Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 26 years old female with a Cerebral Palsy as a consequence of a perinatal vascular accident. She was admitted in August 1996 with a left hemiplegia due to a right M1 median artery thrombotic occlusion, as demonstrated by magnetic resonance imaging angiography. Transesophagical bi-dimensional echocardiography showed a right atrial myxoma and ruled out the persistence of an oval foramen. The study of coagulation disorders lead to the diagnosis of a primary antiphospholipid syndrome. We postulate that interleukin-6 produced by the myxoma could trigger an immunological reaction leading to the primary antiphospholipid syndrome.
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PMID:[Myxoma and antiphospholipid antibody syndrome]. 977 76

Reports on patients with hemiparalysis indicate the importance of the nervous system for the pathophysiology of rheumatoid arthritis (RA) or osteoarthritis (OA). Norepinephrine (NE) and opioids seem to be more antiinflammatory neurotransmitters whereas substance P is proinflammatory. The study aimed to investigate the direct noradrenergic nerve-immune cell interaction in human synovial membrane. We used a recently developed superfusion technique with electrical stimulation of synovial membrane to elicit local NE from synovial membrane slices. The readout parameter of synovial immune cells was interleukin-6 (IL-6). IL-6 was spontaneously secreted from RA and OA synovial membranes. Electrical field stimulation intensively reduced IL-6 secretion. In patients with OA or RA, this electrically induced reduction of IL-6 secretion was not significantly changed by alpha- or beta-adrenergic antagonists. The study demonstrates that local endogenous NE seem to play a minor role, which may be due to a depletion of NE or loss of noradrenergic fibers during chronic RA and OA.
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PMID:In vitro superfusion method to study nerve-immune cell interactions in human synovial membrane in long-standing rheumatoid arthritis or osteoarthritis. 1041 20

We report a 2-year-old boy who developed hemiconvulsion-hemiplegia syndrome with left-sided hemiplegia after a seizure lasting 35 minutes. The interleukin-6 level in the cerebrospinal fluid 2 hours after seizure onset was elevated to levels seen in patients with encephalitis. At 1 year after onset of the seizure, the patient remained hemiplegic on the left side, and magnetic resonance imaging showed severe right hemispheric atrophy. Acute changes seen on imaging studies and electroencephalograms in this patient were consistent with seizure-induced brain damage. Elevation of cerebrospinal fluid interleukin-6 may be related to the severe neurologic sequelae of our patient despite the relatively short seizure duration.
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PMID:Hemiconvulsion-hemiplegia syndrome and elevated interleukin-6: case report. 1250 51

Hemiconvulsions-hemiplegia (HH) syndrome is an acquired condition in which hemiplegia develops after a preceding febrile unilateral status epilepticus in a previously healthy child. Although viral encephalitis or vascular diseases may be the underlying etiology, the pathogenesis remains unknown in the majority of cases. We measured both plasma and cerebrospinal fluid cytokine levels in a girl with HH syndrome, and found elevated plasma concentrations of soluble interleukin-2 receptor and tumor necrosis factor-alpha, and a slightly increased plasma level of interleukin-6. Furthermore, she had a high serum concentration of soluble E-selectin, which is a marker of inflammatory endothelial activation. These findings suggest that proinflammatory cytokine-induced cerebrovascular endothelial injury could play a role in the pathogenesis of HH syndrome.
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PMID:Hypercytokinemia in hemiconvulsions-hemiplegia syndrome associated with dual infection with varicella zoster and Epstein-Barr viruses. 1253 69

Cardiac myxoma is a source of emboli to the vascular tree, especially to the central nervous system. Although it is rare, its early recognition is particularly important because of its unique clinical features of subsequently leading to intracerebral or subarachnoid hemorrhage, even brain metastases, and its potential for surgical cure. Missing the diagnosis may lead to devastating results, including stroke, even sudden death. A 40-year-old male with no other conventional vascular risk factors such as hypertension, diabetes or hyperlipidemia presented with right hemiplegia, global aphasia, vomiting, and fever. Infarction over the left middle cerebral artery was disclosed on magnetic resonance imaging study, and echocardiogram showed a huge mass, about 5cm in size, on the mitral valve which was histopathologically proved to be a cardiac myxoma. He also presented with multiple emboli to the kidneys and the left eye. There is uncertainty about the role of anticoagulation. The treatment of choice remains surgical excision of the cardiac myxoma which may lead to normalization of serum interleukin-6 levels and resolution of constitutional symptoms, and the intracranial aneurysms may regress and resolve.
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PMID:Young stroke, cardiac myxoma, and multiple emboli: a case report and literature review. 1699 1

A 10-year-old boy with psychomotor developmental delay and cerebellar vermis atrophy developed right hemiplegia with vomiting, unconsciousness, convulsions, and late-onset fever. Slow delta activity was noted over the left hemisphere on electroencephalography, and neuroimaging revealed swelling of the left temporo-occipital cerebral cortex with restricted diffusivity, successive transient cortical atrophy, and hyperperfusion over the left cerebral hemisphere. Interleukin-6 was elevated in the cerebrospinal fluid. The acute symptoms resolved completely within 3 weeks after onset, but hypoperfusion persisted in the left posterior cortex thereafter. Another episode with transient left hemiplegia appeared 7 months later, followed by recurrence of migraine attacks. Analysis of the CACNA1A gene revealed a mutation of c.1997 C>T (p.T666M). None of his family members had migraine. This case represents an unusual evolution of sporadic hemiplegic migraine with manifestations of acute encephalopathy, for which the role of migraine-related inflammatory process is assumed.
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PMID:Sporadic hemiplegic migraine presenting as acute encephalopathy. 2213 90

Progressive multifocal leukoencephalopathy (PML) is a central nervous system infection caused by John Cunningham (JC) virus reactivation in an immunocompromised patient. PML has various neurologic symptoms and has very poor prognosis. A 36-year-old man developed transverse myelitis and had a psychiatric disorder at the age of 26. He was diagnosed with systemic lupus erythematosus (SLE) and neuropsychiatric SLE (NPSLE), on the basis of leukopenia and presence of anti-DNA and anti-nuclear antibodies. Treatment with glucocorticoid (GC) was started, and remission was introduced. Six months before PML onset, his condition was complicated with hemophagocytic lymphohistiocytosis (HLH) due to exacerbation of SLE. Remission re-induction therapy by GC, cyclosporine-A, intravenous cyclophosphamide, and rituximab (RTX) was initiated and HLH improved. However, interleukin-6 levels of the cerebrospinal fluid (CSF) continued to rise. We thought that the disease activity of NPSLE worsened; thus, we introduced mycophenolate mofetil (MMF) 4 months before the PML onset. He developed progressive dysarthria and right hemiplegia. He was diagnosed with PML via magnetic resonance imaging and JC virus polymerase chain reaction in CSF. Considering that immunosuppressants, including RTX and MMF, are precipitating factors of PML, we discussed the RTX removal using plasma exchange (PEx), but we did not introduce PEx, because it was expected that the concentration of RTX was already lowered when he was diagnosed with PML. Treatment for PML with mefloquine and mirtazapine saved his life, but severe residual disabilities remained. This is the first report of a patient who developed PML during combination therapy with RTX and MMF.
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PMID:A case of developing progressive multifocal leukoencephalopathy while using rituximab and mycophenolate mofetil in refractory systemic lupus erythematosus. 2998 69