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 report the use of endoscopic techniques for successful diagnosis in a case of atypical esophageal tuberculosis. Tuberculosis of the esophagus is an unusual presentation of this disease, having been estimated to occur in 0.15% of the people who die of tuberculosis. A few cases of possible primary tuberculous esophagitis have been described. This report describes a patient with dysphagia who appeared to have esophageal tuberculosis without HIV and in the absence of other signs of tuberculosis. The patient responded promptly to treatment with tuberculostatics.
Infection 2003 Jun
PMID:Mediastinal mass with Dysphagia in an elderly patient. 1278 77

Complications following endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) biopsy are rare. A 75-year-old man underwent EUS-FNA biopsy of an enlarged mediastinal lymph, which histologic investigation revealed to be a metastasis of a hepatocellular carcinoma. The patient developed the postinterventional complication of suppurative infection within the mediastinum. Under EUS guidance, a pigtail catheter and a soft tube were inserted to respectively drain and rinse the mediastinal lesion for 8 days. The remaining esophagomediastinal fistula was closed by gathering the fistula margins, using band ligations and an Endoloop. The fistula healed with no further complaints or dysphagia. Infection is a possible complication of endoluminal FNA biopsy. An endoscopically guided therapeutic approach can be favored as the initial treatment of choice and as a reasonable alternative that avoids surgical intervention.
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PMID:Successful endoscopic management of iatrogenic mediastinal infection and subsequent esophagomediastinal fistula, following endosonographically guided fine-needle aspiration biopsy. 1565 65

We report a case of previously healthy student with acute rhombencephalitis and brainstem abscess caused by Listeria monocytogenes. The disease begun with uncharacteristic prodromal symptoms of gastrointestinal infection followed by headache and vertigo. After hospital admission the patient rapidly deteriorated, presenting pronounced dysphagia and respiratory failure requiring mechanical ventilation. The diagnosis was established upon clinical symptoms of infection, brainstem involvement, typical MRI findings and positive for L. monocytogenes blood culture. Infection was complicated by acute, demyelinating neuropathy, diagnosed upon clinical symptoms of frail palsy confirmed by ENG. Initially introduced empirical doxycyclin/ceftriaxon treatment was subsequently changed to targeted ampicillin/gentamycin therapy, mechanical ventilation, intravenous human immunoglobulin treatment, tracheostomy and endoscopic gastrostomy. Prolonged dysphagia resolved after rehabilitation. After one year the patient remains well with only slight dysmetria.
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PMID:Prolonged dysphagia due to Listeria-rhombencephalitis with brainstem abscess and acute polyradiculoneuritis. 1626 41

Dysphagia in stroke is linked with increased risk of pneumonia, increased length of stay and poorer outcomes. This study followed a cohort of 88 acute ischaemic stroke patients admitted to hospitals in Perth, Western Australia, over 30 days. There were 8/88 deaths (9%). Infections were treated in 25/80 survivors (31%). Presence and severity of dysphagia were measured at 2 and 7 days post-stroke. Respiratory tract infections occurred at significantly higher rates for dysphagics (p<0.05). At 2 days post-stroke, the odds ratio (OR) of chest infection for dysphagics was 1.45 (95% CI=1.07-1.98). Survivors who were "nil by mouth" 2 days post-stroke were significantly more likely to develop pneumonia (p=0.01). At 7 days post-stroke, dysphagics were again more likely to develop pneumonia (p=0.014) with OR=1.77 (95% CI=1.26-2.49). The total anterior circulation infarcts demonstrated more severe and prolonged dysphagia than other stroke subtypes.
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PMID:Dysphagia in acute ischaemic stroke: severity, recovery and relationship to stroke subtype. 1743 10

The relation between acute ischaemic stroke and infection is complex. Infection appears to be an important trigger that precedes up to a third of ischaemic strokes and can bring about stroke through a range of potential mechanisms. Infections that present subsequent to stroke also complicate up to a third of cases of stroke and might worsen outcome. Inflammatory responses, which are a defence mechanism against infection but can also be a pathogenic mechanism that precipitates stroke and neurological sequelae, are important features. Although factors such as stroke severity and dysphagia are important predictors of poststroke infection, there is evidence from experimental and clinical settings of impaired immunity or brain-induced immunodepression after stroke. Greater understanding of the relation between inflammation and both infection and ischaemic mechanisms is needed. This might be particularly important because new treatment strategies for acute ischaemic stroke are being investigated, including those that modulate cytokines and the immune system.
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PMID:Acute ischaemic stroke and infection: recent and emerging concepts. 1833 49

Infections of the laryngeal cartilages occur clinically as local pain, dysphonia, dysphagia or dyspnoea and may lead to destruction of the laryngeal skeleton. We present positron emission tomography/computed tomography (PET-CT) as a new method for detection and monitoring of laryngotracheal chondritis. We prospectively analyzed all patients undergoing PET-CT examination, of whom we were clinically suspicious of laryngeal cartilage chondritis. When a chondritis had been confirmed by PET, therapy was started, and the course of inflammation was monitored. Three patients were selected, where application of PET is demonstrated. We analyzed nine patients, five of them suffering from a present or past cancerous disease of the neck region. Four patients suffered from symptoms that occurred after percutaneous tracheotomy and long-term intubation. Chondritis of the laryngeal skeleton or upper parts of the trachea was diagnosed in seven of nine subjects by using PET-scan. PET-CT provides a reliable tool in diagnosis of laryngeal cartilage chondritis. Furthermore, it is an excellent tool in monitoring objectively presence and grade of an infection. This may play a decisive role in tracheal surgery or to estimate success of conservative therapy.
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PMID:Positron emission tomography/computed tomography as a method for detection and monitoring of laryngeal chondritis. 1836 26

