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 57-year-old woman developed muscular stiffness and painful cramps, which were relieved by administration of dantrolene sodium. Her serum level of antibodies to glutamic acid decarboxylase (GAD) was markedly elevated and continuous muscular activities were observed on resting surface EMG. These features were compatible with those in stiff-person syndrome (SPS). She was found to have thymoma on CT scan. Immediately after thymomectomy, which was histologically diagnosed as a benign hyperplasia, she developed head retraction reflex-like movements evoked by sensory stimulation to the face, which were followed by severe bulbar symptoms with dysphagia and respiratory arrest. Postoperative myasthenia gravis was excluded clinically. While somatosensory evoked EMG on splenius muscle initially showed biphasic responses with latency of 15 msec and 55 msec, respectively after oral angle non-painful electric stimulation, the late potential phase disappeared after the patient recovered from bulbar symptoms. This suggests that head retraction reflex-like movements of this patient reflected the attenuation of inhibitory potentials from the brainstem.
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PMID:[Head retraction reflex-like movements with severe bulbar symptoms in a patient with stiff-person syndrome]. 1450 49

The aim of this research is to produce a compactable self-sealing chewable tablet of verapamil hydrochloride. Tablets were prepared by compressing beads coated with multiple layers including drug, hydroxypropyl methylcellulose, polyethylene oxide, ethylcellulose, lactose, and sodium starch glycolate. Dissolution studies were carried out according to the USP XXII paddle method for 14 h. A new tablet formulation was evaluated in three different forms: 1) whole tablet, 2) crushed tablet using a commercial tablet crusher, and 3) tablet chewed in the mouth and then expelled into dissolution fluid. Sustained release from the new formulation was maintained and was similar in all three different treatments, and similar to drug release from intact commercially available Isoptin SR, but crushing or chewing destroyed the sustained release property of Isoptin SR (as expected). This new formulation can be administered either by swallowing the whole tablet or by first crushing or chewing the tablet. Controlled release properties of this new formulation do not change by chewing or crushing the tablet first. Such a tablet could be valuable for all patients including those who have difficulty swallowing, such as pediatrics and geriatrics.
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PMID:Novel chewable sustained-release tablet containing verapamil hydrochloride. 1520 77

Esophageal squamous papillomatosis is a rare condition associated with human papilloma virus infection and has been complicated by the development of squamous cell carcinoma. Photodynamic therapy using porfimer sodium has been used for the treatment of esophageal cancer but has not been utilized in the treatment of esophageal squamous papillomatosis. We report here the first case of papillomatosis and obstructing squamous cell carcinoma of the esophagus palliated with porfimer sodium photodynamic therapy indicating successful photosensitizer uptake in papilloma-laden tissue. Extensive debulking of papilloma and tumor allowed esophageal recanalization and placement of a self-expanding metal stent for long-term dysphagia palliation. This unique case highlights the combined use of endoscopic techniques for optimal treatment results.
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PMID:Photodynamic therapy and endoscopic metal stent placement for esophageal papillomatosis associated with squamous cell carcinoma. 1523 Jul 38

