VEGF Levels in Diagnosis of Vasculitic Neuropathy

Manolov, V.; Petrová, I; Vasilev, V.

doi:10.7754/clin.lab.2013.130622

Cited by 7 publications

(8 citation statements)

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“…This publication was a small, unblinded case-control study that showed plasma VEGF levels to be higher in five patients with poly arteritis nodosa-associated vasculitic neuropathy than in eight healthy controls, confirming a previously identified study that compared patients with disease controls 108 .…”

Section: Clinical Diagnosissupporting

confidence: 82%

The nonsystemic vasculitic neuropathies

2017

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The vasculitides are a clinically diverse group of diseases with the histopathological signature of blood vessel-centred inflammation that results in vascular damage and ischaemic injury to the affected tissues 1 . Vasculitis can be caused by drugs, infections and cancers, but diagnostic workup reveals no trigger in most patients. Autoimmune mechanisms are active in all vasculitides, except those caused by direct infection of vessel walls. Most vasculitides are systemic and involve multiple organs and tissues. Those affecting small-to medium-sized vessels often manifest with a vasculitic neuropathy. For example, neuropathies occur in 60-70% of patients with polyarteritis nodosa, eosinophilic granulomatosis with polyangiitis and cryoglobulinaemic vasculitis, and 40-50% of those with microscopic polyangiitis and rheumatoid vasculitis 2 .Vasculitic neuropathy can also occur without systemic vasculitis. This single-organ vasculitis of the PNS has commonly been referred to as nonsystemic vasculitic neuropathy (NSVN), but other forms of clinically isolated PNS vasculitis are now recognized and can be considered variants of NSVN 3 . Although NSVN is classically an acute, relapsing, multifocal neuropathy, it can present as a slowly progressive neuropathy without distinct asymmetries. As such, it should be considered as a possible cause of any progressive axonal neur opathy. NSVN can be diagnosed only with a nerve biopsy, with or without a concomitant muscle or skin biopsy; as nerve biopsies are seldom performed, the condition is under-recognized. The disorder must be distinguished from many other causes of multifocal neuropathy, the definition of which is itself not standardized and requires clarification.A Peripheral Nerve Society guideline group reviewed the literature on vasculitic neuropathy and published consensus recommendations on the classification, diagnosis and immunosuppressive treatment of NSVN in 2010 (REF. 4) Abstract | Nonsystemic vasculitic neuropathy (NSVN) is an under-recognized single-organ vasculitis of peripheral nerves that can only be diagnosed with a nerve biopsy. A Peripheral Nerve Society guideline group published consensus recommendations on the classification, diagnosis and treatment of NSVN in 2010, and new diagnostic criteria for vasculitic neuropathy were developed by the Brighton Collaboration in 2015. In this Review, we provide an update on the classification, diagnosis and treatment of NSVN. NSVN subtypes include Wartenberg migratory sensory neuropathy and postsurgical inflammatory neuropathy. Variants include diabetic radiculoplexus neuropathy and -arguably -neuralgic amyotrophy. NSVN with proximal involvement is sometimes termed nondiabetic lumbosacral radiculoplexus neuropathy. Cutaneous polyarteritis nodosa and other skin-nerve vasculitides overlap with NSVN clinically. Three patterns of involvement in NSVN have been identified: multifocal neuropathy, distal symmetric polyneuropathy, and overlapping multifocal neuropathy (asymmetric polyneuropathy). These patterns lack standard defi...

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Section: Clinical Diagnosissupporting

confidence: 82%

The nonsystemic vasculitic neuropathies

2017

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“…VEGF is also capable of activating PKC-β which phosphorylates the tight junction protein, occludin. The phosphorylated occludin is then ubiquitinated and targeted for degradation leading to an increased vascular permeability ( Lai et al, 2005 ; Murakami et al, 2012 ; Manolov et al, 2014 ). VEGF is made by many types of retinal cells, including RPE, Muller, ganglion, glial, and endothelial cells ( Huang et al, 2011 ; Sun et al, 2012 ) and it has been studied extensively.…”

