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)

Two patients with systemic lupus erythematosus had intermittent episodes of dysphagia associated with severe nonpleuritic chest pain. Esophageal manometry disclosed abnormalities characteristic of diffuse esophageal spasm. The findings suggest that diffuse spasm should be considered in the differential diagnosis of unexplained chest pain and dysphagia in patients with lupus.
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PMID:Esophageal motor dysfunction in systemic lupus erythematosus. Two cases with unusual features. 48 Jun 25

Tc-99m DTPA aerosol is often swallowed during inhalation for lung ventilation scans. The authors evaluated a 16-year-old girl with a known history of mixed collagen disorder (positive lupus anticoagulants) for symptoms of cough and acute shortness of breath. Tc-99m DTPA accumulated in the distal esophagus during aerosol inhalation and remained there at the end of the perfusion study, a period of approximately 1 hour. This serendipitous observation antedates clinical signs and symptoms of dysphagia.
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PMID:Esophageal dysmotility as a serendipitous observation on ventilation-perfusion imaging of the lungs. 161 36

Neurologic manifestations, afflicting up to 70% of SLE patients, include psychosis, seizures, chorea, neuropathies, and stroke. MRI is useful in evaluation of lupus patients and several reports have documented cerebral atrophy or focal hyperintensities. We report an unusual MRI appearance in a 56-year-old woman with SLE, diagnosed on the basis of pleuritis, lymphopenia, anti-DNA antibodies, and neurologic involvement. She reported recent onset of Raynaud's phenomenon and generalized macular rash. She presented after two months of gradual deterioration with memory loss, flattened affect, dysphagia, dysarthria, anomia, and somnolence, without focal neurologic signs. Investigations included elevated ESR, reduced complement, normal CSF without oligoclonal bands, negative viral serology, normal hormone and vitamin levels, normal renal and hepatic function. Neuropsychologic testing showed widespread impairment (WAIS-R: FSIQ-63; WMS-69; DRS-98; RCPM-14; WAB AQ-78.8). CT was normal but MRI showed strikingly symmetric, confluent hyperintensities extensively involving cerebral and cerebellar white matter on T1 and T2 weighted scans. Basal ganglia and subependymal and subcortical white matter were spared. Treated with prednisone, the patient made a gradual, but incomplete, recovery. These MRI findings may reflect widespread vasculopathy or direct immunologic brain insult with or without immunologic blood-brain barrier disruption.
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PMID:Dementia with leukoencephalopathy in systemic lupus erythematosus. 191 71

A patient presented with dysphagia, arthralgias, and a peculiar skin eruption characterized by histopathologic features of sarcoidal granulomas and lupus erythematosus occurring in the same lesion. Sarcoidal granulomas were also found in skeletal muscle. The unique histopathologic features of this case suggest that coexistence of sarcoidosis with autoimmune collagen vascular diseases may be more than coincidence. A review of the immunologic status of patients with sarcoidosis and autoimmune collagen vascular disorders is presented with speculations on the relevance of potential disease-sustaining immunologic patterns of both groups of diseases.
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PMID:A unique case of sarcoidosis with coexistent collagen vascular disease. Possible result of a compatible disease-sustaining immunologic environment. 406 28

In the gastroenterological diagnostic armamentarium, dysphagia is considered as an important symptom for diseases of the esophagus. Concerning the history of illness, symptoms such as retrosternal pain and heartburn are often associated with gastroesophageal reflux disease. Morphological changes of the mucosa can be diagnosed by flexible endoscopy and radiographic examinations. Investigation with 24-h pH monitoring, manometry, and pharmacological tests is necessary for the diagnosis of functional disorders. Additionally, dysphagia can be associated with multiple internal diseases, including muscular diseases such as dermatomyositis, progressive systemic sclerosis, as well as lupus erythematosus. Difficulties in swallowing associated with hypo- and hyperthyroidism can also be interpreted as muscular lesions. Metabolic disorders such as alcoholism, and diabetes mellitus can be the cause of dysphagia. Increasing importance in the differential diagnosis of dysphagia is attached to infections of the upper GI tract. Especially in immunocompromised patients, infections of Candida albicans, mycobacterias, herpes, varicella zoster, and cytomegaloviruses can produce dysphagia and odynophagia. The differential diagnosis of the "angina-like chest pain" has to differentiate between cardiac disease and a noncardiac genesis. Therefore, besides the cardiac diagnostic investigation, endoscopy, radiography, and manometry are often indicated.
Dysphagia 1993
PMID:The gastroenterologist's approach to dysphagia. 846 28

