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)

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

Body composition and energy expenditure were investigated before and 10-14 days after surgery in 44 patients with upper gastrointestinal cancer (23 esophageal and 21 gastric cancer) in order to assess the impact of preoperative weight loss on metabolic adaptation to the surgical trauma and on postoperative complications. Patients were divided in three groups with I: 0-5%, II: 5-10% and III: greater than 10% preoperative weight loss related to the usual body weight. 50% of the patients presented with no or just minor weight loss. Even in case of weight loss greater than 10% no decrease below the ideal body weight was observed. Body cell mass and fat mass were significantly (p less than 0.05) reduced in group III when compared with I. Since energy expenditure and substrate oxidation rates were rather normal in most patients weight loss was considered to be due to tumor related stenosis and dysphagia. More than 50% of the energy requirements were gained from fat oxidation. General criteria of malnutrition were not fulfilled. Perioperative weight loss was lowest (1.6 +/- 4.9 kg) in patients of group III related to group I (2.9 +/- 1.7 kg) and II (5.0 +/- 6.9 kg). Similar elevation of energy expenditure and lipid oxidation with concomitant reduction in glucose oxidation was observed in all groups of patients. This led to a similar decrease of body cell mass. Independent of preoperative weight loss major complications occurred in 8 cases--pneumonia in 6 and leakage of the anastomosis in 2 patients; no patient died. From this study can be concluded that with regard to perioperative weight loss the metabolic response to surgical trauma is adequate even in patients with marked preoperative weight loss. These patients remain compensated and preoperative weight loss is without major effect on postoperative complication rate.
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PMID:[Significance of preoperative weight loss for perioperative metabolic adaptation and surgical risk in patients with tumors of the upper gastrointestinal tract]. 156 4

Cystic hygromas are large lymphangiomas that are most often found in the posterior triangle of the neck and the axilla in children. They are most frequently found before age 2 and may be massive. After upper respiratory infection, they may become infected and enlarged, causing dysphagia and toxemia. The diagnosis can usually be made by history and physical examination and confirmed by biopsy. Treatment is by surgical excision of small lesions and staged debulking excisions in more severe cases. A patient with a cystic hygroma having many clinical characteristics of a plunging ranula is presented. The cyst fluid was aspirated and analyzed for its amylase, sodium, potassium, chloride, urea nitrogen, glucose, and total protein content. The characteristics of the fluid were also compared with those of lymph and saliva. This report demonstrates the difficulty in determining the diagnosis of a tumor that has the clinical features of a cystic hygroma, as well as a plunging ranula. The necessity of a proper presurgical diagnosis is essential since the form of therapy for each is different and conflicting. A method that distinguishes between the cervical cystic hygroma and a plunging ranula by means of aspirated fluid is discussed.
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PMID:Submandibular cystic hygroma resembling a plunging ranula in a neonate. Review and report of a case. 199 19

The rapid diagnosis and immediate intervention required in patients with serious drug overdose or poisoning makes toxicological screening of limited value to the emergency department physician. Instead, a careful clinical evaluation using the history, physical examination, and the more readily available laboratory tests may allow a tentative diagnosis and the initiation of life-saving treatment. Laboratory tests should include serum osmolality, electrolytes, glucose, BUN and an estimation of the anion and osmolar gaps. The ECG can also provide useful information. Clinical findings of important include altered blood pressure, pulse, respiration and body temperature, the presence of coma, agitation, delirium or psychosis, and muscular weakness. An ophthalmological examination is also of importance in the acutely poisoned patient. Oral burns or dysphagia may occur following ingestion of any strongly reactive substance, but the absence of oral burns does not preclude the possibility of oesophageal or stomach injury. Odours and skin colour may also contribute to the diagnosis. Comprehensive toxicology screening may not be immediately available, or may be inaccurate, thus adding little to the information obtained during the initial evaluation of the poisoned patient.
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PMID:Physical assessment and differential diagnosis of the poisoned patient. 354 6