PRESENTING FEATURES: A 53-year-old man who had human immunodeficiency virus (HIV) presented to the Johns Hopkins Hospital with a 3-month history of increasing dysphagia, cough, dyspnea, chest pain, and an episode of syncope. His past medical history was notable for oral and presumptive esophageal candidiasis that was treated with fluconazole 6 months prior to presentation. Three months prior to presentation, he discontinued his medications, and his symptoms of dysphagia recurred. During that time he developed intermittent fevers and chills, progressively worsening dyspnea on exertion, and a cough productive of white sputum. He also reported a 40-lb weight loss over the past 3 months. On the day prior to presentation, he had chest pain and shortness of breath followed by weakness, dizziness, and a brief syncopal episode. He denied orthopnea, paroxysmal nocturnal dyspnea, lower extremity edema, jaundice, hemoptysis, hematemesis, melena, hematochezia, or diarrhea. There was no history of alcohol use, and he stopped smoking tobacco approximately 1 month previously. He smoked cocaine but denied injection drug use. The patient had never been on antiretroviral therapy and had never had his CD4 count or viral load measured. On physical examination, the patient was a thin, cachectic man who appeared older than his stated age. His vital signs were notable for blood pressure of 102/69 mm Hg, resting tachycardia of 102 beats per minute, resting oxygen saturation of 92% on room air, normal resting respiratory rate, and a temperature of 38.1 degrees C. His oropharynx was clear, with no signs of thrush or mucosal ulcers. His pulmonary examination was notable for diminished breath sounds in the lower lung fields bilaterally. Cardiac, abdominal, and neurologic examinations were normal. His skin was intact, with no visible petechiae, rashes, nodules, or ulcers. Laboratory studies showed a total white blood cell count of 3.2 x 10(3)/microL, with a total lymphocyte count of 330/microL, hematocrit of 30.2%, a serum sodium level of 129 mEq/L, and a serum lactate dehydrogenase level of 219 IU/L. The patient had an absolute CD4 count of 8 cells/mm3 and a HIV viral load of 86,457 copies/mL. His arterial blood gas on room air had a pH of 7.51, a PCO2 of 33 mm Hg, and a PO2 of 55 mm Hg. Electrocardiogram and serial serum cardiac enzymes were normal. A chest radiograph showed bilateral upper lobe patchy infiltrates with left upper lobe consolidation. Computed tomographic (CT) scan of the chest with contrast showed bilateral ground glass infiltrates with focal consolidation (Figure 1) and no evidence of pulmonary embolism. Induced sputum was negative for Pneumocystis carinii, fungi, or acid-fast bacilli. A bronchoalveolar lavage was performed. What is the diagnosis?
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PMID:Cases from the Osler Medical Service at Johns Hopkins University. Diagnosis: P. carinii pneumonia and primary pulmonary sporotrichosis. 1533 85

Dysphagia affects a large and growing number of individuals in the United States, particularly the elderly and those who are neurologically impaired. Swallowing difficulties may be due to age-related changes in oropharyngeal and esophageal functioning as well as central nervous system diseases such as stroke, Parkinson disease, and dementia. Among institutionalized individuals, dysphagia is associated with increased morbidity and mortality. An appreciation of the physiology of swallowing and the pathophysiology of dysphagia is necessary for proper patient management. Careful history, physical examination, and evaluation of radiologic and endoscopic studies should differentiate oropharyngeal and esophageal etiologies of dysphagia and distinguish mechanical (anatomic) disorders from functional (motor) disorders. A significant percentage of patients with dysphagia have concomitant acid-related disorders that are managed best with proton pump inhibitor (PPI) therapy. Three of the currently available PPIs are manufactured as capsules containing enteric-coated granules that may be mixed with soft foods or fruit juices before oral administration to those with swallowing difficulties. In addition, omeprazole and lansoprazole may be administered via gastrostomy or nasogastric feeding tubes as suspensions in sodium bicarbonate. Novel dosage formulations of lansoprazole that may be appropriate for patients with dysphagia include the commercially manufactured lansoprazole strawberry-flavored enteric-coated granules for suspension and lansoprazole orally disintegrating tablets.
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PMID:Management of acid-related disorders in patients with dysphagia. 1547 52

A 75-year-old man was admitted to our hospital with dysesthesia of the right lip, dysphagia and gait disturbance. He presented with right Wallenberg syndrome and brain MR image showed a fresh infarction in the right lateral medulla. Therapy with heparin and ozagrel sodium was started. For a time his symptom improved a little, but after 8 days he developed re-infarction, thrombocytopenia and DIC, while being treated with heparin for cerebral infarction. Heparin was discontinued, and these symptoms improved quickly. The clinical course and the positive anti-platelet factor 4-heparin complex antibody suggested that these symptoms were caused by heparin-induced thrombocytopenia (HIT). HIT should be included as a differential diagnosis for progression of ischemic stroke under heparin therapy.
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PMID:[A case of heparin-induced thrombocytopenia that worsened preexisting cerebral infarction]. 1551 11