We report a patient with medial medullary infarction who showed deep sensory impairment as his prominent neurological manifestation. A 54-year-old man with a history of hypertension was admitted to our hospital with numbness of the bilateral upper and lower extremities, followed by dysarthria and right hemiparesis. Physical examination revealed no abnormalities except for high blood pressure. He hiccuped continuously. On neurological examination, he exhibited dysarthria, mild dysphagia and right hemiparesis without facial or lingual paresis. Sensitivity to light touch and pinprick was normal, but sensitivity to vibration and joint position was severely decreased in the bilateral upper and lower extremities, predominantly in the lower extremities and on the right side in the upper extremities. He had been treated with antiedema agents and thromboxane synthetase inhibitor. His hiccups stopped within two weeks, and his right hemiparesis gradually improved within one month. However, his deep sensory impairments remained prominent. Blood examinations disclosed positive lupus anticoagulant. MRI showed bilateral infarction at the medial portion of the upper medulla oblongata, extending to both pyramids, especially on the left. Somatosensory evoked potentials (SEP) after median nerve stimulation showed P14 and the later components with prolonged latency. No SEP were recorded after posterior tibial nerve stimulation. The latency of P14 was well correlated with the severity of deep sensory impairments in the upper extremities. Neurological manifestations of our patient are not typical of medial medullary infarction, and are informative about the functional anatomy of the deep sensory tract in the medulla oblongata. We discuss the relation of the intractable hiccups to the bilateral medial medullary lesions, and emphasize the importance of lupus anticoagulant as one of the risk factors in brainstem infarction.
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PMID:[A case of medial medullary infarction with prominent deep sensory impairment]. 892 33

We report a 54-year-old woman who received interferon alpha for haematological relapse of Ph-positive CML, 7 years after allogeneic BMT from an HLA-identical brother. Eighteen months after relapse, cytogenetic and molecular remission was achieved. She received interferon therapy for 25 months and it was discontinued when she developed skin lesions on her face and trunk, dysphagia and fever with respiratory failure and bilateral patchy airspace consolidation of the lung without microbiologic findings. Histologic features showed discoid lupus erythematosis, oesophagitis with pseudomembranes and a mixed pattern of lymphocytic bronchiolitis involving the alveoli and interstitial spaces all compatible with chronic GVHD. The patient was commenced on immunosuppressive therapy with complete clinical and radiological resolution. The available evidence supports an atypical presentation of chronic GVHD and suggests a role for interferon alpha in the pathogenesis of GVHD. To the best of our knowledge, this is the first case reported of severe chronic GVHD occurring during the course of interferon therapy for relapsed CML.
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PMID:Atypical chronic graft-versus-host disease following interferon therapy for chronic myeloid leukaemia relapsing after allogeneic BMT. 1124 42

We present the case of a 71-year-old man with inclusion body myositis combined with subacute cutaneous lupus erythematosus and dysphagia. Although inclusion body myositis is usually resistant to immunosuppressive therapy, this patient improved under treatment with corticosteroids. The presented case is discussed in the context of earlier reports of inclusion body myositis and lupus erythematosus.
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PMID:Association of inclusion body myositis with subacute cutaneous lupus erythematosus. 1173 63

A 61-year-old woman with a history of photosensitive dermatitis and recurrent mouth ulcers presented with progressive weakness typical of amyotrophic lateral sclerosis (ALS), and subsequently underwent extensive neurologic and rheumatologic testing. We investigated whether ALS-like motor neuron disease associated with a positive antinuclear antibody (ANA) is really ALS or rather neuropsychiatric systemic lupus erythematosus (NPSLE). On neurologic evaluation, she had prominent bulbar involvement with dysarthria and dysphagia associated with profound lingual fasciculations and a denervating pattern on electromyogram. MRI showed no evidence of cerebral ischemia. Laboratory studies revealed a positive ANA (1:2560 titer), positive antiphospholipid antibodies (GPL and MPL), circulating lupus anticoagulant, and depressed C3 and C4. Repeat MRI studies at 4 and 11 mo revealed an evolving infarct in the paramedian pons consistent with the presence of NPSLE. Therapy was initiated with corticosteroids and intravenous cyclophosphamide, and the neurologic condition did not improve, but also did not progress inexorably as would be expected with ALS. NPSLE, presumably through the mechanism of ischemic vasculopathy, may present as motor neuron disease clinically indistinguishable from ALS.
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PMID:Neuropsychiatric systemic lupus erythematosus presenting as amyotrophic lateral sclerosis. 1190 83

Dysphagia is not infrequent in patients with connective tissue diseases such as scleroderma, polymyositis or systemic lupus erythematosus (SLE). It is usually the result of gastro-oesophageal reflux but dysmotility can equally be responsible. A case of dysphagia is described in a patient with SLE, who had developed a rare variety of bullous mucous disease affecting the whole length of oesophagus with spontaneous extrusion of an oesophageal cast. Histological features were suggestive of a variant of rare form of bullous disease in SLE called epidermolysis bullosa acquisita (EBA). This rare association of SLE and EBA involving the oesophagus has not been described in the literature.
Lupus 2002
PMID:Dysphagia in a patient with lupus and review of the literature. 1287 55


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