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

Over the past 30 years human magnesium (Mg) deficiency has become an accepted fact in most medical circles. Our index patient had striking neurological manifestations including generalized tremulousness, grimaces and fibrillary twitches of facial muscles, athetoid and choreiform movements of upper extremities, dysphagia, inability to speak, repeated convulsions, and confusion. She had received glucose in water and saline intravenously for several months. A patient with chronic alcoholism was noted to have almost identical symptoms and signs as the index patient. He also responded dramatically to MgSO4 injections. This resulted in a series of studies on patients with chronic alcoholism. The evidence of Mg deficiency in alcoholism includes the following: significant hypomagnesemia, strongly positive Mg balance during recovery, significant decrease in muscle Mg, a deficit of total exchangeable 28Mg quantitatively similar to deficit by balance studies, often a dramatic response of symptoms to therapy with Mg, and diuresis of Mg produced by ingestion of alcohol. Lipolysis with high levels of long-chain free fatty acids (FFA) occurs in withdrawal of alcohol in chronic alcoholism, withdrawal of certain addictive drugs, after trauma, surgery, administration of adrenergic compounds or theophylline, exposure to cold, and an adverse environment as in grass staggers. Concentrations of Mg fall when FFA increase in all of the above circumstances. This phenomenon has wide implications in health and disease. Better awareness of Mg deficiency in a wide variety of clinical conditions will result in life-saving treatment and less morbidity of other patients.
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PMID:Magnesium deficiency in human subjects--a personal historical perspective. 398 38

After a corrosive burn of the upper gastrointestinal tract leading to a severe dysphagia and to a weight loss of 15 kilograms, a 21-year-old female was treated by total parenteral nutrition (TPN) during the last 7 weeks of pregnancy. TPN by complete nutritive mixtures comprised daily crystalline amino acid solutions and as energy sources glucose plus lipids, the latter representing 43% of the nonprotein calories. A term normal 2800 gram female was delivered by cesarian section. This case report demonstrates the absence of any side effects on pregnancy related to fat emulsions used in usual proportions. Among the nutritional parameters studied here, the variations of weight and creatinine height index seem to be the best indicators of the maternal nutritional status in these cases. Approximately 50 kilocalories and 220 milligrams of nitrogen per kilograms body weight daily seem to be sufficient to restore and to maintain the maternal nutritional conditions and fetal growth.
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PMID:Total parenteral nutrition with fat emulsions during pregnancy--nutritional requirements: a case report. 682 80

We report a 49-year-old man who presented progressive dysarthria, dysphagia, and left hemiparesis. The patient was well until June 28th of 1993 when he noted 'weakness' in his both legs; despite his weakness, he could play golf on that day. In the beginning of July, he noted difficulty in swallowing solid foods. He was admitted to the neurosurgery service of our hospital on July 15th of 1993 and a neurologic consultation was asked on July 17th. Neurologic examination at that time revealed an alert but somewhat childish man who appeared to have some difficulty in paying attention to questions. He was disoriented to time and showed difficulty in recent memory and calculation. Higher cerebral functions were intact. The optic fundi were normal; pupils were isocoric and reacted to light promptly; ocular movements were intact, however, he showed difficulty in convergence. Facial sensation and facial muscles were intact. He had no deafness. He showed slurred speech and difficulty in swallowing solid foods. The remaining cranial nerves were intact. Motor-wise, he was able to walk normally and no weakness or atrophy was noted. Mild ataxia was noted in the finger-to-nose and the heel-to-knee test on the left. Muscle stretch reflexes were normal and symmetric, however, the plantar response was extensor bilaterally. Sensation was intact and no meningeal signs were noted. General routine laboratory findings were unremarkable. CSF was under a normal pressure containing 1 cell/microliter, 68 mg/dl of protein, and 54 mg/dl of glucose. Cranial CT scan showed low density areas involving the pons, midbrain, left thalamus, and the left parietal cortex. In MRI, these areas presented low signal intensity in T1-weighted images and high signal intensity in T2-weighted in images. The brain stem appeared swollen. Gadolinium enhancement was negative. He was given a course of steroid pulse with 1 g/day of DIV methylprednisolone for three days followed by oral steroid. He showed only temporary improvement in swallowing. In the subsequent course, he showed progressive deterioration in dysarthria and dysphagia. A biopsy was performed on the left parietal lobe lesion. After biopsy, he was treated with steroid and glycerol without improvement. A course of chemotherapy with procarbazine, MCNU, and vincristine was given; he did not respond to chemotherapy. His left hemiparesis deteriorated. He developed aspiration pneumonia from dysphagia and expired on October 22, 1993. The patient was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had astrocytoma grade III involving the pons, midbrain, thalamus, and the parietal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 49-year-old man with progressive dysarthria, dysphagia, and left hemiparesis]. 749 19