Central pontine myelinolysis (CPM) is a demyelinating disease of the pons often associated with the demyelination of extrapontine areas of the central nervous system. Although the etiology and pathogenesis are unclear, CPM is usually associated with hyponatremia or its rapid correction, and chronic alcoholism is also a common underlying condition. We observed a 43-year-old man with diabetes mellitus who developed central pontine and extrapontine myelinolysis with no apparent evidence of hyponatremia, serum hyperosmolality or associated rapid correction, or history of alcohol abuse. On admission, the patient was lethargic with dysarthria, dysphagia, and mild tetraparesis and his face and lower extremities were severely edematous. Laboratory examination showed normoglycemia and normonatremia, although hypokalemia, elevated HbA1c, and nephrotic syndrome were also present. Magnetic resonance imaging (MRI) revealed abnormal signal intensity in the pons, the deep layers of the cerebral cortex, and the adjacent white matter consistent with central pontine and extrapontine myelinolysis. Generalized edema was reduced by the use of diuretics and extracorporeal ultrafiltration without significant changes of serum sodium or osmolality. His consciousness level and paresis gradually improved within a few weeks. Our patient is a rare case of CPM associated with diabetes without apparent evidence of sodium or glucose imbalances.
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PMID:Central pontine and extrapontine myelinolysis associated with type 2 diabetic patient with hypokalemia. 1581 68

We describe an 89-year-old woman who presented with an abrupt onset of headache and right hemiparesis. With the initial diagnosis of cerebral infarction, we started therapy using sodium ozagrel. The right hemiparesis worsened, however, and a continuous intravenous heparin injection showed no effect. Furthermore, nystagmus in the bilateral eyes, dysphagia, left hemiparesis, and central ventilation disorder appeared one after another in three weeks. A magnetic resonance images (MRI) of the head, performed on the fifth hospital day with regular intervals of axial sections, disclosed no lesion responsible for right hemiparesis. MRI of the brainstem and upper cervical cord, performed after two weeks with smaller intervals of axial sections, revealed a T2 high signal lesion in the left side of the medulla oblongata and upper cervical cord. After about five weeks from the onset of the disease, she died of pneumonia. With the pathological examination, we diagnosed as glioma originated in the left ventral part of medulla oblongata. Five similar cases of brainstem glioma have been reported so far. Our patient, the oldest one, showed an exceptionally rapid clinical course, instructing us to consider the possibility of medullary glioma even in the elderly patients presenting with acute onset hemiparesis followed by rapid and progressive appearance of brainstem signs.
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PMID:[An autopsied case of medullary glioma with an abrupt onset of headache and hemiparesis]. 1596 Jan 73

Photodynamic therapy (PDT) is a form of photochemotherapy requiring the simultaneous presence of a photosensitiser, activating light of the proper wavelength and molecular oxygen in order to produce a localised therapeutic effect thought to be due to high-energy singlet oxygen generation. Neither drug nor light alone are effective as therapeutic agents and thus PDT treatment methods should be looked upon as true, necessary, drug and device combinations ('systems'). Selectivity of treatment is imparted by a combination of factors, including accumulation of photosensitiser by the target lesion and targeted application of activating light. The most common systemic side effect of systemically administered photosensitisers is cutaneous photosensitivity of varying periods of time. Local toxicities depend on the area of treatment. Sources of light which have been used in PDT include lasers, arc lamps, light-emitting diodes and fluorescent lamps. PDT has been used for a wide variety of clinical applications. In 1995, the first PDT system, using porfimer sodium (Photofrin, Axcan Pharma, Inc.), lasers and fibre optic light delivery methods, developed by QuadraLogic Technologies, was approved in the US for endoscopic palliation of malignant dysphagia caused by oesophageal cancer. A topical PDT system, aminolevulinic acid HCL (Levulan Kerastick) and the large-area BLU-U PDT Illuminator, was developed by DUSA Pharmaceuticals, Inc. for the treatment of actinic keratoses of the face and scalp and approved in the US in 2000. Topical PDT has applicability to a wide variety of skin cancers and precancerous conditions. In 2001, Novartis launched the systemically administered verteporfin (Visudyne) laser-based PDT system in the US as the first pharmacologic treatment for age-related macular degeneration. Development programmes are continuing to investigate PDT for the potential treatment of a variety of diseases, yielding therapeutic results with minimal toxicity.
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PMID:Photodynamic therapy systems and applications. 1598 54

