuropeptides, and prostaglandins that modulate feeding. Many of these neurotransmitters appear to produce their anorectic effects through the adenosine monophosphate kinase/methylmalonyl coenzyme A/fatty acid system in the hypothalamus. Dynamin is a guanosine triphosphatase that is responsible for internalization of melanocortin 4 receptors and prostaglandin receptors. Dynamin is up-regulated in a mouse model of cancer anorexia. A number of drugs, e.g. megestrol acetate, cannabinoids, and ghrelin agonists, have been shown to have some ability to be orexigenic in cancer patients.
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PMID:Pathophysiology of anorexia in the cancer cachexia syndrome. 2667 62

The intricate sensorimotor neural circuits that control swallowing are heavily reliant on serotonin (5-hydroxytryptamine [5-HT]); however, the impact of 5-HT deficiency on swallow function remains largely unexplored. We investigated this using mice deficient in tryptophan-hydroxylase-2 (TPH2), the enzyme catalyzing the rate-limiting step in 5-HT synthesis. Videofluoroscopy was utilized to characterize the swallowing function of TPH2 knockout (TPH2-/-) mice as compared with littermate controls (TPH2+/+). Results showed that 5-HT deficiency altered all 3 stages of swallowing. As compared with controls, TPH2-/- mice had significantly slower lick and swallow rates and faster esophageal transit times. Future studies with this model are necessary to determine if 5-HT replacement may rescue abnormal swallowing function. If so, supplemental 5-HT therapy may have vast applications for a large population of patients with a variety of neurologic disorders resulting in life-diminishing dysphagia, particularly amyotrophic lateral sclerosis and Parkinson's disease, for which 5-HT deficiency is implicated in the disease pathogenesis.
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PMID:Mice Lacking Brain-Derived Serotonin Have Altered Swallowing Function. 3103 61