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)

In two cases of chronic schizophrenia complicated by diabetes mellitus, the concomitant use of the neuroleptica and oral antidiabetics was attended by the appearance of symptoms simulative of syndrome malin, i.e. hyperpyrexia, tachycardia, blood pressure instability, disturbances of consciousness, muscle rigidity, tremor, dysphagia, salivation and urinary incontinence. In one of these cases, the patient, a 47-year-old man, died 10 days later. In the other case, a 62-year-old woman, almost all the symptoms subsided after 14 days, and oral dyskinesia persisted for only one additional month. In both cases, hypoglycemia due to oral antidiabetics was not seen. In Case 2, a combined regimen of oral antidiabetics and neuroleptica was later resumed. Again, a similar set of symptoms as seen initially were noted, along with an elevation of the serum CPK level. Parenterally administered biperiden proved to be highly effective in the control of the symptoms. The pathogenetic mechanism of these symptoms might possibly be explained as potentiation of the action of the neuroleptica by oral antidiabetics.
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PMID:"Syndrome malin"-like symptoms probably due to interaction between neuroleptica and oral antidiabetic agents. 65 48

A 43-year-old man who presented parkinsonism due to pontine and extrapontine myelinolysis was reported. Late in February, 1990, the patient presented suffered from a flu-like illness and was seen at a community hospital. Physical finding showed the pigmentation on the whole body and hypotension, and laboratory examination revealed severe electrolyte imbalance (serum sodium 100 mEq/l, serum potassium 6.9 mEq/l, serum chloride 68 mEq/l) and hypoglycemia (postprandial serum glucose 78 mg/dl). Given these results, adrenal failure was strongly suspected. Prompt correction of electrocyte imbalance was performed by the infusion of sodium chloride, and four days later the serum sodium level reached 131 mEq/l. On the other hand, the patient was noticed lethargic and showed parkinsonism i.e., rest tremor, cog-wheel rigidity, and hypokinesia. Fourteen days after the onset of neurological abnormalities, the patient was referred to our hospital for further evaluation of parkinsonism. Additionally, neurological examination revealed dysphagia, mutism and positive pyramidal tract sign. On admission brain computed tomography was unremarkable, but on the 14th hospital day it showed low density area in the pons. Brain magnetic resonance imaging also showed a striking increase in T2-weighted signal from the pons, the midbrain, and the bilateral thalamus. Based on these findings, a diagnosis of parkinsonism due to pontine and extrapontine myelinolysis was made, and levodopa therapy was started. After the initiation of levodopa therapy, improvement of tremor, rigidity, and hypokinesia ensued with marked functional benefit, and the patient was discharged on the 49th hospital day. Levodopa was stopped three weeks after discharge but, all neurological abnormalities were not recurrent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of parkinsonism due to pontine and extrapontine myelinolysis]. 130 Feb 56

Allgrove syndrome (isolated glucocorticoid deficiency, achalasia and alacrima) was found in eight members of an inbred French Canadian/North American Indian pedigree. The high degree of consanguinity supports an autosomal recessive mode of inheritance for this disorder. Six patients presented with hypoglycaemia and other evidence of cortisol deficiency between 2.5 and 8 years of age; however, two others became cortisol deficient after initial testing showed normal cortisol responses to ACTH, evidence that the glucocorticoid insufficiency of this syndrome may not be congenital, but may develop as late as the third decade. No evidence of mineralocorticoid deficiency has been found during 65 patient-years of follow-up. Alacrima was the earliest and most consistent clinical sign of Allgrove syndrome. Other manifestations of peripheral or autonomic neuropathy were found in four patients. The patients showed similar facial features, and three had significant velo-pharyngeal incompetence. All showed oesophageal dysmotility even in the absence of symptomatic dysphagia. In-vitro studies of lymphocyte ACTH binding showed no differences from normal controls. If such lymphocyte binding, as has been suggested, reflects adrenal ACTH receptor activity, these data would suggest that the glucocorticoid deficiency of Allgrove syndrome is not the result of a defect in that receptor. However, the observation that ACTH does not elicit increased adenylate cyclase activity even in normal lymphocytes casts considerable doubt on the physiological significance of ACTH binding to lymphocytes. It seems likely, therefore, that true ACTH receptors are not expressed on peripheral lymphocytes, and any conclusions regarding a possible receptor defect in Allgrove syndrome must await studies of receptor expression on adrenal cell membranes.
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PMID:Allgrove syndrome: an autosomal recessive syndrome of ACTH insensitivity, achalasia and alacrima. 185 Jun 71