The first pyrethroid pesticide, allethrin, was identified in 1949. Allethrin and other pyrethroids with a basic cyclopropane carboxylic ester structure are type I pyrethroids. The insecticidal activity of these synthetic pyrethroids was enhanced further by the addition of a cyano group to give alpha-cyano (type II) pyrethroids, such as cypermethrin. The finding of insecticidal activity in a group of phenylacetic 3-phenoxybenzyl esters, which lacked the cyclopropane ring but contained the alpha-cyano group (and hence were type II pyrethroids) led to the development of fenvalerate and related compounds. All pyrethroids can exist as at least four stereoisomers, each with different biological activities. They are marketed as racemic mixtures or as single isomers. In commercial formulations, the activity of pyrethroids is usually enhanced by the addition of a synergist such as piperonyl butoxide, which inhibits metabolic degradation of the active ingredient. Pyrethroids are used widely as insecticides both in the home and commercially, and in medicine for the topical treatment of scabies and headlice. In tropical countries mosquito nets are commonly soaked in solutions of deltamethrin as part of antimalarial strategies. Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature. In addition, mammals are protected by poor dermal absorption and rapid metabolism to non-toxic metabolites. The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with either piperonyl butoxide or an organophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of pyrethroids are on sodium and chloride channels. Pyrethroids modify the gating characteristics of voltage-sensitive sodium channels to delay their closure. A protracted sodium influx (referred to as a sodium 'tail current') ensues which, if it is sufficiently large and/or long, lowers the action potential threshold and causes repetitive firing; this may be the mechanism causing paraesthesiae. At high pyrethroid concentrations, the sodium tail current may be sufficiently great to prevent further action potential generation and 'conduction block' ensues. Only low pyrethroid concentrations are necessary to modify sensory neurone function. Type II pyrethroids also decrease chloride currents through voltage-dependent chloride channels and this action probably contributes the most to the features of poisoning with type II pyrethroids. At relatively high concentrations, pyrethroids can also act on GABA-gated chloride channels, which may be responsible for the seizures seen with severe type II poisoning. Despite their extensive world-wide use, there are relatively few reports of human pyrethroid poisoning. Less than ten deaths have been reported from ingestion or following occupational exposure. Occupationally, the main route of pyrethroid absorption is through the skin. Inhalation is much less important but increases when pyrethroids are used in confined spaces. The main adverse effect of dermal exposure is paraesthesiae, presumably due to hyperactivity of cutaneous sensory nerve fibres. The face is affected most commonly and the paraesthesiae are exacerbated by sensory stimulation such as heat, sunlight, scratching, sweating or the application of water. Pyrethroid ingestion gives rise within minutes to a sore throat, nausea, vomiting and abdominal pain. There may be mouth ulceration, increased secretions and/or dysphagia. Systemic effects occur 4-48 hours after exposure. Dizziness, headache and fatigue are common, and palpitations, chest tightness and blurred vision less frequent. Coma and convulsions are the principal life-threatening features. Most patients recover within 6 days, although there were seven fatalities among 573 cases in one series and one among 48 cases in another. Management is supportive. As paraesthesiae usually resolve in 12-24 hours, specific treatment is not generally required, although topical application of dl-alpha tocopherol acetate (vitamin E) may reduce their severity.
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PMID:Poisoning due to pyrethroids. 1618 Sep 29


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