Section: Retinal Neovascularization Leads To Blindness During Diabetimentioning

confidence: 99%

Remodeling of Retinal Architecture in Diabetic Retinopathy: Disruption of Ocular Physiology and Visual Functions by Inflammatory Gene Products and Pyroptosis

et al. 2018

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Diabetic patients suffer from a host of physiological abnormalities beyond just those of glucose metabolism. These abnormalities often lead to systemic inflammation via modulation of several inflammation-related genes, their respective gene products, homocysteine metabolism, and pyroptosis. The very nature of this homeostatic disruption re-sets the overall physiology of diabetics via upregulation of immune responses, enhanced retinal neovascularization, upregulation of epigenetic events, and disturbances in cells’ redox regulatory system. This altered pathophysiological milieu can lead to the development of diabetic retinopathy (DR), a debilitating vision-threatening eye condition with microvascular complications. DR is the most prevalent cause of irreversible blindness in the working-age adults throughout the world as it can lead to severe structural and functional remodeling of the retina, decreasing vision and thus diminishing the quality of life. In this manuscript, we attempt to summarize recent developments and new insights to explore the very nature of this intertwined crosstalk between components of the immune system and their metabolic orchestrations to elucidate the pathophysiology of DR. Understanding the multifaceted nature of the cellular and molecular factors that are involved in DR could reveal new targets for effective diagnostics, therapeutics, prognostics, preventive tools, and finally strategies to combat the development and progression of DR in susceptible subjects.

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“…CSF analyses demonstrated increased IL-6, IL-8 and IL-10 in a cohort of vasculitic neuropathy patients prior to treatment, in support of the Th2 cytokine shift in vasculitic neuropathy in contrast to the Th1/ Th17 shift in AIDP and CIDP [79,84]. DNA microarray analysis of nerve biopsy specimens from vasculitic neuropathy patients showed increased gene expression of immunoglobulin lambda joining 3, immunoglobulin heavy constant gamma 3, immunoglobulin kappa constant, immunoglobulin lambda locus, CXCL9, CCR2 and CX3CR1, with reduced gene expression of Krüppel-Like Transcription Factors KLF2, KLF4 and the nuclear orphan receptor NR4A1 (involved in endothelial activation).…”

Section: Introductionmentioning

confidence: 96%

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

Ubogu

2015

Acta Neuropathol

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Inflammatory neuropathies encompass groups of heterogeneous disorders characterized by pathogenic immune-mediated hematogenous leukocyte infiltration of peripheral nerves, nerve roots or both, with resultant demyelination or axonal degeneration or both. Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating polyradiculoneuropathy variant), Chronic inflammatory demyelinating polyradiculoneuropathy and nonsystemic vasculitic neuropathy (or peripheral nerve vasculitis). Despite major advances in molecular biology, pathology and genetics, the pathogenesis of these disorders remains elusive. There is insufficient knowledge on the mechanisms of hematogenous leukocyte trafficking into the peripheral nervous system to guide the development of specific molecular therapies for immune-mediated inflammatory neuropathies compared to disorders such as psoriasis, inflammatory bowel disease, rheumatoid arthritis or multiple sclerosis. The recent isolation and characterization of human endoneurial endothelial cells that form the blood-nerve barrier provides an opportunity to elucidate leukocyte-endothelial cell interactions critical to the pathogenesis of inflammatory neuropathies at the interface between the systemic circulation and peripheral nerve endoneurium. This review discusses our current knowledge of the classic pathological features of inflammatory neuropathies, attempts at molecular classification and genetic determinants, the utilization of in vitro and in vivo animal models to determine pathogenic mechanisms at the interface between the systemic circulation and the peripheral nervous system relevant to these disorders and prospects for future potential molecular pathology biomarkers and targets for specific therapeutic intervention.

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VEGF Levels in Diagnosis of Vasculitic Neuropathy

Cited by 7 publications

References 0 publications

The nonsystemic vasculitic neuropathies

The nonsystemic vasculitic neuropathies

Remodeling of Retinal Architecture in Diabetic Retinopathy: Disruption of Ocular Physiology and Visual Functions by Inflammatory Gene Products and Pyroptosis

Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention

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