Eating related difficulties and symptoms and postprandial serum glucose levels were studied in 11 patients (44 to 70 years old) five to 48 months after total gastrectomy and Roux-en-Y reconstruction for carcinoma of the stomach with no signs of metastasis or residual tumor. Three tests were used. The first contained 150 milliliters of 50 per cent glucose alone, the second had 150 milliliters of 50 per cent glucose with 5 grams of guar gum (viscose dietary fiber) and the third was a vegetable meal containing 75 grams of glucose. All of the patients with total gastrectomy had eating related symptoms, such as dumping and difficulties with the large volume of a meal. They had to eat small meals and the most usually experienced postprandial symptoms were abdominal pain, nausea and faintness. The postprandial serum glucose level was highest after drinking glucose alone and the lowest after eating the vegetable meal (as the highest 9.4 +/- 2.0 and 6.2 +/- 1.6 millimole per liter, respectively, 50 minutes postprandially, p less than 0.01). Hyperglycemia was associated with nausea, sweating, faintness, reduction of blood pressure and increase of pulse rate. The large volume of the vegetable meal produced difficulties (dysphagia and abdominal distension) in eating for everyone except one patient. Guar gum eaten with glucose reduced the postprandial hyperglycemia near to the level found after the vegetable meal. Also, the symptoms experienced after glucose with guar gum reduced from that after glucose alone, five patients became symptomless. Four of these five patients have supplemented guar gum regularly for several months into their daily meals with the result of reduction of the postprandial subjective symptoms. The dose has been adjusted individually from 2 to 7 grams of guar gum three times daily. Loose stools and diarrhea may occur at the beginning. These are avoided by a gradual increase of the dose during an adaptation period of two weeks. Sometimes glucose with guar gum may result in hypoglycemia with prolonged symptoms after immediate hyperglycemia. It is concluded that guar gum gives a possibility to avoid the symptoms related to a large volume of a meal and to reduce those produced by a high glucose content of a meal in patients after total gastrectomy. Guar gum also works in practical prolonged use when the dose is estimated from postprandial symptoms.
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PMID:Postprandial hyperglycemia after different carbohydrates in patients with total gastrectomy. 358 24

Honey mesquite (Prosopis glandulosa) is distributed across a large portion of the southwestern United States. Ingestion of young leaves, pods, or beans can cause toxicosis in cattle and goats if they comprise a substantial portion of their diet. Goats, as browsers, are most likely to develolp mesquite toxicosis. Sheep appear to be more resistant to the plant's toxic effects. Consistent clinical signs include weight loss, ptyalism, mandibular tremors, tongue protrusion, and dysphagia. Diagnosis of mesquite toxicosis is largely made on the basis of history and clinical signs with exclusion of appropriate differentials. Laboratory findings are nonspecific but may reveal a mild anemia and hypoglycemia. Postmortem findings suggestive of mesquite toxicosis are limited to fine vacuolation of neurons in the trigeminal motor nucleus. Treatment consists of an alternative diet and supportive care. The disease is treatable in cattle and sheep but has a high case fatality rate in goats.
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PMID:Honey mesquite toxicosis in a goat. 1209 60

The report presents a definition and causes of syncope in children. Syncope differs from other states with loss of consciousness by causes leading to decreased perfusion and resultant transient cerebral dysfunction with decreased muscle tone. The most common causes of syncope noted in almost 15% of children are neurocardiogenic. This group includes vasovagal, carotid sinus reflexive, situational (coughing, dysphagia, micturation and defecation disturbances) and post-exercise syncope. Another group is represented by orthostatic syncope that may be triggered by primary and secondary dis-autonomy, decreased blood volume (hemorrhage, diarrhea, Addison's disease), some medications and substances of abuse (alcohol). An important group, accounting for 2%-6% of all cases, are cardiogenic syncope, caused mainly by congenital/acquired obstructive cardiac sub- and valvar heart defects, various cardiomyopathies, some heart tumors (e.g. myxoma), exudative pericarditis, pulmonary embolus and hypertension, congenital and acquired coronary anomalies, various significant brady-tachyarrhythmias (sick sinus syndrome, supra- and ventricular tachycardias, congenital and acquired atrio-ventricular blocks). Subclavian steal syndrome as the cause of syncope is exceptional in children. Syncope does not include loss of consciousness due to neurological and metabolic (hypoglycemia) causes, hypoxia, hyperventilation with hypocapnia or CO intoxication. Differential diagnosis should also include pseudo-syncope (hysteria). Preliminary diagnostic management should include a detailed medical history, including family history, on the frequency and circumstances of syncope, sudden deaths, a physical exam with orthostatic assessment of peripheral blood pressure and standard ECG (heart rate, intraventricular and atrioventricular conduction defects, cardiac hypertrophy, arrhythmias, L-QT, changes in ST-T). Further specialist tests depend on preliminary findings.
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PMID:[Syncope in children and adolescents]. 1843 21

Glycogen storage disease type Ib (GSD Ib, OMIM 232220) is an inborn disorder of glucose metabolism, caused by mutations in the G6PT gene, encoding a glucose 6-phosphate transporter (G6PT). GSD Ib is mainly associated with fasting hypoglycaemia and hepatomegaly. Most GSD Ib patients also show neutropenia and neutrophil dysfunction and therefore are at risk of developing severe infections and inflammatory bowel disease (IBD). An increased risk for autoimmune disorders, such as thyroid autoimmunity and Crohn-like disease, has also been demonstrated, but no systematic study on the prevalence of autoimmune disorders in GSD Ib patients has ever been performed. We describe a 25-year-old patient affected by GSD Ib who developed 'seronegative' myasthenia gravis (MG), presenting with bilateral eyelid ptosis, diplopia, dysarthria, severe dysphagia, dyspnoea and fatigue. The repetitive stimulation of peripheral nerves test showed signs of exhaustion of neuromuscular transmission, particularly evident in the cranial area. Even in the absence of identifiable anti-acetylcholine receptor antibodies, seronegative MG is considered an autoimmune disorder and may be related to the disturbed immune function observed in GSD Ib patients.
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PMID:Myasthenia gravis in a patient affected by glycogen storage disease type Ib: a further manifestation of an increased risk for autoimmune disorders? 1843 26