Recurrent respiratory papillomatosis (RRP), which is caused by human papillomavirus types 6 and 11, is the most common benign neoplasm of the larynx among children and the second most frequent cause of childhood hoarseness. After changes in voice, stridor is the second most common symptom, first inspiratory and then biphasic. Less common presenting symptoms include chronic cough, recurrent pneumonia, failure to thrive, dyspnea, dysphagia, or acute respiratory distress, especially in infants with an upper respiratory tract infection. Differential diagnoses include asthma, croup, allergies, vocal nodules, or bronchitis. Reports estimate the incidence of RRP in the United States at 4.3 per 100,000 children and 1.8 per 100,000 adults. Infection in children has been associated with vertical transmission during vaginal delivery from an infected mother. Younger age at diagnosis is associated with more aggressive disease and the need for more frequent surgical procedures to decrease the airway burden. When surgical therapy is needed more frequently than four times in 12 months or there is evidence of RRP outside the larynx, adjuvant medical therapy should be considered. Adjuvant therapies that have been investigated include dietary supplements, control of extra-esophageal reflux disease, potent antiviral and chemotherapeutic agents, and photodynamic therapies; although several have shown promise, none to date has "cured" RRP, and some may have serious side effects. Because RRP, although histologically benign, is so difficult to control and can cause severe morbidity and death, better therapies are needed. The potential for a quadrivalent human papilloma vaccine is being explored to reduce the incidence of this disease.
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PMID:Recurrent respiratory papillomatosis: a review. 1849 62

Infection of the central nervous system with Nocardia sp. usually manifests as supratentorial abscesses. Supratentorial and cerebellar abscesses from infection with Nocardia sp. following immunosuppression with long-term corticosteroids for idiopathic thrombocytopenia (ITP) have not been reported. An 83 years-old, human immunodeficiency virus (HIV)-negative, polymorbid male with ITP for which he required corticosteroids since age 53 years developed tiredness, dyspnoea, hemoptysis, abdominal pain, and progressive gait disturbance. Imaging studies of the lung revealed an enhancing tumour in the right upper lobe with central and peripheral necrosis, multiple irregularly contoured hyperdensities over both lungs, and right-sided pleural effusions. Sputum culture grew Nocardia sp. Neurological diagnostic work-up revealed dysarthria, dysphagia, ptosis, hypoacusis, tremor, dysdiadochokinesia, proximal weakness of the lower limbs, diffuse wasting, and stocking-type sensory disturbances. The neurological deficits were attributed to an abscess in the upper cerebellar vermis, myopathy from corticosteroids, and polyneuropathy. Meropenem for 37 days and trimethoprime-sulfamethoxazole for 3 months resulted in a reduction of the pulmonary, but not the cerebral lesions. Therefore, sultamicillin was begun, but without success. Long-term therapy with corticosteroids for ITP may induce not only steroid myopathy but also immune-incompetence with the development of pulmonary and cerebral nocardiosis. Cerebral nocardiosis may not sufficiently respond to long-term antibiotic therapy why switching to alternative antibiotics or surgery may be necessary.
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PMID:Cerebellar nocardiosis and myopathy from long-term corticosteroids for idiopathic thrombocytopenia. 2004 27

Infection is the commonest complication of stroke and has a major impact on morbidity and mortality. The relationships between susceptibility to infection after stroke and the influence of infection on stroke outcome are complex, but have considerable clinical relevance. Both pharmacological and non-pharmacological interventions in acute stroke may affect the risk of developing infection by influencing potentially modifiable risk factors, for example exposure to infectious organisms (dysphagia/aspiration), or immune susceptibility to infectious challenge. Treatment of infection itself may also reduce ischaemic injury, and influence outcome following stroke. In this review we discuss the role of current and emerging treatments for stroke and their effects on infection, considering possible underlying mechanisms and implications for the development of new therapies.
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PMID:Current and emerging treatments for acute stroke: relationships with infection. 2016 69

Infections occur commonly following stroke and adversely influence outcome. Dysphagia, greater stroke severity and increasing age are associated with post-stroke infection, but post-stroke immunodepression is now recognised as an independent factor associated with increased susceptibility. Counter-regulatory responses, triggered by the pro-inflammatory response to stroke, appear to effect systemic immunodepression via suppression of both innate and adaptive immune responses. Experimental and clinical studies have identified a range of anti-inflammatory and immunosuppressive changes, including reduced mononuclear phagocyte and natural killer cell function, induction of anti-inflammatory cytokines, apoptotic lymphocyte loss and altered T lymphocyte activity. A range of mechanisms has been proposed, including hypothalamo-pituitary-adrenal axis (HPAA) and sympathetic nervous system (SNS) activation. The post-stroke balance of pro- and anti- inflammatory mechanisms may be aimed at restricting the extent of inflammation and contributing to the restoration of immune homeostasis. However, severe inflammation in the brain may trigger major systemic, counter-inflammatory responses that ultimately compromise immune mechanisms required to combat pathogens. Although key pathways have been identified, the extent to which the various elements of post-stroke immunodepression are clinically relevant remains to be discovered. The identification of markers of immunodepression in the early post-stroke phase may prove useful for identifying patients that may have increased susceptibility to infection. It also seems likely that post-stroke immunodepression will need to be taken into account where stroke treatments impact upon inflammatory and immune pathways.
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PMID:Post-stroke immunodepression and infection: an emerging concept. 2016 72


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