We report a 74-year-old man with a lung cancer, who developed right leg weakness, neurogenic bladder, and multiple cranial nerve palsies. The patient was well until December of 1992, when he was 74-year-old, when he noted transient double vision; in February of 1993, he noted numb sensation and weakness in his right leg. Later in the same month, he developed overflow incontinence of urine and weakness in his right face. He also noted deafness in his left ear (he had a marked loss of hearing in his right ear since childhood because of otitis media). His weakness in his right leg had progressed, and he was admitted to our service on March 19, 1993. On admission, he was afebrile and BP was 130/50 mmHg. General physical examination was unremarkable. On neurologic examination, he was alert and oriented to all spheres; no dementia was noted nor were detected aphasia, apraxia, and agnosia. His optic fundi were unremarkable; ocular movement appeared normal, however, he complained of diplopia in far vision. Sensation of the face was intact. He had right facial palsy of peripheral type; he was unable to close his right eye, and Bell's phenomenon was observed on attempted eye closure. On the left side, he had facial spasm. He had marked bilateral deafness. He had no dysarthria or dysphagia. The remaining of the cranial nerves were intact. Motor wise, he was unable to stand or walk alone; weakness did not appear to account for his difficulty in gait; manual muscle testing revealed 4/5 weakness in his tibialis anterior muscle, 1/5 in the peroneus longus, 0/5 in his extensor hallucis longus and extensor digitorum longus, all on the right side. Brachioradial and quadriceps femoris reflexes were increased to 3/4; plantar response was equivocal on the right side, and flexor on the left. Sensory examination revealed loss of touch and pain sensation in the L5 and S1 distributions in his right leg: vibration and position sensations were also diminished in his right foot. He had overflow urinary incontinence with loss of bladder sensation. Marked nuchal stiffness was noted, however, no Kernig's sign or eye ball tenderness was present. Pertinent laboratory findings were as allows; WBC 8,100/microliters, Ht 42.5%, platelet 326,000/microliters, TP 6.8 g/dl, BUN 16 mg/dl, creatinine 0.54 mg/dl, glucose 95 mg/dl, Na 136 mEq/l, K 4.4 mEq/l, Cl 100 mEq/l; liver profile was normal; CEA 436.6 ng/ml, CA19-93 U/ml; urinalysis was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 74-year-old man with urinary incontinence, right leg weakness and multiple cranial nerve palsies]. 766 22

Liquid esophageal transit and gastric emptying, mouth-to-cecum transit, and whole gut transit of a solid-liquid meal were measured in 14 patients with PSS, 16 control subjects (esophageal transit), and 20 control subjects (gastrointestinal transit), respectively, by using scintigraphic techniques, the hydrogen breath test, and stool markers. In patients with PSS, the glucose hydrogen breath test for detection of small intestinal overgrowth was performed and various gastrointestinal symptoms were determined. Esophageal transit and gastric emptying were significantly prolonged in PSS patients with 11 of 14 PSS patients (79%) disclosing delayed esophageal transit and eight of 14 PSS patients (57%) disclosing delayed gastric emptying. All PSS patients with prolonged gastric emptying also had delayed esophageal transit and there was a significant positive correlation between esophageal transit and gastric emptying (r = 0.696, P < 0.01). No significant differences between PSS patients and controls were detected concerning mouth-to-cecum transit and whole gut transit, but abnormally delayed mouth-to-cecum transit was found in four of 10 PSS patients (40%) and abnormally prolonged whole gut transit was detected in three of 13 PSS patients (23%). Small bacterial overgrowth was diagnosed in three of 14 PSS patients (21%). Delayed esophageal transit and gastric emptying were associated with dysphagia, retrosternal pain, and epigastric fullness, while prolonged whole gut transit was associated with constipation. It is concluded that delayed gastric emptying is frequently associated with esophageal transit disorders in PSS patients and may be one important factor for the development of gastroesophageal reflux disease in these patients.
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PMID:Gastrointestinal transit through esophagus, stomach, small and large intestine in patients with progressive systemic sclerosis. 792 44


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