This paper describes severe hyperinsulinemic hypoglycemia during bolus enteral feeding in two neurologically impaired children. Both children were affected by dysphagia with swallowing difficulties; caloric intake was inadequate. For these reasons, percutaneous endoscopic gastrostomy had been positioned during the first months of life. In one patient due to persisting vomiting, after a few months, a gastrojejunal tube (PEG-J) was inserted. Hypoglycemia was revealed by routine blood tests, without evidence of specific symptoms. Continuous subcutaneous glucose monitoring showed wide glucose excursions, ranging from hypoglycemia to hyperglycemia. Extremely high levels of insulin were detected at the time of hypoglycemia. A diagnosis of dumping syndrome (DS) was suspected in both children. In the child with PEG, the tip of the gastrostomy catheter was found to be lying in the bulbus duodeni. Once this had been pulled back, hypoglycemic episodes disappeared. The child with PEG-J needed continuous enteral feeding to reach a normal glucose balance. DS is a relatively common complication in children with gastrostomy, but extremely irregular glucose levels, ranging from hypoglycemia to hyperglycemia, and increased insulin secretion had not been previously demonstrated. The incidence of DS is probably underestimated in children receiving enteral feeding for neurological impairment. In these patients intensive monitoring of blood glucose levels should be performed to calibrate meals. Repeated underestimated hypoglycemic episodes could worsen neurological damage and cause a deterioration in clinical conditions.
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PMID:Dumping syndrome: an unusual cause of severe hyperinsulinemic hypoglycemia in neurologically impaired children with gastrostomy. 2131 31

Insulin resistance is a characteristic feature of glucose intolerance in myotonic dystrophy type 1 (DM1). DM1 patients with dysglycaemia have liver insulin resistance as well as muscle insulin resistance, and also abnormality of insulin secretion. Insulin resistance in DM1 might result in multiple metabolic defects. Low level of fasting plasma glucose is a characteristic feature in the early stage of glucose intolerance in DM1, Early intervention against insulin resistance in DM1 is suggested because glucose intolerance could deteriorate in a certain degree of cases. Metformin treatment is useful to improve insulin resistance in DM1. Diabetic patients with DM1 usually show mild hyperglycemia. However, poorly controlled patients with hyperglycemic pattern tending to rise from morning to evening exist. Intensive insulin therapy might be necessary in such cases. We should pay attention to hypoglycemia due to hyperinsulinemia, pseudo improvement of glucose control according to exacerbated dysphagia, and acute aggravation caused by infections, at a bedside.
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PMID:[Glucose intolerance in myotonic dystrophy type 1]. 2319 82

Stroke is a public health problem of the first order. In developed countries is one of the leading causes of death, along with cardiovascular disease and cancer. In addition, stroke is the leading cause of permanent disability in adulthood. Many of the patients who survive do so with significant sequelae that limit them in their activities of daily living. Most strokes (80-85%) are due to ischemia, while the rest are hemorrhagic. We have identified many modifiable risk factors, some with an important relationship with dietary factors or comorbidities in wich the diet has a significant impact. The incidence of malnutrition in stroke patients is not well known, but most likely impacts on patient prognosis. Furthermore, the nutritional status of patients admitted for stroke often deteriorates during hospitalization. It is necessary to perform a nutritional assessment of the patient in the early hours of admission, to determine both the nutritional status and the presence of dysphagia. Dysphagia, through alteration of the safety and efficacy of swallowing, is a complication that has an implication for nutritional support, and must be treated to prevent aspiration pneumonia, which is the leading cause of mortality in the stroke patient. Nutritional support should begin in the early hours. In patients with no or mild dysphagia that can be controlled by modifying the texture of the diet, they will start oral diet and oral nutritional supplementation will be used if the patient does not meet their nutritional requirements. There is no evidence to support the use of nutritional supplements routinely. Patients with severe dysphagia, or decreased level of consciousness will require enteral nutrition. Current evidence indicates that early nutrition should be initiated through a nasogastric tube, with any advantages of early feeding gastrostomy. Gastrostomy will be planned when the enteral nutrition support will be expected for long-term (4 weeks). Much evidence points to the importance of glycemic control during hospitalization for stroke. Hyperglycemia at diagnosis and during the first hours of admission impact on patient prognosis. The goal of glycemic control necessary to modify this bad prognosis without adding risk by iatrogenic hypoglycemia is still matter of debate.
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PMID:[Nutritional support in stroke patients]. 2507 46


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