The Zenith Syndrome

Supplemental data at www. Ray report no disclosures. National Center for Biotechnology Information , U. Maloney , BS, J. Long , BS, B. Author information Article notes Copyright and License information Disclaimer. From the Departments of Neurology D. Address correspondence and reprint requests to Dr. Received Apr 14; Accepted Dec This article has been cited by other articles in PMC. Table Genes implicated in both Alzheimer disease and autism. Open in a separate window.

Supplementary Material Data Supplement: Click here to view. Intention tremor, parkinsonism, and generalized brain atrophy in male carriers of fragile X.

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Lessons from fragile X regarding neurobiology, autism, and neurodegeneration. J Dev Behav Pediatr ; The mGluR theory of fragile X mental retardation. Trends Neurosci ; Early acceleration of head circumference in children with fragile x syndrome and autism. PLoS Biol ; 5: Peripheral biomarkers in autism: Int J Clin Exp Med ; 1: Mullan M, Crawford F.

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Nat Neurosci ; 9: Pickett J, London E. The neuropathology of autism: J Neuropathol Exp Neurol ; Elevated cytokine levels in children with autism spectrum disorder. J Neuroimmunol ; Elevation of tumor necrosis factor-alpha in cerebrospinal fluid of autistic children. Pediatr Neurol ; Annu Rev Med ; Macrocephaly and the control of brain growth in autistic disorders.

Taken together, these two cases provide an important lesson that a monophasic illness is not inevitable in anti-GBM disease, and detection of anti-GBM antibodies can be quite variable depending on the assay used.

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These observations extend the phenotype of antic-GBM disease. A common feature in these two cases is the continuing exposure to pulmonary irritants and prominent manifestations of PH with relapses. This might explain the repeated bouts of PH in the presence of a low and undetectable by conventional assays levels of possibly low-affinity anti-GBM antibodies.

These antibodies might have been detected by WB or bio-sensor-based assays, which were not performed. The continued presence of linear deposits of IgG in the case of Gu et al. WB or chemiluminescence assays are preferred when the ELISA assays are inextricably negative; however, these assays may be of limited availability. The observation of a response of PH to PLEX, cyclophosphamide and steroid therapy despite the absence of detectable anti-GBM antibodies implies that removal of some substance or replacement of a missing factor was involved.

While this may have been low-affinity anti-GBM antibody, other factors might also be involved, such as complement components or cytokines. But this is pure speculation. In any case, while many questions cannot be answered, these two exceptional cases re-emphasize the broad spectrum of anti-GBM disease and illustrate the limitations of presently available unstandardized assays for anti-GBM antibody.

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The option of bilateral nephrectomy has been largely abandoned as a maneuver to prevent recurrent anti-GBM disease in renal allografts [ 31 ], but anecdotes of improvement in the activity of native disease and refractory, persistently high anti-GBM antibody levels following bilateral nephrectomy have been reported [ 32 ]. The evidence that the diseased kidneys somehow are involved, in provoking continued autoantibody production resistant to immunosuppressive therapy perhaps by release of altered GBM antigens, is weak and unsubstantiated.

Finally, every effort should be made to remove subjects from exposure to pulmonary irritants of any kind in patients with a diagnosis of anti-GBM disease, regardless of the presence or absence of detectable circulating anti-GBM antibodies. All patients with anti-GBM disease also deserve regular and close follow-up, even for years after the initial episode, even though only a very few will pursue a course revealed by these two highly instructive cases.

See related article by Liu et al. Multiple recurrences of anti-glomerular basement membrane disease with variable antibody detection: Clin Kidney J 9: Frequently relapsing anti-glomerular basement membrane antibody disease with changing clinical phenotype and antibody characteristics over time. National Center for Biotechnology Information , U.

Journal List Clin Kidney J v. Published online Jul Author information Article notes Copyright and License information Disclaimer. Correspondence and offprint requests to: Received Jun 28; Accepted Jun For commercial re-use, please contact journals.

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See " Multiple recurrences of anti-glomerular basement membrane disease with variable antibody detection: This article has been cited by other articles in PMC. Abstract Anti-glomerular basement membrane GBM disease usually pursues a self-limited course, at least from the immunological perspective. Conflict of interest statement None declared. The role of anti-glomerular basement membrane antibody in the pathogenesis of human glomerulonephritis.

Autism, Alzheimer disease, and fragile X

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THROUGH YOUR SILENCE - The Zenith Distance [Full Album]

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