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 presented a case of acute inflammatory demyelinating polyneuropathy associated with autoimmune chronic active hepatitis (AI-CAH). This is the third case report of neuropathy in AI-CAH. A 64-year-old male with chronic liver dysfunction was admitted to the hospital because of high fever, distal weakness and sensory disturbance of all extremities, bilateral facial weakness and dysphagia. On neurologic examination, there was bilateral weakness of the upper and lower facial muscles, bulbar palsy and severe distal weakness of all extremities. The deep tendon reflexes were absent and the sensation of touch, pinprick, temperature, and vibration was impaired bilaterally symmetrically in all extremities. Serum biochemistry revealed hyperproteinemia, hypergammaglobulinemia and elevated liver enzymes. Rheumatoid factor, antinuclear antibody anti-smooth muscle antibody were positive. Serological tests for hepatitis B surface antigen and its antibody hepatitis B core antibody, and hepatitis C antibody were all negative. Serum anti-GM1, anti-GD1b, anti-GQ1b and anti-MAG antibodies were negative. Liver biopsy findings were consistent with AI-CAH with marked lymphocytic infiltration in the portal tracts. Albuminocytologic dissociation was noted in CSF. Motorconduction velocity of the median, ulnar and facial nerves were markedly reduced with temporal dispersion. No motor response was evoked in the lower extremities. Needle electromyography revealed denervation and reinnervation potentials in the arm and leg. The sural nerve biopsy showed segmental de- and re-myelination and deposition of IgG components in endoneurium. Neurological symptoms and liver dysfunction improved with corticosteroid treatment. In this case, hypergammaglobulinemia associated with an exacerbation of AI-CAH may be responsible for the acute inflammatory demyelinating neuropathy through an unknown autoimmune mechanism.
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PMID:[A case of acute inflammatory demyelinating neuropathy associated with autoimmune-type chronic active hepatitis]. 950 66

Inclusion body myositis has been recognized as a major form of idiopathic inflammatory myopathy. An old male patient with insidious onset and slowly progressive muscular weakness and artrophy has been reported in this article. The duration of symptom before biopsy was 23 years. The first symptom was dysphagia, and muscular weakness developed seven years later. Muscular atrophy was predominant symmetrically and proximally, particularly the quadriceps femoris muscles. Cervical and abdominal muscles were also affected. Myalgia was absent. Electromyogrophy showed myopathic alterations. Erythrocyte sedimentation rate, creatine kinase, immunoglobulins G increased slightly or moderately. Rheumatoid factor was positive, and he had been diagnosed as having rheumatoid arthritis for 23 years. Inclusion body myositis was ultimately diagnosed based on the muscle biopsy which showed mononuclear cell invasion of nonnecrotic muscle fibers, the characteristic rimmed vacuoles in cryostat sections and cytoplasmic inclusion bodies consisted of plenty of tubulofilaments by electron microscope.
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PMID:[Inclusion body myositis: clinical and myopathological features]. 1043 72

We describe a patient who developed an ataxic sensory syndrome associated with xerophthalmia and progressive dysphagia with regurgitation. Electrophysiological findings were consistent with an axonal sensory neuropathy, and superficial peroneal nerve biopsy showed a reduction in number of myelinated fibers with epineurial inflammation. Rheumatoid factor, anti-SSA/SSB and antinuclear antibodies were positive and a diagnosis of Sjogren's syndrome was made. An endoscopic investigation revealed esophageal achalasia. We suggest that there may be a common autoimmune mechanism directed to different targets on the basis of this rare association.
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PMID:Sensory ataxic neuropathy and esophageal achalasia in a patient with Sjogren's syndrome. 1722 76